Scientific Foundations

and Principles of Practice

in Musculoskeletal
Rehabilitation
This page intentionally left blank
 SCIENTIFIC FOUNDATIONS
AND PRINCIPLES OF PRACTICE
IN MUSCULOSKELETAL
REHABILITATION

Editors

David J. Magee, PT, PhD

Professor
Department of Physical Therapy
Faculty of Rehabilitation Medicine
University of Alberta
Edmonton, Alberta, Canada

James E. Zachazewski, PT, DPT, SCS, ATC

Clinical Director
Physical Therapy
Massachusetts General Hospital
Boston, Massachusetts

William S. Quillen, PT, PhD, SCS, FACSM

Professor
Associate Dean, College of Medicine
Director, School of Physical Therapy and Rehabilitation Sciences
University of South Florida
Tampa, Florida

Editorial Consultant
Bev Evjen
Swift Current, Saskatchewan, Canada
11830 Westline Industrial Drive
St. Louis, Missouri 63146

SCIENTIFIC FOUNDATIONS AND PRINCIPLES OF PRACTICE IN MUSCULOSKELETAL ISBN-13: 978-1-4160-0250-5

REHABILITATION ISBN-10: 1-4160-0250-2

Copyright © 2007 by Saunders, an imprint of Elsevier Inc.

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Notice

Neither the Publisher nor the Editors assume any responsibility for any loss or injury and/or damage to persons or property arising out of or
related to any use of the material contained in this book. It is the responsibility of the treating practitioner, relying on independent expertise
and knowledge of the patient, to determine the best treatment and method of application for the patient.

The Publisher

ISBN-13: 978-1-4160-0250-5
ISBN-10: 1-4160-0250-2

Acquisitions Editor: Kathy Falk

Publishing Services Manager: Julie Eddy
Project Manager: Rich Barber
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Printed in the United States

Last digit is the print number: 9 8 7 6 5 4 3 2

 Contributors
Gary P. Austin, PT, PhD, CSCS Brian D. Busconi, MD
Associate Professor Professor of Orthopaedic Surgery
Department of Physical Therapy and Human Movement University of Massachusetts Medical School
Science Worcester, Massachusetts
Sacred Heart University
Fairfield, Connecticut David S. Butler, BPhty, GDAMT, MAppSc
Adjunct Lecturer
J. Bradley Barr, DPT, OCS University of South Australia
Assistant Professor Australia
Department of Physical Therapy Director
Creighton University Medical Center Neuro Orthopaedic Institute
Omaha, Nebraska Australia

Marie K. Hoeger Bement, PT, PhD Judy T. Chen, PharmD, BCPS

Assistant Professor Assistant Professor of Pharmacy Practice
Physical Therapy Department School of Pharmacy and Pharmaceutical Sciences
Marquette University Purdue University
Milwaukee, Wisconsin West Lafayette, Indiana

Robert E. Berg, MD, PT, MA Terese L. Chmielewski, PT, PhD, SCS

Radiologist Assistant Professor
Department of Radiology Department of Physical Therapy
University of Nebraska Medical Center University of Florida
Omaha, Nebraska Gainesville, Florida
Instructor and Musculoskeletal Fellow
Department of Musculoskeletal Radiology Daniel J. Cipriani, BPT, PhD
University of Nebraska Medical Center Assistant Professor
Omaha, Nebraska Department of Exercise and Nutrition Sciences
San Diego State University
Cal Botterill, BPE, PhD San Diego, California
Professor
Department of Kinesiology and Applied Health Sandra L. Curwin, BScPT, PhD
University of Winnipeg Adjunct Associate Professor
Winnipeg, Manitoba School of Physiotherapy
Faculty of Health Professions
Lori Thein Brody, PT, PhD, SCS, ATC Dalhousie University
Graduate Program Director Halifax, Nova Scotia
Orthopaedic and Sports Physical Therapy
Rocky Mountain University of Health Professions Sérgio Teixeira da Fonseca, BPT, ScD
Provo, Utah Associate Professor
Senior Clinical Specialist Physical Therapy
Sports Medicine and Spine Physical Therapy Universidade Federal de Minas Gerais
University of Wisconsin Health Belo Horizonte, Minas Gerais, Brazil
Madison, Wisconsin
Paula Lanna Pereira da Silva, BPT, MSc
Marybeth Brown, PT, PhD, FAPTA Doctor Student
Professor, Physical Therapy Program Center for the Ecological Studies of Perception and Action
Professor, Biomedical Sciences University of Connecticut
University of Missouri-Columbia Storrs, Connecticut
Columbia, Missouri

v
vi CONTRIBUTORS

Cecília Ferreira de Aquino, BPT, MSc David A. Hart, PhD

Assistant Professor Professor of Surgery, Medicine, and Microbiology and
Physical Therapy Department Infectious Diseases
Fundação Educacional de Divinópolis (FUNEDI/UEMG) Chairman, Joint Injury and Arthritis Research Group
Divinópolis, Minas Gerais, Brazil University of Calgary
Calgary, Alberta
Juliana de Melo Ocarino, BPT, MSc Grace Glaum Professor in Arthritis Research
Assistant Professor The Calgary Foundation
Departamento de Ciências Biológicas, Ambientais e da Saúde Calgary, Alberta
(DCBAS)
Centre Universitário de Belo Horizonte (UNI-BH) Mark J. Haykowsky, BPE, PhD
Belo Horizonte, Minas Gerais, Brazil Assistant Professor
Doctor Student Canadian Institutes of Health Research (CIHR) New
Rehabilitation Science Program Investigator
Universidade Federal de Minas Gerais (UFMG) Department of Physical Therapy
Belo Horizonte, Minas Gerais, Brazil Faculty of Rehabilitation Medicine
University of Alberta
Bruce H. Dick, MD Edmonton, Alberta
Orthopaedic Associates of Saratoga
Saratoga Springs, New York Timothy E. Hewett, PhD, FACSM
Director, Sports Medicine Biodynamics Center
Jeffrey E. Falkel, PhD, PT, CSCSD The Human Performance Laboratory
VDP Enterprises Cincinnati Children’s Hospital Medical Center
Littleton, Colorado Cincinnati, Ohio
Associate Professor, Departments of Pediatrics, Orthopaedic
Frances A. Flint, PhD, CAT(C), ATC Surgery and Biomedical Engineering
Faculty Adjunct Associate Professor, Department of Rehabilitation
Coordinator, Athletic Therapy Certificate Sciences
School of Kinesiology and Health Science University of Cincinnati College of Medicine
York University Cincinnati, Ohio
Toronto, Ontario
Kevin A. Hildebrand, MD, FRCS(C)
Cyril B. Frank, MD, FRCS(C) Associate Professor
Professor and Alberta Heritage Scientist Department of Surgery
Department of Surgery University of Calgary
University of Calgary Calgary, Alberta
Calgary, Alberta
Scientific Director Ellen A. Hillegass, EdD, PT, CCS
Institute of Musculoskeletal Health and Arthritis President
Canadian Institutes for Health Research Cardiopulmonary Specialists, Inc.
Ottawa, Ontario Atlanta, Georgia
Co-Vice Chair
Alberta Bone and Joint Health Institute Wendy J. Hurd, PT, PhD, SCS
Calgary, Alberta Department of Physical Therapy
University of Delaware
William E. Garrett, MD, PhD Newark, Delaware
Professor of Orthopaedic Surgery
Duke University Medical Center
Durham, North Carolina

Douglas P. Gross, BScPT, PhD

Assistant Professor
Department of Physical Therapy
University of Alberta
Edmonton, Alberta
 CONTRIBUT0RS vii

Lydia Ievleva, PhD, MAPS Barbara J. Loitz-Ramage, PT, PhD

Lecturer Coordinator, C.H. Riddell Family Movement Assessment
School of Leisure, Sport and Tourism Centre
Faculty of Business Alberta Children’s Hospital
University of Technology, Sydney Research Associate, McCaig Centre for Joint Injury and
Sydney, NSW, Australia Arthritis Research
Chair University of Calgary
College of Sport Psychologists Calgary, Alberta
Australian Psychological Society
Melbourne, VIC, Australia Katie Lundon, BSc(PT), MSc, PhD
Consultant Program Coordinator, Advanced Clinician Practitioner in
Integrated Medicine Clinic Arthritis Care (ACPAC) Program
YourHealth Manly St. Michael’s Hospital and The Hospital for Sick Children
Manly, NSW, Australia Toronto, Ontario
Lundon Orthopaedic Physical Therapy Consulting
Joseph Jordan, PharmD Oakville, Ontario
Assistant Professor of Pharmacy Practice
College of Pharmacy and Health Sciences Lorrie L. Maffey, BMRPT, MPhty, DipManipPT
Butler University Clinical Physiotherapist
Indianapolis, Indiana Researcher: Injury Prevention
Kinesiology, Sport Medicine Centre
Deanna S. Kania, PharmD, BCPS University of Calgary
Assistant Professor of Pharmacy Practice Calgary, Alberta
School of Pharmacy and Pharmaceutical Sciences
Purdue University David J. Magee, BPT, PhD
Indianapolis, Indiana Professor
Department of Physical Therapy
William J. Kraemer, PhD Faculty of Rehabilitation Medicine
Professor University of Alberta
Human Performance Laboratory Edmonton, Alberta
Department of Kinesiology
Department of Physiology and Neurobiology Terry R. Malone, PT, EdD, ATC
University of Connecticut Director
Storrs, Connecticut Physical Therapy Program
University of Kentucky
Chandramouli Krishnan, PT, MA Lexington, Kentucky
Research Assistant
Musculoskeletal Research Laboratory Linda L. Marchuk, BSc
Graduate Program in Physical Therapy and Rehabilitation Research Associate
Science Department of Surgery
University of Iowa University of Calgary
Iowa City, Iowa Calgary, Alberta

Ai Choo Lee, BEd, MSc Elizabeth Matzkin, MD

PhD Student, Rehabilitation Science Department of Orthopaedic Sports Medicine
Faculty of Rehabilitation Medicine Duke University Medical Center
University of Alberta Durham, North Carolina
Edmonton, Alberta
Laura A. May, BHScPT, PhD
Associate Professor
Department of Physical Therapy
University of Alberta
Edmonton, Alberta
Research Affiliate
Glenrose Rehabilitation Hospital
Edmonton, Alberta
viii CONTRIBUT0RS

Paula F. McFadyen, MSc Michael S. Puniello, DPT, MS, OCS, FAAOMPT

Department of Physical Education
University of Victoria
Victoria, British Columbia
Ross A. McFadyen, BScPT, FCAMT, CAFCI
Yates Orthopaedic and Sports Physiotherapy Clinic
Victoria, British Columbia
Mark A. Merrick, PhD, ATC
Associate Professor and Director
Division of Athletic Training
School of Allied Medical Professions
The Ohio State University
Columbus, Ohio
Clinical Assistant Professor
Graduate Programs in Physical Therapy
MGH Institute of Health Professions
Boston, Massachusetts
South Shore Physical Therapy Associates
Hingham, Massachusetts
William S. Quillen, PT, PhD, SCS, FACSM
Professor
Associate Dean, College of Medicine
Director, School of Physical Therapy and Rehabilitation
Sciences
University of South Florida
Tampa, Florida

Laura Middleton, MSc Jerome B. Rattner, PhD

Department of Physical Education Professor
University of Victoria Department of Anatomy and Cell Biology
Victoria, British Columbia University of Calgary
Calgary, Alberta
Marilyn Moffat, DPT, PhD, FAPTA, CSCS
Physical Therapy Department Ellen M. Schellhase, PharmD
New York University Assistant Professor of Pharmacy Practice
New York, New York School of Pharmacy and Pharmaceutical Sciences
Private Practice Purdue University
Locust Valley, New York Indianapolis, Indiana

Jeffrey B. Noftz II, PT, MD Brian M. Shepler, PharmD

Head Team Physician Intercollegiate Athletics Assistant Professor of Pharmacy Practice
Athletic Department School of Pharmacy and Pharmaceutical Sciences
Bowling Green State University Purdue University
Bowling Green, Ohio West Lafayette, Indiana
Private Practice Physician
The Bowling Green Clinic Kathleen A. Sluka, PT, PhD
Bowling Green, Ohio Professor
Graduate Program in Physical Therapy and Rehabilitation
Brian R. Overholser, PharmD Science
Assistant Professor of Pharmacy Practice Pain Research Program
School of Pharmacy and Pharmaceutical Sciences Neuroscience Graduate Program
Purdue University College of Medicine
Indianapolis, Indiana University of Iowa
Iowa City, Iowa
Poonam K. Pardasaney, PT, DPT, MS
Physical Therapy Services Lynn Snyder-Mackler, PT, ScD, FAPTA
Massachusetts General Hospital Alumni Distinguished Professor, Department of Physical
Boston, Massachusetts Therapy
Director, Graduate Program in Biomechanics and Movement
Sachin K. Patel, MD Sciences
Assistant Professor of Orthopaedic Surgery University of Delaware
Albany Medical College Newark, Delaware
Albany, New York
Kevin M. Sowinski, PharmD, BCPS, FCCP
Associate Professor of Pharmacy Practice
School of Pharmacy and Pharmaceutical Sciences
Purdue University
Indianapolis, Indiana
 CONTRIBUTORS ix

Barry A. Spiering, MS Howard A. Wenger, PhD

Doctoral Fellow
Human Performance Laboratory
Department of Kinesiology
University of Connecticut
Storrs, Connecticut
Patricia E. Sullivan, DPT, PhD
Associate Professor
Graduate Programs in Physical Therapy
MGH Institute of Health Professions
Boston, Massachusetts
Jill M. Thein-Nissenbaum, MPT, SCS, ATC
Faculty Associate
Physical Therapy Program
Department of Orthopedics and Rehabilitation
University of Wisconsin-Madison
Madison, Wisconsin
John P. Tomberlin, MPhySt (Manip), PT, OCS,
CSCS, FAAOMPT
North American Instructor
Neuro Orthopedic Institute
Cedar Rapids, Iowa
Jason D. Vescovi, PhD
Postdoctoral Fellow
Women’s Exercise and Bone Health Laboratory
Faculty of Physical Education and Health
University of Toronto
Toronto, Ontario
Joan M. Walker, PT, PhD, FAPTA, FNZSP
Professor Emeritus
School of Physiotherapy
Dalhousie University
Halifax, Nova Scotia
Professor
Department of Physical Education
University of Victoria
Victoria, British Columbia
Craig D. Williams, PharmD, BCPS
Associate Professor of Pharmacy Practice
School of Pharmacy
Oregon State University
Corvallis, Oregon
Glenn N. Williams, PT, PhD, ATC, SCS
Assistant Professor, Physical Therapy and Rehabilitation
Science
Assistant Professor, Department of Orthopaedics and
Rehabilitation
Director of Research, University of Iowa Sports Medicine
Center
University of Iowa
Iowa City, Iowa
James E. Zachazewski, PT, DPT, SCS, ATC
Clinical Director
Physical Therapy
Massachusetts General Hospital
Boston, Massachusetts
Adjunct Assistant Clinical Professor
MGH Institute of Health Professions
Charlestown, Massachusetts
Ronald F. Zernicke, PhD
Professor, Faculty of Kinesiology
Wood Professor in Joint Injury Research, Faculty of Medicine
Professor, Schulich School of Engineering
University of Calgary
Calgary, Alberta
 Dedication

“To teach is to learn twice.”

To those who invested in us that we might in turn pass on their
knowledge and wisdom to future generations of students.
 Preface
Musculoskeletal Rehabilitation Series
Musculoskeletal conditions have an enormous impact on
society. Today, musculoskeletal conditions have become
the most common cause of disability and severe long-
term pain in the industrialized world. As we approach the
second half of the Bone and Joint Decade, it is apparent
that the knowledge and skill required by the community
of health care providers involved in managing the impair-
ments and functional limitations resulting from acute or
chronic musculoskeletal injury/illness has grown expo-
nentially as the frequency of visits to practitioners’ offices
for musculoskeletal system complaints has risen.
The art and science of musculoskeletal rehabilitation
began as a consequence of the injuries suffered on the
battlefields of Europe during World War I. Since that
time, numerous textbooks have been published regard-
ing musculoskeletal rehabilitation. These texts have
encompassed the areas of basic science, evaluation, and
treatment. However, these books have most often been
developed and written in professional “isolation” (i.e.,
from a single discipline’s perspective). As a consequence,
topics have either been covered in great depth but with
a very narrow focus, or with great breath with very little
depth. Our goal in the development and production of
this series was to develop a series of textbooks that com-
plement and build on one another, providing the reader
with the needed depth and breath of information for this
critical area of health care.
Volume I of the series is the 5th edition of David
Magee’s Orthopedic Physical Assessment. This now classic
text provides the clinician with the most comprehensive
text available on this topic. First published in 1987, it
has withstood the test of time and is the most widely
used text in this area. In 1996, we developed and pub-
lished Athletic Injuries and Rehabilitation. Based upon
feedback from both students and clinicians, we have
expanded and broadened the scope of Athletic Injuries
and Rehabilitation into two new volumes. Volume II,
Scientific Foundations and Principles of Practice, pro-
vides clinicians with currently available science regard-
ing musculoskeletal issues and principles of practice that
should guide clinicians regarding therapeutic interven-
tion. In Volume III, Pathology and Intervention, we have
attempted to provide readers with a comprehensive text
containing information on the most common mus-
culoskeletal pathologies and the best evidence behind
contemporary interventions directed towards the treat-
ment of impairments along with limitations associated
with acute, chronic, and congenital musculoskeletal
conditions that occur across the lifespan.
International contributors have provided their unique
perspectives on current diagnostic methodologies, clini-
cal techniques, and rehabilitative concerns. We hope that
our continued use of interdisciplinary author teams has
firmly broken down the professional “territorial turf”
barriers that have existed in past decades of health care.
Health care professionals involved in the contemporary
care of musculoskeletal conditions must continue to
share and learn from one another to advance the provi-
sion of the most time- and cost-efficient care possible in
21st century society.
Each volume in our series is liberally illustrated. Key
concepts in each chapter are highlighted in text boxes,
which serve to reinforce those concepts for the reader,
and numerous tables summarize chapter information for
easy reference. Readers will find that references are not
contained on printed pages at the end of chapters, but
rather contained as part of a comprehensive electronic
resource on CD-ROM (provided with each volume),
which allows the reader to link to MEDLINE abstracts
where possible. Because of the comprehensive nature of
this multi-volume series, each text, although complete in
itself, has been edited to build and integrate with related
chapter materials from the other volumes in the series. It
is the editors’ hope that this series will be used by faculty
as a basis for formal coursework as well as a friendly com-
panion and frequently consulted reference by students
and those on the front lines of clinical care.
As with our previous collaborations, we look forward
to the feedback that only you, our colleagues, can provide,
so that we may continue the development and improve-
ment of the Musculoskeletal Rehabilitation Series.
David J. Magee
James E. Zachazewski
William S. Quillen
xi
 Preface
Scientific Foundations and Principles
of Practice
As clinicians, we examine and treat patients with similar
diagnoses. However, if we look at them closely, none are
the same. There are differences in how each patient pres-
ents to us and what they seek from us to return to an opti-
mal level of health and physical function. All patients are
truly different. Given these differences (some profound,
yet most subtle), how do we proceed forward to decide
how to evaluate them, to design the most appropriate
treatment program for them, and to implement that pro-
gram in the most effective way for that particular patient?
How do we decide who is the most appropriate provider
of care, what is the most appropriate care to provide,
when do we initiate and progress the plan of care, where
is the most appropriate environment to provide that care,
why are we doing what we are doing, and how can our
intervention affect the patients’ goals most efficiently?
The practice of musculoskeletal rehabilitation must
be built upon a sound scientific foundation with firm
principles that can be applied across the broad spectrum
of patients who will present to clinicians with muscu-
loskeletal disease, dysfunction, and/or injury. We have
attempted to provide students and practicing clinicians
with a summation of the scientific foundations and
principles of practice that can be used throughout their
careers in this volume of our series.
xii
In Section I, “Scientific Foundations,” we have brought
together authors who are exceptional basic scientists and
clinicians. We believe that the content of these chapters
and the authors’ style of writing will readily and easily allow
the reader to understand very complex critical informa-
tion, most often derived from bench research, and allow
the clinician to apply it in the real world of patient care.
In Section II, “Principles of Practice,” we have
brought together authors who are able to present broad
conceptual basics of practice, supported by the literature,
that provide the reader with a framework from which to
evaluate their patients and develop intervention strate-
gies and programs that can be built upon from patient
to patient.
Our expectation is that we have developed a text that
will allow the student and the practicing clinician to
answer some of their questions concerning musculoskel-
etal rehabilitation related to the who, what, when, where,
why, and how. Our sincere hope is that our text and the
series will stimulate them to ask more questions and pro-
vide clinicians with the necessary foundations and princi-
ples to develop their clinical practice, thereby answering
those questions.
David J. Magee
James E. Zachazewski
William S. Quillen
 Acknowledgments
We would like to gratefully acknowledge the ongoing professional assistance of the following
individuals who have steadfastly supported this series from its inception.
Kathy Falk – Senior Editor, Health Professions, Elsevier
Marion Waldman – Former Acquisitions Editor, Elsevier
Rich Barber – Project Manager, Elsevier
Bev Evjen – Editorial Assistant
Ted Huff – Artist

xiii
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 Contents
SECTION I
SCIENTIFIC FOUNDATIONS
Chapter 1. Injury, Inflammation, and Repair: Tissue
Mechanics, the Healing Process, and Their Impact on the
Musculoskeletal System—Ai Choo Lee, William S. Quillen,
David J. Magee, James E. Zachazewski, 1
Chapter 2. Ligament Injuries: Pathophysiology, Healing,
and Treatment Considerations—Kevin A. Hildebrand,
David A. Hart, Jerome B. Rattner, Linda L. Marchuk,
Cyril B. Frank, 23
Chapter 3. Tendon Pathology and Injuries: Pathophysiol-
ogy, Healing, and Treatment Considerations—Sandra L.
Curwin, 47
Chapter 4. Adaptability of Skeletal Muscle: Responses to
Increased and Decreased Use—William J. Kraemer,
Barry A. Spiering, Jason D. Vescovi, 79
Chapter 5. Skeletal Muscle: Deformation, Injury, Repair,
and Treatment Considerations—Elizabeth Matzkin, James E.
Zachazewski, William E. Garrett, Terry R. Malone, 97
Chapter 6. Bone Biology and Mechanics—Barbara J.
Loitz-Ramage, Ronald F. Zernicke, 122
Chapter 7. Cartilage of Human Joints and Related
Structures—Katie Lundon, Joan M. Walker, 144
Chapter 8. Peripheral Nerve: Structure, Function, and
Physiology—David S. Butler, John P. Tomberlin, 175
Chapter 9. Articular Neurophysiology and Sensorimotor
Control—Glenn N. Williams, Chandramouli Krishnan, 190
Chapter 10. Pain: Perception and Mechanisms—Marie
K. Hoeger Bement, Kathleen A. Sluka, 217
Chapter 11. Physiological Basis of Physical Agents—Mark
A. Merrick, 238
Chapter 12. Pharmacology and Its Impact on the Reha-
bilitation Process—Ellen M. Schellhase, Judy T. Chen, Joseph
Jordan, Deanna S. Kania, Brian R. Overholser, Brian M.
Shepler, Kevin M. Sowinski, Craig D. Williams, 255
Chapter 13. Effects of Aging-Growth Changes and
Life Span Concerns (0-40) —Lori Thein Brody, Jill M.
Thein-Nissenbaum, 282
Chapter 14. Effects of Aging-Growth Changes and Life
Span Concerns Ages (40+)—Marybeth Brown, 305
SECTION II
PRINCIPLES OF PRACTICE
Chapter 15. Rehabilitation Program Development:
Clinical Decision Making, Prioritization, and Program
Integration—Patricia E. Sullivan, Michael S. Puniello,
Poonam K. Pardasaney, 314
Chapter 16. Clinicians’ Roles in Health Promotion,
Wellness, and Physical Fitness—Marilyn Moffat, 328
Chapter 17. Physiological Principles of Conditioning for
the Injured and Disabled—Howard A. Wenger, Paula F.
McFadyen, Laura Middleton, Ross A. McFadyen, 357
Chapter 18. Principles of Neuromuscular Control for
Injury Prevention and Rehabilitation—Terese L.
Chmielewski, Timothy E. Hewett, Wendy J. Hurd, Lynn
Snyder-Mackler, 375
Chapter 19. Principles of Stabilization Training—
David J. Magee, James E. Zachazewski, 388
Chapter 20. Integration of the Cardiovascular System in
Assessment and Interventions in Musculoskeletal
Rehabilitation—Mark J. Haykowsky, Ellen A. Hillegass, 414
Chapter 21. Physiological Principles of Resistance
Training and Functional Integration for the Injured and
Disabled—Daniel J. Cipriani, Jeffrey E. Falkel, 432
Chapter 22. Psychology of the Injured Patient—Cal
Botterill, Frances A. Flint, Lydia Ievleva, 458
Chapter 23. Integration of Stresses and Their Relation-
ship to the Kinetic Chain—Sérgio Teixeira da Fonseca,
Juliana de Melo Ocarino, Paula Lanna Pereira da Silva,
Cecilia Ferreira de Aquino, 476
xv
xvi CONTENTS

Chapter 24. Arthrokinematics and Mobilization of Mus- Chapter 28. Fracture Management—Sachin K. Patel,
culoskeletal Tissue: The Principles—Lorrie L. Maffey, 487 Bruce H. Dick, Brian D. Busconi, 607

Chapter 25. Range of Motion and Flexibility—James E. Chapter 29. Functional Testing and Return to Activity—
Zachazewski, 527 Gary P. Austin, 633

Chapter 26. The Utility of Orthopedic Clinical Tests for Chapter 30. Rehabilitation Outcomes: Measuring Change
Diagnosis—Daniel J. Cipriani, Jeffrey B. Noftz II, 557 in Patients to Guide Clinical Decision Making—Laura A.
May, Douglas P. Gross, 665
Chapter 27. Imaging Joints and Musculoskeletal Tissue:
Pathoanatomic Considerations—J. Bradley Barr, Robert E.
Berg, 568

SECTION I SCIENTIFIC FOUNDATIONS
I NJURY , I NFLAMMATION , AND R EPAIR :
T ISSUE M ECHANICS , THE H EALING
P ROCESS , AND T HEIR I MPACT ON THE
M USCULOSKELETAL S YSTEM
Ai Choo Lee, William S. Quillen, David J. Magee, and James E. Zachazewski
Introduction
The study, diagnosis, and management of musculoskeletal
injuries have evolved into a multidisciplinary field involv-
ing physicians, therapists, and other health care profes-
sionals who have an interest in the area of musculoskeletal
injury prevention and care. Thus, a multitude of health
care professionals, researchers, and educators devote all or
part of their respective professional careers and practices
toward the prevention, treatment, and rehabilitation of
musculoskeletal injuries and the return of the individual
to the highest level of function possible.1–15
The goal of treatment of musculoskeletal injuries has
been the restoration of function, to the greatest degree
possible, in the shortest time possible.3–5,8,14,16–20 The safe
and successful return of an individual to his or her pre-
injury level of function remains the desired outcome for
any practitioner. Scientifically based practice, focused on
managing the time course of initial inflammatory reac-
tion and subsequent healing processes, recognizing the
healing constraints of neuromusculoskeletal soft tissues,
and based on an appreciation of joint mechanics, per-
formance physiology, and psychology of the individual
regarding the injury, has accelerated the resolution of
many injuries.8,21,22
1
C H A P T E R
Normal Tissue
Tissues in the body are designed to function while
responding to the stresses of everyday living. Under
normal circumstances, human tissue, most of which
has viscoelastic properties, responds to stress or load
in different ways depending on the rate at which the
load is applied, the magnitude of the load, and its dura-
tion. Maintaining a level of homeostasis and staying
within the tolerances of the tissues enable the tissues
to remain healthy and viable. Each tissue is different in
terms of its makeup, and how it responds to stress will
be different. For example, in general, muscle is able to
respond to loads better than bone because of its con-
tractile properties. Connective tissue is primarily made
up of collagen and responds differently depending on
whether it is loose or dense collagen (Table 1-1). The
tissue response is dictated by the effect of any applied
load on the tissue’s physical and mechanical properties,
such as viscosity, elasticity, creep, and tissue relaxation.
If tissue tolerance is exceeded by excessive internal or
external loading, or both, the tissue fails. In rehabilita-
tion, clinicians use controlled loading to increase the
body’s ability to withstand stress and to strengthen
tissues. This controlled loading can be produced by
1
2 SECTION I • Scientific Foundations
Table 1-1
Connective Tissue Differences
Dense Connective Tissue Loose Connective Tissue
Supports or limits motion Very flexible
Found in bone, Found in capsules, muscles,
ligament, tendon, nerves, fascia, and skin
aponeuroses (areolar tissue, reticular
tissue, adipose tissue,
fibroelastic tissue)
Parallel, tightly Random fiber orientation
aligned fibers
Elastic stretch → Greater lengthening (≥80%)
plastic stretch → rupture without tension buildup
(10% lengthening
before tearing)
weight bearing, using the effects of gravity, by modi-
fying muscular forces, and by external factors such as
weights, tubing, sand bags, and exercise machines.
Protective Tissue Responses to Stress
There are several protective mechanisms that inher-
ently exist in the tissue to help it respond to stress or
strain, including level of stiffness, viscoelasticity, creep,
uncrimping, and stress relaxation, all of which increase
joint flexibility by approximately 6% to 8%.23–26 Should
any of these protective tissue mechanisms be overstressed
or exceed the tissue’s tolerance, injury will result.
Collagenous fibers normally have a slightly wavy
appearance in a relaxed state under the microscope.27
This crimp is the slack in collagen tissue and, in reality, is
collagen tissue’s first line of response to stress. Collagen
fibers may be curved or wavy and run obliquely when
relaxed, but with load the fibers line up in the direction
of the applied force.25,28–30
This realignment is called the “taking up of the micro-
scopic slack” or “uncrimping.” When stress is placed on the
tissue, the crimp is removed, and when the stress is removed,
the collagen returns to its previous state. Crimping is seen
primarily in ligaments, capsules, and tendons and allows
collagen to stretch by about 2% with no change in structure.
This uncrimping occurs when any joint is taken through a
range of motion and as stress is applied to the tissue early in
physiological movement. In fact, the crimp is taken up in
the neutral zone (“toe” region of the stress–strain curve),27
so that when the crimp has been taken up, the change in
resistance can be called the crimp barrier, which is also the
end of the neutral zone25 (Figure 1-1).
Viscoelasticity is the primary mechanism used by
tissues, including ligaments, capsules, and muscle, to
increase their length.30–32 Elasticity, part of the visco-
elastic continuum, is the property that enables the tissue
to return to its original shape when a force is removed,
thus imparting a springlike behavior to the tissue.33 This
is the tissue’s second line of response to stress. Elastic
deformation allows about a 4% stretch in collagen, but
this varies depending on the amount of elastic tissue pres-
ent23 (see Figure 1-1). Like crimp, the tissue’s elasticity
allows collagen to return to its normal length and dimen-
sions when the stress is removed. It occurs throughout
the active range of physiological movement. Clinicians
use joint play mobilization to increase range of motion.
The cyclic loading of oscillations allows a certain amount
of relaxation (hysteresis) to occur in the tissues.24,27
Elastic properties can be seen in bone as well as other
collagen and muscle tissue, but the amount of elasticity var-
ies.27,34 If the elastic limit is exceeded because too great a
load is applied, plastic deformation begins to occur and the
tissue will no longer return to its original shape or length
because some of the collagen fibers will have been broken.
Creep, the third line of response, is the second part of
the viscoelastic continuum. It is the continuous or viscous
deformation, or “plastic flow,” in a tissue in response to
a maintained or constant load. Creep allows a constant
lengthening to occur in the tissue in response to stress,
which, in turn, increases the stiffness of the tissue.27,30,31
If too great a load is applied to the tissue, although creep
begins, the excessive load causes the collagen fibers to
“give” (i.e., collagen cross-links begin to fail) and the
tissue begins to tear.35 In this case, plastic deformation or
tearing/breaking of the tissue occurs. The ability of the
collagen to respond to different loads depends on its ten-
sile strength, but in general, approximately a 4% increase
in length due to creep can occur before failure.23
Protective Tissue Mechanisms
● “Uncrimping”
● Elastic deformation
● Creep
● Stress reaction
● Stress or force relaxation
With plastic change, the linear deformation produced
by stretching remains when the stretching force is
removed, resulting in permanent elongation. This plas-
ticity can be seen in the capsule and ligaments as well as
other collagenous tissues, although the amount of plas-
ticity (and elasticity) in each tissue varies.27,34 If a small
load is applied for a long period (10 to 60 minutes) and
the tissue is heated, the collagen will lengthen and remain
intact, but is weakened.33,36 This mechanism is used by
clinicians to lengthen tight collagen tissue in the fibro-
plasia and consolidation phases of healing or in cases of
hypomobile tissue.37 This type of lengthening is a result
 CHAPTER 1 • Injury, Inflammation, and Repair 3

Failure (3o)

Some injury 1o-2o

Some microfailure
Load

Toe region

2% 4% 6% 8%
Uncrimping
+
macroscopic Elasticity
slack Plasticity Total failure
Physiological ROM

Beginning of End of End of

movement neutral zone Physiological movement

Physiological loading 1-2 degree

injury
Figure 1-1
Role of crimp, elasticity, and plasticity in allowing collagen to adapt to stress. Note that some authors state that the plasticity phase (microfailure)
starts at 3% stretch, others at 4%. These differences are probably due to the makeup of the different tissues tested.

of tissue creep or plastic flow and, ultimately, plastic
deformation if applied long enough or repeated often
enough. This lengthening technique, when performed
properly, is very painful and is noted clinically as going
through the stages of being uncomfortable, to aching, to
hurting, to painful, to almost unbearable, but the pain
then disappears shortly after the stress is removed (within
1 to 2 minutes). If, however, a large or sudden load is
applied that exceeds the load capacity of the collagen, the
tissues are overloaded and they tear. This can be called
plastic deformation. It is important to understand that
for both cases, permanent plastic change occurs in the tis-
sue. In reality, however, plastic flow and plastic deforma-
tion are the same process. They are differentiated here to
help clarify the changes that occur under different condi-
tions: whereas plastic flow is used by clinicians to lengthen
tissues, plastic deformation results in tissue injury. When
the first method is used clinically, the clinician must be
careful that the tissue does not become overstressed.
The amount of stress (how often it is applied, and how
much) must be controlled. Once a new range of motion
is achieved, further plastic flow stretching should not be
attempted until the patient has gained muscular control
of the new range and the collagen has strengthened and
adapted to its new length.33,38 This repeated, controlled
application of stretching with a period devoted to achiev-
ing muscular control enables the patient to build up suffi-
cient muscular strength to support the newly lengthened
tissue, and provides time between each load session for
the lengthened collagen to remodel to accommodate
to the stress applied (Figure 1-2). Thus, therapeutically
applied prolonged stretching must be used with care to
prevent overload and injury to the collagen tissue. Which
type of plastic change (flow or deformation) will occur
depends on how much force is being applied and the state
of the tissues when the load is applied.
Stress or force relaxation is another response
mechanism commonly seen in viscoelastic tissue when
4 SECTION I • Scientific Foundations
Quick movement
Uncontrolled movement
Plastic deformation (failure)
Large load
“Cold tissue”
Slow movement
Plastic flow
Small load (controlled stress)
(lengthening)
Warm tissue
Figure 1-2
Outcomes of stress in the plastic zone.
it is stretched to the end of its passive range into the
pathophysiological zone.24,31,39 This phenomenon is one
of the reasons serial casting is frequently used to treat
hypomobility and why casts must be adjusted from time
to time to readjust the load and continue lengthening
of the tissues.40 To increase length, the clinician must
continually apply small loads to a tissue until the desired
length is achieved. The greatest stress relaxation occurs
within 6 to 8 hours of loading.25
Stress reaction is a method by which the body responds
to repeated stresses in an attempt to make itself stronger so
that it can adequately respond to the stress. Wolff’s law40,41
states that bone or collagen will respond to the physical
demands placed on it, resulting in remodeling or realign-
ment along lines of tensile force or stress.42 To strengthen
tissue, it is critical to expose the tissue to progressively
increasing loads; for injured tissue, this is particularly true
during the remodeling phase of injury repair.
Plateauing and increased symptoms during treatment are
two signs of overtreatment that may indicate an excessive
stress reaction. The only way to alleviate the excessive stress
reaction is to relieve the cause. This is a primary consider-
ation when treating overuse or repetitive stress injuries.
In conclusion, when a load is applied to collagen tissue,
the tissue’s first response is to “uncrimp,” followed by elon-
gation of the elastic fibers. As elongation progresses into
the linear zone of the stress–strain curve (see Figure 1-4),
there may be some tearing of the small collagen fibers, but
for the most part, this is an elastic response and the tissue
returns to its original length when the deforming force is
removed. Finally, in the plastic phase, which occurs at the
end the linear part of the stress–strain curve, if an appro-
priate load is applied in a controlled manner, the tissue will
assume a new length (plastic flow) through cyclic loading
(hysteresis), creep, and stress relaxation. Some collagen
fibers will be broken and some cross-links destroyed, but
these changes tend to be microscopic. If the stress applied
is too great, the tissue will fail (plastic deformation), with
rupture or tearing. The last two mechanisms are essentially
the same process, but are given different names for ease of
understanding.
Trauma Injury
Creep/stress Tissue Tissue
relaxation lengthening remodeling
Tissue Injury
Different types of loads may be applied to tissues in the
body. In the right circumstances, the body is able to
respond to these loads. However, if the body is not able
to respond appropriately to the stresses, an injury occurs.
High, rapidly applied loads are more likely to lead to tissue
damage. In fact, rapid deformation is sometimes referred to
as a rupture (i.e., third-degree sprain, third-degree strain).
Similarly, frequent repetitions or cyclic stress loading can
lead to failure of the tissue because of the accumulated
weakness in that tissue, hence the term fatigue failure.
Factors Affecting the Degree of Injury
or Stress on Tissues
The degree of injury or the stress applied to tissues may
be affected by many factors that can be used by the clini-
cian to ensure proper treatment and prevent the recur-
rence of injury.31,43 Information about the degree of
injury and tissue stress can also be used as part of an edu-
cation program to teach the patient to protect an injury
while it is healing.
The degree of injury suffered by a patient depends on
the magnitude, duration, and velocity of the applied force
and whether the force exceeds tissue tolerance limits.
A glancing blow causes less damage than a force that
strikes the body directly (location). Rotation or move-
ment away from a force can decrease injury through
absorption of force by involving the whole kinetic chain.
On the other hand, rotation away from the force may
cause an injury to occur farther from the actual site of
the blow if distal tissues are overstressed by the rotation
or movement away from the force. Increasing the length
of the lever arm can cause similar injuries. If a tissue tol-
erance is exceeded, the longer a given force is applied
(duration), the more likely it is to cause greater damage.
Likewise, the more often force that has the potential to
exceed tissue tolerance limits is applied (frequency), the
greater is the potential for more extensive injury due to
fatigue, as described earlier.

Factors Affecting Injury Probability
● Magnitude, duration, frequency, and velocity of applied force
● Tissue tolerance limits
● Direction of applied force
● Movement relative to applied force
● Length of lever arm
● Muscle action
● Area of force application
● Awareness of impending injury
The rate of force development (velocity) and the dura-
tion the force is applied can both affect the stress on tis-
sues. The body and its tissues are more tolerant of forces
that develop slowly, over time, compared with rapidly
applied forces, because there is a more gradual absorp-
tion of the load with the former. By allowing the patient
more time or by increasing the distance she or he has
in which to stop or slow down, the deceleration forces
applied to the body will be decreased, rebound will be
less, and there will be a more gradual decrease in velocity.
Contracting muscles, through their passive (connective
tissue) and active (contractile) components, act as energy
shock absorbers by working eccentrically to decrease the
stress on tissues.
The larger the area over which the force is spread on
the body, the less damage there is likely to be because
there is less force per unit area. The heavier an object is
and the faster it is moving, the more likely it is to cause
damage. Similarly, with an increase in velocity, the body
has less chance to react and prepare itself for the load.
If a rough, uneven object hits the body, it is more likely
to cause damage, as is a more pointed object, which will
penetrate deeper.
Awareness of impending injury can also play a role in
the severity of the injury. In most cases, awareness enables
the person to brace himself or herself and, provided the
force is not too great, the person is able to dissipate the
forces. People hurt in a rear-end automobile collision are
a good example of this. Most commonly, it is the person
who is hit who suffers the injury, not the person in the
vehicle doing the hitting.
Mechanisms of Injury
There are several mechanisms by which tissues can be
injured. These mechanisms give the clinician a very
strong indication of what tissues might be injured, how
the injuries may have occurred, and the potential severity
of the injuries. With all of these mechanisms, the degree
of injury depends on the tissue’s ability to tolerate load
and deformation due to an imposed force of a certain
magnitude, at a certain velocity, at a certain angle of
CHAPTER 1 • Injury, Inflammation, and Repair 5
application, with a certain duration of application, and
at a certain frequency of application. These forces can
result in tissue overload of a dynamic nature from accel-
eration or deceleration forces (e.g., sprains and strains),
repetition and overuse (repetitive stress), compression
or crushing (contusions), or transection (lacerations or
surgical incisions).
Macrotraumatic versus Microtraumatic Injury
Macrotrauma results from the application of an acute,
one-time force of sufficient intensity and duration to
cause injury to the tissue at that time. Stress applied to
the tissue exceeds the tissue’s tolerance limits or is applied
too quickly for the tissue to adapt. Tensile failure in the
tissue results. For example, a tendon is most likely to fail
when tension is applied quickly at an oblique angle. This
type of failure is due to dynamic overload. Dynamic
overload is the most common mechanism of injury for
bones, tendons, ligaments, and muscles. Dynamic over-
load of tissue can be a result of an acceleration or a decel-
eration injury. An acceleration injury occurs when the
body or body parts are stationary or moving slower than
the applied force. The injury producing force accelerates
the body or body part beyond the tissue’s ability to with-
stand the force. This type of injury is commonly seen
when someone is hit from behind, as in whiplash-type
injuries, or when the body is stationary and hit by a mov-
ing object, such as a football player being tackled. In the
case of a deceleration injury, the body or body parts are
rapidly decelerated. An example of a deceleration injury
is tearing the anterior cruciate ligament as one tries to
stop and go in another direction while running.
Mechanisms of Injury
● Dynamic overload (acceleration or deceleration)
● Microtrauma (cumulative overload)
Microtraumatic injuries are a result of a cumulative
load or repetitive stress being applied to a tissue over time.
Although these forces are small and by themselves would
not cause injury, their cumulative effect is to exceed the
tissue’s load tolerance and ability to repair itself. This
overload usually results in an acute inflammatory process.
Unchecked, it can become a chronic condition, progress-
ing even to the point of tissue rupture.
Injury Classification
Injuries may be classified as acute, subacute, chronic,
acute on chronic, or subclinical adaptation. The dura-
tion and “time lines” used for each stage of healing are
6 SECTION I • Scientific Foundations
arbitrary, and the reader must understand that these time
lines commonly vary. There is little objective basis for
deciding when an injury passes from one stage to another.
This determination is often based on the experience of
the clinician—a very subjective decision.
Injury Classification
● Acute
● Subacute
● Chronic
● Acute or chronic
● Chronicity
Acute injuries usually are caused by macrotrauma and
indicate the early phase of injury and healing. Typically,
the acute phase lasts approximately 7 to 10 days. Acute
tissue disruption with bleeding provides the best model
for the classic acute inflammatory phase seen in tissue
healing. Sudden macrotrauma (e.g., a collision or contact
injury) commonly results in an acute injury. However,
an acute inflammatory response can also result from
sudden overuse with repetitive activity that is associated
with peritenonitis or bursitis. As the inflammatory pro-
cess begins, symptoms manifest 8 or more hours after the
event. Symptoms of severe pain, muscle spasm, decreas-
ing range of motion, and functional impairment gradually
subside as the inflammation decreases.
In children, many acute injuries result in fractures of
the growth plate or avulsion at the physis because these
areas are weaker than the bone itself, whereas injuries
experienced by adults are clustered in the joints of the
lower extremity, with the knee, ankle, and lower back
being the anatomic regions most commonly involved.44
In sports involving the upper limb, the shoulder, because
of its extensive mobility and minimal inherent stability, is
the primary focus of injuries.
A subacute injury is one that has passed through the
acute phase and is now in the healing (proliferation) phase
of regeneration and repair. It typically lasts from 5 to 10
days after the acute phase (12 to 20 days after injury).
The term chronic injury has different meanings.
It may indicate the final stage of healing (time depen-
dent), in which the injury has reached the maturation
phase and is going to resolution to complete the healing
cycle. The final stage of healing occurs 26 to 34 days
after injury and is usually complete in about 2 weeks,
although achieving preinjury strength and resolution
of the tissue to near-normal strength can take up to
2 years. Chronic injury may also be applied to an injury
that lasts longer than a month and does not appear to
be improving (injury or disease state). This is termed
chronicity. An example would be a chronic wound. The
Wound Healing Society45 has arbitrarily defined chronic
wounds as “wounds that have failed to proceed through
an orderly and timely process to produce an anatomic
and functional integrity, or proceed through the repair
process without establishing a sustained and functional
result.” Chronicity implies excessive scarring with intra-
articular or extra-articular adhesions; decreased range of
motion, strength, and function; and a tendency to rein-
jure, with a psychological overlay often playing a role.
Chronicity probably results from the body’s inability to
fight prolonged disease, or is due to the overloading of
tissues in a pathologic state caused by cumulative micro-
trauma (repetitive stress) or macrotrauma. Chronicity is
a persistent inflammatory state that promotes extended
fibroplasia and fibrogenesis.8 With chronicity, healing
is much slower because of accumulation of repetitive
scar adhesions, degenerative changes, and other harm-
ful effects. This type of chronic injury demonstrates
subclinical adaptation, with its associated pathophysi-
ologic changes. Subclinical adaptation is seen in repeti-
tive stress injuries when the tissue does not have time to
adapt to the stresses applied to it. An acute on chronic
injury is an acute exacerbation of a chronic injury—in
effect, a reinjury of the tissue.
Certain types of injuries are more prevalent in differ-
ent populations as lifetime sports and fitness activities have
become more common. For example, Matheson and col-
leagues46 reviewed sports-related injuries in a large series of
both young and older patients presenting to a sports med-
icine clinic. They found that the older population expe-
rienced certain types of injuries more frequently, such as
metatarsalgia, plantar fasciitis, and degenerative meniscal
lesions. However, no clear relationship between the injury
and the given sport or fitness activity was demonstrated.
Common osseous, soft tissue, nerve, and joint injuries
are summarized in Table 1-2.46 Fractures are simply a com-
plete or incomplete loss of continuity of bone or cartilage,
or both. A variety of descriptions have been applied to
delineate further the degree of discontinuity or the specific
structure involved.47,48 Joint injuries primarily involve
dislocations and subluxations. Soft tissue injuries include
trauma to skin (e.g., laceration, abrasion), underlying tissue
(e.g., contusion), fascia (e.g., fasciitis), musculotendinous
units (e.g., strains, peritenonitis, tendinosis), and ligaments
(e.g., sprains). Most often, they are clinically assessed as
mild (first-degree), moderate (second-degree), or severe
(third-degree [rupture]) based on severity and extent of
loss of structural integrity.1,12,47 These injuries primarily
result from macrotraumatic forces imposed on the body.
They are among the most frequent injuries seen and are the
classic “lumps, bumps, and bruises” whose accompanying
morbidity is sometimes disproportionate to the severity of
the injury.21,49 Microtraumatic injuries involve osseous and
musculotendinous structures and result from the repeti-
tive overloading of the body due to repetitive activity or
 CHAPTER 1 • Injury, Inflammation, and Repair 7

Table 1-2
Common Injuries Involving Neuromusculoskeletal Tissues
Bone Soft Tissue Nerve Joint

Fractures Contusion Neurapraxia Dislocation

Closed Hemorrhage Axonotmesis Subluxation
Open Hematoma Neurotmesis Internal derangement
Comminuted Muscle strain Meniscus
Avulsion Ligament sprain Loose body
Incomplete Myositis ossificans Plica
Torus Peritenonitis
Greenstick Tendinosis
Bow Bursitis
Stress Osteochondritis
Pathologic

high functional levels.44,46,50 Injuries to the peripheral or

central nervous system usually result from macrotraumatic
forces, and those involving the central nervous system are
potentially catastrophic or life-threatening.

The Healing Process

The soft tissue healing process is a complex one, involving
several steps. Figure 1-3 summarizes the cycle of an injury
and related events. A basic understanding of the process
is necessary so that it can be taken into account in the
development of an appropriate rehabilitation program.
The healing process can be either hampered or enhanced
by the clinician, so he or she must have a full apprecia-
tion and knowledge of this process. This understanding
encompasses the different phases of healing and the events
proper to each stage, so that a treatment program that is
appropriate, efficient, and effective can be established.
Healing is a dynamic process that results in the restoration
of anatomic continuity of the tissue through an orderly
biological process.51,52 Two types of healing—regeneration
and repair—commonly occur together, although repair
more commonly predominates. Regeneration is a form of
healing that produces new tissue that is structurally and
functionally identical to normal tissue,45,52,53 and would be
considered as the ideal wound healing response. Repair,
on the other hand, is the restoration or replacement of
damaged or lost cells and extracellular matrices with new Figure 1-3
cells and matrices,45 resulting primarily in scar formation. Cycle of injury. (From Booher JM, Thibodeau G: Athletic injury
assessment, ed 3, St. Louis, 1994, Times Mirror/Mosby College
Publishing.)
Phases of Healing
Tissue and cell injury occurs when there is a severe external
or internal trauma or disease affecting the body. After ing is similar, although the cells involved may be different.
microtrauma, macrotrauma, or a disease process occurs, The general process of healing is described here, whereas
the body tries to heal itself through a routine sequence of healing of specific structures is described in subsequent
overlapping events. Whether it is a skin, muscle, tendon, chapters (ligament, Chapter 2; tendon, Chapter 3; mus-
ligament, or capsular injury, the process for soft tissue heal- cle, Chapter 5). The process of bone healing is somewhat
8 SECTION I • Scientific Foundations

different, but it too goes through different stages and is
discussed in Chapters 6 and 28.
The healing process or repair cascade can be broken
down into four phases: the clotting phase, the inflamma-
tory phase, the proliferative/fibroplasia phase, and the
maturation/remodeling phase. In reality, healing is a con-
tinuous process with the stages merging and overlapping,
so there are no definitive beginning or end points in soft
tissue healing54–56 (Figure 1-4).
Phases of Healing
● Clotting
● Inflammatory
● Proliferative/fibroplasia
● Maturation/remodeling/cicatrization
Clotting Phase
When an injury occurs, especially from macrotrauma,
blood and lymphatic vessels are ruptured at the wound
site and the cellular and plasma components of blood and
lymph enter the wound. The extravasated (forced out)
blood and lymph cause swelling, and the vascular cellu-
lar components (i.e., platelets, red blood cells, and other
blood-borne cells) die. Swelling plus initial vasospasm
leads to anoxia (secondary hypoxic injury) due to stasis
of the blood and the foreign environment outside the
blood vessels.57 The blood congeals and, through several
steps, a clot is formed.
Among the blood and lymph components, there are
exudates of plasma fibrinogen, fibronectin, prothrombin,
and other clotting proteins. Clotting is initiated by the
interaction of plasma and tissue components once the
plasma constituents enter the interstitial tissues. Two
enzymes, prothrombinase and thromboplastin, cause

Injury
Clotting
Phase Inflammatory Response

Inflammatory Maturation Phase

Phase (up to 2 years)
Proliferation Phase

Clot formation Fibrinolysis

and resolution

Inflammation Macrophages
PMNS

Epithelization
(skin) Maturation
Coverage
Response

Amount
Granulation tissue
formation
Fibroblasts Endothelium
Collagen type I
Fibroblast secretion
products Collagen type III
GAGs
Collagen secretion 70-80%
Tensile strength Collagen cross-linking
clot

Wound contraction
Force, rate
Remodelling Collagenase (?)
Devascularization

7 14 28+
Time (days)
Figure 1-4
Although the healing process is commonly divided into cycles, it is in reality a series of overlapping phases. This illustration shows a hypothetical
sequence of soft tissue repair. (Modified from Davidson JM, Buckley-Sturrock A, Woodward SC: Growth factors and wound repair.
In Abatangelo G, Davidson JM, editors: Cutaneous development, aging and repair, p 116, Padova, Italy, 1989, Liviane Press.)

the conversion of prothrombin to thrombin, an active
enzyme. Thrombin then turns fibrinogen in the presence
of fibronectin into very sticky fibrin, which combines with
platelets and other cellular debris to form a hemostatic
or platelet plug called a clot (Figure 1-5). This platelet
plug, which is an insoluble water-binding gel, acts like
a low–tensile-strength “glue” to hold the wound edges
together and localize the injury.58–60 Under the skin, the
clot remains soft and gel-like, whereas on the surface, it
dehydrates and hardens and is most commonly termed a
scab. On the surface of the skin, the clot acts as a barrier
to foreign bodies, infectious agents, and transcutaneous
water loss; restrains local hemorrhage; and provides the
wound with its only source of tensile strength. Over time,
the gel is transformed into granulation tissue and eventu-
ally into dense, relatively acellular collagen (scar tissue).61
The damaged tissue releases and the clot contains che-
moattractants (chemotactic factors) that attract vasoactive
amines or mediators that increase vascular permeability
by up to 10 times normal, which allows further extravasa-
tion of plasma products into the injury site. These vaso-
active mediators come from plasma and damaged cells
(e.g., platelets, leukocytes, and mast cells), and are the
main causes of the soft tissue inflammatory response that
consists of redness (erythema), heat, swelling or edema,
pain or tenderness, muscle spasm, and, finally, dysfunc-
tion, whereas in joints and periarticular structures, there is
effusion, redness, heat, synovial hypertrophy, occasional
hemarthrosis, pain, loss of function, and, if unabated,
degeneration. Inadequate immobilization, improper
Prothrombin
(plasma protein)
Prothrombinase
+ Ca++
thromboplastin
Thrombin
(soluble)
Fibronectin
Fibrinogen
Fibrin
(insoluble)
Platelets
Clot
Figure 1-5
Clotting stage of soft tissue healing.
CHAPTER 1 • Injury, Inflammation, and Repair 9
treatment and care, and further trauma or reinjury will
perpetuate the injury cycle.
Clinical signs and symptoms may have their origin at
the chemical level but affect the cellular level. With the
presence of exudates in the extracellular spaces as a result
of increased vasodilation, vascular permeability, and the
leakage of fluids from damaged tissues, signs of inflam-
mation occur. A combination of increased pressure on
tissues and an increased sensitivity of the pain receptors
to the chemical substances in the area results in pain.
Bradykinin, histamine, and prostaglandins are believed
to sensitize pain receptors so that their level of activation
becomes lower (lower pain threshold) and they are more
easily excitable62 (Figure 1-6). At the same time, these and
other mediators or chemoattractants (Table 1-3) attract
neutrophils, which in turn begin to attract leukocytes
and other macrophages. The clot, degraded platelets,
and vasoactive mediators combine to form a provisional
matrix or ground substance for healing to begin.
Serous fluid accumulates as edema in the extracellular
spaces because of the blocked lymphatic vessels, or, if a
joint is injured, synovial fluid accumulates with swelling
because of the action of the vasoactive mediators on the
synovial membrane. When tissues expand immediately
after injury, it is primarily because of blood in the inter-
stitial spaces, and the bleeding is controlled by the mech-
anisms mentioned previously. If, however, the damage
is extensive (e.g., fracture), more blood will be released
into the surrounding tissues or joint because the clot-
ting mechanism cannot respond sufficiently to the injury.
Trauma
Cell damage
Inflammation
Stimulation Direct nerve
of nerve damage and
endings stimulation
Second line First line
of warning of warning
Delayed pain Immediate pain
(2nd pain) (1st pain)
Figure 1-6
Causes of pain in soft tissue healing.
10 SECTION I • Scientific Foundations

Table 1-3
Some Chemotactic Factors and Their Functions
Chemical Mediators Functions

Histamine Vasodilator
Causes short-lived increase in permeability of venules
Serotonin (5-hydroxytryptamine) Vasodilator
Involved in fibroblastic proliferation
Bradykinin Vasodilator (plasma kinin)
Causes increased microcirculation permeability
Kallidin Vasodilator (plasma kinin)
Causes increased microcirculation permeability
Substance P (sP) Sensitizes pain receptors
Prostaglandin E1 Vasodilator
(PGE1) Causes increased vascular permeability
Sensitizes pain receptors
Prostaglandin E2 Vasodilator
(PGE2) Attracts leukocytes to inflamed area
Sensitizes pain receptors
Leukotrienes Increase vascular permeability
Cause cellular adhesions
Thromboxane A2 Vasoconstrictor
Mediates platelet aggregation
Leukotaxin Causes margination in which leukocytes line up along cell walls
Increases cell permeability
Affects passage of fluids by diapedesis (passage of red or white blood cells through vessel
walls) to form exudates; amount of swelling is directly related to amount of vessel damage
Necrosin Causes phagocytic activity
Lactic acid Byproduct of energy metabolism
Plasmin Dissolves fibrin clots
K +
Maintains acid–base balance
Maintains water balance
H+ Maintains acid–base balance

Thus, the presence of significant edema or effusion early Inflammatory Phase

is a good indication of a major injury that may require
extra care. Synovial swelling, commonly the result of
inflammation, is a process that occurs later (usually at
least 6 to 8 hours postinjury) because of irritation of the
synovial membrane by the vasoactive amines. Similarly,
swelling due to infection shows up later because it results
from a combination of direct bacterial action and the
white blood cells trying to contain the bacteria during
the inflammatory phase.
The clotting mechanism normally is complete 5 minutes
after injury, but may take up to 48 hours.60,63 The process
can be sped up by protection, rest, ice, compression, and
elevation (PRICE).
During the healing process, inflammation must not
be considered as a negative occurrence but rather as
a necessary part of the healing cascade.52,55,56,64–66 The
inflammatory response is necessary for healing to be
initiated but, paradoxically, healing does not commence
until the inflammatory response begins to subside. This
response involves a complex system of events at the bio-
chemical and cellular levels and is the first stage in injury
recovery.58
With injury, a number of localized factors in the dam-
aged area are activated. Many of these chemotactic factors
are induced by the Hageman (XIIa) factor, an enzyme
in the blood. This process is known as chemotaxis and

is essential to the process of inflammation. As shown in
Table 1-3, many chemotactic factors or substances are
intimately involved in the inflammatory process. For
example, bradykinin, a potent vasodilator produced by
plasma enzymes, becomes active in the wound, increas-
ing vascular permeability. In addition, bradykinin triggers
the release of prostaglandins, which are among the most
powerful chemicals in the human body.17 Prostaglandins
in turn have a number of effects within the damaged area,
including vasodilation, increased vascular permeability,
pain, and fever, as well as some actions related to the
clotting mechanism.67,68 Two prostaglandins exert their
effects predominantly during the inflammatory phase,
namely, prostaglandin E1 (PGE1) and PGE2. Whereas
PGE1 increases vascular permeability, PGE2 attracts
leukocytes (Figure 1-7).
Leukocytes are migratory white blood cells that
are attracted to the wound area by the inflammatory
response and the vasoactive amines released from the
damaged cells. The more common white blood cells
are the lymphocytes, monocytes (macrophages), and
granulocytes (neutrophils [most common], basophils,
and eosinophils). The macrophages and granulocytes act
INJURY
(microtrauma, macrotrauma)
Vasoactive Histamine
mediators Bradykinine
Serotonin
Kallidin
K+
Increased vascular
permeability
Cytokines Arachidonic
acid
metabolites
Prostaglandins (PGE, PGE2)
Leukotrenes
Leuotaxin
Pain
Swelling
CHAPTER 1 • Injury, Inflammation, and Repair 11
as phagocytes and clean the wound of dead tissue and
detoxify toxic proteins seen with cellular injury and allergic
reactions. These leukocytes gain access to the injury site
because of the vasodilation associated with inflammation,
and release powerful enzymes that hasten the breakdown
of the injured cellular structures and damaged tissue out-
side the cells through degradation. The macrophages
and granulocytes debride the injured area of necrotic
tissue, debris, and foreign material within 24 hours and
continue acting for the next few days (commonly 2 to
5 days). Macrophages are central to the healing process
because they produce substances (e.g., growth factors,
cytokines, and chemokines) that modulate the inflam-
matory response. In early inflammation, the neutrophils,
macrophages, and other leukocytes clean the wound
site by phagocytosis, destroying and degrading bacteria,
denatured matrix, and damaged cells.
As the wound is cleansed of debris, there is a shift
from the inflammatory phase to the proliferative or heal-
ing phase, in which fibroblasts (for repair) and specialized
cells such as myoblasts and tenoblasts (for regeneration)
migrate into the area, facilitated by chemoattractants and
other molecules (e.g., glycoproteins). As the fibrin clot
Chemotactic factors
Leucocyte Substance P
activation
Proteases Oxidants
Figure 1-7
The inflammatory process.
12 SECTION I • Scientific Foundations

breaks down, the original provisional matrix is replaced of immobilization to an absolute minimum.17,20,71,72
by an extracellular matrix called granulation tissue. Without proper care, a “vicious cycle” will result and the
Granulation tissue consists of capillaries, myofibroblasts, injury will go to chronicity (Figure 1-9). By this stage,
macrophages, fibrin matrix, endothelial cells, and a nutri- the wound should progress to the healing or prolifera-
tive matrix. It is red and consists of a granular mass of tion phase, but may go to chronicity because of impeding
connective tissue that fills in the gaps in the wound during factors (see later; Figure 1-10). In the normal healing
the healing period. The endothelial cells in the granula- response, both repair and regeneration begin to occur
tion tissue begin to produce new capillary buds (angio- with restoration of “normal” and scar tissue; pain disap-
genesis). In the later part of the inflammatory phase, it pears and, strength, endurance, and range of motion are
appears that prostaglandins may initiate early repair as restored, leading to normal function.
well as continue the inflammatory reaction.69 The change
from the inflammatory phase to the proliferative phase is Proliferative/Fibroplasia Phase
not an abrupt one. In fact, an inflammatory response As the inflammatory process subsides, true tissue repair
can continue well into the proliferative phase (see Figure and regeneration begin to occur.52,55,56,64,65 The healing
1-4), but with normal healing, inflammatory effects in process involves a “competition” or “race” between
the proliferative phase grow increasingly less prominent.
If the inflammatory process does not subside, chro-
nicity, often with persistent, low-grade inflammation that
can be resistant to treatment, results. Attempts to signifi-
cantly alter the time course of the acute inflammatory
phase through pharmacological or physical means can
be problematic,59,63,70 and require care in looking for the
cause of the problem and modifying the treatment to
deal with it.
The injury cycle (Figure 1-8) demonstrates the
absolute necessity for the clinician to moderate the
inflammatory response symptoms and keep the period

Figure 1-9
Ischemia Vicious cycle of injury. (From Stokes M, Young A: The contribution
of reflex inhibition to arthrogenous muscle weakness, Clin Sci
67:7–14, 1984.)

Injury cycle of pain and spasm

Trauma Infection

Pain Inflammation Spasm Inflammation

Joints and Muscles and

ligaments tendons Chronicity Healing

Scarring Repair
Intra- and extraarticular Regeneration
Effusion Edema adhesions Hypertrophy
Synovial Hemorrhage Tendency to reinjure No pain
Hypertrophy Atrophy Loss of function Full range
Hemarthrosis Necrosis Loss of range Full strength
Degeneration Adhesions Loss of power (atrophy) Normal movement pattern
Fibrosis Contracture Psychological problems No psychological residue
ROM
Figure 1-8 Figure 1-10
The injury cycle. Pathways of inflammation.

repair, which is the replacement of the original tissue by
scar tissue that starts as an emergency effort to restore
mechanical integrity, some degree of barrier function,
and some limited functionality to the area, and regenera-
tion, which is replacement of the damaged tissue with
the same type of tissue having the same function as the
original tissue. Both processes occur simultaneously, but
invariably repair “wins” because it is supported more by
the inflammatory process, with formation of scar tissue
outpacing regeneration of the original type of tissue.21,73
This period of scar formation is known as fibroplasia, and
may last from 4 to 6 weeks, and in some cases longer.
Growth of endothelial capillary buds into the wound
is stimulated by the low oxygen tension caused by the
lack of local blood supply. As the capillary buds form
capillaries, the wound becomes capable of healing aero-
bically because of the improved blood supply, which, in
turn, leads to increased oxygen delivery and delivery of
nutrients essential for tissue regeneration and better heal-
ing in the area.74
Fibroblasts accumulate at the wound site as the
capillaries continue to grow into the wound area.
Fibroblastic cells begin to synthesize an extracellular
matrix that contains collagen protein fibers (which resist
tensile loads), elastin, a ground substance (consisting
of nonfibrous proteins called proteoglycans that resist
compression), glycosaminoglycans, and fluid. Fibroblasts
produce collagen fibers (primarily type III collagen) that
are deposited in a random fashion, with the greatest rate
of collagen accumulation occurring between 7 and 14
days. The tensile strength of the wound quickly increases
in proportion to the rate of collagen synthesis as the col-
lagen continues to proliferate. Type III collagen, which
forms rapid cross-links and stabilizes the wound,31,36 is
gradually replaced by type I collagen, which is a major
constituent of scar, and the ratio of type III to type I
collagen decreases over time (Table 1-4). Depending on
the type of tissue (Tables 1-5 and 1-6), different types of
collagen are laid down and aligned in bundles, and cross-
links are established for enhanced stability. Mobilization
and controlled movement at the right time will lead to a
smaller scar with better structural organization and capil-
lary growth.
Maturation/Remodeling/Cicatrization Phase
The number of fibroblasts diminishes and the tensile
strength of the wound increases, signaling the start of the
maturation phase.52,55,56,65 The normal sequence of events
in the repair phase leads to the formation of minimal scar
tissue. The amount and extent of scarring depend on such
factors as the site of injury, the tissue or organ injured, the
nature of the injury, the direction of the tearing/incision,
the patient’s genetic background and race, the care and
treatment given to the wound and damaged tissue, and
presence or lack of complications (e.g., infection). In some
CHAPTER 1 • Injury, Inflammation, and Repair 13
cases, excessive scar tissue may be laid down, which can
interfere with the rehabilitation process. For example, in
the skin at least two pathologic scar types are seen, hyper-
trophic and keloid scarring, in which excessive scar tissue
forms. Hypertrophic scarring (Figures 1-11 and 1-12)
consists of normal scar, but the scar tissue is excessive and
the scar appears stretched, although it remains within
the wound margins. Keloid scarring (Figure 1-13; see
Figure 1-11) usually manifests as overgrown, dense, fibrous
tissue that spreads beyond the wound margins.75 Rich vas-
culature, high mesenchymal cell density, and a thickened
epidermal cell layer differentiate keloid and hypertrophic
scars from healthy skin. Differentiating keloid from hyper-
trophic scars can be difficult, especially in their early forma-
tive phases. Keloid scars grow beyond the original wound
or scar margins and can become progressively larger, but
hypertrophic scars do not. Histologically, keloid scars are
differentiated by the presence of broad, dull, pink bundles
of keloid collagen.76
The maturation phase is a long-term process, extend-
ing 1 year or more from the time of injury.77 At 12
months, the tissue has regained approximately 70% to
80% of its original tensile strength.26 This is important
to remember because the potential for reinjury remains
high and patients should be made to understand that it
can take a year or longer until they feel “normal” again
(Figure 1-14).
The cells in the wound area, abundant during the
clotting and inflammatory phases, decrease in number.
As collagen becomes denser, its vascularity is dimin-
ished, and the initially vascularized red scar begins to
turn white. As some capillaries are “cut off” as the tis-
sue matures over time, the new tissue loses its sensitivity.
At the same time, myofibroblasts contribute to wound
contracture, which can be by as much as 40% to 80%,
making an initially large scar much smaller. The maturity
of the collagen correlates to the tensile strength of the
scar, as the fibers become more organized along the lines
of stress. More type I collagen is added and the num-
ber of cross-links increases, so the tissue is better able
to respond to stress within normal activity limits. This
is an example of the principle of specific adaptation to
imposed demand (SAID). In this case, it demonstrates
a remodeling response to stress.
During this final phase of healing, new tissue is remod-
eled until a strong, permanent structure is formed, some-
times restoring the area with its original structure (e.g.,
tendon regeneration) and sometimes replacing the original
structure with a scar (repair). Scar formation—a “patch,”
in effect—allows the tissue to return to normal use, but
the tissue is never completely normal in appearance or
function. It is generally agreed that most soft tissues heal
through the repair process, using primarily scar tissue to
replace damaged structures.12,78,79 In humans, regenera-
tion occurs on a limited basis and is widely believed to be
 Table 1-4
Collagen Types Known or Suspected to Be Directly Involved in Bone, Tendon, or Ligament Healing
Collagen
Type Tissue Distribution
I Dermis, bone, tendon, teeth,
fascia, sclera, organ capsules,
fibrous cartilage
II Hyaline and elastic cartilage,
intervertebral disk, vitreous
humor
III Bone, skin, smooth muscle,
arteries, uterus, liver, spleen,
kidney, lung, tendon,
periosteum, endoneurium
V Skin, bone, tendon, synovial
membrane, liver, vascular tissue,
placenta, teeth
IX Uniform throughout
cartilage matrix; vitreous humor
X Fetal and adolescent skeleton;
transient intermediate in
cartilage replaced by bone;
growth plate
XI Fetal and adolescent skeleton;
transient intermediate in
cartilage replaced by bone;
growth plate
XII Ligament, tendon,
perichondrium, periosteum,
periodontal ligament, fetal
bovine cartilage, reticular
dermis
XIV Codistributed with type I
in skeletal and cardiac
muscle, tendon, periosteum,
dermis, perineurium, placenta
N/A, information not available.
From Liu SH, Yang RS, al-Sheikh R et al: Collagen in tendon, ligament and bone healing: a current review, Clin Orthop Relat Res 318:267, 1995.
Optical Microscopy
Closely packed, thick,
nonargyrophilic fibers;
strongly birefringent red
or yellow
Loose collagenous
network visible only
with picrosirius stain
and polarizing microscopy
Loose network of thin,
argyrophilic fibers; weakly
birefringent green;
reticular
N/A
N/A
N/A
N/A
N/A
N/A
Ultrastructure
Densely packed,
thick fibrils with
marked variation
in diameter
No fibers; very thin
fibrils embedded
in abundant
ground substance
Loosely packed, thin
fibrils with more
uniform diameter
Form quarter-
staggered fibrils
Covalently cross-linked
to type II collagen
fibrils
Sheetlike
Form quarter-
staggered fibrils
Covalently cross-linked
to type I collagen fibrils
Covalently cross-linked
to collagen fibrils
14
SECTION I • Scientific Foundations
Site of Synthesis Function
Fibroblast, osteoblast, Resistance to tension
odontoblast
Chondroblast Resistance to tension
Fibroblast, smooth Structural maintenance in
muscle cells, expansile organs; wound
Schwann cells, healing; mediate
hepatocytes, attachments of tendon,
mesenchymal ligament, and periosteum
precursor cells to bone cortex
Fibroblasts, osteoblasts Control of fiber diameter
Chondrocytes Contributes mechanical
stability and resistance to
swelling to type II
collagen framework
Hypertrophic N/A
chondrocytes during
endochondral ossification
Chondrocytes Control of fiber diameter
Fibroblast, myoblast, Control of fiber diameter
osteoblast, endoneural and interaction with
and perineural cells proteoglycans
Fibroblast, myoblast, Control of fiber diameter
osteoblast, endoneural and interaction with
and perineural cells proteoglycans
 CHAPTER 1 • Injury, Inflammation, and Repair 15

Table 1-5 restricted to labile and stable cells, such as in lung and liver
Makeup of Collagenous Structures that Resist Tensile tissue. Recent evidence of regeneration on a small scale
Deformation has been observed in minor skeletal muscle strains11,79–82
and in the meniscus.83 In greater muscle injuries, the site
Each collagenous structure contains the following substances,
heals primarily through the repair process.
but in different amounts:
Collagen (strength and stiffness; 5× stronger than elastin)
Elastin (elasticity) Factors Impeding Healing
Reticulin (bulk)
Nonfibrous ground substance (reduces friction between Many factors determine the outcome of a given injury.
individual fibers) The major factors that impede wound healing can be
divided into local (intrinsic), systemic, and extrinsic
factors (Table 1-7).

Local (Intrinsic) Factors

Table 1-6
The extent or amount of tissue damaged will deter-
Comparison of Tendons and Ligaments mine the subsequent inflammatory response and the
Tendons Ligaments Both extent of repair. Microtears of soft tissue associated with
overuse involve only minimal damage and a prolonged
Have fewer cells Have dense closely Show crimp
Bundles are packed collagen Have poor blood
more aligned (70%–80%) supply relative to
Have more Have more elastin other tissues
type I collagen (3%–5%) Have relatively Keloid
Have more Have periligamentous low metabolic
collagen membrane rates
Scar volume

cross-links Have duller, Hypertrophic scar

Have better white color
blood supply
(sheath)
Normal scar
Have glistening
white color 0 2 4 6 8 10 12 14 16 18 20 22 24
Months
Data from Whiting WE, Zernicke RF: Biomechanics of musculoskeletal Figure 1-11
injury, Champaign, IL, 1998, Human Kinetics; and Butler DL, Growth of scar tissues. (From Nicoletis C, Bazin S, Le Lous M:
Grood ES, Noyes FR et al: Biomechanics of ligaments and tendons, Clinical and biochemical features of normal, defective, and pathologic
Exerc Sport Sci Rev 6:125–181, 1978. scars, Clin Plast Surg 4:350, 1977.)

Figure 1-12
A transverse scar on the anterior chest wall
after a simple mastectomy that healed without
complications. Note alternating areas of “normal”
healing and hypertrophic scarring within the same
wound. (From Peacock EE: Wound repair, ed 3,
p 234, Philadelphia, 1984, WB Saunders.)
16 SECTION I • Scientific Foundations

Table 1-7
Factors Affecting Healing
Local Systemic Extrinsic

Degree of tissue Age Medications

damage Concurrent illness Humidity
Type and size Nutritional state Temperature
of wound Obesity
Blood supply Stress
Amount of stress
applied to tissue
Presence of
swelling
Amount of pain
Stabilization of
Figure 1-13 wound
Typical keloid scar. Blacks develop keloids most commonly on the Tissue characteristics
earlobes and face. (From Habif TP: Clinical dermatology, ed 4, p. 709, Presence of infection
St. Louis, 2004, Mosby.)

inflammatory response, whereas macrotears cause greater

destruction of soft tissue and result in more significant
clinical symptoms and greater functional limitation.62
Regeneration and Tissue injury Normal injury
compensatory A clean, sterile wound caused by a sharp scalpel (incision)
hyperplasia heals faster than a wound caused by a blunt instrument,
where the wound edges commonly also suffer injury (lac-
eration). Small wounds heal faster than large ones, and
wounds that occur in areas with a rich supply of blood
Wounds that never heal Wounds that heal too much
(e.g., face or skeletal muscle) heal faster than wounds in
(uncontrolled proliferation) areas that have poor vascularization (e.g., foot or tendon).
Adhesions or scarring of bony surfaces can prevent wound
Hyperplasia Cutaneous lesions
Neoplasia Keloid contraction and adequate apposition of the wound edges.
Tumor growth Hypertrophic scar For a wound to heal properly, there is an obvious need
3! burns for a good blood supply. Wounds heal poorly and at a
Fibrosis
Adhesions slower rate when the blood supply is inadequate.84 A poor
blood supply leads to a weak initial inflammatory stimu-
lus (fewer platelets and macrophages result in low growth
factor concentrations; low fibrin and fibronectin content
Wounds that heal properly results in low rates of chemotaxis) and impaired haptotaxis
(fibroblasts moving up the gradient of extracellular matrix
Cutaneous ulcers density). Complications to healing occur when there is
Decubitus an inadequate blood supply for the high metabolic needs
Diabetic
Venous stasis of granulation tissue.11 Tendon degeneration, especially
Arterial in the supraspinatus portion of the rotator cuff, in the
Non-fractures Achilles tendon, and at sites of extrinsic bone pressure,
Tendon rupture
has long been thought due to poor vascularity.85,86
Figure 1-14 During the inflammatory phase, excessive stress or
The range of tissue responses to injury. Damage to tissues can result
in either functional repair (normal repair) or, in the case of liver and movement may cause new trauma to a wound. The
fetal tissue, regeneration. Numerous pathologic states can result from wound may split open (dehiscence) and begin bleed-
tissue injury, including poorly controlled or uncontrolled proliferation ing again, or there may be increased cellular synthesis of
(wounds that never heal), excessive accumulation of scar tissue and matrix degradation enzymes, a condition clinically known
extracellular matrix (wounds that heal excessively), and the many
as tissue breakdown.87 Thus, the clinician must take
examples of retarded wound healing. (Modified from Davidson JM:
Wound repair. In Gallin JI, Goldstein IM, Snyderman R, editors: extreme care during the inflammatory stage to ensure
Inflammation: basic principles and clinical correlates, ed 2, p 810, the injured tissue is protected and not overstressed. This
New York, 1992, Raven Press.) does not necessarily mean immobilization, although

that may play a role in treatment. Any treatment must
be carefully controlled so as not to reinjure or overstress
the tissue, and should be geared toward restoring normal
tissue homeostasis.
Excessive effusion in joints or edema in the interstitial
tissues slows the healing process, whether caused by
bleeding or increased synovial or lymphatic fluid. The
increased pressure causes separation of the tissues, inhib-
its neuromuscular control, leads to reflexive neurologic
changes, and impedes nutrition to the injured part.
In a wound, the degree and type of tissue separation
have an impact on the course of healing. Clean, smooth-
edged wounds heal faster with minimal scarring. Wounds
with jagged, serrated edges heal with more granulation tis-
sue filling the defect and result in excessive scarring.88 For
example, with skin wounds, immediate suturing of wound
edges is called primary closure or primary intention,
whereas the term delayed primary closure is used when
a wound has partially healed with granulation tissue and
then is sutured. Healing by secondary intention means
the wound is allowed to heal itself with no suturing.64
Healing by primary closure has the advantages of the tis-
sue healing closer to its normal length, blood supply is
restored sooner, healing by creeping substitution is more
likely allowing a better chance of regeneration, less scar
tissue and a decreased period of disability. With secondary
healing, the resulting scar can often end up as small as with
primary healing because of wound contracture. However,
if secondary healing occurs in tight tissue areas or across
joints, the results can be poor because of contractures.
Muscle wasting or atrophy begins immediately after
injury because of disuse due to either pain or immobilization.
To retard atrophy, early strengthening and mobilization of
the injured structure are necessary. Prolonged immobili-
zation (i.e., 6 to 12 weeks) can lead to profound atrophy
of the muscles as well as collagen tissue, and recovery may
require months or even a year or two. A study by Noyes
and McGinnis89 showed that 12 weeks of immobilization
of the medial collateral ligament in the growing rabbit led
to extreme atrophy. There was a 30% decrease in collagen
mass as a result of increased collagen degradation.
There have been few investigations into the cause of
decreased strength and elastic stiffness of the anterior
cruciate ligament associated with immobilization, apart
from the classic study of Noyes and colleagues90 in which
the effects of immobilization on the anterior cruciate liga-
ment of a primate were studied. Tipton et al.91 reported a
decrease in the number and size of collagen fiber bundles
in immobilized dogs. This was the suggested cause of the
decreased cross-sectional area seen in immobilized rabbit
medial collateral ligaments.3 After 6 weeks of immobili-
zation of the medial collateral ligament in rats, there was
a decrease in the number of small-diameter fibrils.92
Structural variability in connective tissues, as observed in
animal models and clinically, may provide the explanation
CHAPTER 1 • Injury, Inflammation, and Repair 17
for differences in response to injury and adaptive capa-
bilities. Mechanical demands and local nutritional sup-
ply probably are the main reasons for the structural and
biochemical differences between ligaments and tendons45
(see Table 1-6). Ligaments tend to be composed of
tightly packed collagen (70% to 80%) with approximately
3% to 5% elastin, whereas tendons have fewer cells, more
closely aligned bundles, more cross-links, more type I
collagen, and a better blood supply, although relative to
other tissues (e.g., muscle), both have a poor blood sup-
ply and a lower metabolic rate.93 Microscopic studies of
rotator cuff tendons in cadavers have shown a complex,
interwoven, multilayered orientation of both tendons
and ligaments.94 These characteristics affect recovery
from injury as well as the location of the original injury.
Depending on the strain rate placed on a ligament, its
failure pattern can range from osseous detachment to
intrasubstance tearing.
Microorganisms can enter the body through wounds,
and a badly infected wound or preexisting infectious
disease can delay or even reverse the healing process.
This is due to the destruction of tissues by bacterial and
enzymatic action, and prolongation of the inflammatory
phase of healing.95 Bacteria in the wound delay healing,
causing granulation of tissue and often leading to large,
deformed scars or keloid formation. As the immune sys-
tem and the inflammatory process become less effective,
wound infection becomes more likely.96
Irradiation may delay tissue healing by interfering
with the blood supply. Ionizing radiation, such as x-rays,
alpha and beta rays, and neutrons, causes a reaction at the
wound site that may also block cell division.
Systemic Factors
The ability to heal injuries decreases with age. This may
be due to poor microcirculation, which results in poor
perfusion of the wound area. Another reason is the relative
inability of aged fibroblasts to synthesize matrix compo-
nents.97 With aging, metabolic processes slow down and
skin loses its elasticity, which prolong tissue repair. There
is also a decreased concentration of glycosaminoglycans in
tendons, ligaments, and other connective tissues as a result
of aging, and this loss is coincident with decreased tissue
hydration.23,98 It has been thought that collagen synthe-
sis decreases with age, but this decrease is not intrinsic
because collagen synthesis can be stimulated with ascorbic
acid.99 In general, changes in matrix integrity and slower
rates of wound healing go hand in hand with aging. It has
been well documented that morphologic, immunologic,
and biochemical changes are associated with aging.100 With
age, collagen fibers thicken, and there is overall increase in
insoluble collagen.101 Morphologic changes correspond to
biochemical changes. These changes include a decrease in
water and proteoglycan content and changes in the elas-
tic fibers.100 With age, the process of adaptation requires
18 SECTION I • Scientific Foundations
a longer period of rest and recovery.102 Aging, however,
does not prevent adequate wound healing.
Many older patients have a chronic concurrent illness
that requires drug therapy, both of which may delay
healing. Degenerative diseases such as diabetes and
arteriosclerosis also affect wound healing. Diabetes causes
delayed wound healing by affecting both the macrocircu-
lation and microcirculation, leading to less oxygenation
and perfusion in the tissues.103 Diabetic patients are more
prone to wound infection. Their overall ability to fight
infection is reduced (i.e., altered immune status) because
increased blood glucose levels affect polymorphonuclear
leukocyte function. The dietary patterns of a diabetic
patient should be monitored. There should be caloric
restrictions, balanced with additional vitamins and nutri-
ents to aid the healing process. The psychological impact
of diabetes should not be discounted; emotional stresses
such as depression, frustration, and sadness have neuro-
hormonal effects at the local microvascular level. Oxygen
is essential for wound healing. In the presence of cardio-
vascular or pulmonary disorders, wound healing is further
delayed because there may not be sufficient oxygen for
the healing tissues. Uremia may cause a wound to split
open owing to low levels of collagen deposits, and granu-
lation may be delayed. Slow metabolic rates as a result of
thyroid or pituitary deficiency may also delay healing.
Obesity and malnutrition can delay wound healing
as well. Oxygen pressure in the tissues is lower in
obese patients.104 Wound healing is commonly affected
by obesity, poor nutrition, or malnourishment.104 In
general, the most common problem in wound care is
protein malnutrition rather than any single nutrient or
vitamin deficiency. Protein is lost in wound exudates,
and the healing process may place a higher-than-usual
demand on the patient’s energy resources. The elderly
can be at a significant disadvantage because of physiolog-
ical changes (e.g., loss of appetite, difficulties in eating
and swallowing) and social limitations that hinder their
access to food and water. Patients with poor nutritional
status may need dietary supplements; these can be tablets
(e.g., zinc supplements, multivitamins), injections (e.g.,
Neocytamen, iron), or food supplements or replace-
ments. In particular, vitamins C (for collagen synthesis
and immune system), K (for clotting), and A (for the
immune system); zinc (for enzyme systems); and amino
acids play very important roles in the healing process.
Hormones affect the composition and structure of a
variety of tissues. For example, estrogen affects the devel-
opment of bone, muscle, and connective tissues. Wound
healing is known to be blocked by the biochemical effects
of psychological stress. Like surgical stress, psychological
stress also can cause cellular dysfunction.105 Any form of
stress, whether related to family, workplace, study, rela-
tionships, or finances, can lead to hormonal changes and
result in slower healing.106 Hormonal changes are seen in
all stressful situations, and it is the sympathetic nervous
system that is responsible for these changes. Under stress,
the catecholamines norepinephrine and epinephrine are
released, causing vasoconstriction and decreased tissue
perfusion. Besides decreased perfusion, there is evidence
that an increase in catecholamines stops the growth of
fibroblasts, resulting in less granular tissue formation.107
The hormonal effects of stress also exert an immunoreg-
ulatory effect on lymphocyte activity.108
One of the recognizable aids to patients with soft tissue
injury is rest. Exactly how rest contributes to well-being
during the inflammation/repair process is unknown,
and it remains an empirical observation. Although rest
does not itself heal,109 it can be said that cell repair efforts
“catch up” during rest periods. The effects of rest are
multiple and may include improved blood supply to the
healing tissue and improved structural balance of matrix
degradation and production.110
Extrinsic Factors
Drugs can play an important role in tissue healing. For
example, nonsteroidal anti-inflammatory drugs (NSAIDs)
and corticosteroids decrease inflammation and swelling,
resulting in decreased pain. Such medications must be
used judiciously, however, because long-term use can
have adverse effects, and the loss of pain as a protective
mechanism can lead to overstressing of the tissues. In the
early stages of healing, the use of steroids inhibits fibro-
plasia, the spread of capillaries, and collagen synthesis.
The effectiveness of steroids in the later stages of heal-
ing with chronic inflammation is doubtful. Excessive use
can lower the effectiveness of the immune system, caus-
ing complications and potentially masking other disease
processes (e.g., infection).111
With use of absorbent dressings, the degree of humid-
ity greatly affects the process of epithelialization. In a
moist environment, the epithelium regenerates twice as
quickly as in a dry environment, so no crust or scab can
form. Scabs form on dehydrated wounds; with the for-
mation of scabs, wound drainage is trapped, thus encour-
aging infection. In a moist wound, dead cells move more
readily to the surface and are removed. Oxygen ten-
sion plays a significant role in neovascularization of the
wound, which provides for optimal saturation and maxi-
mal tensile strength development.70
Wound healing is also affected by temperature.
Hypothermia, which is common during the presurgical
period, has a negative effect on healing. Hypothermic
stress causes vasoconstriction, leading to decreased cuta-
neous blood flow and subcutaneous oxygen tension.111,112
Hypothermia also affects the immune system, increas-
ing the potential for infection. Hypothermia weakens
chemotaxis and phagocytosis, and impairs macrophage
mobility.113 It has also been known to cause abnormalities
in coagulation, especially platelet dysfunction.114

Facilitation of Wound Healing
All wounds heal by the series of organized and complex
biologic events leading to the formation of connective tissue
to resurface the wound and restore tensile strength (repair).
These processes can be facilitated by several factors.
Nutrition
In every stage of wound healing, protein is needed.
Cytokines produced by macrophages in the inflamma-
tory phase, collagenases and integrins in the prolifera-
tive phase, and matrix secretion and remodeling in the
final maturation phase all require amino acids for synthe-
sis and, later, angiogenesis.115 Prolonged lack of protein
risks wound dehiscence because of impaired fibroplasia.
Protein depletion also results in hypoalbuminemia with
secondary edema. Edema slows down healing because
the diffusion distance for nutrients increases, which delays
the nutrients reaching the intended areas.116 Prolonged
protein depletion ultimately reduces lean body mass,
resulting in reduced cardiac and respiratory muscular
strength, impaired cellular immunity, and increased risk
of infection, sepsis, and tissue hypoxia.117,118
The structural and functional components of cell
membranes are made up of fats. Polyunsaturated fatty
acids are involved in the production and release of eico-
sanoids (any of the biologically active substances derived
from arachidonic acid, including the prostaglandins and
leukotrienes) during the inflammatory phase. As fatty
acids are metabolized, prostaglandins are produced. The
type of prostaglandin produced depends on the substance
the enzyme acts on in the fatty acid.119 Omega-3 fatty
acids are found in fish oil, whereas omega-6 fatty acids
come from vegetable oils. When there is a predominance
of omega-6 fatty acids, PGE1 and PGE2 are formed. In
addition to their anti-inflammatory actions, PGE1 and
PGE2 also act as vasodilators. PGE3 and leukotrienes are
formed when there is a predominance of omega-3 fatty
acids. PGE3 and leukotrienes function as mediators in
the inflammatory response, vasoconstriction, and plate-
let aggregation.120 Fat is also the main provider of energy
and is a primary source of stored energy and essential
fatty acids. The dietary intake should consist of adequate
fat along with carbohydrates to provide for energy needs.
With sufficient dietary fats and carbohydrates, amino acids
will not be oxidized but will be used in tissue repair.
The main source of energy for healing is glucose. It
provides energy for leukocyte activity and phagocytosis.
Fibroblasts use glucose to combine hexosamines and
proteoglycans for tissue repair.120
Adequate nutrition and stores of trace elements are
required for the physiological process of wound healing.
Minerals important in wound healing are zinc, copper,
and iron. Zinc functions as a constituent in enzyme sys-
tems and the immune system, as well as in the formation
CHAPTER 1 • Injury, Inflammation, and Repair 19
of collagen. It also helps stop bacterial growth. It plays
a key role in the reconstruction of matrix in a wound.121
Experimental studies have shown that an increase in
zinc helps skin wound healing.122 As one of the metal-
loenzymes, copper, like zinc, influences healing. In the
enzyme lysyloxidase, copper catalyzes the oxidation of
lysyl residues in collagen. This helps cross-linkage and
ultimately develops scar strength. Copper is also neces-
sary for the production of the enzyme superoxide dis-
mutase, which is present in every cell in the body.120
Superoxide dismutase, an intracellular enzyme produced
endogenously, reduces scar tissue, heals wounds and
burns, lightens hyperpigmentation, has anti-inflamma-
tory properties, and protects against harmful ultraviolet
rays from the sun. This enzyme regulates collagen and
elastin formation, which keeps the skin thick, strong, and
supple.120 Finally, as a critical component of hemoglobin,
iron is necessary for the transport of oxygen. In enzyme
systems, iron also is necessary for the oxidation of glucose
to provide energy in the cell. It is an essential cofactor for
lysyl and prolyl hydroxylase. Collagen synthesis through
the procollagen peptide is impaired in iron deficiency.120
Adequate nutritional intake and body stores of all vita-
mins are essential to the physiological processes involved
in wound healing. Vitamin A, a fat-soluble vitamin,
produces an increase in cell adhesion and membrane
microviscosity. Vitamin A stimulates the deposition of
matrix glycosaminoglycans,123 and is an essential cofac-
tor for collagen synthesis and cross-linkage. During the
inflammatory stage of healing, vitamin A mediates the
anti-inflammatory response, acting as a glucocorticoid
antagonist, and also stimulates cellular differentiation in
fibroblasts and collagen.115 Wound healing is delayed and
susceptibility to infection increased in patients with vita-
min A deficiency.124
The various B vitamins have a positive effect on wound
healing. As cofactors acting in a wide variety of enzyme
systems involved in the release of energy from carbohy-
drates, B-complex vitamins are central to cell metabolism.
B-complex vitamins such as thiamine, riboflavin, and
pyridoxine are important cofactors in the cross-linkage of
collagen. Riboflavin is involved in the synthesis and oxida-
tion of fatty acids and the deamination of amino acids.
In all stages of wound healing, vitamin C plays an
essential role, most importantly during the proliferation
and maturation phases. Vitamin C is a cofactor for the
hydroxylation of proline and lysine residues in procolla-
gen, which is an essential prerequisite for the subsequent
development of collagen. Vitamin C also protects iron-
and copper-containing metalloenzymes and is essential
for the cross-linkage of collagen. In the formation of
glycosaminoglycans, vitamin C acts as a carrier for sul-
fate groups.125 The function of vitamin C as a scavenger
of free radicals becomes increasingly important dur-
ing healing. During injury, oxygen free radicals can be
20 SECTION I • Scientific Foundations
generated that can inflict damage by peroxidation of the
lipid components of cell membranes. During the inflam-
matory response, these radicals can cause degradation of
collagen and disruption of enzyme systems.126
As an antioxidant, vitamin E is also a free radical scav-
enger and acts synergistically with vitamin C to prevent
oxidation of cell membrane polyunsaturated phospholip-
ids. Some evidence supports that the tensile strength of
irradiated wounds can be improved by using vitamin E
supplements.127
In summary, a patient recovering from an injury
should consume a well-balanced, nutritious diet that
provides the necessary vitamins and minerals for tissue
repair along with sufficient calories to support the energy
expended during the rehabilitation process.
Pharmacology
For specific injury conditions, oral anti-inflammatory
medications may play a role in the therapeutic regimen.
The healing process can be enhanced by the NSAIDs.
The primary value of NSAIDs may be in reducing the
disability produced by painful and reflexively controlled
muscle spasm. NSAIDs have a domino effect on other
events occurring in the inflammatory phase. NSAIDs act
to inhibit prostaglandin production.128 When local noci-
ceptors are stimulated by prostaglandins, the sensation
of pain occurs. Prostaglandins’ effect on vascular perme-
ability can enhance edema. By restricting the production
of prostaglandins, the NSAIDs can decrease pain and
edema. Therefore, NSAIDs have a positive impact on the
initial inflammatory reaction. With decreased local pain
and edema, there may be less loss of function. The overall
result of NSAID therapy is a less extensive inflammatory
reaction, but at the risk of weakened tissue and delayed
healing.128,129
The NSAIDs have several indications and fewer
potential side effects than more potent corticosteroids
because they work in a different area of the arachidonic
acid cycle. The common sources of chronic inflammation
include inflammatory cell reactions, chemical mediator
release, and mechanically induced cell death. Activation
of polymorphonuclear cells can be stimulated by fibro-
nectin and breakdown products of collagen, favoring fur-
ther mediator release and neutrophil activation. NSAIDs
enter into this cycle in a variety of ways to stabilize cell
membranes and reduce the effects of arachidonic acid
release. Although there is some concern about the slow-
ing down of wound healing by NSAIDs, it is balanced by
their lack of adverse effects on the function of fibroblasts
and tissue macrophages. Because the NSAIDs interfere
directly with inflammatory cell hyperactivity, they may be
less efficacious in injury settings where such activity is not
provoked. This explains their relative lack of effective-
ness in treating inflammation caused by acute rather than
chronic injury.
There is some evidence that the NSAIDs increase
collagen strength,106,107,130 either through an increase in
the number of cross-links between collagen molecules
or an increase in the amount of insoluble collagen.
The end result of either of these processes is enhanced
biomechanical strength of the new tissue.
Physical Modalities
Various physical modalities are recommended to promote
an efficient healing environment for an injury. They
may be used individually, in combination with other
modalities, or with exercise.
Acute symptoms can be reduced by the selective
application of cold. This is thought to be due to a dimi-
nution of cellular metabolic activity, which decreases the
oxidative requirements of the cells and thus decreases the
level of tissue hypoxia. The end result is an overall reduced
inflammatory process in which there is less edema, pain,
debris, and tissue damage. Because of the effect of cold
on the inflammatory process, ice may be the therapeutic
agent of choice after acute injuries.58
Cryotherapy may ameliorate the secondary necrotic
effects of the initial trauma by reducing local tissue tem-
perature and local blood flow to an injured area. Cellular
responses continue to be conjectural, although such pro-
cesses are readily implied in acute injury by the resulting
decreased edema and pain.131
The physiological effects produced by thermotherapy
or heat application include vasodilation and increased
muscle temperature and blood flow to stimulate analgesia.
This modality may also increase nutrition at the cellular
level, as well as enhance enzymatic activity. Removal of
inflammatory process metabolites and reduced edema
can be expected after heat application.132 There is evi-
dence that the application of exogenous heat increases
the synthesis of collagen.133 The secondary symptoms of
inflammation, such as spasm, also may be relieved with
thermotherapy.134
Exercise
“Wolff’s law of soft tissue” states that tissue remodeling
and the response to therapeutic exercise are determined
by the specific adaptation of the tissue to the imposed
level of demand.40 Positive cellular and biomechanical
responses to exercise, including changes in collagen fibril
size, stiffness, and strength, are documented in ligament,
tendon, and muscle.131
Studies demonstrate that, in general, cells in tendon,
ligament, muscle, skin, and cartilage respond to increased
loading by increasing matrix synthesis, replication rates,
and metabolic activity, and by modifying the produc-
tion of matrix components. An important concept is that
pathologic loading effects (excessive loading or no load)
can increase degradative activity, reduce cell synthesis,
or both. In animal models, controlled mobilization has

been shown to be superior to immobilization for scar
formation, muscle regeneration, revascularization, and
reorientation of muscle fibers and tensile properties.73
As healing progresses to the repair phase, controlled
activity is directed toward return to normal strength and
flexibility. As the remodeling phase begins, aggressive
but controlled active range-of-motion and strengthen-
ing exercises should be incorporated to facilitate tissue
remodeling and realignment.
Each individual responds differently to exercise.
Progression therefore should be performance based.
Some patients must be cautioned repeatedly about being
overly aggressive, whereas others must be encouraged
to do more. Much of the individual response hinges on
a person’s response to pain and on “taking responsibil-
ity” for his or her own rehabilitation. If pain is defined
as a discomfort that alters normal movement mechanics,
then two guidelines for progression can be established:
(1) active therapeutic exercise should be pain free, and
the injured individual should be able to repeat the next
day what was done before; and (2) pain during or after
treatment is a sign that excessive stress is being applied
to the healing structure and that the duration, frequency,
and intensity of the activity should be reduced.135
Conclusion
Healing of soft tissues is a continuous process involving
clotting, inflammation, proliferation, and maturation or
remodeling. It should be recognized that in a wound,
these processes usually overlap both spatially and tempo-
rally (see Figure 1-4). Although the clotting phase should
be completed within 5 minutes to 24 hours, the inflam-
matory phase may last anywhere from 3 to 6 days. It is
during this time that the body attempts to minimize and
stabilize the injury. The next phase of healing may occur
from days 6 or 7 to 21. During this time, the cellular struc-
tures at the injury site are changing and replacing tempo-
rary structures that were formed during the inflammatory
phase with more permanent structures. The reparative
process for injured soft tissue involves a complex series of
interrelated physical and chemical activities. Because the
normal healing process takes place in a regular and pre-
dictable fashion, various signs and symptoms exhibited at
the injury site should be observed to monitor the progress
of healing. In the maturation or remodeling phase, which
is the final phase of healing, tissue continues to grow
and develop, undergoing either a repair process whereby
scar tissue is formed or a regeneration process whereby
damaged tissue is replaced with essentially new functional
tissue. This process may take as long as 2 years.
Rehabilitation requires not only the complete resto-
ration of preinjury performance of the injured limb or
joint but also maintenance of cardiovascular conditioning
of the body as a whole.3–5,7,9,10,17 Injury rehabilitation is
CHAPTER 1 • Injury, Inflammation, and Repair 21
founded on the science of tissue healing constraints and
a knowledge of joint biomechanics, the physiology of
muscular strength and endurance, and the neurophysi-
ological basis of skill retraining. Physical change, such
as muscle hypertrophy, trails functional performance
improvement by many weeks. Each activity, whether
activities of daily living, work, recreation, or sport,
imposes unique demands on the body. Successful reha-
bilitation programs are constructed on an understand-
ing of tissue healing constraints, which, when properly
applied, permit the progressive stressing of joints and
muscles. Muscular strength, endurance, and power can be
redeveloped while the necessary structural flexibility and
general cardiovascular fitness are maintained.5,9,12,17,19,20
Goals for rehabilitation of an injury should be structured
in an ordered sequence that builds on the successful attain-
ment of each preceding stage;20 each step should contrib-
ute to the larger goal of return to the work, home, or sport
environment5,9,17 (Figure 1-15). A close patient–clinician
relationship, built on mutual goal setting and attain-
ment, can facilitate the necessary attention to the patient’s
“emotional rehabilitation.”11 Because an injury may result
in a profound loss of self-worth and even identity for the
individual, providing emotional support during the early
days of rehabilitation helps the patient regain a sense of
competence, achievement, and acceptance. Clinicians
must convey a genuine sense of care and concern during
this period.11
Restoring proprioceptive control and balance along with
motor skill reacquisition precedes a planned sequence of
activity-specific skills—a functional activities progression.121
Progressing from general to specific, simple to complex,
easy to difficult, with ever-increasing repetition and inten-
sity, the patient’s injured limb or joint is reintroduced to
the performance demands of his or her work and leisure
environment. Determining when the end point has been
reached in the rehabilitation of an injury can be a difficult
task. Clinical tests and measurements, however sophisti-
cated, cannot predict the complex interactions of a reha-
bilitated joint or limb in response to the specific demands
imposed by the patient’s environment.12,20 Careful obser-
vation of the patient’s bodily control, maintenance of car-
riage or form, and confidence in the performance of the
activity can be critical in determining readiness for return
to activity.20
The demand to return to former levels of performance
or activity drives individuals to expect a full recovery after
even the most severe injuries. The pressure to enhance heal-
ing or to speed recovery may lead the patient or clinician
to embrace unconventional treatment regimens. Proper
rehabilitation of injuries requires (1) immediate and accu-
rate initial diagnosis of the nature and severity of the injury,
with the specific tissues involved; (2) immediate initiation
of appropriate treatments directed toward moderating
the secondary effects of the inflammatory reaction; (3) an
22 SECTION I • Scientific Foundations

Figure 1-15
The rehabilitation pyramid. (From Quillen WS,
Magee DJ, Zachazewski JE: The process of athletic
injury and rehabilitation. In Zachazewski JE,
Magee, DJ, Quillen WS, editors: Athletic injuries
and rehabilitation, p 7, Philadelphia, 1996,
WB Saunders.)

ordered sequence of rehabilitation, including a regimen of
progressive exercise, to enhance the healing of soft tissue
structures; (4) integration of functional activities to assist
in the restoration of coordinated movement patterns; and
(5) the successful completion of activity-specific tasks with
confidence and bodily control.12,20
Goals should be jointly established by the patient and
clinician, always keeping in mind the patient’s psycho-
logical status.11 Successful rehabilitation is an active,
participatory process in which the patient is motivated
to meet successive criteria, thereby progressing through
a rehabilitation continuum that is highly structured
yet truly individualized.9,12 Contemporary rehabilita-
tion is a team process shared by a variety of health care
professionals.2 To be effective, the process must be evi-
dence-based and founded in anatomy, biomechanics,
applied and performance physiology, and rehabilitative
therapeutics.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever pos-
sible. There are a total of 187 references for this chapter.

L IGAMENT I NJURIES :
P ATHOPHYSIOLOGY , H EALING ,
AND T REATMENT C ONSIDERATIONS
Kevin A. Hildebrand, David A. Hart, Jerome B. Rattner, Linda L. Marchuk, and Cyril B. Frank
Normal Ligaments
Definition and Anatomy
The word ligament is derived from the Latin ligare,
meaning “to tie” or “to bind.”1 Skeletal ligaments have
thus been defined historically as bands of grossly paral-
lel, fibrous, dense connective tissue that “tie” or “bind”
bones together at or near the margins of bony articula-
tion.2 Because well over 120 moveable bones make up the
major diarthrodial or synovial joints of the human body,
with a number of ligaments connecting each articulation
between these bones, it can be estimated that there are
several hundred ligaments.3
The majority of the ligaments that have been defined in
this way have been named for the bones into which they
insert (e.g., glenohumeral, scapholunate, coracoacromial).
However, other features, such as their shape (deltoid),
relationships to a joint (collateral, on either side), and
relationships to each other (cruciate, crossed), also have
been used. These well-characterized ligaments are, by def-
inition, anatomically quite distinct and are therefore often
portrayed schematically as typical ligaments (Figure 2-1).
Such descriptions suggest that ligaments are rather simple
structures both anatomically and, by implication, func-
tionally. This is almost certainly not the case.
The first evidence that ligaments are not simple is that
each of the aforementioned “anatomically distinct,” “sim-
ple” ligaments, upon more careful inspection, can be seen
to insert into very specific and geometrically complex areas
2
C H A P T E R
on the bones.4 These insertion sites and the movements
of insertions relative to each other in three-dimensional
space during typical joint function have a great deal of
influence on ligament parts, with different parts appear-
ing to tighten or loosen during movement. These obser-
vations during joint movement have made it clear that
ligaments contain “functional subunits,” components that
tighten or loosen in different joint positions (Figure 2-2).
These functional subunits have been described best in the
ligaments of the knee joint, including the anterior cru-
ciate ligament (ACL) and the medial collateral ligament
(MCL).5–9 There is every reason to believe that functional
subdivisions will be found in all ligamentous structures.
Therefore, each apparently “simple” ligament is designed
to function effectively in numerous positions of its parent
joint. This fact by itself has profound functional, diagnos-
tic, and therapeutic significance.
The second piece of evidence in support of ligament
complexity is that many ligaments are parts of anatomi-
cally inseparable structures known as joint capsules.3
These sheetlike capsules are so named because they
clearly “encapsulate” a major diarthrodial joint. Some
of these capsules contain relatively discrete fibrous
bands with functionally distinguishable roles (e.g., the
insertion of the semimembranosus tendon into the pos-
teromedial aspect of the knee joint capsule contributes
to the so-called posterior oblique ligament).10 Owing
to the complex interdigitation of fibers in other parts
of these capsules, however, no attempt has been made
23
24 SECTION I • Scientific Foundations
Figure 2-1
Typical schematic showing the four “anatomically distinct”
ligaments of the knee joint. (From Frank CB: Ligament injuries:
pathophysiology and healing. In Zachazewski JE, Magee DJ, Quillen
WS, editors: Athletic injuries and rehabilitation, p 10, Philadelphia,
1996, WB Saunders.)
to distinguish individual ligaments. Rather, it has been
more convenient to consider the capsule as the functional
unit. Because capsules clearly tighten or loosen in differ-
ent joint positions, this too is a gross oversimplification.
Many of the “ligaments” within joint capsules have, at
least thus far, probably escaped specific anatomic defini-
tion while no doubt sharing in some of the functions of
their more anatomically obvious neighbors.
The third piece of evidence supporting ligament
complexity comes from a variety of sources showing
that many ligaments share functions.11–13 The ACL, for
example, is the primary restraint to anterior translation
of the tibia relative to the femur (it prevents the tibia
from sliding forward).14–16 To a lesser extent, the collat-
eral ligaments of the knee and the posterior capsule of
the knee also share this function.15,17,18 In other words,
because the anatomic subunits of a variety of ligamen-
tous structures around a joint are likely to be oriented in
functionally similar ways, ligaments work together to
stabilize joints and control their movements. Thus, in a
functional sense, ligaments are not the discrete units per-
ceived during anatomic dissection. This perspective has a
profound effect on our understanding of ligament func-
tion, injury, and therapy.
Figure 2-2
Schematic of the functional subunits of the anterior cruciate ligament
(ACL) and the medial collateral ligament (MCL). At approximately
15° of flexion, the anterior portion of both the ACL and MCL is
relatively “loose” compared with the “tight” posterior parts. (From
Frank CB: Ligament injuries: pathophysiology and healing. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 10, Philadelphia, 1996, WB Saunders.)
Ligament Functions
Ligaments have long been thought to have two primary
roles: the passive guidance of bone position during nor-
mal joint function and joint stabilization (i.e., prevention
of abnormal bony displacements) during the application
of extrinsic load. There is little doubt that these func-
tions are served by ligaments because when ligaments
are torn or cut, bones no longer maintain normal kine-
matic relationships15–18 and can be shown to displace in
abnormal directions during the application of external
forces.15,16,19 This fact is a main feature in the clinical
diagnosis of ligament injuries, with ongoing investiga-
tions continuing to explore the relationship between
these complex mechanical changes and the onset and rate
of osteoarthritis development.
In addition to their obvious mechanical role in main-
taining joint stability, ligaments have equally important
sensory functions as proprioceptors or position sen-
sors.20–22 Ligaments contain a variety of sensory nerve
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
endings (mechanoreceptors)23,24 that, when activated,
feed back information through the central nervous system
to the periarticular muscles, thereby affecting muscular
function.25 Studies in animals26–28 and humans29–31 have
documented the presence of these proprioceptive nerve
endings in most ligaments, along with evidence that joint
motion can cause periarticular nerve signals. Further, the
denervation of joints that are ligament deficient appears
to increase the incidence of arthritis.32,33 Ligaments alone
are not responsible for joint proprioception, and future
work in this area will need to focus on defining the actual
proprioceptive contributions of ligaments within the
joint (see Chapter 9).
Role of Ligaments
● Provide passive guidance when moving through range of motion
● Provide joint stabilization, primarily at end range
● Provide sensory (proprioceptive) feedback through
mechanoreceptors
Gross Appearance
The anatomically well-defined ligaments are dense white
bands or cords of connective tissue that run between spe-
cific sites on bones (Figure 2-3). From a gross perspec-
tive, they look like juxta-articular tendons, which are also
dense and white but are more often cordlike. Tendons, of
course, connect muscle to bone, whereas ligaments con-
nect bone to bone. Their anatomic locations and orienta-
tions are subsequently almost always clearly different.
On closer inspection, even with the naked eye, many
ligaments can be seen to be composed of roughly parallel
fibers that tighten or loosen in different joint positions
or as different forces are applied to the joint. Not all liga-
ments, however, have easily distinguishable fibers, at least
Figure 2-3
Gross appearance of the New Zealand white rabbit (medial collateral
ligament).
25
not without considerable fine dissection. The removal of
surrounding tissues or surface layers of ligaments dur-
ing their anatomic dissection has never been thought to
have any particular significance because these tissues are
believed to be nonligamentous. However, those obscur-
ing surface layers may, in fact, be a very important com-
ponent of the ligament. For example, in some models the
MCL has been shown to have a very thin superficial layer
of tissue attached to it that obscures the view of its fibrous
architecture.34 This layer is analogous to the synovial layer
on the surface of the ACL, which is similarly attached to
its outer surface and often obscures the gross view of the
ACL structure in the joint. The main concept that must
be appreciated is that, even at a gross level, ligaments are
not homogeneous tissues. As alluded to earlier, there are
many ligaments that are much less distinct than those
commonly described. These capsular ligaments are note-
worthy because despite their relative lack of definition,
they clearly have major functional roles.10,35–37
Blood Supply and Innervation
Ligaments are not as richly endowed with blood vessels or
nerves as many other tissues, with estimates of only 1.5%
of the extracellular matrix of the rabbit MCL being occu-
pied by blood vessels.38 This does not mean that their vas-
cularity or innervation is not important. Ligaments have
a ligament-specific blood and nerve supply that is impor-
tant for normal function and to promote healing.
The popliteal artery gives rise to a number of branches
that supply the tibiofemoral joint (Figure 2-4). The
Popliteal artery
Medial superior
genicular artery
Lateral superior
Semimembranosus genicular artery
Middle
Oblique popliteal genicular artery
ligament
Medial inferior Lateral inferior
genicular artery genicular artery
Popliteus
Figure 2-4
Schematic drawing illustrating the most common level of origin
of the middle geniculate artery (clasped) from the popliteal artery
and the point at which it usually penetrates the joint through the
oblique popliteal ligament and the posterior capsule. (Redrawn from
Scapinelli R: Vascular anatomy of the human cruciate ligaments and
surrounding structures, Clin Anat 10:152, 1997; with permission
from John Wiley & Sons Canada, Ltd.)
26 SECTION I • Scientific Foundations

ACL receives its major arterial supply from the middle
geniculate artery, with the distal ligament receiving some
blood supply from the inferior geniculate artery.38–40 As
with the blood supply to other ligaments, it appears that
these vessels give branches to the synovial tissue that cov-
ers the cruciates. Small blood vessels originate from these
branches, penetrate the ligament substance in a central-
izing direction, and anastomose with the longitudinally
oriented endoligamentous network. The distribution of
blood vessels to the ACL is not homogeneous, with the
middle of the ligament being somewhat avascular and
the proximal and distal ends enjoying a richer blood sup-
ply. Innervation of the cruciate ligaments (Figure 2-5) is
derived from the tibial nerve, which branches to form the
posterior articular nerve. Branches of this nerve usually
accompany the blood vessels supplying the ligaments and,
similar to the blood vessel distribution, the insertional
ends of the ligament are more highly innervated than the
midsubstance.
The MCL receives its blood supply from branches of
the superior and inferior genicular arteries. Its microvascu-
lature, like that of the ACL, appears to enter the substance
of the ligament through the epiligamentous (surface) layer,
ramifying deeper within the substance of the ligament
into smaller neurovascular bundles that run parallel to the
dominant fibrous structure.41–43 The surface of the MCL,
including its epiligamentous layer (like the synovium of
the ACL), is thus highly vascular (Figure 2-6). Deeper
levels of the ligament are less vascular but still appear to
contain neurovascular elements at regular intervals (see
Figure 2-6). The longitudinal distribution of vessels in the
MCL is somewhat similar to that in the ACL. No vessels
cross the bony interface in the mature ligament. In the
soft tissue part of the ligament, near the bony insertions,

a d

d
b f

b e
c

c f
Figure 2-5
Coronal section of a rat knee joint showing the femoral and tibial attachments of the cruciate ligaments, and the femoral attachment of the lateral
collateral ligament (LCL; original magnification ×25). Side images (a-f) show typical fluorescent-labeled protein gene product (PGP) profiles.
a, Femoral attachment of LCL; b, meniscal attachment of LCL; c, tibial attachment of cruciates; d-f, cruciate attachment points in femoral
groove. (Section stained with hematoxylin, safranin O, and fast green; original magnification ×400). Corresponding areas of immunofluorescent
slide images a-f are visible in the outlined boxes found within the corresponding outlined areas shown above. (Courtesy of Dr. Paul Salo,
University of Calgary, Alberta, Canada.)
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
Figure 2-6
Vascular perfusion of the New Zealand white rabbit lateral collateral ligament with an ink/gelatin solution. Collagen and matrix are unstained and
therefore not visible. Bar = 50 µm. A, The surface (epiligamentous) layer. Note the high number of branching blood vessels. B, Deep substance.
Double arrows indicate long axis of ligament; bar = 50 µm. Note the large area devoid of vessels. (From Bray RC, Fisher AWF, Frank CB: Fine
vascular anatomy of adult rabbit knee ligaments, J Anat 172:69–79, 1990.)
vessels enter the surface of the ligament substance, mak-
ing these areas relatively richly vascularized. Vessels enter
the remaining length of the MCL at various locations.44
The MCL receives its innervation from the medial articu-
lar nerve, which is a branch of the saphenous nerve.45 Like
the blood supply, MCL innervation is greatest in the epi-
ligament.34 The insertions of the MCL are more highly
innervated than the midsubstance and the nerves generally
are in close proximity to the vasculature of the ligament, a
similar pattern to that seen in the ACL.
From a functional view, ligaments therefore have the
innervation to perceive pain and, as noted previously,
are likely to possess nerves to assist with position sense
and feedback through specialized sensory organs such as
mechanoreceptors (Ruffini endings, pacinian corpuscles,
Golgi receptors, bare nerve endings).46–48 Complete liga-
ment tears probably disrupt the pattern of innervation
completely. Ligaments also have a sufficient number of
blood vessels both in their substance and on their surface
to cause local bleeding (seen as bruising or as a hemar-
throsis, depending on whether bleeding tracks outward
toward the skin or inward into the adjacent joint).
Microscopic and Ultrastructural
Organization
At a microscopic level, a ligament is defined as extending
from insertional bone at one end, through its major soft
tissue portion, to the bone at the other end. Ligaments
are heterogeneous from surface to depth both in their
substance and along their length.
The ligament is composed of collagen fibers separated
and surrounded by several types of ligament cell arrays.
Although some differences in ligament organization have
27
been noted, there is a general organization that is com-
mon to most, if not all ligaments.15,49–52 Closely spaced col-
lagen fibers (fascicles) are aligned along the long axis of
the ligament and are arranged into a series of bundles that
are delineated by a cellular layer, the endoligament, that is
more apparent in some ligaments (e.g., the ACL) than in
others (e.g., the MCL).50 The entire ligament is also encased
in a neurovascularized cellular layer, the epiligament, and
collagen fibers in this region are less organized and gener-
ally aligned perpendicular to the long axis of the ligament.53
Epiligament cells are roughly spherical in shape and display
long cytoplasmic extensions that generally run perpendicu-
lar to the long axis of the ligament. These extensions con-
nect adjacent cells by gap junctions. A similar organization
is thought to exist in the endoligament region.
The third and most prominent type of cellular array
consists of ligament cells that commingle with the colla-
gen fibers in a bundle and are organized into rows that
run along the long axis of the ligament (Figure 2-7A).
Adjacent rows are interconnected by cytoplasmic exten-
sions.50,54–58 This arrangement produces a complex array of
cells that are interconnected and extend from one end of
the ligament to the other. This array has been termed the
cellular matrix.55 The cellular matrix is thought to facili-
tate the transfer of information throughout the ligament
and coordinate the tissue’s response to both biochemical
and biomechanical information. Cells in the cellular matrix
are connected at two sites: along the cellular row where
two adjacent cells abut one another, and at sites where
cytoplasmic extensions impinge on another cell. Where
adjacent cells abut one another, adherens junctions as well
as gap junctions interconnect the cells54 (Figure 2-7B). To
date, only gap junctions have been localized to the cyto-
plasmic extension–cell interface. Although historically the
28 SECTION I • Scientific Foundations

Figure 2-7
A, A frozen section of a rabbit medial
collateral ligament stained with DAPI
(4',6-diamidino-2-phenylindole)
illustrating the arrangement of nuclei
and hence cells into rows; these rows are
aligned along the long axis of the ligament.
B, Transmission electron micrograph of a C
rabbit MCL illustrating two cells in a row,
as shown in A. The cells are connected
by a gap junction (box), and this region is
shown at higher magnification in the right
panel. C, Scanning electron micrograph of
a portion of a rabbit MCL that has been
torn to reveal several rows of cells aligned
along the ligament and embedded in the
collagen fibers. Each cell (one is denoted
by the arrow) has an extensive and irregular D
shape. Note that the cells pass in and out
of the plane of the tear. D, Transmission
electron micrograph of a region of a rabbit
MCL illustrating the presence of vesicle- NU
filled seams (arrow) between bundles of
collagen fibers. E, Transmission electron
micrograph of a region of a ligament cell
near the nucleus (NU). Note the presence
of a centriole (large arrow) associated with
a primary cilium (small arrow). The cilium
extends out of the plane of the section into
a region associated with the extracellular
matrix. E

does not extend along a single plane within the tissue, and
Microstructure of Ligaments thus it is difficult to follow a single row of cells for long
● Fascicles distances in sections prepared along the long axis of the
● Cellular matrix tissue (see Figures 2–7A and D). Also from a historical
● Endoligament perspective, ligaments have been described as hypocellular.
● Epiligament Hence, the cells have been considered only a minor com-
ponent of the tissue. Although ligaments are hypocellular
compared with some other tissues, this type of descrip-
tion does not convey the complex and extensive nature
cells of the cellular matrix have been described as fusiform, of individual cellular matrix cells (see Figure 2-7C). It is
more recent studies indicate that the morphology of these now appreciated that cells extend through and commingle
cells varies and, as a result, the center-to-center spacing of with a major portion of the ligament and thus are a major
adjacent cells can vary (Figure 2-7C). In addition, a row component of ligament tissue.
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
The relationship between the cells and the extracel-
lular matrix is complex. Some surfaces of the ligament
cell are closely apposed to collagen fibers, whereas other
regions of the cell, including the cytoplasmic extensions,
are surrounded by a pericellular matrix (see Figure 2-7).
This matrix contains both collagen fibers and abundant
vesicles. The collagen fibers vary in diameter but are gen-
erally smaller than those found in the extracellular matrix
and are similar to those found in ligament scar tissue. The
fibers do not display a consistent orientation and repre-
sent only a minor component of the pericellular matrix.
As previously mentioned, the matrix also follows the
cytoplasmic extensions and thus extends into the region
between collagen fibers and collagen fiber bundles. This
region can be identified in thin sections as vesicle-filled
seams (see Figure 2-7D). These seams, which follow the
subdivisions of the ligament, may be sites of interbundle
shearing. Another point of interest is that elastin fibers
also appear to run along the seams, although it is unclear
exactly what function they have (Dr. Richard Boorman,
personal observation).
Close examination of the surface of ligament cells and
their cytoplasmic extensions reveals that they are the site
of endocytosis and exocytosis and are populated by abun-
dant caveolae. Thus, there appears to be an interchange
of material between the cellular and extracellular matrix
that occurs in the pericellular matrix and the vesicle-filled
seams. This structural arrangement may form the foun-
dation for the maintenance of tissue homeostasis.
Although the cell biology of ligament cells is still in its
infancy, the basic organization of the cells of the cellular
matrix is known in some detail. Each of these cells contains
a single nucleus that is flattened and roughly spherical.
Adjacent to the nucleus is a centrosome containing two
centrioles. The mother centriole functions as a basal body
and gives rise to a primary cilium (Figure 2-7E). This
cilium extends out into the extracellular matrix, and this
structure is thought to have a sensory and signal transduc-
tion capacity that allows it to sense changes in the pericel-
lular and extracellular matrix.59,60 Information obtained at
the cilium may be relayed to the nucleus through micro-
tubules and actin filaments that extend between these two
structures. The daughter centriole is often found several
microns from the mother centriole and does not display
a close association with the mother centriole, a configu-
ration that is common in other tissues. These cells also
contain a prominent Golgi complex that characteristi-
cally surrounds the centrosome. The cytoplasm contains
an extensive microtubule and actin cytoskeleton as well
as other thin filament systems, such as those composed
of vimentin. These cytoskeletal elements are thought to
play an important structural role as well as participating
in the transmission of biomechanical and chemical infor-
mation. Both these cytoplasmic elements are also present
in the cytoplasmic extensions. In addition to being the
29
site of endocytosis and exocytosis, the plasma membrane
of these cells is also folded in certain regions to form
depressions or bays that appear to be the sites of collagen
fibrillogenesis.61 Occasionally, membrane-bound as well
as non–membrane-bound intracellular collagen fibers of
varying sizes are also found in the cytoplasm. Finally, the
plasma membrane of the cells is not homogeneous and
contains various types of lipid rafts.
There appears to be a gradual change in ligament
architecture as the ligament approaches bone that
involves a modification of both the cellular and extra-
cellular matrix.47,62–66 Collagen fibers that make up the
ligament appear to be cemented into the bone during
ligament growth and development,64,67,68 forming so-
called Sharpey’s fibers at the ligament insertions. The
cells at the bone–soft tissue interface in ligaments are
different from those in the midsubstance.64 It appears
that the ligament cells undergo a transition from fibro-
blasts (cells that produce and maintain the ligament mid-
substance), through fibrocartilaginous cells (producing
fibrocartilaginous material withi n 100 µm of the bone
interface), to an area where fibrocartilage calcifies (at the
surface of the bone), finally merging into an area with
bone (Figure 2-8). From a functional point of view, this
transition permits a progressive stiffening of the liga-
ment, thus decreasing the likelihood of concentration of
stresses at the ligament–bone interface and minimizing
the chance of failure at this site.
Biochemical Composition
Ligaments are roughly two-thirds water and one-third
solid (Table 2-1). Water is therefore a critical compo-
nent, contributing to cellular function (the distribu-
tion of nutrients, removal of wastes, and other potential
movement-related influences) and viscoelastic behav-
ior.69–71 The amazing ability of normal ligaments to adapt
to loads and load histories within seconds is due in part
to this water content.
Of the solid components of ligaments, the major
family of proteinaceous constituents is the collagens.
Collagen makes up roughly 75% of the dry compo-
nent. The structures and definitions of the collagens
can be found in a number of reviews.54–58,72–76 In sum-
mary, approximately 27 different types of collagen with
42 distinct polypeptide chains have been characterized
biochemically, with specialized structures and func-
tions. Ligaments have been shown to be composed of
six genetically distinct types of collagen,77 with type I
collagen representing the major fibrillar component
(approximately 85%). Type III collagen (an embryonic,
vascular, more microfibrillar type) and type V collagen
are quantitatively smaller components, along with a very
small percentage of type VI collagen (also microfibrillar
and found in the pericellular and interfibrillar spaces).78
30 SECTION I • Scientific Foundations
Figure 2-8
Top, a direct insertion with its four morphological zones: tendon (T),
uncalcified fibrocartilage (UF), calcified cartilage (CF), and bone (B).
The femoral insertion of the medial collateral ligament is an example
of a direct insertion. Bottom, an indirect insertion where the deep
fibers of the ligament (L) pass into bone through a well-defined zone
of fibrocartilage (F). The arrow represents the line of calcification.
(From Woo SL-Y, Debski RE, Withrow JD et al: Biomechanics of
knee ligaments, Am J Sports Med 27:537, 1999.)
Types XII and XIV collagen have also been described
in ligament and are thought to localize predominantly
in the insertions.
The second family of solid components, as found in
other connective tissues, is the proteoglycans.79 These
protein–sugars have major water-binding properties and
appear to be at least partially responsible for controlling
water composition and distribution in ligaments. In
addition, they appear to contribute to the structural
integrity of the extracellular matrix and to play an impor-
tant role in the organization of the microfibrillar colla-
gen networks that contain type VI collagen, fibrillin, or
tropoelastin. There is now evidence that proteoglycans
can control collagen fibrillogenesis by controlling fibril
diameter and the rate of fibril formation. Both small,
leucine-rich proteoglycans such as decorin and biglycan
and larger, aggregating proteoglycans such as versican
and aggregan are found in ligaments. Although decorin
Table 2-1
Ligament Biochemical Composition
Constituent Percentage Composition
Water 65
Type I collagen 20
Other collagens
(III, V, VI, XII, XIV) 3–5
Proteoglycans (90% decorin) <3
Elastin 1–2
Fibronectin, other
glycoproteins 1–2
Uncharacterized ∼3
Rabbit medial collateral ligament biochemical constituents
(percentage of wet weight). Note the large percentages of water and
collagen, which are the major constituents of the ligament.
is the most abundant proteoglycan found in the tensile
regions of the ligament, with smaller amounts of versi-
can, in the fibrocartilaginous regions, the large proteo-
glycan aggrecan is more abundant. Together, the large
and small proteoglycans make up a very small proportion
of the ligament by weight (<3%).
The third solid component of ligaments, present in
very small proportions, is elastin. Elastin makes up less
than 2% of most ligaments but may be an important con-
tributor to their low load recovery.
Other proteins and glycoproteins have been described
in ligaments, including actin, laminin, and the integrins,
although their quantities, qualities, and relationships to
the other components of the matrix remain the subjects
of ongoing investigation. A large percentage of the dry
weight of ligaments remains uncharacterized.
Biomechanical Behaviors
Ligaments are typical of all connective tissues in the body
in having very complex but functionally very impor-
tant biomechanical behaviors. The interested reader is
referred to other sources for a detailed discussion of these
behaviors.80–83 In this section, only those attributes that
have clinical significance are discussed. We familiarize the
reader with some of the engineering terminology com-
monly used in the literature to describe connective tissue
properties in order to demystify the language to some
extent. It is hoped that those familiar with engineering
terminology will forgive the simplification.
There are three fundamentally different biomechanical
attributes of connective tissues that have a clinical signifi-
cance: structural (load–deformation) behavior, material
(stress–strain) behavior, and viscoelastic (relaxation and
creep) behavior.
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations 31

displacement continues. The parts of the ligament that

Biomechanical Behavior of Connective Tissue were tightest when the load began are likely to be the first
● Load–deformation to fail.
● Stress–strain Until recently, the reasons for differing degrees of
● Viscoelastic (relaxation and cyclic loading) tightness or looseness of ligament parts were not entirely
clear. It is now apparent that several reasons probably
account for these behaviors. The first reason for the rela-
tive looseness of part of a ligament is the presence of
crimp, as noted earlier. Straightening of collagen fiber
Structural (Load–Deformation) Behavior crimp occurs at relatively low strains with low amounts
Structural behavior refers to how a ligament behaves in of force. Thus, there is effectively a small amount of rela-
its entirety, regardless of its composition or its geometry, tive slack built into the fibrillar system that allows some
when it is mechanically tested in a particular way. For elongation to occur with low amounts of energy and
example, if one ligament is isolated between two bones without any damage to the fibrils themselves. At higher
and the two bones are pulled apart, that ligament will loads, there are greater displacements, and fibrils them-
exhibit specific structural properties. It resists the dis- selves begin to carry increasing loads. As the distraction
placement with an increasing stiffness until some part of of ligament ends continues beyond this crimp region,
that ligament complex fails. The ligament itself may fail, an increasing number of ligament fibers are recruited
as could its insertions into bone or the bones themselves. into tension. As the number of fibers increases, the
The structural strength of the ligament complex does not stiffness of the ligament also increases. At the point of
take into consideration which part of the complex was the maximal ligament stiffness, the maximum number of
weak link, but refers only to the load and deformation at
the point where the ligament did fail. This load is usually
the number quoted by many authors as the strength of
that tissue.84,85
The structural behavior of a ligament is, therefore,
entirely dependent on the “boundary conditions” of
the test. The direction of load (relative to the ligament
or bone axis) is a particularly important determinant of
apparent ligament complex strength. In other words,
the direction in which a ligament is pulled can change
its apparent strength by as much as 50% to 100%.85 The
obvious clinical significance is that ligament complex
strengths depend, to a certain extent, on the direction in
which the joint (and its ligaments) are loaded. This also
has significance for the interpretation of any experimental
comparisons of ligament strength. Results must be nor-
malized, or at least qualified, to the boundary conditions
of the test, with joint angle being a particularly important
factor. Quoting “ligament strengths” in absolute terms is
therefore a risky business!
The increasing tensile resistance (stiffness) of ligaments
as they are distracted is known as nonlinear structural
behavior. The farther the ligament is pulled, the more
force it takes to continue the displacement (up to the point
of yield and failure). This increasing stiffness is due to the Figure 2-9
recruitment of parts of the ligament (i.e., tightening of Graph illustrating the structural behavior of ligaments subject to
tensile deformation. As the ligament complex is distracted, fibers
fibers) as the ligament ends are pulled apart86 (Figure 2-9). become progressively recruited into tension (A) until all the fibers
Exactly how and when the parts of the ligament become are tight (B). The parts of the ligament that tightened first are likely
tight depends on how the ligament is pulled. If different to be the first to fail (C) as the ligament reaches its “yield point.”
parts of each ligament are tight in different joint angles, Progressive fiber failure quickly results in catastrophic ligament
then it is clear that those parts will be the first to be loaded rupture (D). (From Frank CB: Ligament injuries: pathophysiology
and healing. In Zachazewski JE, Magee DJ, Quillen WS, editors:
if the ligaments ends are distracted suddenly with the joint Athletic injuries and rehabilitation, p 15, Philadelphia, 1996, WB
fixed at that angle of flexion or rotation. The relatively Saunders; adapted from Curwin S, Stanish WD: Tendinitis: its etiology
loose parts of the ligament will then become tight as the and treatment. Lexington, Mass, 1984, Collamore Press.)
32 SECTION I • Scientific Foundations

fibers in the ligament (for that joint position) have been

recruited. Yield and failure of the ligament then result Force and Displacement Ligaments Can Withstand,
from progressive fibril failure in the ligament. If loads Depend On:
are sustained, or if distraction continues to increase, the ● Size of ligament
amount of stress (force per unit area) on the remaining ● Age of individual
ligament increases dramatically as the number of fibrils ● Position of joint
present that can carry load drops. Catastrophic rupture
then occurs very quickly.
Most clinical tests of joints are really structural tests.
The joint is gripped and displaced in some direction,
and the examiner feels the stiffness of the joint (its resis-
tance to load) under those conditions. The ligaments
of the joint will be recruited to resist the force being
applied, depending on the position of the joint. The
feeling of stiffness that the examiner perceives is clearly
an aggregate of whichever ligaments (or parts thereof)
resist force in that direction (plus, of course, the con-
tributions to resistance of all nonligamentous tissues,
which may be considerable in some joints and some joint
positions). The examiner simulates forces that the joint
would encounter during function, hoping to reveal an
abnormally low stiffness of the joint in that plane of dis-
placement. Forces during a clinical examination are, of
course, very much lower than forces that the joint would
encounter during an injury (probably in the range of
about 10% of their failure loads). Clinical examinations
are therefore being conducted in what is known as the
toe region of a load–deformation curve for the joint
(see Figure 19-1).
To summarize, both joints and isolated ligaments
exhibit nonlinear load–deformation behavior. In the
case of isolated ligament tests, as the ligament ends
move apart, the ligament begins to take up a load.
With increasing distraction, the load increases slowly.
At some point, the amount of load increase in the liga-
ment is linearly proportional to the amount of displace-
ment. With further distraction, however, the ligament
begins to yield. Catastrophic rupture of the ligament
Figure 2-10
occurs. The amount of force and the amount of dis- Changes in knee ligament load-sharing patterns after a typical
placement that it takes to rupture any ligament depend injury with the knee at approximately 15° of flexion. The portions
on the size of the ligament (usually related to the size of the ligaments that are taut at the time of injury (see Fig. 2–2)
of the individual), the age of the host (ligaments reach are likely to be the first to rupture. Once the rupture has occurred,
neighboring portions of affected ligaments must assume load-bearing
peak energy-absorbing ability at the time of skeletal
responsibilities. Compare with Figure 2-2. (From Frank CB: Ligament
maturity), and the position of the joint when loads are injuries: pathophysiology and healing. In Zachazewski JE, Magee DJ,
applied (which determines how and when fibers in the Quillen WS, editors: Athletic injuries and rehabilitation,
ligament will be recruited).11,85,87–89 When entire joints p 16, Philadelphia, 1996, WB Saunders.)
are being loaded, the “load-sharing pattern” of liga-
ments under the conditions in which the load is applied
(direction, magnitude, and rate) determines which lig- Material Properties
aments or parts of ligaments will be damaged. Thus, The material properties of a ligament are those load–
the nonlinear load–deformation behavior of ligaments deformation behaviors that have been normalized for the
explains why the majority of joint injuries are actu- size of the ligament and for local changes in its length,
ally combined injuries, involving parts of a number of known as its stress–strain behavior. Stress is the amount
ligaments (Figure 2-10). of force per unit area in the ligament and is thus derived
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
by measuring cross-sectional areas and calculating force
(load being carried) per unit area of the ligament. Strain
is the change in length divided by the original length of
the part of the ligament being measured and is thus a very
localized measure. Like the load–deformation behavior,
the stress–strain behavior of ligaments is nonlinear, with
increasing material stiffness (known as the modulus of
elasticity of the material) as stress and strain increase.
Material measures allow ligament tissue to be com-
pared with other biologic materials (e.g., tendons)
or artificial materials and are generally of more inter-
est to researchers (who are trying to duplicate normal
ligament material behaviors) than to clinicians (who
are more interested in reproductive structural proper-
ties). A large amount of an inferior material can pro-
duce a structure with reasonable structural stiffness and
strength. The duplication of normal ligament material
behaviors,90,91 however, would allow structural behaviors
to be achieved with a replacement that is the same size
as the original.
Viscoelastic Behavior
Ligaments exhibit a combination of viscous and elastic
behaviors, besides having an interesting ability to change
the proportions of each behavior as conditions demand.
Being viscous means that the ligament behaves as though
it contains a thick fluid that is being squeezed through
a porous medium. Being elastic means that the ligament
has complete recoverability to its resting length after
being stretched (like an elastic band or a spring). The
combination produces a range of behaviors that lie on a
continuum between these two properties.92 The ligament
absorbs energy as it stretches and recovers in a nonlin-
ear way; at lower loads the viscous behaviors dominate,
whereas at higher loads elastic behaviors dominate. At all
levels of load, both behaviors can be measured, but dur-
ing clinical tests, viscous behaviors are so subtle that they
are usually not appreciated. As is discussed later, however,
they are likely to influence some clinical impressions of
joint laxity, particularly those due to changes in ligament
lengths or loads after different load histories.
When a ligament is pulled to a fixed length, a certain
amount of force is required. If the ligament is held at that
length, the amount of load in it decreases. This decrease
is due to the load relaxation (stress relaxation) of the vis-
cous component of that ligament. The ligament behaves
as if some component of the ligament adjusts to the new
length by flowing to a new location. This relaxation
behavior minimizes the amount of force in the ligament
within seconds to minutes (although the phenomenon
can continue to a lesser extent for hours to days); it has
clinical significance in that it is likely to be one means by
which the joint adjusts loads within a tissue to decrease
its chances of injury. The same behavior occurs with the
cycling of a ligament to a fixed deformation. The load
33
in the ligament decreases with successive cycles until the
load in the whole structure achieves a new equilibrium.
When a ligament experiences a fixed load, the liga-
ment length continues to increase, up to either a new
equilibrium or the point of ligament failure (depending
on the magnitude of the load), a behavior known as liga-
ment creep (increase in strain over time in a material
from the initial elastic strain, when the material is subject
to constant strain; Figure 2-11).20,93–95 Cyclic loading to
a fixed level similarly increases the ligament length. From
a clinical point of view, it can be seen that cyclic loading
of a joint during exercise will effectively alter the lengths
of the ligaments that were experiencing loads and hence
alter subsequent clinical impressions of their length (e.g.,
joint laxities). Fortunately, from a clinical point of view,
these adjustments in length are likely to be only a few
millimeters in normal cases and probably do not greatly
influence clinical impressions.
Nonetheless, the functional significance of viscoelas-
tic behavior is that ligaments demonstrate an amazing
ability to adjust their length (or intrinsic load) according
to actual loads or loading history. Adjusting the balance
between viscous and elastic behavior allows ligaments to
function within a fairly wide range of loads without being
damaged and probably contributes considerably to the
homeostatic balance of loads in all the joint tissues.
Effects of Aging
As with all connective tissues, all the aforementioned
structural, material, and viscoelastic properties of liga-
ments change as a function of age. In general, ligaments
reach their peak performance, in a mechanical sense,
shortly after the time of skeletal maturity (i.e., age 18 to
Figure 2-11
An idealized creep and creep recovery curve of strain (ε) plotted
against time. “Elastic” is used instead of “initial,” and thus includes
both viscous and true elastic responses. Ci, peak strain of the first cycle
in the cyclic creep test; Cf, strain at the end of the static creep test; Ri,
strain at the beginning of the recovery period; Rf, strain at the end
of the recovery period. (From Thornton GM, Boorman RS, Shrive
NG et al: Medial collateral ligament autografts have increased creep
response for at least two years and early immobilization makes this
worse, J Orthop Res 20:348, 2002.)
34 SECTION I • Scientific Foundations
20 years) owing to an optimization of their cellular and
matrix behaviors.85
Before skeletal maturation, ligaments are slightly
more viscous.96–98 These ligaments have smaller cross-sec-
tional areas and are thus relatively compliant (low stiff-
ness). Joints thus appear to be relatively loose on clinical
manipulation. At higher loads, insertions are common
sites of weakness because the ligaments are not yet firmly
cemented into bones.64,94,99 Insertions are thus common
injury sites in children.
After skeletal maturation, ligament cell metabolic func-
tions begin to slow, probably resulting in a less efficient
replacement of ligament substance over time. At this point,
ligaments reach their maximum size and structural stiff-
ness and are less viscous (more elastic) than their immature
counterparts. In middle age, both ligaments and bone inser-
tion sites begin to weaken, resulting in progressive losses in
structural strength. Ligament viscosity decreases further,
and the collagen in ligaments becomes more highly cross-
linked.100 Ligaments thus become even less compliant, and
joints appear to become tighter over time.
In old age, bones are usually more fragile than ligaments
and become clinically significant sites of weakness in joint
injuries. Ligaments lose mass, stiffness, strength, and
viscosity in the elderly. Probably because of decreasing
loads on the ligaments and decreasing activity levels in
the elderly, these changes in the ligaments are usually not
part of any obvious clinical problem. If joints deform as a
result of changes in bone shapes, however, and if ligaments
experience excessive loads as a result, ligaments may creep
excessively and contribute to pathologic joint laxities.
For a more detailed description of the effects of growth,
maturation, and aging on ligament properties, the reader
is referred to specific references on this topic.101–103
Sexual
Birth maturation
Optional factors
1 Pregnancy
2 Multiple pregnancies
3 Lactation
Sexual
maturation
Figure 2-12
Schematic of the potential gender-specific influences on musculoskeletal health across the life span. Note the different hormonal influences at each
stage of life for both males and females and the possible effects these could have on ligament function.
Influence of Hormonal Environment on Ligament
Regulation
Ligaments have been shown to express receptors for
hormones such as estrogen, progesterone, and andro-
gens.104,105 This information suggests the possibility
that ligament function in men and women could be
regulated in part by hormones, and that there might be
gender-specific aspects to such regulation. As depicted
in Figure 2-12, women and men experience different
“transition points” with regard to their hormonal envi-
ronment. Both males and females are exposed to hor-
mones in utero, and both go through puberty with
different hormones being elaborated. However, in
women, hormone levels cycle during sexual maturation,
and some of them cease after menopause. After sexual
maturation, ligaments of women could also be subjected
to unique hormonal influences during pregnancy both
quantitatively and qualitatively (i.e., relaxin).106,107 Thus,
ligaments in women and men are likely to be regulated
by hormonal variables in quite different manners, con-
tributing to gender-specific environments that affect
functioning of the tissues.
Evidence in support of the aforementioned possibilities
comes from both human populations and experimental
models. In humans, excessive ligament laxity (also called
benign joint hypermobility syndrome [BJHS]) is much
more common in women than men.108–111 The frequency
of BJHS in women versus men has been reported to be
5:1 in some studies, with some significant differences in
incidence between different ethnic populations. The inci-
dence also varies between women from different origins,
and in some families there appears to be a genetic com-
ponent112 responsible for the laxity that differs from those
Menopause Aging
Optional
1 HRT
Andropause (?)
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
responsible for Marfan’s and Ehlers-Danlos syndromes.
Some reports113 indicate BJHS may be due to altered reg-
ulation of normal genes rather than to alterations in the
coding sequences of gene products, whereas others are
focusing on other candidate genes that may be mutated
in the coding sequence.114,115 Interestingly, the extent of
the laxity can diminish during aging, and thus there is
an apparent interplay between the factors responsible for
BJHS and those involved in age-related changes such as
stiffness. A direct role for hormones in BJHS is yet to be
defined, but because the condition is more prevalent in
women, this possibility is viable.
A role for hormonal involvement in ligament laxity
has also been implicated in studies of ligament laxity dur-
ing different phases of the menstrual cycle and during
pregnancy. Although still somewhat controversial, several
reports116–119 have indicated that joint and ligament laxity
can change during different phases of the menstrual cycle
in a subset of sexually mature women. Laxity changes
have been noted between the follicular and luteal phases
of the cycle.119 The fact that such variation is evident
in only a subset of women may indicate that the hor-
monal influence is superimposed on some as yet unde-
fined genetic contribution(s). To date, the mechanisms
responsible for the menstrual cycle–dependent changes
in ligament laxity have not been defined. However, some
studies with ligament cells have indicated that somewhat
supraphysiologic concentrations of estrogen can influ-
ence collagen synthesis.120 The relationship of such find-
ings to the in vivo situation is uncertain because collagen
components of ligaments have usually been associated
with high-load behaviors of the tissues rather than low-
load behaviors and laxity, which have been ascribed more
to proteoglycans, and it is difficult to understand how
estrogen-induced changes in collagen synthesis could
relate to rapid changes in laxity during the menstrual
cycle.121 Whatever the mechanism, it is clear that it is
readily reversible and likely does not compromise over-
all functioning of the tissues. The reports that implicate
hormonal variation in ligament regulation also raise the
possibility that ligament regulation in women taking oral
contraceptives may also be influenced by those hormonal
“supplements.”122
Ligament and joint laxity also has been reported to
vary during pregnancy. In humans, a number of joints
and ligaments can be affected,123,124 and not all women
are affected to the same degree (again indicating involve-
ment of a potential genetic component). In the study by
Schauberger and colleagues,123 the changes in laxity did
not correlate with serum relaxin concentrations, but such
observations do not eliminate a role for this pregnancy-
associated hormone in the phenomenon. Somewhat
reversible changes in knee ligament laxity have also been
reported in experimental animals, such as in the rab-
bit MCL, during pregnancy 4 (Hart, Frank, and Shrive,
35
unpublished observations). These changes were accompa-
nied by changes in messenger RNA (mRNA) expression
patterns in cells in knee ligaments,125,126 but an association
between specific changes in gene expression and laxity
could not be deduced. Interestingly, in the postpartum
period, the molecular changes did not revert to the pre-
pregnancy levels, possibly indicating that the ligaments
did not return to the prepregnancy state, findings con-
sistent with anecdotal reports from human populations.
Thus, ligament function in women who have been preg-
nant one or more times may be regulated differently than
in women who have never been pregnant.
Although there are still many details to be worked out
with regard to hormonal influences on regulation of liga-
ment function, it is clear that gender-specific factors affect
regulation of these tissues and the hormonal history of
ligaments is an important aspect of their functioning.
Effects of Immobilization and Exercise
Although the mechanisms are not clear, ligament
complexes are extremely sensitive to load and load his-
tory. Load deprivation (joint immobilization) causes a
rapid deterioration in ligament biochemical and mechan-
ical properties, partially because of atrophy (a decrease
in ligament mass), which causes a net loss in ligament
strength and stiffness.127–130 Experimental evidence sug-
gests that immobility causes a net shift in ligament cell
metabolism from a balanced (homeostatic) state or a net
anabolic (building) state to a more catabolic (destruc-
tive) state.131 A few weeks of immobilization causes the
ligament matrix to decrease in quantity. Ligament cells
also apparently produce inferior-quality ligament mate-
rial, which contributes to the structural weakening of
the ligament complex. Bone begins to resorb, causing a
focal weakness at the sites of insertion. The loss of liga-
ment complex strength with immobilization appears to
be exponential over time.132–134 Although there is only
slight weakening in the first few weeks, ligament com-
plexes that have been completely immobilized for peri-
ods of 6 to 9 weeks are only about 50% as strong and stiff
as normal controls.135,136 From a functional therapeutic
view, this implies that periods of joint immobilization
should ideally, for the sake of the ligaments at least, be
minimized.
Joint stiffness after immobilization is probably not
caused by ligament deterioration; in fact, ligaments are
less stiff after periods of immobilization. Joint stiffness is
probably caused by the binding together (cross-linking)
of the nonligamentous periarticular tissues. Joint stiffness
is not, therefore, a good index of ligament function after
immobilization because nonligamentous structures con-
tribute to this impression. In fact, true ligament function
cannot be tested for a long time in intact joints after the
remodeling of this nonligamentous tissue.
36 SECTION I • Scientific Foundations
Prevention of Atrophy Caused by Immobilization
To date, it is not clear how much movement is required
to maintain normal ligament behavior. If ligaments were
analogous to bone, only a minimal number of cyclic
loads (e.g., only a few cycles of a joint per day) would be
required to maintain baseline ligament behaviors.90–92
Recovery from Immobilization
Experimental evidence suggests that different parts of the
ligament complex recover at different rates after a signifi-
cant period of immobilization.135,137,138 The bony inser-
tions appear to recover more quickly than the substance
of the ligament itself. The former occurs in a period of
weeks after the removal of immobilization. The recovery
of the latter occurs over many months (Figure 2-13).
It is not clear what dose–response relationship may exist
between the recovery of ligament behavior after immo-
bilization and the exercise protocol used. Presumably
there is some, as yet undefined, optimal amount of load
or optimal number of loading cycles that would, in turn,
optimize the metabolic recovery of ligament cells in each
ligament. Until this information is available, the proto-
cols for joint recovery must remain empirical.
Effects of Exercise
Ligaments respond to joint exercise by becoming slightly
stronger and stiffer.139 In most cases, however, ligaments
receive the minimum amount of mechanical stimula-
tion necessary for them to maintain a substantial base-
line (which appears to be roughly 80% to 90% of their
mechanical potential). Exercise, therefore, appears to
Figure 2-13
Schematic diagram illustrating ligament responses to immobilization
and exercise. (From Woo SL-Y, Gomez MA, Sites TJ et al: The
biomechanical and morphological changes in the medial collateral
ligament of the rabbit after immobilization and remobilization, J Bone
Joint Surg Am 69:1200–1211, 1987.)
have the potential to increase ligament strength and stiff-
ness by probably no more than an additional 10% to 20%
(see Figure 2-13). As with immobilization, the effects of
exercise may be ligament specific. A certain “window of
loading” is likely to be positive for each ligament, whereas
loads outside that window (too much or not enough)
probably result in ligament deterioration.
Ligament Injury
Mechanisms of Injury
Based on the foregoing understanding of ligament struc-
tures and functions, it is now possible to provide a clearer
understanding of how ligaments are injured and how
clinical diagnostic methods work (or fail to work).
In any particular position of any joint, it should be clear
that parts of several ligaments around that joint are likely
to be in a taut state. In other words, a certain proportion
of specific ligament fiber bundles will have been recruited
and will be somewhere within the relatively linear por-
tion of their load–deformation curve (see Biomechanical
Behaviors, earlier). Because ligaments share loads around
the joint to maintain a mechanical equilibrium, it is
unlikely that only one ligament will be loaded at any
point in time. If an extrinsic load is then applied to the
joint (e.g., a twisting injury to a knee joint), the tight
(loaded) portions of those restraining ligaments absorb
the greatest amount of energy. They will deform past
their elastic (recovery) limit and fail. Other fibers in those
structures simultaneously become recruited into tension.
Depending on how far the bones are allowed to displace
(from the forces being applied and resistance of other
periarticular structures, e.g., muscles), a certain propor-
tion of several ligaments will be damaged. The ligament,
the primary restraint to a force being applied (e.g., the
MCL is the main restraint to a valgus knee force), will be
the primary structure damaged. Secondary ligamentous
restraints will be damaged to a lesser degree. It is there-
fore unlikely for a truly “isolated” ligament injury ever to
occur. There is often some (possibly minor and subclini-
cal) damage to other ligaments around a damaged joint,
which should be sought in a careful history and physical
examination. More than one ligament may be partially
torn while the functional part of one anatomic structure
is completely torn.
Ligament “sprains” must therefore be reevaluated
in this context. Ligament injuries have historically been
graded according to the severity of a tear, grade I being
an incomplete tear (no joint instability noted), grade
II being a more significant tear that is not complete
(some instability), and grade III being a complete tear
(complete instability). The grade III case, almost by
definition, involves the tearing of multiple ligaments,
making joint instability obvious on clinical examination.
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
Some structures are likely to be partially torn in these
types of instabilities (structures that were secondary
restraints to the injury forces). Grade II injuries, which
also have some obvious clinical instability, may be due
to complete tearing of one structure (e.g., the MCL)
plus incomplete tears of other structures (e.g., capsu-
lar ligaments or ACL). Alternatively, instability could
be due to only partial tears of several structures, which
may have a different clinical prognosis than the previ-
ous scenario. Grade I injuries are the most difficult for
the clinician to detect. It is possible that ligaments have
been damaged so minimally that the joint is not clini-
cally unstable. On the other hand, it seems possible that
some of these injuries are simply not being examined in
the right way with respect to joint position or direction
of force, causing a latent instability to be missed. It is
possible that these types of injury become the chronic
instabilities that are so often seen clinically. A high index
of suspicion and a very careful examination will prob-
ably lead to further refinements in defining ligament
injuries in all joints.
The fact that partial ligament injuries are likely to
be very common has one extremely important clini-
cal consequence—clinicians must be aware that partial
injuries are common and that they must be extremely
careful in examining a joint to discover them. The most
important principle in this regard is that the joint will
be unstable only in the position in which it was injured.
A knee that was injured with the knee flexed at 20° is
therefore likely to be unstable (i.e., the ligaments will
not provide normal resistance to forces) only in that
degree of flexion and in the direction in which the
injury forces were applied. This is the basis on which
the Lachman test140,141 has proved to be a much more
sensitive test for torn ACLs than the anterior drawer
test. The former tests the knee at the degree of flexion
in which most knees are injured (slight flexion). Few
knees are ever injured at 90° of flexion (the anterior
drawer position). In fact, the portion of the ACL that
is taut at 90° of flexion142 is often uninjured in most
first-time knee injuries, and knees will still be stable in
that position when tested clinically. The clinician should
also be aware that a second injury often “finishes off”
a ligament (e.g., the remaining part of the ACL) if it
has become the main restraint in the direction needed
to pathologic bony displacement. Prevention of second
injuries should therefore become the focus of treatment
by attempting to protect the joint within its range of
stability during, and subsequent to, its healing.
When testing ligaments, always test them in the position in which
they have been injured
37
This principle is almost certainly true of all joint inju-
ries and is based on the knowledge that individual liga-
ments (as perceived anatomically) do not have single,
simple functions.
Gender-Specific Factors in Ligament Injuries
and Response to Injury
Earlier discussion in this chapter indicated that the
hormonal environment can affect ligament functioning,
and thus gender-specific aspects to ligament regulation
likely exist. That such hormonal variation appears to con-
tribute to risk for ligament injuries is a further extension
of that impact. Several reports have indicated that female
athletes experience a much higher rate of non–contact-
initiated ACL injuries than do male athletes participating
in the same sports at the same level.127,143–145 Additional
studies have again indicated that the incidence of such
injuries does not occur randomly across the menstrual
cycle.127,146,147 Although some of the knee ligament inju-
ries may in part be due to anatomic considerations, and to
a running and cutting maneuver style that is correctable,
the fact that changes in hormonal levels have been impli-
cated indicates that such fluctuations contribute to the
risk environment.145 Furthermore, individuals with BJHS
are at greater risk for knee and ligament injuries, likely
because of the ligament laxity and possibly proprioceptive
and other considerations.148 Whether such injury risk is a
general feature of the condition or whether women with
BJHS also exhibit further menstrual cycle–dependent
variation in laxity is as yet unknown, but if so, this would
certainly impose further risk for injury.
Interestingly, there are no reports of increased inci-
dence of ligament injuries in pregnant women with
altered ligament laxity. This may be due to altered pat-
terns of activity during later stages of pregnancy, but
many women continue high levels of activity during the
early stages of pregnancy without an apparent increased
risk for ligament injuries. There are a few reports of
pregnancy affecting the response to ligament injury and
reconstruction. In a rabbit model, it was found that preg-
nancy did affect cells in the healing ligament, but the
experimental protocol did not allow for conclusions to be
made regarding the long-term impact of the pregnancy
on the functioning of the healed tissue. In a case study,
it was reported that pregnancy affected the laxity of a
reconstructed ACL, but again, no long-term impact on
the functioning of the autograft was reported. Because
the reconstructed ACL likely undergoes a process not
unlike that occurring in a healing ligament,149 long-term
follow-up of such individuals may be warranted because
many younger women of childbearing age are having
their damaged ACLs reconstructed.
Although there is a relative paucity of information
regarding the mechanistic basis for the relationship
38 SECTION I • Scientific Foundations
between risk for ligament injuries and gender-specific
variables, it is clear from a variety of studies that inflam-
matory processes, and by extension healing processes,
differ in sexually mature women and men, and such dif-
ferences are affected by menopause in women.150,151 Thus,
it is very likely that the response to ligament injuries will
exhibit some gender-specific aspects. Whether these dif-
ferences would affect the rate of healing or the quality of
the healed tissue remains to be elucidated.
From the preceding discussion, it is fairly clear that
gender-specific and hormone-related variables affect
both the risk for ligament injuries as well as potentially
the response to such injuries. Much of the basic science
associated with identifying the mechanistic basis for both
the risk for injury and the response to injury, as well as
how to manipulate it, remains to be investigated.
Phases of Healing
Bleeding and Inflammation
When ligaments tear, there is immediate local pain
(because of pain fibers in the ligament) and bleeding
(because of tearing of vessels in and around the ligament).
As with bleeding anywhere, an immediate inflammatory
response is initiated. With extra-articular ligaments,
bleeding occurs into a subcutaneous space, where tam-
ponade can ensue. With intra-articular ligaments (e.g.,
cruciate ligaments), bleeding proceeds unchecked into
the joint space until either clotting occurs spontaneously
or pressure builds to the point that ligament vascular
pressure is exceeded and tamponade also occurs. The
next steps are, to some extent, ligament and environ-
ment specific.
In all cases, platelets promote clotting. A fibrin clot is
deposited and substances (growth factors) are released
that promote an inflammatory cascade. Local vessels
dilate, acute inflammatory cells infiltrate, and fibroblas-
tic scar cells begin to appear. The first phase of ligament
healing, lasting for hours to days, comprises this acute
cascade of events.
Stages of Ligament Healing
● Bleeding
● Inflammation
● Proliferation of bridging material (production of scar matrix)
● Matrix remodeling
Proliferation of Bridging Material
The second phase of ligament healing involves the produc-
tion of scar matrix.127 Unfortunately, there is no evidence
that normal ligament matrix can be produced during this
phase of healing, for any ligament. Different quantities
(and possibly qualities) of scar matrix can be produced
(which can be altered by different therapies, as discussed
later), but there appears to be some fundamental inability
for completely disrupted ligaments to regenerate normal
ligament matrix. Thus, the proliferating scar fibroblasts
(whose source remains unknown, but probably involves
some combination of local fibroblasts and the differen-
tiation of circulating cells, e.g., macrophages) become
the local workers, attempting to produce a new bridging
matrix for the torn ligament. Inflammatory cells simul-
taneously remove damaged ligament and clot debris and
attempt to leave only a dense scar matrix in place of the
gap in the ligament.
The gap in extra-articular ligaments (e.g., the MCL)
probably becomes filled with a very viscous scar matrix
within days. The scar progressively becomes less viscous
and more elastic over several weeks as inflammation
decreases.
Contrary to popular belief, which seems to hold that
the ACL is incapable of any healing response, scar tissue
is apparently produced in many ACL injuries. Based on
observations, bridging scar appears to occur frequently
between the torn ACL and the posterior cruciate liga-
ment (PCL), or between the torn ACL and some other
location in the intercondylar notch in the joint.152
Unfortunately, the scar tissue appears to arise in func-
tionally useless locations and probably often involves the
same inferior-quality scar that is found in extra-articular
ligament healing. The combination of inferior-quality
material in the wrong position in the joint likely explains
the high incidence of failure to heal in the ACL. The
principle, however, is that in this phase of healing, healing
material must connect torn ligament ends to the correct
anatomic locations. The failure to reconnect appropri-
ate locations on bones (i.e., between the anatomic inser-
tions that were presumably optimized by nature for that
ligament) is one cause of healing failure. The failure to
produce enough scar is a second cause of failure (i.e.,
the scar tissue is structurally inadequate). The third cause
is the failure to produce the correct material (probably
the cause of failure in ligaments that have been surgically
repaired).
Matrix Remodeling
The third phase of ligament healing is matrix remodeling.
Once bridging has occurred, the scar matrix contracts,
becomes less viscous, and becomes both denser and more
highly ordered. Defects in the scar (e.g., debris, fat cells,
loose matrix, hypercellular inflammatory areas, and areas
without matrix) are filled in.153,154 Although ligament
scar matrix becomes more ligament-like with time, it still
has some major differences in composition and architec-
ture.155–157 Improvement in scar quality occurs over time,
depending on a variety of factors, including, for example,
joint motion.
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
For those interested in more detailed reviews of the
morphological, biochemical, metabolic, and biome-
chanical events that occur during ligament healing in
experimental models of healing, some specific articles are
recommended.158–162
Diagnostics
Two new methods to evaluate ligament physiological
function or biomechanical/kinematic outcomes have
recently been reported.163–168 The physiological function
measures blood flow to intra-articular tissues, whereas
the biomechanical/kinematic methodology describes
knee joint motions with ACL deficiency/reconstruction.
Although these methods are in the development stage,
future applications could include determining healing
potential of tissues with blood flow measures and evalu-
ating techniques for ACL reconstruction.
The new method used to measure blood flow in joint
structures is called endoscopic laser speckle perfu-
sion imaging (eLSPI).166,168 The eLSPI method is an
adaptation of laser Doppler imaging that allows quicker
resolution times that are also more sensitive to hyper-
emic responses in joint structures after reperfusion of
the joint with release of a tourniquet.167 Studies of rab-
bit joint capsule show a linear response in blood flow
detection from 0 to 800 µL/minute, with high resolu-
tions and rapid response rates.168 Occlusion of the fem-
oral artery decreased blood flow by 59% in the rabbit
knee MCL.168 One study in human knees using eLSPI
found that changes in perfusion were detected in the
synovium, medial meniscus, and medial femoral condyle
with tourniquet occlusion of blood flow and reperfusion
after tourniquet release, and in response to increasing
Figure 2-14
Endoscopic laser speckle perfusion images of the human knee showing blood flow. A, Standard endoscope image with color camera.
B, Corresponding color-coded perfusion image showing low flow to the avascular central zone of the meniscus and higher flow to the
vascular zone at the perimeter. (Image courtesy of Dr. R. B. Bray, Dr. K. R. Forrester, and C. Leonard, University of Calgary, Alberta,
Canada.)
39
concentrations of epinephrine (a vasoconstrictor) in the
arthroscopic fluid166 (Figure 2-14). The measures in the
human knees were relative measures, and further work is
required to obtain more quantitative values.
Several investigators are using different methods
and models to evaluate the results and techniques of
ACL reconstruction. The various methods use markers
attached to the femur and tibia. In a sheep model, the
group headed by Tapper and colleagues169 use an optical
marker system attached to plates on the femur and tibia.
Knee kinematics and joint forces are measured before
and after ACL reconstruction. Future directions include
evaluation of ACL reconstructions and determination of
in situ ligament forces using robotic technology to repro-
duce kinematics obtained with the optical tracking sys-
tems.170 Tashman and coworkers165 have used high-speed
biplanar videoradiography to monitor implanted tanta-
lum bead movement in the femur and tibia of dogs. They
have monitored knee kinematics and moments before and
after ACL transection. In both animal models, kinemat-
ics and forces/moments about the knee remain abnormal
for up to 2 years.165,170,171 Tashman and coworkers163,164
have applied their high-speed biplanar videoradiography
system in humans (Figure 2-15). Tantalum beads were
placed in the tibia and femur bilaterally during unilat-
eral ACL reconstruction. Kinematic evaluation (run-
ning downhill on a treadmill) showed the reconstructed
knees were on average more externally rotated and more
adducted compared with the contralateral uninjured
limbs.164 The values of the differences were small (3.8° ±
2.3° for external rotation, and 2.8° ± 1.6° for adduction)
but consistent. A finite-element model of the lower limb
is being constructed from this work.163 These kinematic
measures offer the opportunity to gather data during
40 SECTION I • Scientific Foundations
Figure 2-15
Knee kinematics assessed with dynamic radiographic stereo-
photogrammetric analysis, using a high-speed biplanar radiographic
system configured for downhill treadmill running. Images are
acquired simultaneously at 250 frames/sec for the two views (60°
separation). (From Tashman S, Collon D, Anderson K et al: Abnormal
rotational knee motion during running after anterior cruciate ligament
reconstruction, Am J Sports Med 32:977, 2004.)
more functional activities (e.g., walking, running), but
the work is preliminary and requires further investigation
before they are introduced in everyday clinical practice.
Effects of Various Treatments on Ligament Healing
From a clinical point of view, to be effective, treatments
must both improve joint function and decrease second-
ary disability caused by ligament injuries. Unfortunately,
the quantitative proof that any treatment results in true
improvement of either of these areas is plagued by the
lack of quantitative assessment tools, the myriad of
clinical variables that can influence the natural history
of healing in any individual case, and the unknown
contributions of other structures (which can compensate
to variable degrees) in the healing process. The reader
should therefore not have any false illusions. To date,
there is no clear picture of what any treatment truly
does in a clinical setting. At best, there are general ideas
about what some commonly used clinical modalities do
to alter the healing processes of ligamentous tissues in
some circumstances. These have been derived using ani-
mal models under certain boundary conditions and with
some very specific markers as indices of improvement.
Based on the foregoing discussions of ligament structure
and function, it should be appreciated that ligaments
have many structural elements, a complex composition
and organization, and a complicated mechanical behav-
ior. Further, they never act in isolation in a joint. Only a
few of these features can be studied in any experiment,
and none should be portrayed as the most important
characteristic of the ligament. In other words, the reader
should be cautioned that any given parameter (e.g., liga-
ment strength), although important, may not be the most
important outcome measure. Similarly, collagen content,
or types of collagen present, may not have any functional
meaning. Because one cannot say which behaviors are
most important, discussions usually revolve around how
“healing is different from normal.”
The current understanding of experimental effects of
various therapies on ligament healing is summarized in
the following, but the reader is cautioned to be critical
of this interpretation and should refer to other sources
for a more in-depth appreciation of this very complex
subject.4,6,172–174
Immobilization
The immobilization of an injured joint almost certainly
decreases the load and load history of injured ligaments
in that joint. As noted previously, immobilization has
detrimental mechanical effects on noninjured ligaments,
making them weaker and less stiff. This is a long-lasting
effect that takes months to reverse after remobilization.
The effects of immobilization on the other tissues in
the injured joint should also be considered. Long-term,
rigid immobility has been shown to have detrimen-
tal effects on diarthrodial joints.175 Cartilage surfaces
become damaged, bones atrophy, and the joint becomes
fibrosed (stiffened). A joint that has been destabilized
owing to a significant ligament injury appears to undergo
other types of damage. Bones form osteophytes; cartilage
fibrillates, then erodes; and the joint becomes inflamed.
These changes are known as osteoarthritis.176 In fact,
certain ligament deficiencies, such as ACL deficiency,
have been used to produce osteoarthritis in animal mod-
els.177,178 In these cases, joint immobilization has some
beneficial effects. Short-term periods of immobilization
decrease these osteoarthritic changes.178 If the joint does
not move, it appears to be kinematically stable and is
thereby relatively protected. Presumably, the detrimental
effects of immobilization are present, but they do not
appear to be as rapid or as destructive as those seen with
instability in the same models. It is not known whether
there are any long-term protective effects of such immo-
bilization on the joint surfaces once these unstable
joints are remobilized because these experiments, to the
authors’ knowledge, have not yet been performed. It can
be assumed, however, that if the period of immobility
does not facilitate increased stability of the joint (e.g.,
allow the damaged structure to heal, or produce some
compensatory net stiffening of other structures), the
instability will subsequently cause osteoarthritis as well.
The immobilization of ligament scar tissue appears
to inhibit scar mass and scar quality.155,179 Scars in legs
that have been immobilized are thus smaller, structurally
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
weaker, and less stiff than are larger scars from knee
joints that have been allowed to move (Figure 2-16).
Immobilized scars are also less viscous (relax less), creep
more, and are materially weaker than their nonimmobi-
lized counterparts.93,180 At equal points in time, these scars
are therefore less able to resist stresses without straining.
They would, presumably, be more subject to subsequent
reinjury at comparable levels of load or deformation on
the joint.
The biggest unknown regarding ligament immobi-
lization (or exercise) is the effect on ligament length.
Ligament length refers to the amount of bone defor-
mation that must occur in the normal plane of the liga-
ment in question before that ligament takes up any load.
This would correspond to the clinical term laxity. It is
clear that in certain joint instabilities, healing ligaments
are effectively much “longer” than their normal coun-
terparts. In the combined MCL/ACL-deficient rabbit
knee, for example, the healing MCL is initially much
more lax.178 Immobilizing the joint during the early
phase of healing prevents this laxity and may thus con-
fer some degree of low-load stability to the knee. On
the other hand, it simultaneously prevents scar mass and
inhibits scar qualities that would allow that MCL scar to
resist higher loads. On balance, it would appear that this
Figure 2-16
New Zealand white rabbit medial collateral ligament scars subject
to immobilization (A) and exercise (B). Note that the scar from
the immobilized ligament is small compared with the scar from
the exercised ligament. (From Frank CB: Ligament injuries:
pathophysiology and healing. In Zachazewski JE, Magee DJ, Quillen
WS, editors: Athletic injuries and rehabilitation, p 21, Philadelphia,
1996, WB Saunders.)
41
short-term benefit does not compensate for the resultant
disability. This appears to be borne out by clinical stud-
ies, which have thus far failed to show that immobilizing
MCL/ACL-injured joints provides any long-term ben-
efit to the outcome.181 This clearly remains controversial,
however, and is worthy of further investigation.
Exercise
As with normal ligaments, exercise has some powerful
influences on ligament scars. Joint movement during
ligament healing definitely has some beneficial effects on
the joint tissues, the uninjured ligaments, and the healing
ligament as long as forces on the healing tissues are not
too great. What force is too great, however, is unknown.
Further, it is not clear in most cases how loads on healing
ligaments can be modified, because it is not even clear
how much load a normal ligament carries in a joint, let
alone when it or some of its load-sharing partners have
been damaged.
The current concept is that very low cyclic loads on
a ligament scar promote scar proliferation and material
remodeling, thus making the scar stronger and stiffer
structurally160,173 and, possibly, materially. As far as is
known, the definitive experiment demonstrating that the
loading of a ligament scar can accelerate either the rate
of its material improvement or achievement of its mate-
rial end point has not yet been carried out. It has been
shown, however, that animals that are presumably more
active during healing (dogs) form better-quality scars
in collateral ligaments than do less active animals (rab-
bits).182,183 Canine MCL scars apparently can reach 75% of
normal material strength, whereas those in rabbits appear
to reach their peak at 30% to 40% of normal. If these dif-
ferences are real and if they are due to joint movement,
there is experimental support for controlled motion dur-
ing ligament repair. Loads can presumably be increased
slowly as the stiffness of ligament scars increases, in terms
of load-resisting ability, for several months after injury.
Until the limits of load are defined, and until loads
on ligaments of interest in the clinic can be determined
under both normal and pathologic (injured) conditions,
the current empirical forms of controlled motion should
probably still be used.184–187
Ice and Heat
Based more on clinical than experimental evidence, it
appears that the use of ice immediately after ligament injury
decreases bleeding, swelling, and inflammation.188–190 This
is certainly helpful in minimizing the masking signs of pain
and swelling. The inhibition of inflammation may also
limit secondary damage to the other joint structures,
which may decrease secondary stiffness of the joint if
periarticular scar formation is inhibited.
The effects of ice on scar formation are unknown. If scar
mass depends on inflammatory mediators, ice-mediated
42 SECTION I • Scientific Foundations
scar inhibition may also inhibit the structural maturation of
a ligament scar. Bleeding and inflammation may be impor-
tant to the healing process itself. As with many aspects of
therapeutic intervention, this requires further study.
The anecdotal and experimental results suggesting
that ice can be used to manipulate blood flow to a tis-
sue191 could be invoked to suggest that ligament healing
may be influenced through that mechanism, even during
the chronic phases of healing. This has not been stud-
ied in ligaments, and it remains unknown whether blood
flow is a limiting factor in their healing at all.
The same holds true for heat. In the short term, heat
increases inflammation, swelling, and blood flow. It is
not known what the consequences are of these changes
on the quality or quantity of ligament healing. Similarly,
the effects of ultrasound on scar tissue remain controver-
sial and require further study at both the basic and clini-
cal science levels.192–196
Surgical Repair
The surgical repair of torn ligament ends has been noted
in the past to induce faster and stronger healing through
a process that was likened to regeneration rather than scar
formation.197,198 Subsequent work, however, has shown
that even in cases in which ligament ends are surgically
apposed immediately, scar tissue still forms between the
ends and may or may not withstand subsequent loads. In
the case of the ACL, such reapposition usually fails, both
in the clinic and experimentally.198–201 In the case of the
MCL, apposition of ends makes the MCL complex slightly
stronger and stiffer at comparable points in time,91 but it
does not cause true regeneration. Even in this best-case
scenario (immediate overlapping repair of a Z-plasty cut
in an extra-articular rabbit ligament), the complex recov-
ers only to approximately 80% to 90% of normal structural
strength. Larger gaps in the rabbit model cause a relative
weakness of the MCL complex owing to the increased
prevalence and size of defects in the scars.153 These defects
(see Phases of Healing, earlier) are removed over time but
cause bigger scar gaps to be weaker than smaller ones for
the first few months of healing.91
If repair could be shown to restore immediate nor-
mal joint kinematics while the scar forms and remodels,
it would probably be an advantage. However, because
repairs are unlikely to provide enough initial tensile
resistance, this is seldom the case. Further, because it
appears that in most cases (at least for most extra-articu-
lar ligaments) ligament ends are likely to be in reasonable
apposition, repair is probably not justifiable for the small
degree of structural improvement that gap minimization
would create.
In situations in which gaps are known to be large
(e.g., if ends are seen to be far apart on a magnetic
resonance imaging scan), in which large forces may main-
tain a ligament gap (e.g., arm weight distracting ends of
coracoclavicular ligaments), or in which a large anatomic
gap may exist (e.g., the ACL), the surgical repair of liga-
ment ends may be justified. Because it appears that, in
at least some cases, scars are capable of contracting to
minimize joint laxity202 and most of the foregoing condi-
tions occur only rarely, the operative approach to repair
of ligaments should probably remain restricted.
Surgical Replacement (Grafting)
There has been a great deal of work on the surgical
replacement of ligament complexes with both nonbio-
logical (i.e., artificial) and biological (i.e., tendons, fascia)
substances.203 It is beyond the scope of this chapter to
review all these results. A few points, however, are worth
making.
No ligament replacement has ever been shown to
restore normal function totally. Most replacements
have been aimed primarily at restoring ligament com-
plex strength or stiffness and secondarily at restoring
low-load behaviors such as joint laxity. None has been
aimed at restoring viscoelastic behaviors, and none has
even begun to look at the possibility of restoring pro-
prioceptive functions. Even the most successful ligament
replacements have achieved only 80% to 90% of normal
ligament strength and stiffness under optimal circum-
stances.152–155 The best replacements of the ACL in ani-
mals have achieved only approximately 50% of normal
ACL strength, even after many months of healing.156,157
Ligament grafts, if performed acutely and if fixed
with adequate means to ensure immediate joint motion,
offer a distinct advantage in facilitating healing of the
joint according to the principles espoused previously. If
the graft controls joint kinematics in the same way as its
damaged predecessor did, and if the joint can be cycli-
cally loaded within the window of acceptable forces after
the replacement, joint healing will presumably be facili-
tated. The potential advantages and disadvantages of this
approach are, of course, the subject of many ongoing
investigations.158–160,201
Current Directions in Ligament Healing
Recent biological approaches to improve ligament repair
or ligament graft healing have used growth factors and
gene therapy. Some of these investigations have com-
bined the approaches, so these approaches are considered
together here. This section begins with growth factors
and then progresses to gene therapy.
Growth factors are molecules that modify cell prolif-
eration or secretion of proteins (matrix, other growth fac-
tors). It has been shown that various growth factors, such
as platelet-derived growth factor-BB, transforming growth
factor-β, and epidermal growth factor, modify fibroblasts
isolated from intra-articular (ACL) and extra-articular
(MCL) ligaments.204–206 Several studies have evaluated the
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations
effects of growth factors on ligament repairs or ligament
reconstructions using animal models.207–213 The outcomes
reported have been largely biomechanical and histologic.
The results have been variable, such that certain biome-
chanical parameters were improved whereas others were
unchanged,207,211 or there were no improvements in some
studies.213,214 The effects of the growth factors were dose
dependent in some studies,209,211 but there was no effect
of dose in others.213 Histologically, the alignment of colla-
gen was altered on light microscopy, as were the collagen
fibril diameters on electron microscopy.207–209 Studies of
ligament graft incorporation in bone tunnels have shown
beneficial effects using bone morphogenetic protein
(BMP)-2.210 Interestingly, intramuscular administration
of BMP-13 leads to the formation of ligamentous and
tendinous tissue in the muscle.212
An all-encompassing characterization of growth factor
effects on ligament healing or grafting is not possible; the
most that can be said at this time is that growth factor
application can modify ligament repair or graft replace-
ment, but several influences in this process are unknown
and likely contribute to the variable results reported
so far. These influences include type of growth factor,
dose, method of administration, the complex milieu of
the healing/remodeling environment, the ligament in
question, biomechanical loads on the healing environ-
ment (isolated versus combined ligament injuries), and
other factors unknown at this time. The issue of delivery
serves as a connection between growth factors and gene
therapy.
Gene therapy refers to the modification of the genetic
expression of cells. Several recent reviews go into more
depth on the subject, and several highlights are empha-
sized here.215–217 Gerich and colleagues218 tested several
viral vectors on fibroblasts from the rabbit MCL, ACL,
Antisense treatment
Antisense oligonucleotide
Antisense binds to mRNA
Breakdown of mRNA
No translation into protein
43
and PCL, showing that these cells were susceptible to
genetic manipulation using these vectors. Several different
groups have shown that marker genes can be expressed
in the MCL and ACL of rabbits and mice.219–221 The first
growth factor delivery using gene therapy to enhance
ligament healing was by Martinek and coworkers,210 who
showed that delivery of BMP-2 improved soft tissue inte-
gration of semitendinosus grafts in bone tunnels used for
ACL reconstructions in a rabbit model.
Other strategies have been used to modify ligament
healing with gene therapy. Oligodeoxynucleotides
(ODN), segments of DNA approximately 15 to 25 base
pairs long, have been synthesized that modify translation
of mRNA to protein217,222,223 (Figure 2-17). One method
of doing this is to conjugate the ODNs to lipids and then
encase these lipid vesicles with an inactivated virus, which
can then be delivered to the target tissue (Figure 2-18).
This strategy can be used to overexpress or underexpress
proteins with the ODN method. There are several other
methods for achieving the same result (see Figure 2-18).
In ligament, blocking or decreasing expression of mol-
ecules with antisense ODNs is promising. Two groups
have shown decreased expression of decorin and type
V collagen, two molecules whose increased expression
has been associated with decreased collagen fibril diam-
eters.222,223 It was shown in a rabbit MCL repair model
that antisense decorin gene therapy was associated with
a return to more normal matrix histology (Figure 2-19)
and the reversal of small fibril diameters (Figure 2-20)
to a more normal bimodal distribution of collagen fibril
diameters222 (Figure 2-21). Antisense decorin therapy
also improved biomechanical measures, including less
creep at lower loads and increased peak failure forces.222
Growth factors and gene therapy offer new biological
methods to enhance ligament repair or reconstruction.
mRNA
Normal
Ribosome
Figure 2-17
Schematic diagram depicting antisense
strategy using oligonucleotides (ODNs)
as the intervention in messenger RNA
Translation into protein translation.
44 SECTION I • Scientific Foundations

ATGCTATG ATGCTATG ATGCTATG

HVJ liposomes Catonic lipids Adenovirus

Figure 2-18
Schematic diagram depicting methodologies that can be used to facilitate antisense oligonucleotide (ODN) delivery to the cell nuclei of ligament
scar fibroblasts, where they can couple to the sense messenger RNA (mRNA) strand and block mRNA translation. Examples of transfection
strategies include hemagglutinating virus of Japan (HVJ) liposomes, cationic lipids, and adenovirus preparations that can be injected into early
ligament scars by hypodermic syringe with a repeater assembly using an injection grid overlaid on the ligament scar area. (Courtesy of Dr. Paul
Sciore, University of Calgary, Alberta, Canada.)

Work remains to determine the best method of delivery
as well as the length and timing of the delivery, and to
understand better the healing environment. It is clear that
growth factors and antisense gene therapy have multiple
effects in a healing environment characterized by many
metabolic systems with some degree of redundancy.224
Thus, a specific intervention focused on one molecule
may have multiple (unforeseen) effects. Other directions
use gene therapy, cells, and growth factors to engineer
replacement tissues or scaffolds for later implantation to
replace missing or dysfunctional tissue.216,217,225 An area of
interest currently receiving a great deal of attention is the
use of mesenchymal stem cells, specialized adult cells that
have the potential to differentiate into various mesenchy-
mal lineages, including ligaments.226 These cells continue
to be the focus of cell-mediated gene therapy for skel-
etal tissue regeneration, where they could be engineered
to express and respond to growth factors in vivo and
 CHAPTER 2 • Ligament Injuries: Pathophysiology, Healing, and Treatment Considerations 45

A C E G

B D F H
Figure 2-19
Hematoxylin and eosin staining of normal medial collateral ligament (A), 6-week injection control scar (C), sense-treated control scar (E), and
antisense-treated scar (G). B, D, F, H are polarizing microscopic images in the corresponding fields to A, C, E, and G, respectively. Relatively
well-aligned collagenous matrix (G) with limited but distinct restoration of crimp pattern (H) is observed in the antisense-treated scar, whereas
only disorganized collagenous matrix with a microcrimp pattern is observed in the injection (C and D) and sense-treated (E and F) control scars
(original magnification, ×250). (From Nakamura N, Hart DA, Boorman RS: Decorin antisense gene therapy improves functional healing of early
rabbit ligament scar with enhanced collagen fibrillogenesis in vivo, J Orthop Res 18:519, 2000.)

A B

C D
Figure 2-20
Transmission electron micrographs of normal medial collateral ligament (A), sense-treated control scar (B), 6-week injection control scar (C), and
antisense-treated scar (D). Both the injection control and sense-treated scars contained only small-diameter collagen fibrils, whereas the antisense-
treated scar contained larger-diameter collagen fibrils, some of which were of comparable size to those in normal ligament (original magnification
×30,000).
46 SECTION I • Scientific Foundations
70
60
50
Relative frequencies (%)
40
30
20
10
0
0-25 25-50 50-75 75-100
Figure 2-21
Distribution of collagen fibril diameters in normal medial collateral ligaments, 6-week injection and sense-treated controls, and antisense-treated
scars. Note the shift in fibril diameter sizes in the antisense-treated scars (circled graph area) to larger fibrils over 125 nm in diameter. This shift is
not seen in the injection and sense-treated scars.
possibly to differentiate into skeletal specialized cells that
could actively participate in tissue regeneration. Perhaps
in the future the patient could become the donor for his
or her own engineered replacement tissues, but much
work remains to make this a reality!
Summary
Ligaments are biologically complex connective tissues
that are only beginning to be understood. They are het-
erogeneous both structurally and functionally, and many
share functions with other ligaments in any given joint.
Ligaments are metabolically active and are constantly
changing over time. Normal ligaments respond to their
environment, including the therapeutic modalities of
immobilization and exercise.
Ligaments are rarely injured in isolation, and it is com-
mon for different parts of ligaments to be damaged in a
joint injury. Ligaments do not regenerate when injured.
They appear to heal, when able, with variations in scar
tissue quality and quantity.
Ligament scars respond to therapeutic modalities.
Exercise and immobilization are powerful modifiers of
scar quantity and probably scar quality. Controlled joint
Normal MCL
Antisense treated
Sense control
Injection control
(n=6 for each group)
100-125 125-150 150-175 175-200 200-225 225-250 250-275 275-300
Fibril diameter sizes (nm)
motion, within a (yet to be defined) “window” of stress
on the healing tissues, appears to be the optimal way to
enhance ligament healing. Other modalities have more
speculative effects.
A great deal of clinical and experimental work remains
to be done before a scientifically rational approach to
therapy for all ligament injuries is possible.
Acknowledgments
The authors acknowledge the financial support of the
Canadian Institutes of Health Research (Institutes
of Musculoskeletal Health and Arthritis and Gender
Health), The Arthritis Society of Canada, the Alberta
Heritage Foundation for Medical Research, and the
Health Research Foundation. David A. Hart is the
Calgary Foundation Grace Glaum Professor. Cy B. Frank
is the McCaig Professor.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 226 references for this chapter.
 3
C H A P T E R

T ENDON P ATHOLOGY AND I NJURIES :

P ATHOPHYSIOLOGY , H EALING ,
AND T REATMENT C ONSIDERATIONS
Sandra L. Curwin

Introduction This chapter explores the structure, physiology, and

mechanics of normal and injured tendon, explains how
Tendons are important structures in the musculoskel-
tendons can be injured, describes the evidence support-
etal system. They transmit force between muscle and
ing different approaches to the treatment of tendon
bone1,2 and, when stretched, store elastic energy that
overuse injuries, and provides guidelines for the exercise
contributes to movement.3,4 They are relatively small
treatment of chronic tendon injuries. An ideal treatment
but are tremendously strong—perhaps half as strong
strategy will deal with the current injury, prevent its
as steel. Despite their strength, tendons do become
recurrence, and be cost-effective. The design of such a
injured. Some injuries are the result of accidents, such as
strategy requires knowledge and understanding of ten-
the severing of flexor tendons in the hand. More com-
don structure and function, changes after injury, and
monly, the gradual onset of pain and tenderness signals
the success rates and costs of various interventions. One
a lesser tendon injury. Various names have been used for
can then use this knowledge to successfully treat tendon
these injuries; the most common are tendonitis, tendi-
injuries. To avoid confusion, the term “chronic tendi-
nosis, and tendinopathy (these terms are defined later
nopathy” will be used when referring to chronic tendon
in the chapter). Tendon injuries can cause prolonged
injuries of uncertain onset and without obvious signs of
disability for the competitive client or worker and cre-
inflammation.
ate a dilemma for both clients and health profession-
als. Despite (or perhaps because of) advances in tendon
research since the mid-1990s, considerable uncertainty Structure and Function
remains about the pathophysiology of tendon injuries
Structure and Elements of the Tendon
and how best to treat them or even what name to use
to identify them. Junctions with Bone
Tendons are part of the connective tissue subcategory
called “dense, parallel-fibered connective tissues” that
Function of Tendon also includes bone and ligaments.1 Tendons are com-
posed of cells and extracellular matrix (ECM) and are
● Transmit force between muscle and bone unique because their behavior is determined primarily by
● Store elastic energy the amounts, types, and organization of their extracel-
lular components (in contrast with, for example, nervous

47
48 SECTION I • Scientific Foundations
tissue or muscle). While the details of the fine structure
of tendons may vary among species and even between
different tendons in the same animal,1,2,5 all tendons
are alike in attaching muscle to bone at each end of the
muscle. The tendon can thus be divided into three main
sections: (1) the muscle-tendon junction (MTJ), (2) the
bone-tendon junction (BTJ), and (3) the tendon mid-
substance. At most tendon-bone interfaces, the collagen
fibers insert directly into the bone, in a gradual transition
in material composition (over a distance of about 1 mm)
through four zones: tendon, fibrocartilage, mineralized
fibrocartilage, and bone.6–8 Some fibers join the bone at
an acute angle, blending gradually into the periosteum.6
The ultrastructure of most bone-tendon junctions is sim-
ilar, but they may vary widely in gross anatomic appear-
ance, from a flat aponeurosis to a rounded cord. The
structure of the bone-tendon junction is illustrated in
Figure 3-1.
Muscle-Tendon Junction
The muscle-tendon junction (MTJ) or myotendinous
junction comprises numerous interdigitations between
muscle cells and tendon tissue, like interlocked fin-
gers.9–12 This overlapping allows the terminal actin fila-
ments within the sarcomeres to connect, via the cell
membrane, to tendon collagen fibers. There are at least
two mechanisms for this connection: (1) via transmem-
brane proteins (integrins) and (2) via other protein-cell
membrane-ECM interactions.13 The infoldings increase
the surface contact area so that stress is reduced, ensure
that junctions are loaded in shear rather than tension (to
provide friction), and minimize areas of stress concentra-
tion.10 Muscle cells also are surrounded by collagenous
Figure 3-1
The bone-tendon junction of the supraspinatus tendon. There are
four distinct zones: tendon (T), fibrocartilage (FC), mineralized
fibrocartilage (C-FC), and bone. Blood vessels (BV) are observed in
the tendon but not in the fibrocartilage areas. There is a prominent
line, the tidemark (TM) between the two areas of fibrocartilage. (From
Benjamin M, Evans EJ, Copp L: The histology of tendon attachments
to bone in man, J Anat 149:89, 1986.)
tissue, so the entire surface of the muscle fiber, not just
the tapered end, is capable of transferring tension across
the cell membrane to the tendon; otherwise there would
be an enormous concentration of stress at the tip of the
muscle cell.9,10,13 The geometry of these attachments is
illustrated in Figure 3-2.
Composition of Tendon
Tendons are cell-matrix complexes composed primarily of
collagen and other proteins, proteoglycans, elastin, gly-
colipids, cells, and water.14–17 Collagen is the major load-
bearing component in the tendon.14 Collagen is a family
of molecules that is divided into two major groups, the
fiber-forming and nonfibrillar collagens. There are at least
13 types of collagens, numbered via Roman numerals,
which are the products of more than 30 distinct genes.18
The type of collagen is often unique to the tissue—for
example, cartilage contains largely type II collagen, while
over 95% of the collagen in tendons is type I. Type III
collagen, found in fairly large amounts in immature or
healing tendons, constitutes less than 5% of the total col-
lagen found in mature tendons.18 Small amounts of other
collagen types also are present (such as VI and XI), usu-
ally connecting the large type I fibrils to the fibroblast
cells within the tendon. The type of collagen indicates
the types of forces applied to the tissue, with type II
Figure 3-2
Longitudinal section through myotendinous junction of frog
semitendinosus muscle cell. Note that the cell and surrounding
connective tissue appear to interdigitate at the end of the cell. Also
note that the dense, fibrillar material extends from the terminal Z disc
to the junctional plasma membrane. (From Tidball JG: Myotendinous
junction: Morphological changes and mechanical failure associated with
muscle cell atrophy, Exp Mol Pathol 40:1–12, 1984.)
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
reflecting compressive loads and type I reflecting tensile
loads. Because type I collagen is the major load-bearing
component in dense connective tissues,19–21 tendons and
ligaments provide an excellent opportunity to explore
the mechanical properties of this collagen.
The tendon also contains ground substance, a mix-
ture of water and proteoglycans. The ground substance
surrounds the collagen fibrils, providing the friction
that causes collagen fibrils to adhere to one another, yet
allowing lubrication and spacing so that fibrils can slide
past one another.15,17,22 Proteoglycans (PGs) are formed
from a protein core to which are attached disaccharide
amino sugars called glycosaminoglycans (GAGs). The
GAGs form only about 1% of the tendon’s material, but
are important because they bind the water that forms
65% to 75% of the total weight of the tendon. Like col-
lagen type, the proportion and type of GAG and PG in a
tissue also appear to reflect its mechanical environment.
Cartilage has very large PGs with many GAG chains,
attracting large amounts of water and enabling cartilage
to resist compression. Tendon proteoglycans (PGs) are
much smaller than those found in cartilage and have a
different GAG composition.22,23 PGs associate with the
surface of the collagen molecule,22 probably in the gap
zone near where the collagen molecules overlap in a
head-to-tail fashion. PGs play a role, as yet undefined, in
the organization of collagen into fibrils by both directing
and limiting this organization.22,24
Cellular and Extracellular Processing
Many proteins are “processed” inside the cells that pro-
duce them and remain largely unchanged after leaving
the cell (enzymes and hormones, for example). Protein
processing may include such functions as hydroxyl-
ation or glycosylation of amino acids, cleaving of ter-
minal peptides, folding into a tertiary formation, and
covalent bonding.20 Collagen undergoes many of these
same intracellular processes but also undergoes a num-
ber of extracellular modifications that create the unique
mechanical properties of connective tissues such as
skin, ligaments, and tendons.18 Extracellular modifica-
tions include removal of propeptides and cross-linking
between molecules, allowing organization into a fibril-
lar structure that gives collagen its unique load-bearing
properties.18–21,25 This is an extremely important feature
of dense connective tissues such as tendon because the
amount of tissue depends largely on intracellular events,
whereas the quality of the final tissue is determined
outside the cell (Figure 3-3).
Cross-linking between and within collagen molecules
prevents their enzymatic, mechanical, or chemical break-
down, helps direct the organization of collagen molecules
into fibrillar structures, and contributes to the tissue’s
ability to resist being stretched.25–29 Some cross-links
49
have a short-lived function, such as the disulfide bonds
in the amino- and carboxy-terminals of the procollagen
chain that keep the collagen alpha chains close enough
to allow the triple helix arrangement of the molecule to
form.25 The terminal propeptides of the procollagen mol-
ecule are removed outside the cell by peptidase enzymes,
leaving the tropocollagen molecule. Propeptide removal
is essential for the subsequent extracellular assembly of
the collagen triple helix molecules into larger fibrillar
structures.
Most collagen cross-links form after the molecules
leave the cell, and they take time to form. The earliest
cross-links (called immature or reducible) form between
modified lysine or hydroxylysine amino acid residues in
adjacent amino acid chains from the same or neighbor-
ing collagen molecules.25,29 These cross-links are chemi-
cal rearrangements of adjacent amino acids, facilitated by
the enzyme lysyl oxidase. Lysine-derived cross-links pre-
dominate in some tissues, while hydroxylysine-derived
cross-links predominate in other tissues such as tendons
that are subjected to higher tensile loads.29 The number
of hydroxylysine-based cross-links is directly proportional
to the load on a tendon, suggesting some sort of feed-
back mechanism.29 The early cross-links, derived from the
hydroxylysine-based immature cross-links, gradually rear-
range over weeks or months to form cross-links, such as
hydroxypyridinium, that link three collagen molecules.29
These cross-links reflect the mature load-bearing ability
of the tendon, giving the tendon its ability to withstand
deformation under high levels of tensile force.1,29
Defects in Collagen Processing and Organization
A number of defects in collagen metabolism can lead to
clinical disorders (Table 3-1). Some are genetic disorders,
such as the various forms of Ehler-Danlos syndrome,30
osteogenesis imperfecta (OI), chondrodysplasias, some
forms of epidermolysis nervosa, Marfan syndrome, and
others.31 Some gene mutations cause decreased cross-
linking, resulting in weaker tissues that elongate readily
when force is applied. Others cause defects in collagen
molecular structure or organization. There is a wide
spectrum of severity of these disorders, depending on the
location of the gene mutation.31 Milder phenotypes may
appear as the more common disorders of osteoarthritis,
osteoporosis, and some disorders of vascular integrity.
Increased cross-linking is more likely to occur in diabetic
clients and appears to be due to an increase in nonenzy-
matic cross-linking related to glycosylation of hydroxyly-
sine residues as the procollagen alpha chains pass through
the rough endoplasmic reticulum or Golgi complex of
the cell. The increased cross-linking creates stiffer tissues
that require more force to stretch, which may explain
why adhesive capsulitis is up to 10 times more prevalent
in diabetic clients compared with age-matched control
50 SECTION I • Scientific Foundations

Assembly into triple helix Hydroxylation of

lysine and proline
Intracellular events

Disulfide bonding

Glycosylation

Procollagen molecule

Cleavage of propeptides

Collagen molecule
Extracellular events

N-Propeptidase Fiber assembly C-Propeptidase

Intramolecular Intermolecular
bond bond Cross-linking

Overlap zone
Quarter stagger

Hole zone

Hiearchical structure with crimp appearance

Figure 3-3
Intracellular and extracellular modifications of collagen. Collagen synthesis, hydroxylation, and triple helix formation occur inside the cell. In the
extracellular space, while still close to the cell, the terminal propeptides are removed, and the collagen molecules then overlap in a head-to-tail or
tail-to-tail manner to form collagen microfibrils, fibrils, and so on. Cross-linking occurs within the fibrils between adjacent molecules. (Modified from
Curwin SL: Tendon injuries: pathophysiology and treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and rehabilitation,
p 30, Philadelphia, 1996, WB Saunders. Adapted from Prockop D, Guzman NA: Collagen diseases and the biosynthesis of collagen, Hosp Pract
12:61–68, 1977.)
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations 51

Table 3-1
Some Disorders of Collagen Metabolism
Levels of
Defect Collagen Defect Reason Clinical Manifestations Clinical Name

Regulation of Decreased or Lack of gene, or Fragile bones and Osteogenesis imperfecta (OI)
synthesis abnormal type I mutation soft tissues, multiple (several types exist)
collagen fractures, blue sclera;
variable in severity
depending on genetic
pattern
Decreased or Lack of gene, or Weak arteries, skin, Ehler-Danlos syndrome
abnormal type III mutation intestine, uterus (organs type IV
collagen may rupture); easy
bruising
Decreased type I Severe vitamin C Growth suppression, Scurvy
collagen deficiency, fasting poor wound healing,
fragile skin
Structural Decreased collagen Structural mutation Skin fragility and Ehler-Danlos syndrome
defects fibril formation, in one procollagen hyperextensibility, easy type VI
failure to remove chain bruising, bilateral hip
amino-terminal dislocation
propeptide
Decreased Vitamin C deficiency Same as above Scurvy
hydroxyproline (cofactor for
prolylhydroxylase
enzyme)
Enzyme defects Decreased Decreased lysyl Loose skin, hypermobility Ehler-Danlos syndrome
cross-linking oxidase enzyme in joints of digits type V
Decreased Decreased lysyl Skin hyperextensibility, Ehler-Danlos syndrome
cross-linking hydroxylase enzyme poor wound healing, type VI
musculoskeletal
deformities
Lysyl oxidase Decreased Copper deficiency, As for Ehler-Danlos
inhibition cross-linking decreased lysyl type V
oxidase activity
Decreased Poisoning because As for Ehler-Danlos Lathyrism
cross-linking of β-amino- type V
propionitrile
ingestion

From Curwin SL: Tendon injuries: pathophysiology and treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and
rehabilitation, p 31, Philadelphia, 1996, WB Saunders.

subjects.32 Immature cross-links also increase in capsular
tissues after joint immobilization, whereas they decrease
in tendons and ligaments around the same joint.33,34 This
leads to decreased joint range of motion and increased
friction with joint movement, thus requiring a greater
muscle effort to produce the same range of motion.33–35
Assembly into a Fibrillar Structure
Self-assembly into a fibrillar structure begins outside the
cell as the collagen molecules aggregate linearly in an
overlapping head-to-tail fashion after leaving the fibro-
blast.5,14,20,21 The first step is removal of the terminal
pieces. Outside the cell, but still within infoldings of the
cell membrane, the ends of the triple helix molecules
are enzymatically removed, leaving collagen (tropocol-
lagen). This step is essential for subsequent assembly into
fibrils; without it, collagen simply accumulates but does
not form a load-bearing structure. Once the propeptides
are gone, linear and lateral aggregation of the molecules
begins. The molecules assemble laterally in groups of five
(microfibrils), overlapped linearly in a head-to-tail fash-
ion that is dictated by cross-linking ability and by the type
and amount of GAGs already present.5,14,22 Each micro-
fibril is about 4 nm wide. A variable number of micro-
fibrils associate to form collagen fibrils ranging from
52 SECTION I • Scientific Foundations
30 to 400 nm in diameter. It is at the subfibrillar levels
that intermolecular cross-linking normally occurs.14,25
The space between fibrils is usually too large to allow
cross-linking between adjacent fibrils, although this may
sometimes occur under atypical conditions such as limb
immobilization.33 The interfibrillar matrix (ground sub-
stance) probably plays a large role in adhesion between
collagen fibrils.17,21 The exact nature of collagen supra-
molecular organization varies among tissues, even if the
collagen type is the same. The reasons for the differences
are not known.
Collagen fibrils are the smallest tendon units capa-
ble of resisting load under laboratory conditions.14,21
Tissue strength, especially during healing, closely cor-
relates with collagen content, but this collagen must
be organized and cross-linked before it can function as
a load-bearing unit.36–38 Masses of nonorganized col-
lagen molecules are incapable of resisting tensile force
application.38 Thus, even if a large amount of procol-
lagen is produced, but the molecules are not enzymati-
cally modified to become collagen (tropocollagen),
no structural benefit is obtained from the newly syn-
thesized collagen (this occurs, for example, in Ehler
Danlos syndrome type VI). The ground substance
molecules, especially the small leucine-rich proteogly-
cans like decorin, attach to the surface of the fibrils
and both direct and limit their growth.22,24 New micro-
fibrils may be added to existing nearby fibrils, increas-
ing their size, or they may associate to form new fibrils,
which are typically much smaller in diameter than the
older fibrils.37 Fibroblasts become squeezed between
the growing fibrils and end up as columns of flattened,
spindle-shaped cells with thin cytoplasmic processes
extending among the fibrils. The strongest tendons
contain large numbers of large-diameter fibrils. These
are generally the oldest fibrils, which also contain the
largest numbers of mature cross-links.5,37,38 Immature
and healing tissues contain larger amounts of type III
collagen, which forms smaller diameter fibrils than
does type I.
Collagen fibrils group together to form successively
larger primary bundles, which are also known as fibers
(Figure 3-4). They are the smallest units visible in light
microscopy, with a diameter of 1 to 10 µm. Groups of fibers
are surrounded by a loose connective tissue sheath called
the endotenon—which also encloses the nerves, lymphat-
ics, and blood vessels supplying the tendon—to form a
fascicle (secondary bundle).5,14,39 The fascicles are consid-
ered the smallest functional (i.e., “real-life”) load-bearing
units within the tendon. Individual fascicles are associated
with discrete groups of muscle fibers (or motor units)
at muscle-tendon junctions. Several fascicles may form a
larger group (tertiary bundle) surrounded by epitenon,
which also surrounds the entire tendon. The sheaths are
differentiated by their location and by their collagen type
content. The endotenon contains more type III collagen,
organized as small-diameter fibrils, while the epitenon,
which contains more type I collagen, has larger diameter
fibrils. An additional double-layered sheath of areolar tis-
sue, the peritenon or paratenon, is loosely attached to the
outer surface of the epitenon. The peritenon may become a
synovial fluid-filled sheath, the tenosynovium, in tendons
that are subjected to friction, for example, when tendons
pass beneath a retinaculum like those found at the wrist
and ankle joints. A simplified version of the hierarchical
organization of the tendon is illustrated in Figure 3-4.5,14
Some evidence suggests that the organization may vary
from place to place within the tendon or among tendons.
For example, the rat tail tendon shown in Figure 3-4 has
a simpler structure than many other tendons, containing
fewer subdivisions and being composed of nearly 100%
type I collagen. These variations may explain why there is
no universally accepted model of tendon organization.5
Microstructure of Tendon
● Fascicles
● Epitenon
● Endotenon
● Peritenon (paratenon)/tenosynovium
Mechanical Behavior of the Tendon
The organization of the tendon determines its mechani-
cal behavior. The resting tendon has a slightly crimped,
or wavelike, appearance1–4 that straightens under load
and reappears as the tendon recovers its original rest-
ing length after the load is removed. The straightening
of the “crimp” results in a “toe” region in the force-
elongation (load-deformation) curve, where little
force is required to change tendon length.40 Little or
no physical deformation of the collagen fibrils takes
place. As the load increases beyond the toe region, the
collagen fibrils stretch, creating the linear region of
the load-deformation curve.1,41 The force-elongation
curve can be transformed into a stress-strain curve by
dividing the force by the tissue cross-sectional area,
and the change in length by the original tissue length
(Figure 3-5).1,40
Structural Properties
The total amount of force (load) the tendon can resist
and the amount it stretches during loading depend on
the size (cross-sectional area), composition, and length
of the tendon, as shown in Figure 3-6.1,40,42 In general,
larger tendons tolerate larger forces, and longer tendons
can stretch further before any damage occurs. These
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations 53

Collagen Molecule Collagen Fibril Collagen Fiber Fascicle Tendon Unit

α1
α2

X
Gly Y

Fibroblast Paratenon
64 nm Nerve and
Blood Vessels

280 nm
Endotenon

Crimp
Epitendinium
A 1 nm 100 nm 1-20 µm 20-200 µm 500 µm

Figure 3-4
Structural hierarchy in tendon.
A, Diagram illustrating the
relationship between collagen
molecules, fibrils, fibers, fascicles,
and tendon units. Although
the diagram does not show
fibril subunits, collagen fibrils
appear to be self-assembled
from intermediates that may be
integrated within the fibril. B,
Scanning electron micrograph
of rat tail tendon showing
fascicle units (asterisk) that
make up the tendon. (From
Silver FH, Freeman JW, Seehra
GP: Collagen self-assembly and
the development of tendon
mechanical properties, J Biomech
B 36(10):1529–1553, 2003.)

size-dependent features are referred to as the structural
properties of the tendon.1 They depend on the physical
dimensions of the tendon. The Achilles tendon is much
stronger than, say, the plantaris tendon. On the other
hand, if one were to cut a piece of Achilles tendon exactly
the same size (area) as plantaris, there might be no dif-
ference between the two when tested mechanically. Such
a finding would indicate that the load and elongation
differences between the tendons were solely due to their
physical dimensions.
54 SECTION I • Scientific Foundations

Material Properties
To account for differences in physical dimensions among
tendons, researchers correct for size and length. Force is
divided by cross-sectional area, and the change in length
during loading is divided by the starting length of the
tissue. This removes the influence of the tissue’s physi-
cal size. If the new variables are plotted, the result is the
stress-strain curve (see Figure 3-5). Because the effects
of size have been removed, any differences in the stress-
strain curves of different tissues must reflect some other
characteristic of the tissue, the so-called material prop-
erties.1 These properties arise from factors like differing
collagen fibril organization, differences in cross-linking,
varying ground substance concentration, and perhaps
different collagen types.30,40 They are dependent on the
material of which the tendon is made, not how much
material the tendon contains. Thus, after correcting for
physical size, mechanical testing results reflect tissue
composition (or organization).

Figure 3-6
Structural properties of tendon (those determined by size and length).
Generally, a larger tendon will withstand greater forces at the same
percentage elongation, while a longer tendon will undergo a greater
overall length change in response to the same magnitude of applied
load. (From Butler DL, Grood ES, Noyes FR et al: Biomechanics of
ligaments and tendons, Exerc Sports Sci Rev 6:144, 1978.)

Consider two tendons, A and B. If A is larger than

Figure 3-5
A stress-strain curve for a tendon loaded until failure. The load (force)
applied to the tissue has been divided by the cross-sectional area to
calculate the stress, while the increase in length is divided by the original
length to give the strain (∆L/L × 100). In the toe region of the curve,
the crimped collagen fibers straighten, which requires little force. In
the linear region, the tendon resists deformation through cross-linking
between molecules and friction between fibrils. The slope of this part
of the curve is the stiffness of the tissue, and it reflects the material
properties of the tissue. Less physical deformation should reduce the
likelihood of injury, which occurs in the region of 6% to 10% strain.
After the linear region, the stress-strain curve becomes irregular as fibrils
begin to fail. (From Curwin SL: Tendon injuries: pathophysiology and
treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic
injuries and rehabilitation, p 33, Philadelphia, 1996, WB Saunders.)
B but has fewer cross-links, A and B may have simi-
lar force-elongation curves but different stress-strain
curves. The larger cross-sectional area of A allows it to
withstand as much force as the smaller B, but when the
effect of size is removed, B will have a steeper stress-
strain curve. B is therefore stiffer than A, though both
tendons can withstand the same load before breaking.
An increase in cross-linking alters the material proper-
ties of a tendon and make it more resistant to stretch
than a tendon of the same size containing fewer cross-
links. Both an increase in area with no change in cross-
linking or collagen concentration and, conversely, an
increase in cross-linking or collagen concentration
with no change in area can create stronger tendons. In
other words, tendons can adapt structurally or materi-
ally to changes in their mechanical environment. For
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
example, the tendons of fusiform muscles (e.g., biceps
or hamstrings) tend to have smaller cross-sectional areas
relative to muscle strength than do tendons of penni-
form muscles (e.g., gastrocnemius or quadriceps), and
different tendons have different stress-strain behavior,
suggesting that tendons may differ in composition as a
result of load conditions.2,40,42
Differences in collagen type also seem to affect tissue
mechanical behavior. Tissues with large amounts of type
I collagen are usually stiffer and stronger than those with
more type III collagen.19,21,38 Whether there is actually
any difference in the tensile strength of type I versus type
III collagen, or whether tissue strength differences are
more closely related to differences in fibril architecture
and cross-link number between the collagen types, is
unknown.38
Physical Changes during Loading
Force application beyond the toe region (2% to 4%
strain) causes deformation of the tendon’s components
and structure.40 The relationship between applied force
and resulting tissue deformation becomes linear, with
stress applied directly to the now-straightened collagen
fibrils.1,14,40 It is in this region of the curve that cross-link-
ing and adhesion between fibrils play the most impor-
tant role, and differences in the slope of the linear region
of the stress-strain curve may be interpreted to reflect
differences in collagen concentration (or type), cross-
linking, or ground substance concentration. X-ray dif-
fraction techniques show that as loading is increased, the
first structural damage is intrafibrillar slippage (between
molecules), then interfibrillar slipping (between fibrils),
and finally gross disruption of the collagen fibrils/fibers
themselves.43–45 Intrafibrillar slippage is probably gov-
erned by cross-linking, interfibrillar slippage by ground
substance and gross disruption by these factors plus fibril
size. After the first fibrils rupture, the force curve plateaus
and then drops off rapidly as the remaining fibrils fail in
sequence. Total mechanical failure (i.e., tendon rupture)
usually occurs at about 8% to 10% elongation from the
starting length.40
Most tendon injuries, however, probably result from
loading that extends into the linear region, not maxi-
mal loads. Increasing severity of injury may be due to a
progressive collapse of lateral cohesion between compo-
nents that begins at the fibrillar level, which could cause
Order of Tendon Structural Damage
● Intrafibrillar slippage
● Interfibrillar slippage
● Disruption of fibers (plastic deformation)
55
a greater reduction in tensile strength than suggested
by the actual number of torn fibrils or fibers observed
on tissue examination.44,45 In other words, the tissue is
more severely damaged than it appears. Such damage
can occur not only during tissue loading but also during
rapid unloading, perhaps as a result of shearing within
the tendon.44 This may explain why both sudden force
application and release are often associated with tendi-
nopathy.
The breaking strength of the tendon (i.e., the mag-
nitude of the force being applied at the point of tendon
rupture) has historically been used to assess the tensile
strength of the tendon.1,2 The value observed is called
the ultimate tensile strength; it can be used to compare
different tendons or ligaments or to assess the effects of
experimental interventions on healing tendon. Breaking
strength may not necessarily reflect everyday loading
conditions, however, since most tendons probably func-
tion in the toe and early linear regions under physiologi-
cal loading conditions. Some authors have suggested that
the slope of the linear portion of the curve (∆F/∆L),
the stiffness, may be a better indicator of the tendon’s
in vivo mechanical behavior.40 Healthy tendons rarely
rupture under normal loading conditions,46 so one can
probably assume that they are seldom loaded in vivo to
the maximum levels used to rupture tendons in labora-
tory testing.1,40,47 Understanding the physical changes
occurring in the linear region of the stress-strain curve
may be more important in explaining the tissue damage
that occurs during tendinopathy than is a knowledge of
the maximum load that the tendon can tolerate before
breaking.
Results of Testing and Indirect Calculations:
Forces on Human Tendons
There is a strong relationship between the size of a tendon
and the maximum force that its attached muscle can pro-
duce, a logical adaptation since larger tendon can with-
stand more force.2,47 It has been estimated that the tensile
strength of a tendon is about four times the maximum
force produced by its attached muscle, so that tendons
in vivo are rarely stressed to more than one-quarter their
maximum physiological strength,2 probably into the toe
region of the stress-strain curve. Such loads should not
damage a normal tendon.
Estimates of in vivo tendon strength have been
extrapolated from in vitro testing, but it is difficult to
calculate in vivo stress-strain behavior. Transducers of
various sorts have been applied to animal and human
tendons, and studies using these transducers implanted
on animal tendons support the theory that tendons are
strained only within the toe region of the stress-strain
curve during normal daily activities such as walking
and trotting.48,49 If such experiments represent typical
56 SECTION I • Scientific Foundations

Table 3-2
Tendon Forces and Stresses during Activity
Activity Tendon Force (N) Stress (MPa)* Reference

Running Achilles 5000 80 Curwin, 198457

Patellar 7500–9000 60–75 Alexander and Vernon, 197552
Jumping Achilles 4000–5000 60–80 Curwin, 198457
Fukashiro et al., 199555
Patellar 8000 70 Alexander and Vernon, 197552
Cycling Achilles 5500 88 Gregor et al., 198750
Kicking Patellar 5000 42 Curwin and Stanish, 1984136
Voluntary Achilles 4000–5000 60–80 Wren et al., 200153
contractions
Eccentric exercise Achilles 2000–4000 30–60 Curwin, 198457
Rupture Patellar 14,000 100 Zernicke et al., 1977123
Mechanical testing Various 5000–10000 80–100 Harkness, 196828
to failure

*Stresses estimated using approximate values of 60 mm2 for Achilles tendon and 120 mm2 for patellar tendon. Actual stress values would depend
on accurate measurement of tendon cross-sectional area, probably via MRI measurement.

loading patterns, it is difficult to see why tendons
would be injured during activities, given such a large
margin between physiological and maximum loading.
A more likely explanation is that these are fairly low
loads, even for animals. Studies from racehorses and
humans suggest that tendons may be loaded to much
higher values during more strenuous activities like run-
ning and jumping.49–57 Gregor et al. and Komi et al.
placed buckle transducers on the Achilles tendon of
volunteers (including themselves!) and recorded forces
in the range of 5000 to 6000 N during cycling and
running.50,54 Achilles tendon forces of up to 4000 N
were recorded during hopping on one foot.55 These
forces were higher than those observed during other
activities.52–57
Transducers are difficult to insert and may limit activ-
ity, so human tendon loading data have usually been
acquired through indirect calculations based on bio-
mechanical models and kinematic (film or video) and
kinetic (force platform) data. Barfred estimated maxi-
mum forces of about 4340 N in a person who, while
running, suddenly changed direction and ruptured his
Achilles tendon;51 ordinary push-offs were calculated
to be about 2000 N. The larger value was similar to
data obtained from in vitro testing of isolated human
tendons, which showed maximum tensile strength of
about 4000 N and suggest that tendons may be loaded
near-maximally during some activities.56 Achilles tendon
forces between 2000 to 5000 N have been estimated
during activities such as running and jumping.57 Other
examples of estimated tendon forces in various tendons
during different activities suggest that tendons may often
be loaded to more than 4000 N during athletic activities
(Table 3-2).52–55 However, these are still only estimates
of tendon force.
The data from estimates and direct measurement of
human tendon forces suggest that tendons may indeed
be subjected to large loads under daily conditions,
probably into the linear region of the stress-strain
curve. The confusion may arise from the definition of
“physiological loading,” which depends on the activi-
ties considered physiological for most people. Forces
during walking and light exercise may be only 20% to
30% of those observed during vigorous exercise such
as fast running, jumping, hopping, or suddenly chang-
ing direction. It appears, then, that clients’ tendons
frequently may be subjected to potentially damaging
loads, yet many clients are symptom free. The reasons
for this paradox remain unknown. Perhaps all clients
have structural defects at the submicroscopic level in
their tendons, and it is only after enough damage has
accumulated that symptoms and dysfunction occur.
This suggests a fatigue of tendon structure, leading to
eventual dysfunction. Such degenerative changes, with-
out clinical signs or symptoms, have been described as
tendinosis.
Effects of Exercise and Disuse
on Tendons
Exercise has mechanical and physiological effects on
specific structures involved in exercise, as well as systemic
effects on other body systems. Blood flow increases
7-fold in tendon during exercise and up to 20-fold in
muscle.58 Tendons are stretched, especially under iso-
metric or eccentric loading conditions, and deformation
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
takes place within the fibrils and between molecules.
Exercise influences cell shape and physiological func-
tions, presumably through direct connections between
the extracellular matrix (ECM) and the interior of the
cell. Even short bouts of exercise have been shown to
increase collagen synthesis in tendon.59
The response to exercise varies among tissues and
depends on the nature of the stimulus, as well as the
amount, type, and frequency of loading. Muscle responds
to increased mechanical load by increasing myofiber
cross-sectional area, primarily by synthesizing more force-
producing protein. An increase in frequency of loading
(with no change in magnitude) results in alterations in
metabolic enzyme profiles.60 Eccentric exercise may pro-
duce muscle damage,61 while sustained increased loading
increases the connective tissue component of the muscle.62
The molecular program of muscle adaptation to endur-
ance exercise and resistance exercise is very different,60,63
but in each case the adaptation improves the muscle’s
ability to function under its new loading conditions. The
tissue adapts in different ways to different stimuli.
The local mechanism of connective tissue (bone,
tendon, ligament, and cartilage) response to exercise
appears to involve cells detecting tissue strain and
modifying the type and amount of collagen and PGs
synthesized.16–24 The volume, nature, and frequency
of deformation are important. Compressive loading
induces cartilage formation,16,23 while tensile loads
result in tissue resembling that found in tendon or liga-
ment.23 Variations in load can occur within a tendon as
tendon wraps around bony structures (like the peroneal
tendon behind the lateral malleolus), and these varia-
tions are reflected in changes in tendon composition to
resemble cartilage.23
Maintenance of the normal mechanical state of con-
nective tissues appears to require repetitive loading to
or beyond a threshold level.64 Loading below this level
results in weaker tissues, and these changes take place
quite rapidly, over a period of days or weeks. The effects
of disuse and immobilization on tissues such as mus-
cle, ligament, joint capsule, and tendon have been well
established.33–35,65–71 In tendons, collagen and cross-link
concentrations decline, and the tendon becomes smaller.
Thus, the tissue becomes weaker through both structural
and material changes. These findings have led to the clini-
cal use of early motion and gradual stress application to
treat bone and soft tissue injuries.72–75
Connective tissues also adapt to increased loading by
becoming stronger, but these changes occur over a lon-
ger time frame (months) than with disuse.75–90 Healing
and normal tendons both adapt to increased loads either
structurally, by becoming larger and hypertrophying as
muscle does, or by changing their material properties to
become stronger per unit area. Other connective tissues
behave in a similar fashion.
57
Various tissues respond differently to exercise, and
there also are variations in the response of a given tissue
to different types of exercise. Different regions of liga-
ments respond differently to immobilization and recov-
ery,69–71 with junctional areas of ligaments responding
more rapidly to immobilization than the midsubstance,
but recovering more slowly. Tendons may behave
the same way,90 perhaps explaining why tendon inju-
ries often occur at bone-tendon junctions. Chronic
mechanical overload (experimentally created via surgi-
cal muscle excision and compensatory hypertrophy) on
a tendon resulted in both structural changes (increased
cross-sectional area) and material changes (alterations
in cross-linking patterns and amounts).29
Running is often used experimentally as a model
of tendon loading, but the results after such endur-
ance exercise are variable, perhaps because the load is
lower or there is a systemic as well as a local response.
Running had little effect on tendon size and composi-
tion in some studies,35,81,83 while others found changes
in tensile strength or stiffness.82,84,90 Swimming showed
little or no effect on healing rat tendon,85 perhaps not
surprising since loading magnitude is much lower in
swimming compared with locomotion.86 The number of
cycles may be important as well as the load per cycle in
tendon adaptation to exercise, and the tissue examined
also may play a part.91 Exercise training attenuated age-
related increases in cross-linking in the left ventricle of
rats but had no effect on the right ventricle.87 Endurance
exercise thus seems to produce variable results, perhaps
because of variations in factors such as model, loading
magnitude, number of cycles, and the accompanying
physiological stress.
Tendon injuries in humans are usually associated with
exercise such as running, jumping, or sudden changes in
direction, or with repeated use. Some sports-related activi-
ties can stress tendons to large percentages of the theoreti-
cal maximum for mammalian tendon (see Table 3-2). The
association of tendon injury with particular sports (such as
Exercise Effects on Tendon
Increased magnitude of load (strength exercise)
● Increased cross-links
● Increased cross-sectional area
● Increased collagen content
● Stronger tendon material
Increased time/frequency of load (endurance exercise)
● Same cross-sectional area
● May decrease cross-links
● Same or decreased collagen content
● Same or weaker tendon material
58 SECTION I • Scientific Foundations

badminton with Achilles tendon rupture) implies that the
high demands placed on tendons during many movements
in sports and dance may cause injury.92–97 The increased
incidence of tendon injuries after sudden increases in the
amount of training, or when training is resumed at a high
level after a period of inactivity, suggests that the tendon is
being subjected to damaging loads.
Most models of tendon injury assume abnormalities
in force application as part of the etiology, and this is
clearly the case in acute tendon injuries. Many clients,
however, appear to develop tendinopathy even though
the loading environment has not changed (e.g., run-
ners training at the same speed and distance or workers
performing the same job). This leads to the question
(usually asked right away by the client) of why loads pre-
viously well tolerated by the tendon would now pro-
duce an injury. Repetitive loading in animals, even at
functional loads, has been shown to induce changes in
motor behavior, such as prolonged or increased motor
unit recruitment, that may cause tendon pathology.98–102
Similar loading patterns are common in human workers,
in whom repetitive strain injuries (RSIs) or work-related
musculoskeletal disorders (WRMDs) now account for a
large percentage of work-related health care costs.103 The
presence or the nature of degenerative changes within
the tendon in such cases is not known, since no correla-
tion has yet to be shown between tendon structure and
clinical presentation.
The fact that normal loads, repeated frequently, appear
to cause tendon damage suggests that the relationship
between training intensity, load, and tendon physiology
is more complex than previously thought. Perhaps the
magnitude of mechanical loading is not the only impor-
tant factor, or different types of exercise induce different
adaptations in tendon. There is evidence to suggest that
cross-linking in the Achilles tendon may be increased
with chronically increased loads but decreased by an
intermittent strenuous running program (even though
the latter would be expected to load the Achilles tendon
and indeed is often used as a model of increased tendon
loading).29,81,83 Perhaps other factors (metabolic, nutri-
tional, immune, hormonal) induce changes in the tendon
such that previously safe levels of loading are now capa-
ble of damaging the tendon.104–108 Animal studies suggest
that the duration of loading is also important, with even
submaximal loads capable of inducing tendinopathy if
repeated over a prolonged period.98–101
Tendon Injury
Forces Causing Tendinopathy
Understanding normal tendon structure and function,
one can predict the changes in tendon structure or
composition that would make a tendon susceptible to
injury (Table 3-3). The development of chronic pain in

Table 3-3
Potential Causes of Tendon Dysfunction
Stimulus Response Possible Effects

Immobilization Atrophy of myotendinous junction Partial rupture, microtears

Increased cross-linking in Increased resistance to joint movement, increased muscle work
joint capsule
Prolonged Hormonal changes leading to Weaker tendon, microtears
endurance increased collagen turnover
exercise
Intense exercise Rupture of cross-links or collagen Inability to withstand forces during daily activities,
fibrils, release of collagen inflammatory response
components into circulation
Prolonged Increased cross-links, Effect on tendon function unknown
increased decreased collagen
mechanical
loading
Injection Mechanical disruption of fibrils, Weaker tendon, possible rupture
decreased collagen synthesis
Nonsteroidal Decreased inflammation Effect on tendon function unknown
medication
Intermittent Unknown Effect on tendon function unknown
resistance
exercise

From Curwin SL: Tendon injuries: pathophysiology and treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and
rehabilitation, p 37, Philadelphia, 1996, WB Saunders.
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
human tendons subjected to prolonged loading (e.g., the
Achilles, patellar, supraspinatus, and forearm extensors,
and the findings from animal studies) suggests that repet-
itive loading leads to injury. A basic principle in most
models of the etiology of tendinopathy is that physical
loading has caused damage to the tendon (i.e., the ten-
don is not strong enough to withstand the loads to which
it is subjected). Few data from human subjects are avail-
able to support this conclusison.59,64 The nature of the
actual damage and the tendon’s subsequent adaptation
(or failure to adapt) probably vary with the type of force
(compressive versus tensile) as well as its magnitude and
pattern of application.
Compressive Forces: Extrinsic Tendinopathy
Tendinopathy may result from outside forces that are
applied directly to the tendon—“extrinsic” tendinopa-
thy. The cause is usually excessive compressive, frictional,
or tension force applied to the tendon by an external
(extrinsic) object or by a change in anatomical align-
ment. Compression may come from an article worn by
the client; for example, tight laces in a hightop sneaker or
skate may cause tenosynovitis of the extensor tendons at
the ankle joint. Friction may come from tight anatomical
structures rubbing on bony projections, such as iliotibial
band friction syndrome or flexor hallucis tenosynovitis.101
A combination of compression and friction from the cli-
ent’s own anatomic structures and movement patterns
also may be responsible. A large acromion process may
cause pressure on the supraspinatus tendon, leading to
shoulder impingement syndrome with repeated overhead
movements. Similarly, retinacula at the wrist can cause
various forms of tenosynovitis, usually in combination
with repeated use during occupational or recreational
Table 3-4
Examples of Extrinsic Tendinitis
Clinical Name Cause
Impingement syndrome Anterior shoulder structures rub on rotator
cuff during overhead movements
Iliotibial band syndrome Friction of IT band on lateral epicondyle of
femur during knee movement
De Quervain’s syndrome Friction on thumb muscles passing under
wrist retinaculum
Achilles tenosynovitis Friction from heel counter
Friction of tendon on sheath
Extensor tenosynovitis Friction from anterior structures at ankle
joint
59
activities.109–111 In some cases of prolonged compression,
the tendon may change its composition and come to
resemble cartilage.112,113 Tenosynovitis also can be caused
by overstretch during movement114,115 or can result from
infection.116,117 Atypical foot alignment, such as forefoot
varus or hindfoot valgus, may increase the stress on the
medial side of the Achilles tendon. These cases of tendi-
nopathy are best treated by early removal of the external
cause (Table 3-4).
Sudden Loading/Excessive Force
Cases of tendon injury that cannot be directly attributed to
an external cause are sometimes referred to as “intrinsic”
tendinopathies. This type of tendinopathy is apparently
caused by loads applied to the tendon during functional
activities. It appears that there is a mismatch between the
tendon’s mechanical properties (material and/or struc-
tural) and the loads it must withstand. This mismatch
could arise from an increase in loads applied to the ten-
don (i.e., tendon structure composition is the same, load
changes) or from changes in tendon composition that make
it weaker mechanically while loading remains the same.
Human tendons can be subjected to fairly large loads dur-
ing normal activities (see Table 3-2), and the association
of tendon injuries with different sports implies a relation-
ship between tendon injury and tensile loading. Achilles
tendon injuries are common in runners,94 and the inci-
dence of Achilles tendon rupture is higher in badminton
players,97 in whom it appears to be associated with a rapid
change in direction from backward to forward movement.
Patellar tendinopathy is more common in jumping clients
such as volleyball and basketball players.92,95
The load on the tendon, of course, may be quite dif-
ferent to the stress on the tendon. The latter is seldom
Possible Solutions
Acromioplasty
Joint mobilization to restore glides at
GH joint
Scapular muscle retraining
Posture correction
Stretch IT band
Realign lower extremity via orthotics
Reduce thumb movement (splint)
Reduce sheath swelling via medication or
modalities
Reconfigure heel counter
Ice, modalities, and medication
Activity reduction until symptoms begin to resolve
Distribute forces via padding
Ice, modalities, and medication
60 SECTION I • Scientific Foundations
calculated, because it is difficult to measure tendon cross-
sectional area. Imaging techniques such as ultrasound
(US) and magnetic resonance imaging (MRI) allow
cross-sectional area to be measured, so that muscle and
tendon stresses can be calculated.56,117–119 Considerable
variability in tendon size, and thus stress, has been
observed between subjects, which may explain why some
people experience injury while others do not.56,90,91 The
distribution of stress within individual tendons is not
known, although it is generally assumed that all areas of
the tendon are loaded equally. It is possible, however,
that this may not always be the case. Force is transmit-
ted to the tendon via connective tissue connections with
muscle fibers. Thus, if only some muscle fibers are active,
they could create an asymmetrical load on the tendon.
Asymmetries in strain have been shown to occur in the
muscle-tendon area during loading.13,119
Situations in Which Tendon Damage May Occur
● Load amount or pattern increases because of changes in
functional demands, and
● Tendon composition and structure are stable
or
● Tendon composition changes, and
● Load remains stable
Role of Eccentric Muscle Activation
Muscle physiology experiments on both isolated and in
vivo human muscle have shown that force increases as
the velocity of active muscle lengthening increases, while
the opposite is true during concentric (shortening) mus-
cle activations (Figure 3-7).120–122 This may explain the
frequent connection between eccentric loading and ten-
don injury.51,95,96,98 The tendon is exposed to larger loads
during eccentric loading, especially if the movement
occurs rapidly.120,122 This is exactly what occurs when one
is landing from or preparing for a jump (patellar tendi-
nopathy),92,95 midstance during running54,57 or during a
demi-plié in ballet96 (Achilles tendinopathy), and when
hitting a backhand in tennis (lateral epicondylitis).
Almost all shortening activations (concentric contrac-
tions) of muscle-tendon units are preceded by lengthen-
ing while the muscle is active (eccentric contractions).122
This activation pattern stretches the elastic elements in
the muscle-tendon unit (MTU), including the tendon,
and contributes to movement if the muscle is allowed to
immediately shorten after being lengthened.3,4,120–122 This
storage of elastic energy allows the muscle to produce
more force at less metabolic cost and is an important
tendon function. It has been estimated that this elastic
energy contributes approximately 6% of the total energy
Figure 3-7
The force-velocity relationship for eccentric and concentric muscle
contractions. As shortening velocity increases, force decreases; as
lengthening velocity increases, force also increases. (From Curwin
SL, Stanish WD: Tendinitis: its etiology and treatment, Lexington,
Mass,1984, DC Heath, 1984.)
for human walking and up to 60% in kangaroo hopping.3
This loading pattern also results in maximum force and
maximum elongation being applied to the tendon, creat-
ing the most likely scenario for physical damage to the
tendon. Figure 3-8 shows the loading patterns on the
Achilles tendon associated with some different activities.
The combination of maximum force and length appears
to create the potential for tendon damage. The filming of
a competitive weightlifter during a lift in which his patel-
lar tendon ruptured revealed that the disruption occurred
as the lifter changed from downward to upward motion
(i.e., the end of the eccentric phase).123 The force on the
patellar tendon was estimated at about 14 kN, over 17
times body weight!
Rapid force application or release is more likely to
cause tendon damage than the same load applied gradu-
ally.43–45,51 The sudden stretch of the muscle, especially if
it is contracting near-maximally, results in a larger than
normal force being rapidly applied to the tendon, per-
haps causing partial or complete rupture. Force is more
likely to cause tendon damage if it is applied suddenly,
rather than gradually increased to the same level. The
sudden removal of force also is more likely to cause dis-
ruption than a gradual reduction of the same force. A
disruption of the relationship between the collagen fibrils
and their surrounding matrix appears to be involved.43–45
Differential loading at the musculotendinous junction
also may be related to variability in motor unit recruit-
ment patterns that causes different strain patterns in the
attached connective tissues. Slow movements, low force
levels, and the maintenance of posture use small motor
units composed of slow muscle fibers. The tendon fas-
cicles associated with these motor units are therefore
regularly loaded during daily activities. Sudden loading
may recruit less frequently used fast motor units. If the
tendon fascicles associated with these motor units have
not been exposed to the same loading history as other
fascicles within the tendon, perhaps they are weaker and
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
Figure 3-8
Achilles tendon forces during three sports-related activities (A) and
a slow and rapid heel drop over the edge of a step. B, Forces were
indirectly estimated using force platform and film data; muscle lengths
for the soleus and gastrocnemius were also estimated from the film
records. Maximum muscle lengths (soleus maximum = ∆, gastrocnemius
maximum = •) usually occur at or near the peak force observed during
the activity. (From Curwin SL: Tendon injuries: pathophysiology and
treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic
injuries and rehabilitation, p 40, Philadelphia, 1996, WB Saunders.)
61
thus more easily injured when a sudden demand is made
on the muscle for rapid force production. It is well known
that muscle damage can be caused by eccentric muscle
contraction,124 presumably because of higher load levels,
and this appears to be true for tendon as well.
Situations in Which Tendon Injury Is More Likely
to Occur
● Loads are suddenly applied or released
● A seldom-used motor unit is recruited in response to a new
movement or load
Diagnosis, Classification, and Terminology
Systemic, metabolic, and genetic disorders that may
cause tendon dysfunction are not included in the classifi-
cation of overuse tendon disorders, although they must
be considered in the differential diagnosis of tendon
injury.104–108 The possibility of somatic referred pain from
spinal structure also should be considered and ruled out
via thorough examination.125
Acute Tendon Injuries
Tendon injuries may be divided into two broad classifica-
tions: (1) acute and (2) chronic. Acute injuries include
those for which the time and method of injury are known.
These injuries generally follow a “traditional” healing
model and are treated according to the phases of healing
(Table 3-5).126 Acute injuries include tendon rupture and
partial tendon tears, as well as other injuries for which the
time of onset is known. Tendonitis, defined as an inflam-
matory tendon response to repetitive loading, probably
fits best in the acute injuries category when the onset of
symptoms is known (Figure 3-9). Such tendon injuries
involve pain, swelling, and tenderness, and they can be
treated like other acute injuries.94
Overuse Injuries: Terminology
Chronic tendon injuries involve repetitive loading that
damages the tendon. The response may, in some cases, be
similar to that seen in acute injuries. The tendon sheath
may swell, for example.101 One difference between acute
and chronic injuries is that the time of onset is not known
with the latter. Typically, symptoms begin gradually after
a tendon-loading activity and progress to interfere with
function.127 The client presents with pain during loading
activities, tenderness on palpation, and thickening of the
tendon. Because of the gradual nature of onset and the lack
of quantitative diagnostic measurements, the exact pathol-
ogy of chronic tendon injuries remains unknown. Few or
no signs of inflammation have been observed.128–131
Tendon injuries also may be classified by the location
of pathology within the overall tendon structure (e.g., the
62 SECTION I • Scientific Foundations

Table 3-5
Acute Tendon Healing and Suggested Therapy
Stage of Healing
Inflammatory Fibroblastic/Proliferation Remodeling/Maturation

Time (days) 0–6 5–21 20 days and onward

Progressive stress on tissue
Suggested Rest, ice Gradual introduction of stress
Therapy Anti-inflammatory Modalities to increase collagen
modalities synthesis
Decreased tension
Physiological Prevent prolonged Increase collagen Increase cross-linking (tendons and
Rationale inflammation Increase collagen cross-linking ligaments)
Prevent disruption Increase fibril size and Decrease cross-linking (joint capsule)
of new blood vessels alignment Increase fibril size
and collagen fibrils
Promote ground
substance synthesis
Main Goals Avoid new tissue Prevent excessive muscle and Optimize tissue healing
disruption joint atrophy

From Curwin SL: Tendon injuries: pathophysiology and treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and
rehabilitation, p 43, Philadelphia, 1996, WB Saunders.

tendon substance or the tendon sheath). Degenerative
changes within the tendon that are not apparent on
visual examination or that cause no symptoms were
called tendinosis in the past, while chronic injuries that
are accompanied by pain were called tendonitis. More
recently, because the presence and role of inflamma-
tion in chronic tendonitis remain unclear, the use of the
term tendinopathy has been recommended.128–130 In most
cases of chronic tendinopathy, the inflammatory process
is absent, either having come and gone or having never
happened. The term tendinosis is used to refer to these
forms of tendinopathy, in an attempt to discourage cli-
nicians from treating an absent inflammatory response
and to denote that the normal time frame for healing
does not apply.129 An overview of the terminology used
to describe tendon injuries is shown in Table 3-6.
In most clinical cases, it is impossible to determine
which portion of the tendon is the source of pain.
Palpation involves both the tendon and its sheath, and
muscle contraction will apply force both to an inflamed
sheath and its damaged tendon. One can perhaps define
tendinopathy as “a syndrome of pain and tenderness
localized over an area of tendon, aggravated by activities
that apply tensile force to the tendon, and either caused
or followed by degenerative changes in tendon struc-
ture.”127–130 The syndrome can include inflammation of
the tendon sheath, as in tenosynovitis (tenovaginitis),
as well as actual inflammation of the tendon substance
itself. The degree of degenerative change can vary from
microscopic to complete rupture.123–130 It is unlikely that
pathologic changes can be determined for most clients,
since such analysis would require a sample of tendon tis-
sue. This means that any classification system for chronic
tendon injury based on pathology alone may not apply to
the vast majority of clinical cases of tendinopathy, since
signs of pathology do not correlate well with clinical
status.131–135 It may be more helpful to use a classifica-
tion system based on pain and function, which can be
determined clinically, even though the exact relationship
between symptoms and pathology remains unknown.
Such a system is presented in Table 3-7.136
The Overuse Model of Tendon Injury: Degeneration
without Inflammation (Tendinosis)
Chronic tendinopathy is considered an overuse injury,
the result of prolonged tensile loading, perhaps extend-
ing into the linear region of the stress-strain curve.43 It
is thought that this repetitive loading causes partial rup-
ture (microscopic failure) of some of the fibrils within
the tendon, or slippage between fibrils, which leads to
tendon injury.44,45 Such injuries have been likened to the
stress fractures that occur in bones subjected to chronic
load.44 The injury is thought to be the result of fatigue
of the loaded structure, just as metal beams will fatigue
with repeated loading. Individual loads may be within the
physiological range but are repeated so often that recovery
cannot occur and the structure fatigues.137 This concept is
supported by animal studies.35,40,45,68 Since tendon structure
recovers with rest, even after loading into the linear region,
time is probably an important element in producing these
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations 63

Increased mechanical these are often referred to as work-related musculoskel-

load beyond etal disorders (WMSDs) and may account for up to 50%
tissue tensile strength of work-related disability costs.103
Descriptions of the pathology of chronic tendon inju-
ries are based on the examination of specimens from
Submaximal Maximal
clients scheduled for surgery for recalcitrant tendinopa-
thy. Samples from various tendons show material that is
Microfailure Macrofailure soft and dull, with an increase in ground substance and
(partial rupture) (complete rupture) a loss of collagen fibril structure.131–134 Fibroblast cell
number was increased, but no inflammatory cells were
seen. These findings led to the conclusion that clients
Failed healing Inflammatory with chronic tendinopathy do not exhibit the typical
response response
signs of an inflammatory response and that a degenera-
tive process is responsible for the tendon damage and
Increased load on
clinical signs and symptoms. The lack of inflammatory
remaining fibers cells led to the recommendation of the name tendino-
sis for chronic tendon injuries.129 The uncertainty about
Healing this conclusion stems from the fact that few clients with
Degenerative
Degenerative chronic tendinopathy require surgery (probably fewer
changes and
changes in
sheath
than 3% to 5%), and those who do have typically had
tendon longstanding tendon dysfunction. Since tissues from
inflammation
these clients represent tendon disorders of long standing
that have resisted other forms of treatment, one must
Tendinosis Tendinitis be cautious in extrapolating findings from such tendons
to the vast majority of tendon injuries that do respond
to nonsurgical treatment. While tendon injuries may be
Pain during loading
more likely in older individuals, this does not appear to
Altered activity with continued loading be a consequence of aging per se but rather of overall
with duration of loading.
less In cases of chronic tendinopathy, it is possible that
loading an inflammatory response may have taken place ear-
Decreased function
lier and resolved, leaving behind degenerative changes,
somewhat analogous to the situation in liver fibrosis, for
Figure 3-9 example. Answering this question will require examina-
The possible progression of tendon injury. Inflammation may be
tion of tissues from the majority of tendinopathy clients
minimal or absent, and the tendon may gradually change even if no
symptoms are present. Pain usually occurs eventually and is possibly who do not require surgery and correlations between
related to neovascularization and neural ingrowth into the tendon. duration of problem and tissue changes. Such examina-
Some tendons may rupture without any previous signs or symptoms. tions are challenging in nonsurgical clients. Biopsies have
(Modified from Curwin SL: Tendon injuries: pathophysiology and been taken from the tendons of clients showing signs of
treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic
tendinopathy, and no overt signs of inflammation were
injuries and rehabilitation, p 42, Philadelphia, 1996, WB Saunders.)
observed.138–140 Microdialysis techniques have been used
to collect fluid samples from injured tendons, and these
samples did not contain indicators of inflammation, such
injuries. Development of chronic injury may be due to fail- as the presence of prostaglandins that accompany inflam-
ure of the tendon to heal the damage.132 This is the type of mation (e.g., PGE2).141 Rather than typical inflamma-
tendinopathy that seems to develop gradually and is often tory mediators, substances such as glutamate, known to
related to high training levels, such as distance running. play a role in central pain generation, have been found.
It is not only high-level clients who are afflicted Imaging techniques, such as MRI and US, can indicate
with this type of tendinopathy, though this group does the presence of a tendon lesion, but they do not cor-
account for many of the eponyms, such as tennis elbow relate with clinical signs and symptoms.133 The concept
and jumper’s knee, that are used for many cases of chronic of a noninflammatory model of chronic tendinopathy
tendinopathy.92,95,131 Many older individuals involved in has been discussed in articles encouraging the use of the
recreational sports also suffer, as well as nonclients109,111 diagnostic term tendinosis rather than tendonitis.128,129
involved in repetitive loading activities. Occupational These authors feel that tendonitis implies an acute, self-
activities in particular are associated with tendon injuries; limited injury that requires minimal intervention and
64 SECTION I • Scientific Foundations

Table 3-6
Chronic Tendon Injury Classification128–130
Suggested Name Former Name Pathology Signs and Symptoms Treatment

Paratendinopathy Paratenonitis (formerly Inflammation of Swelling, pain, crepitus, Anti-inflammatory

one of tenosynovitis paratenon dysfunction, agents: topical or oral
peritendinitis tenderness, warmth NSAIDs, corticosteroid
tenovaginitis) injection into tendon
sheath
Acute tendinopathy Tendinitis Tear of tendon fibers Swelling, pain, Relative rest, modalities
and blood vessels dysfunction, to control symptoms,
with inflammatory tenderness, warmth progressive loading
response
Chronic tendinopathy Tendinosis Increased cellularity, Increased tendon size, Progressive eccentric
fibril disorder, pain, dysfunction exercise loading
neovascularization
Pantendinopathy Paratenonitis with Inflammation of As above As above
tendinosis or sheath plus
tendinitis degenerative
changes in tendon

Table 3-7
Classification of Tendon Disorder Based on Pain and Disability
Intensity Level Pain Disability

Mild 1* No pain No effect on activities

2 Pain with extreme exertion; stops when
activity ceases
Moderate 3 Pain with extreme exertion; lasts
1–2 hours afterward
4 Pain with any moderate exertion; increases
with activity; lasts 4–6 hours afterward
Severe 5 Pain with any exertion; rapidly increases in
intensity; lasts 8–24 hours
6 Pain during daily activities
No effect on activities
Little effect on activities; may limit more intense
physical activities
Performance level decreased; unable to perform some
necessary tasks
Causes immediate withdrawal from activity
Unable to participate in any sports; daily activities
may also be restricted

From Curwin SL: Tendon injuries: pathophysiology and treatment. In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and
rehabilitation, p 43, Philadelphia, 1996, WB Saunders. Adapted from Curwin SL, Stanish WD: Tendinitis: its etiology and treatment, Lexington,
Mass, 1984, DC Heath.
*Level 1 is almost the same as normal tendon but can be reached only from one of the higher levels. There may be some residual strength or
functional deficits, as explained in the text, which should be ruled out before calling the tendon “normal.”

may be drug or modality based, while tendinosis sug-
gests a degenerative problem that requires an exercise
approach to solve.
The Overuse Model of Tendon Injury:
Possible Presence of Inflammation
The possible presence of an inflammatory response ear-
lier in chronic tendon injuries cannot be dismissed out
of hand. Cetti et al. examined surgical biopsy specimens
from ruptured human Achilles tendons, plus biopsy
samples from the unaffected Achilles tendon, and found
signs of degeneration and necrosis in different areas of
the ruptured tendon as well as the contralateral nonrup-
tured tendon, but they also found signs of inflamma-
tion within hours of injury.142 These inflammatory signs
(presence of neutrophils) decreased in tendons with a
longer time lapse between injury and surgery, leading
the authors to conclude that the inflammation had been
triggered by the preexisting degenerative changes in the
tendon, rather than occurring in response to the rup-
ture. Only one of the unaffected tendons showed signs of
inflammation, while signs of degeneration and necrosis
were found in most. Their conclusion was that a thresh-
old level of degenerative change caused an inflammatory
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
response, and this further weakened the tendon and led
to rupture.142
One of the major difficulties in evaluating chronic
tendinopathy is the lack of a suitable animal model to
mimic human chronic tendinopathy. Models are avail-
able to examine acute tendon injuries, usually based on
tendon damage induced by collagenase injection, and an
inflammatory response clearly occurs.143 Repetitive use
(overuse) of tendons in animals has been shown to cause
inflammatory changes in tendon.98 Four weeks of exer-
cise in rabbits, via repetitive flexion and extension of the
ankle caused by electrical stimulation of the triceps surae
muscle, resulted in irregular thickening of the tendon,
degenerative changes within the tendon, thickening of
the tendon sheath (paratenon), and a twofold increase in
blood flow to both the paratenon and the tendon.99,100
Most cellular changes suggestive of an inflammatory
response were found in the tendon sheath, with degen-
erative changes occurring in the central portion of the
tendon. Repetitive reaching and grasping by rats over an
8-week period resulted in decreased motor performance,
as well as local and widespread macrophage infiltration and
increased serum levels of interleukin-1 (signs of inflam-
mation).98 Human patellar tendon fibroblasts have been
shown to produce inflammatory mediators (phospholi-
pases, cyclooxygenases, prostaglandins) when stretched,
especially at higher frequencies.144 Using microdialysis
techniques, healthy human Achilles tendons, when exer-
cised, have been shown to produce inflammatory media-
tors, while chronically injured Achilles tendons do not.145
Injection of corticosteroid into a chronically injured
Achilles tendon led to a rapid reduction in pain and ten-
don swelling, suggesting an inflammatory process was
ongoing.146 Under reverse conditions, the administration
of inflammatory mediators has been shown to induce
tendinopathy.147
It is difficult to know how to interpret these findings.
Perhaps normal tendons do respond with an inflamma-
tory response to repetitive loading, and tendons that fail
to produce this response develop tendinopathy. This is
analogous to the failed healing response proposed by
Leadbetter as an explanation for the development of
chronic tendon injuries.137 It appears that tendons that
develop tendinosis may have a different physiological
response than normal tendons to loading-induced dam-
age (i.e., they fail to repair damage as it occurs). This
hypothesis is difficult to assess without longitudinal,
long-term studies of populations likely to develop tendon
injuries.
The issue of whether inflammation plays a role in
chronic tendinopathy also may depend on the time period
when examination is made. Following the creation of an
Achilles tendon injury in rats by injection of collagenase,
neutrophils and macrophages increased by 46-fold and
18-fold, respectively, 1 day after injury but returned to
65
control values after 7 to 14 days.148 Thus, the presence or
absence of inflammation, based on cell population, could
well depend on when the tissue is examined. The results
of this study suggest that it is unlikely that the pres-
ence of inflammatory cells would be detected weeks or
months after injury. As mentioned earlier, these collage-
nase models more closely represent acute tendonitis, so
whether a similar time response occurs in chronic tendon
injuries is unknown. More advanced biochemical analy-
sis techniques may be required to answer the question
of whether and when inflammation is present in chronic
tendon injury.149,150
Cause of Pain in Tendon Injury
Whether or not inflammation is present in the early
stages of overuse injury, it does not appear to be present
in the later stages of chronic tendinopathy and should
not be a focus of treatment. The pain experienced by
chronic tendinopathy clients was previously attributed to
the presence of inflammatory mediators, but this expla-
nation now appears unlikely.151,152 Nonsteroidal anti-
inflammatory agents (NSAIDs) may influence the pain
experienced by clients, but this is probably via their anal-
gesic rather than anti-inflammatory properties. The rapid
effect of corticosteroid injection in the tendon sheath on
the pain of chronic tendon injuries has been attributed to
other possible mechanisms or to an alteration in neural
factors within the tendon.152
The apparent lack of signs of typical inflammation
in tendon has led to a search for other explanations for
the cause of the pain experienced by clients with chronic
tendinopathy.152–155 Perhaps the pain in chronic tendi-
nopathy comes from the physical disruption of the tis-
sue itself, via noninflammatory biochemical substances
(e.g., collagen fragments, PGs) that may irritate the
free nerve endings within the tendon.155–157 Perhaps
neurotransmitters are released from afferent nerves in
response to abnormal signals from the damaged tendon,
or lactate levels increase and cause pain.158 The release of
neural peptides into the periphery causes a tissue reac-
tion termed neurogenic inflammation.158,159 In contrast
to the classic inflammatory response to tissue trauma or
immune-mediated cell damage, neurogenic inflamma-
tion is driven by events in the central nervous system
and does not depend on granulocytes or lymphocytes
in the tissue. Afferent nerves may become so sensitized
that a low-intensity stimulus such as a slight movement
or minimal deformity of surrounding tissues can gener-
ate pain. This phenomenon, allodynia, has been impli-
cated in chronic degenerative arthritis, low back pain,
and severe irritable bowel syndrome and interstitial cys-
titis, and it also may play a role in complex regional pain
syndrome. This pain mechanism, referred to as the neu-
rogenic model of tendon pain, appears (at the moment)
66 SECTION I • Scientific Foundations
to be a possible explanation for pain in chronic tendi-
nopathy.152
The neurogenic model of tendon pain holds that
neuropeptides such as substance P (SP), calcitonin gene-
related peptide (CGRP), and glutamate are increased in
cases of chronic tendinopathy, and that they are respon-
sible for increased pain responses to mechanical stimuli
from tendon loading. This theory is supported by the
fact that the supply of nerve and blood vessels increases
in chronic tendinopathy,160 and glutamate is increased.161
Glutamate is known to act as a pain neurotransmitter in
the central nervous system, and it has been theorized
that chronic tendon pain may be neurogenic in origin.
Injection of glutamate into muscle causes increased
sensitivity to pain,159 and the central nervous system
role of glutamate in pain transmission is well known.157
Neuropeptides have been shown to be present in heal-
ing tendon and to be related to nociception; they also
have been found in and around human tendons.160–168
Increased levels of these neuropeptides appear to cause,
or accompany, new blood vessel formation, which appears
to correlate with tendon pain.160,162,164
Other Factors in Tendon Injury
There are numerous metabolic factors capable of influ-
encing tendon physiology that remain largely unex-
plored. Some individuals develop tendinopathy despite
an apparently normal loading environment, suggesting
there may be other reasons why tendons, previously
pain free, become symptomatic. Endocrine responses to
stress, such as increased glucocorticoid and catechol-
amine release,106,107 may have negative effects on con-
nective tissue,169–173 increasing turnover and resulting
in decreased cross-linking. Strenuous training, or even
a mild illness imposed on training, has been shown to
alter the immune system and to have negative influences
on several body systems. Hormones can influence con-
nective tissues such as tendon and apparently can even
cause tendinopathy, but no clear relationship has yet
been demonstrated in athletic cases of tendinopathy.171
Nevertheless, tendon injury is closely linked with other
clinical disorders such as renal transplantation,172,173
and it has even been suggested that some blood groups
may be associated with a higher incidence of tendinop-
athy.174,175 It is interesting to speculate that an endo-
crine response to chronic levels of overtraining may be
at least a partial explanation for cases of tendinopathy
that develop spontaneously. Certainly tendons can be
dramatically affected by changes in their metabolic or
biochemical milieu, as illustrated by the relationship
between fluoroquinolone use and a variety of tendon
pathologies.176–180
Adequate amounts of amino acids supplied by a nor-
mal healthy diet are required for all protein synthesis,
including collagen. Cofactors such as vitamin A, vita-
min C, and copper are known to be important in col-
lagen synthesis and cross-linking.20 Iron deficiency can
also have a negative influence on healing.181 There is
some evidence to suggest that collagen synthesis is more
severely affected than some other proteins during fast-
ing,170,182 which may have some implications for individu-
als involved in sports that emphasize a slender build, such
as gymnastics and ballet, or even for people who are diet-
ing. The nutritional influences on chronic tendinopathy,
however, remain largely unexplored.
Treating the Injured Tendon
Acute Tendon Injuries
Much is known about the healing of severed tendons,
mainly from models in which the tendon has been
divided, surgically or accidentally, and the severed ends
approximated and held in place via immobilization or
suture.26,183–189 These models have explained a tremen-
dous amount about tendon healing under these condi-
tions, particularly the timing of the biochemical and
mechanical changes that take place in the healing ten-
don. The initial inflammatory stage triggers an increase
in GAG synthesis within days, rapidly followed by syn-
thesis of types I and III collagen, such that the healing
wound can be subjected to low levels of force within
a matter of days.36,49,183,189 The judicious application of
force encourages the new collagen fibrils to align in
the direction of force application. Healing tissues that
are subjected to graduated loading are almost always
stronger than unloaded tissues, whether the example
is skin, ligament, or tendon.65,68,70,71,73,82 The applica-
tion of these principles in plastic surgery has led to the
design of early motion programs after tendon repair
as well as rehabilitation programs based on scientific
principles.
The healing response must be respected in cases of
acute tendinopathy, and PRICEMM is the treatment of
choice—Protection, Rest, Ice, Compression, Elevation,
Modalities, Medication—as it is in any acute injury. The
inflammatory response should be limited in cases of para-
tendinopathy, since inflammatory changes in the sheath
may lead to degenerative changes within the tendon, and
friction between the sheath and the tendon should be
reduced. In cases of chronic tendinopathy, a therapeutic
focus on limiting inflammation is inappropriate. The out-
line for the treatment of acute tendon injuries was shown
in Table 3-5.
Chronic Tendon Injuries
Some Assumptions about Chronic Tendinopathy
The current understanding of chronic tendinopathy
remains incomplete, so the development of a rational
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
treatment strategy requires making some assumptions,
based on the available evidence. These assumptions may
or may not be true, but they allow the development of
a logical, and successful, approach to the treatment of
tendinopathy.
Assumption 1: Inflammation Is Not a Focus of
Treatment in Chronic Tendinopathy. Despite the
ongoing debate about whether the physiological pro-
cess of tendinopathy involves an inflammatory stage, it
seems clear that inflammation, at least as it is viewed in
wound healing, is not a part of chronic tendinopathy.
This should eliminate the use of most modalities or anti-
inflammatory medications and direct the clinician toward
loading-based rehabilitation.
Assumption 2: Chronic Tendinopathy May Become
Acute and Can Then Be Treated Using the Healing
Model. Acute tendon injuries by definition will pass
through the stages of healing as defined in Table 3-5
and so can be treated using these guidelines. Almost
all cases of acute tendinopathy will be fully resolved in
6 weeks or less if the time of injury is known. Chronic
tendinopathy has either passed through or bypassed the
acute stage but, if returned to it, can also be treated
appropriately. In other words, if a chronically injured
tendon is further damaged to the degree that an inflam-
matory response is produced, it can be treated like an
acute tendonitis. This may explain the success of surgery
or tendon splitting, which could provoke a classic heal-
ing response. The definition of an injury as acute should
not depend solely on the length of time that dysfunction
has been present but rather on the nature of the client’s
signs and symptoms. Whenever marked swelling, ten-
derness, warmth, and redness are present, the injury
should be treated according to acute injury guidelines.
Although most cases of overuse tendinopathy are not
inflammatory in nature, the clinician should not over-
look these signs when present in a client with a long-
standing tendon disorder. This approach minimizes the
chance that the client’s condition may be made worse
through overzealous treatment and a refusal to accept
the possibility of an inflammatory process in longstand-
ing tendon injuries. Acute injuries superimposed on
chronic injuries will generally take a longer time for
complete recovery because the loading progression will
need to be more gradual.
The flare-up that occurs after too vigorous treatment
usually convinces the clinician that a more conservative
approach is required. The advantage is that the time of
tendon injury is now known—it was the last treatment!
If a tendon injury is inadvertently returned to the acute
stage, the treatment progression becomes easier to visu-
alize. The appropriate use of modalities and the progres-
sion of tensile loading can be matched with the stage of
healing, producing an evolving treatment strategy (see
Tables 3-5 and 3-6).
67
Assumption 3: Pain Can Be Used to Monitor
Treatment Progression. Pain is monitored to assess
the progression of tendon recovery, and treatment is
modified as the pain changes. There are drawbacks to
this approach, because pain is a very subjective percep-
tion, but it appears to be the most clinically useful way to
monitor client progress (see Table 3-7). Though clients
may have degenerative changes without inflammation,
all have pain, the reasons for which are as yet unknown.
There is no known correlation between clinical signs and
symptoms and tendon pathology, so this assumption is
based purely on clinical observation.
Assumption 4: The Effects of Exercise and Disuse
Will Be the Same for Chronically Injured Tendons
as for Other Connective Tissue Structures. Exercise
should cause the tendon to adapt to progressive load-
ing, if the effects of exercise and disuse are the same for
chronic tendinopathy as for normal and healing tendons
and ligaments. These adaptations in structural or material
properties will allow the tendon to withstand the forces
to which it is subjected during activities.
There is no way of knowing at present whether
these assumptions are correct. They are theories that
have not been tested. Much research remains to be
done to determine the sequence of events in tendon
healing in tendinopathy and to examine the correla-
tion between clinical symptoms of soft tissue injury
and quantitative measures, such as tissue imaging with
US or MRI, or serum or urine markers of connective
tissue metabolism.
General Principles for Treating Tendinopathy
There are many principles, physiological and mechanical,
that should be considered when treating chronic tendi-
nopathy, such as possible causes of the problem and the
nature of damage to the tendon. It is helpful to develop
a framework that can be applied to all forms of chronic
tendon injury. This reduces the possibility that the clini-
cian will miss something that may be a factor in an indi-
vidual’s case. The following guidelines can be used for
treating all forms of tendinopathy.
General Principles of Tendinopathy Treatment
● Identify and remove negative external forces/factors
● Establish stable baseline treatment
● Determine tensile load starting point
● Use symptoms to guide loading program
● Control pain
● Address use of whole kinetic chain
● Employ specificity
● Use maximum loading
● Load progression
68 SECTION I • Scientific Foundations

1. Identify and Remove All Negative External Forces/
Factors. With extrinsic tendinopathy, the outside force is
usually pressure on the tendon. Treatment involves identi-
fication and removal of the source of pressure. This step is
essential to avoid further tendon damage. Other forms of
treatment, such as modalities, however helpful in relieving
the symptoms of extrinsic tendinopathy, can be considered
only temporary or adjunctive. Eliminating the cause is the
fundamental treatment. A simple example is tenosynovitis
of the extensor tendons at the ankle joint caused by pres-
sure from tight laces in a skate or shoe. Loosening the laces
or using a device to redistribute the force may remove
the pressure. A more complicated example is shoulder
impingement syndrome, in which the appropriate treat-
ment is removal of the cause of impingement. Some causes
of shoulder tendinopathy are presented in Table 3-8. A
compression etiology also has been proposed to explain
some resistant cases of patellar tendinosis.113
In some cases, external factors may be contributing to
tendinopathy more indirectly. Excessive foot pronation
can cause the medial side of the Achilles tendon, or the
tibialis posterior muscle-tendon unit, to be overstretched.
Under these circumstances, the medial side of the Achilles
tendon is forced to elongate more than the lateral side, and
a shoe insert should be used to redistribute the forces.
The most common contributing factor in most cases
of chronic tendinopathy may be a lack of flexibility of the
involved muscle-tendon unit and perhaps others as well.
A thorough and specific stretching program is nearly always
an essential part of the rehabilitation strategy if examina-
tion reveals limited range. Since tendon damage occurs as
the tendon is strained, improving the overall length of the
muscle-tendon unit may decrease deformation within the
tendon during subsequent functional movements.190,191
2. Establish a Stable Baseline for Treatment. The
client’s symptoms should be stable and predictable before
treatment begins, otherwise it will be difficult to assess
the effect of any intervention. This may require a reduc-
tion in activities that load the muscle-tendon unit or the
use of analgesic medications. Once a stable baseline is
achieved (usually within 1 to 2 weeks), exercise inter-
vention can begin. If the client’s symptoms are already
stable, no modification is required and exercise loading
can begin immediately.
3. Determine the Tensile Load Starting Point. This
is an imprecise process, based on the client’s size, strength,

Table 3-8
Examples of Shoulder Tendinitis
Impairment Suggested Mechanism Possible Solution

Weak scapular rotators Lack of scapular lateral rotation Strengthen lateral rotators (lower trapezius, serratus anterior) or
during overhead movements teach proper recruitment during overhead movements
increases demand for Assess via observation and measurement of scapular rotation
glenohumeral motion to during movement
achieve hand position
overhead, possibly causing
anterior impingement
between acromion and
humerus
Excessive shortening of
glenohumeral muscles creates
decreased force production,
requiring recruitment of more
motor units and leading
to fatigue
Adhesive capsulitis Capsule tightness prevents Joint mobilizations to increase capsule tissue length; capsule
humeral head from gliding stretching exercises
during elevation of upper Assess via physiological and accessory range of motion
limb, leading to excessive measurement
upward movement of humerus
and impingement against
acromion
Rotator cuff tear Capsular venting leads to Strengthen rotator cuff muscles to increase humeral head
glenohumeral hypermobility, stabilization against glenoid; may require surgical repair
allowing excessive upward Assess via symptoms during overhead movements and via strength
gliding of humeral head as testing of rotator cuff muscles
deltoid activates during
shoulder abduction
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations 69

and activity patterns, and requires judgment based on
the examiner’s clinical experience to become accurate.
Generally, the more severe the client’s symptoms, the
lower the starting load. Those who have worked with large
numbers of clients may better recognize the appropriate
starting point for loading; however, there is no harm in
underestimating the load and “catching up” over a few
days to a week. If the condition worsens, the clinician can
reduce the load until symptoms have stabilized. Conversely,
if the pain is mild and function only mildly restricted, a
larger starting load is indicated. Recommendations for
starting loads for some representative examples of chronic
tendinopathy are presented in Table 3-9.
4. Progress the Loading Program According to
Client Symptoms. The tendon must be loaded if colla-
gen synthesis, alignment, and maturation via cross-link-
ing are to be ideal, and this loading must be progressed
so that there is a stimulus for further adaptation. The
more severe the injury, the lower the starting force
and the slower the progression.136 Even acute tendi-
nopathies should be treated with progressive loading.
Passive movement produces little tensile force, is safe
immediately after injury, and is known to have benefi-
cial mechanical effects on tendon.74 Gentle stretching
would be the next step, followed by increased stretch-
ing force and then active exercise. For chronic tendi-
nopathy, progressive tensile loading via resisted exercise
should be used.
5. Control Pain. If load is progressed appropriately,
it is unlikely that an acute injury will be produced, but
this may occur. If pain is interfering with activities of daily
living or if a stable baseline of pain and function can-
not be achieved, then the clinician should focus on pain
control. If signs of inflammation are present, additional
help may be needed to reduce a prolonged inflammatory
response. In such cases, medications, ice, and modalities
can be used as adjuncts to treatment.
6. Address the Entire Kinetic Chain. The clinician
should examine the rest of the upper or lower extremity
to determine deficits in range, strength, and motor con-
trol. Strengthening and control of proximal segments,
including “core stability,” may be indicated. A change
in landing pattern is frequently required for clients with
Achilles or patellar tendinopathy, while shoulder and
scapular muscle retraining may be required for clients
with lateral epicondylitis. Since the kinetic chain func-
tions as a multisegment unit, malfunction in one seg-
ment can increase stresses on other segments.

Table 3-9
Examples of Chronic Tendinopathy Starting Points for Loading
Suggested Starting
Example Client Pain Function Point for Loading Other

45-year-old club Lateral elbow 7/10 Decreased playing 2.5 kg, lower and raise Mild to moderate
“A” level tennis with >45 minutes time because of weight slowly tendinopathy, should be
and squash tennis or squash elbow pain If no elbow pain by 30 able to progress fairly
player, elbow Lasts 2-3 hours after Does not enter repetitions, increase rapidly
pain × 3 months onset tournaments speed of movement, No need to specifically
0/10 during daily Overall sense of drop weight rapidly curtail activities, client
activities condition worsening Once symptoms has already adjusted
provoked, slow participation appropriately
movement slightly
for next exercise session
28-year-old 2/10 at rest Working at 75% of Weight on both feet, Severe tendinopathy
bodybuilder with 3/10 during preinjury load heels over edge of step, (pain at rest)
pain in Achilles slow walking because of pain lower slowly Should reduce or
tendon × 6 weeks 6/10 during Unable to run If no change in avoid Achilles tendon
fast walking pain by 30 repetitions, loading during workout
8/10 during drop more rapidly, until no pain at rest
resisted exercise but still controlled May require very
Monitor pain carefully, gradual load progression
should be 2/10 until and careful monitoring
20-30 repetitions, of pain level
then increase to
about 6/10
21-year-old After vigorous practice Normal Unilateral weightbearing, Mild tendinopathy
basketball player or game 4/10 drop rapidly and catch May tolerate more rapid
Lasts 2 hr (drop and stop) progression in loading
70 SECTION I • Scientific Foundations
Specific Forms of Treatment
Modalities
Clinicians employ a wide variety of modalities in treat-
ing soft tissue disorders, including ultrasound, laser, ice,
heat, pulsed electromagnetic current, electromagnetic
field therapy, high-voltage galvanic stimulation, acu-
puncture, and interferential current. Most are proposed
to “decrease inflammation and promote healing.” There
is only limited evidence to date to support these claims.
Ultrasound is one of the most commonly used modal-
ities. Generally, pulsed ultrasound is recommended for
acute injuries to avoid a thermal effect, and continuous
ultrasound is used for more longstanding injuries.192,193
Although there have been reports that ultrasound has
no influence on healing tendon,194 studies have shown
that it increases the fibroblasts’ synthesis of collagen,195
speeds wound healing,192 and increases tensile strength
in healing tendons.196,197 Ultrasound has little or no effect
on inflammation.198 Probably its most important effect is
when the synthetic activity of the fibroblasts is maximal
(i.e., in the proliferative stage of healing).192,195,199 There
is little indication for using ultrasound for prolonged
periods of time. While there is some theoretical basis for
the use of ultrasound in acute tendinopathies, there is
limited evidence to support its use.200 The use of ultra-
sound for chronic tendinopathy is not indicated.
Electrical stimulation is a modality that has also been
demonstrated to have a positive influence on tendon
healing.201–205 Like most studies on modalities, results
were obtained using an acute tendon healing model
and so may not represent chronic tendon injuries. Both
direct electrical stimulation202 and indirect current via
electromagnetic field induction201 seem to augment ten-
don healing. Pulsed electromagnetic fields can treat both
deep and superficial tissues and cover larger areas than
ultrasound or laser.201 Questions about timing and dos-
age remain, but it appears that treatment needs to be
prolonged to several hours daily to have an influence on
tissue, since clinical use for shorter periods has not shown
the same positive effects.205
One of the most widely used modalities for all soft
tissue injuries is ice. Its use is recommended immediately
after injury to prevent excessive soft tissue swelling. Ice is
thought to act mainly by decreasing the activity of inflam-
matory mediators and decreasing the overall metabolic
rate of the injured tissue.206 Another important effect is
analgesia, which allows the use of appropriate forms of
exercise, such as passive motion, that otherwise might
be uncomfortable for the client. The rationale for the
use of ice with chronic injuries is less clear, although it
can be used for its analgesic effect, and it may help offset
inflammatory changes induced by mechanical injury to
the tendon during exercise.
Although the use of modalities is widespread, it remains
largely speculative in the treatment of chronic soft tissue
injuries. Scientific studies suggest that increased synthetic
activity by fibroblasts may be the major effect of most
modalities except ice. Clinicians should keep in mind that
this synthetic activity occurs mainly during the proliferative
phase of healing, and this is probably the phase in which
modalities will have the greatest effect on healing tissues.
The effects of modalities on chronic injuries remain largely
unexplored, and more well-designed clinical trials are
needed to determine their efficacy in the clinical setting.
Transverse Friction Massage
This technique was recommended by Cyriax as a treat-
ment for chronic tendinopathy and is often used by clini-
cians.207,208 Adhesions between tendon and surrounding
tissue may cause continuous tissue irritation and inflam-
mation, and some believe that transverse friction massage
will release these adhesions. An increase in local blood
flow from the hyperemic response to finger pressure is
also thought to occur. Transverse friction massage may
create a tensile force as the downward pressure on the
tendon creates a “bowstring” effect.209 The exact effects of
friction massages are not known, and although both positive
effects and “no effects” have been claimed, the technique is
widely recommended by experienced clinicians.207–210
Manipulation and Mobilization
The use of manipulation or mobilization to treat chronic
tendinopathy has been recommended for lateral epi-
condylitis, where it has been shown to strengthen grip
immediately and to decrease symptoms.211–213 The manip-
ulation may be local, or vertebral if pain is thought to be
referred from the spine.211,214 The mechanism for pain
relief is suggested to be neural. These techniques have
been used to treat some other forms of tendinopathy,215
but this is not a common approach.
Extracorporeal Shock Wave Therapy (ESWT)
ESWT has been used to treat various connective tissue
disorders such as plantar fasciitis, shoulder tendonitis,
Achilles tendinopathy, and lateral epicondylalgia. Both
positive and negative results have been reported.216–225
Systematic reviews support the use of ESWT for calcific
shoulder tendonitis,225 but the evidence for other uses
is still lacking. There is considerable variability in the
dosage parameters used in different studies, which may
account for the different results observed. Further stud-
ies on this modality are required.
Acupuncture
Acupuncture has been recommended for various chronic
injuries, including tendinopathy. It has been reported to be
successful in the treatment of lateral epicondylalgia,226–230
and systematic reviews have found moderate evidence to
support the use of acupuncture to relieve chronic lateral
elbow pain.229,230
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
Orthotics
Various braces and supports are frequently used in cases
of chronic tendinopathy. Most often, the device is applied
and the client’s symptoms assessed for severity during a
function activity, such as gripping in lateral epicondylalgia
or jumping in patellar tendinopathy. If the client’s symp-
toms reduce, the device can be used to allow the client to
participate in functional activities. Elbow taping has been
shown to reduce pain and increase grip strength,231 and
band-type devices have been used for epicondylitis,232
patellar tendinopathy,233 and heel pain.234 The mecha-
nism is thought to reduce slightly the force applied to
the bone-tendon junction.235 These devices have been
recommended on an empirical basis,236 but as yet there is
little evidence to support their use.237
NSAIDs and Topical Medications
Nonsteroidal anti-inflammatory agents (NSAIDs) are
widely used to treat acute soft tissue injuries but less so
to treat chronic injuries such as tendinopathy.238–240 They
limit inflammation by inhibiting prostaglandin synthesis
or release, depending on the drug. Unlike corticoste-
roids, they do not inhibit fibroblast or macrophage activ-
ity.239 Although some evidence shows that preventive use
of indomethacin may reduce subsequent muscle injury in
cases of delayed-onset muscle soreness (DOMS),238 most
clinical studies have not been designed well enough to
firmly conclude whether the use of NSAIDs has a benefi-
cial effect on postinjury recovery.240,241 There is moderate
evidence to support their use in acute tendinopathies.241
Given the noninflammatory nature of chronic tendinop-
athy, the success of NSAIDs in reducing chronic tendon
pain appears to be through their analgesic properties.
They can be useful in reducing pain to establish a stable
baseline for the introduction of gentle loading exercise,
but caution should be exercised in progressing loading
in cases in which analgesics are used to control pain.
Stretching and low-load exercises may be more appro-
priate than progressive exercises, for example. After 1 to
2 weeks of successful exercise without pain, the client
should be weaned from the medication before exercise
is progressed. Topical medications also have been used
successfully to treat chronic extensor tendinosis (lateral
epicondylalgia).242
Iontophoresis and Phonophoresis
This technique has seen renewed interest as equip-
ment and delivery methods have become easier to
use.243 Iontophoresis using corticosteroids has been
reported to decrease pain in acute lateral epicondy-
litis and Achilles tendon pain,244,245 but it does not
seem to be effective in treating plantar heel pain.246,247
Iontophoresis may be an alternative to injection in
cases in which the injured structure lies within 1 to
2 cm of the skin surface.248 Iontophoresis appears to be
71
useful for relieving pain but to have little or no effect
on long-term outcome.
Phonophoresis, or the use of ultrasound to increase
the penetration of topical medications, also has been
recommended to treat tendon disorders.249 Some
researchers have reported that it has positive effects on
pain associated with lateral epicondylitis250 and resolves
calcific tendonitis of the shoulder.251 Others have
reported that phonophoresis is no more effective than
regular ultrasound252 or than other forms of intervention
such as stretching and resisted exercise.253
It appears that neither phonophoresis nor iontophoresis
is effective in the long-term treatment of chronic tendinop-
athy, although either may be of some benefit for relieving
pain in the short term. This pain relief may help establish a
stable baseline and allow the earlier start of progressive ten-
don loading. These techniques probably should not be used
simultaneously because symptoms may worsen.254
Injections
The most potent anti-inflammatory drugs are the cortico-
steroids, which are sometimes used, via local injection, to
treat chronic tendinopathy. The negative effects of systemic
corticosteroid use are well known,95,98 but the effects of
local injection are less clear. Both negative effects and “no
effects” have been reported.255–261 Corticosteroid injec-
tion has been shown to have superior short-term results
in treating lateral epicondylitis, compared to physical
therapy, but not when examined on a longer-term basis.259
There seems to be general agreement that injection into
the tendon substance of larger tendons should be avoided
because of the effects of the drug (which decreases col-
lagen synthesis), the mechanical disruption caused by the
needle and the volume of fluid injected, and the irritant
effect of the solvent in which the drug is dissolved.258,261
Since most inflammatory changes occur in the paratenon,
injection into the tendon sheath may be useful when
inflammation is marked or prolonged.255,256,261 Researchers
have challenged the taboo against intratendinous injection
by injecting corticosteroid into the Achilles tendon and
demonstrating rapid reduction in signs and symptoms,
at least on a short-term basis.147 A more recent injection
technique for treating chronic tendinopathy addresses the
neovascularization that has been observed in chronic ten-
don injuries.262,263 A sclerosing agent is injected into the
tendon, and this appears to decrease pain.
Whatever the injection technique chosen, it may be
wise to consider the injected tendon as having under-
gone a partial rupture. Tensile force should be reduced
for 10 to 14 days, and the tendon should be treated
as if it had suffered an acute injury (i.e., ice, rest, and
modalities) followed by progressive loading starting at
about 2 weeks. Repeated steroid injections into a tendon
are almost certain to result in substantial mechanical
disruption and should be avoided.240
72 SECTION I • Scientific Foundations
Cautions When Using Corticosteroids
● Inject into sheath rather than tendon
● Treat injected tendon like an acute tendon injury
● Avoid repeated injections
Surgery
Perhaps surprisingly, there have been no randomized
controlled trials assessing the efficacy of surgery as a
form of treatment for chronic tendinopathy. Surgery is
typically used when nonsurgical approaches have failed,
and good results are generally reported.264–267 Most tech-
niques involve the removal of scar tissue and the repair of
the injured tendon, but it is possible that the postopera-
tive healing response and carefully progressed treatment,
rather than the surgery itself, cause the improvement in
the client’s condition. Complications, including infec-
tions, deep venous thrombosis (DVT), or worsening of
symptoms, occur in approximately 10% of clients under-
going tendon surgery, while only about 60% to 80% of
clients will experience an improvement in their condi-
tion.266 Most cases (>95%) of chronic tendinopathy can
be successfully treated without surgery, and because a
success rate of >90% can be expected with little or no
risk of complications, nonsurgical approaches should be
exhausted before surgery is performed.
The Role of Exercise in Treating Chronic Tendon
Injuries
Some time ago, Nirschl recommended the regular use of
resisted exercise as a treatment for chronic tendinopathy
(tennis elbow).267 Curwin and Stanish first described an
“eccentric exercise program” (EEP) for the treatment of
chronic tendinopathy.136,268,269 This program was devel-
oped in the early 1980s in response to the frustration of
unsuccessfully treating clients with chronic tendon inju-
ries. Curwin and Stanish had a large series of clients, but
they did not use a control group, nor did they randomly
assign clients to different treatment interventions, primar-
ily because of their clients’ refusal to accept other forms of
treatment that they had already tried without success. This
limited the scientific validity of their results. However, since
they first described the EEP, the eccentric exercise approach
has been used by numerous clinicians and researchers and
has been successful in the treatment of Achilles tendonitis,
patellar tendonitis, and lateral epicondylitis.260–284
All studies examining the EEP have found it effective
in treating chronic tendinopathy, although the design
of the program may vary among studies. Alfredson et
al., for example, used heavy eccentric exercise, with-
out accounting for pain, and obtained excellent results
in about 85% of clients.274 Others have used isokinetic
devices to produce the eccentric load,280 or have modified
the client’s position to increase load on the tendon.281 It
has been this author’s experience that careful attention
to the level of pain during the EEP is crucial for overall
improvement. A high level of pain (8/10 or 9/10 on a
visual analogue scale), or pain too early in the program
(before 20 repetitions), can cause a worsening of symp-
toms during functional activities (Figure 3-10). On the
other hand, if the client completes more than 30 repeti-
tions without pain, their symptoms during activity appear
to plateau (i.e., they neither improve nor worsen). The
ideal pain/load balance, as originally described by Curwin
and Stanish,136 involved three sets of 10 repetitions, with
the onset of tendon pain during the last 10 repetitions.
Whether this careful attention to pain is really necessary
requires further examination.
Though the EEP seems to be successful and is widely
used clinically, the number of well-designed studies com-
paring the EEP with other forms of treatment is still
small. There is still a need for large, controlled studies
that compare various treatment approaches for chronic
tendinopathy.
Basic Principles of Exercise Treatment for Chronic
Tendinopathy
Basic exercise principles must be followed for any exercise
program to succeed. In the treatment of chronic tendi-
nopathy, the following components are most important.
Specificity of Training. Training must be both ana-
tomically and motor specific. The correct muscle-ten-
don unit must be loaded, it must be loaded in a way
Symptoms as percentage of start level
Pain at #20 repetitions
100
No pain
Pain at "20, #30
1 2 3 4 5 6
Time (weeks)
Figure 3-10
Symptom intensity with different levels of loading and symptom
provocation. If pain is felt too early (<20 repetitions), the condition
is usually made worse. If no pain is felt, the condition remains at
the same level. When symptoms are provoked between 20 and 30
repetitions, the condition gradually improves over time, usually taking
6 to 12 weeks to resolve. (Redrawn from Curwin SL: The etiology
and treatment of tendinitis. In Harries M, Williams C, Stanish WD
et al, editors: Oxford textbook of sports medicine, ed 2, p 624, New
York, 1998, Oxford University Press.)
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
that produces controlled tensile loading, and the motor
pattern should resemble the client’s activity. The exer-
cise should, eventually, closely simulate the pattern of
loading during functional activity in the type of load-
ing (tensile; eccentric) and the magnitude and speed of
loading. Specificity is achieved by simulating the move-
ment pattern associated with maximal tendon forces (i.e.,
a lengthening of the active muscle-tendon unit followed
by shortening contraction). The initial magnitude and
speed of loading are based on the estimated stage of heal-
ing. The more acute the injury, the lower the force and
the slower the eccentric loading. The affected tendon
must be subjected to specific, controlled tensile load-
ing, not just a generalized exercise involving use of the
affected muscle-tendon unit. The Achilles tendon, for
example, is loaded by having the client stand at the edge
of a step and drop his or her heels downward rather than
running, even though the latter creates large loads on
the Achilles tendon (Figure 3-11). The patellar tendon
can be loaded via squat-type exercises, while the wrist
Figure 3-11
Increasing Achilles tendon forces during toe-raising exercises over
the edge of a step and three sports-related activities. Slow 1, Fast 1
= weight on one foot; slow or fast speed. Slow 2, Fast 2 = weight on
both feet, slow or fast speed. Fast + Weight = extra weight added to
body. Run = sprint running. Jump = landing from 50 cm. Push-off =
a change in direction from backward to forward running. The slow
and fast movements represent progressive steps in the clinical exercise
program to treat Achilles tendinitis. (From Curwin SL: Tendon
injuries: pathophysiology and treatment. In Zachazewski JE, Magee DJ,
Quillen SW, editors: Athletic injuries and rehabilitation, p 36, 1996,
Philadelphia, WB Saunders.)
73
extensors can be loaded via wrist flexion/extension. The
aim of such specific loading is to isolate the mechanical
effects of the exercise on the tendon from any potentially
negative effects associated with stressful training such as
running.
Maximal Loading. Maximal loading is essential to
induce adaptation in musculoskeletal tissues. In the case
of an injured tendon, maximal loading can be defined
as the force the tendon can withstand without further
injury. Since one cannot measure this clinically, the cli-
ent’s pain/function level is assumed to reflect potential
tendon damage. The client’s pain level during exercise is
assumed to reflect the tendon’s tolerance for load and is
used as a barometer to determine when the load should
be changed. The client should experience pain during
the last 10 repetitions of three sets of 10 repetitions of
the chosen exercise. Curwin and Stanish determined
empirically that the most rapid and consistent improve-
ment occurred if the client experienced pain between
the 20th and 30th repetitions of the specific loading
movement.136 They found that pain before this point
(<20 repetitions) was usually accompanied by overall
worsening of the client’s condition, and they assumed
this indicated overloading. Clients who experienced no
pain or discomfort during the 30 repetitions, yet who
continued to have symptoms during functional activi-
ties, did not see any change in overall status (see Figure
3-10). Curwin and Stanish interpreted this as suggest-
ing that the loading stimulus was inadequate to induce a
change in the tendon and recommended that loading be
increased to induce further adaptation.
Progression of Loading. As the tendon becomes
stronger, loading must be progressed so that maximal
loads continue to be applied and the tissue will continue
to have a stimulus for adaptation. This progress can be
made by increasing the speed of movement (based on
the muscle force-velocity relationship) or by increasing
the magnitude of the tensile force through changing
the external resistance (Figure 3-12). The progression is
from slow to fast at a given load (thus increasing force,
since the movement is eccentric), followed by increas-
ing the load and repeating the slow-to-fast sequence.
Variations of speed versus load may be applied once the
clinician is familiar with the program and with the cli-
ent’s response to exercise progression.
Curwin and Stanish136 established the initial load
progressions for eccentric exercise loading of chronic
tendon disorders based on the assumption that pain
could be used as an indicator of the appropriateness of
exercise intensity. Their main assumption was that the
levels of pain and dysfunction experienced by the client
are a reflection of the degree of injury to the tendon. Pain
is therefore used to titrate the amount of load applied
to the tendon; as pain decreases, load is increased.
There is no direct evidence to support this view. It is
74 SECTION I • Scientific Foundations

Chronic Tendinopathy Eccentric Exercise Program

● Warm up
● Employ flexibility stretching
● Use specific eccentric exercises
● Repeat flexibility stretching
● Apply ice

2. Stretch to improve flexibility. As noted earlier, lack of

Figure 3-12
Flowchart illustrating the progression of the eccentric exercise program
according to the client’s symptoms. Loading should progress whenever
pain diminishes and is not felt by 30 repetitions. Conversely, exercise
should not progress until the pain level reduces. (From Curwin SL,
Stanish WD: Tendinitis: its etiology and treatment, Lexington, Mass,
1984, DC Heath.)
based on trial and error in the treatment of hundreds
of clients diagnosed with chronic tendonitis.136 Some
authors have successfully used heavy loading exercise
to treat tendonitis without basing progression on client
discomfort, suggesting that such careful attention to
pain may not be necessary with all client populations.274
Since the source and mechanism of tendon pain remain
unknown,155 the use of pain as an indicator for treat-
ment is empirical.
Eccentric Exercise for Chronic Tendinopathy
The principles and methods of the eccentric exercise
program were first described by Curwin and Stanish.136
Although others have made modifications, the program
generally reflects the process described here. The program
can be applied to any injured tendon, but it appears to
be most successful in cases in which “overuse” is part of
the etiology. The guidelines for treatment progression
are shown in Figure 3-12. The overall program has five
steps, which are performed in this order:
1. Warm up. A generalized exercise such as cycling
or light jogging is used to increase body tem-
perature and increase circulation. This exercise
is not intended to load the tendon and should
not cause local pain or discomfort. It is possible
that local heating modalities, such as hot packs
or ultrasound, could be used instead to warm the
tendon.
flexibility is a common finding in chronic tendinop-
athy. It is recommended that the client perform at
least two 30-second static stretches of the involved
MTU and its antagonist(s). More stretching may be
done if lack of flexibility is thought to be a major
factor in causing the client’s symptoms (i.e., if func-
tional range of motion is far from normal). In this
case, flexibility and restoration of range of motion
also may become a separate focus of treatment.
3. Complete the specific exercise. The EEP is done fol-
lowing the guidelines presented in Figure 3-12,
based on the principles outlined previously. It is
suggested that the client perform three sets of 10
repetitions, with a brief rest or a stretch between
each set. Symptoms should appear after 20 repeti-
tions (i.e., between 20 and 30 repetitions). The
level of discomfort should be similar to that felt
during activities and should not be severe or steeply
increase in intensity with each repetition (the client
should stop exercising if this occurs). If the client
feels pain before the 20th repetition, reduce the
speed of movement, or decrease the load; if the
client does not experience pain by 30 repetitions,
increase speed or load (not both).
If this is the first exercise session and the initial
level of loading is being determined, the intensity
of exercise (load) may be increased until symptoms
are reproduced. If the client has done >30 repeti-
tions when this occurs, stop for the day and use the
same (final) load for the next exercise session. If the
client has done <20 repetitions when pain occurs,
reduce the load slightly and continue. The amount
of reduction will require clinical judgment, based
on the level of symptoms and the starting load. In
general, a load adjustment of 10% to 20% will be
appropriate.
The response to the initial treatment (severity
of pain) will determine whether subsequent treat-
ment should be more or less vigorous. The client
should note the severity of any pain experienced
and record its duration. An increase in pain during
nonexercise activities is a sign to reduce loading.
Since it is much easier to increase exercise inten-
sity incrementally than to recover from overzealous
loading, clinicians should err on the side of under-
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
loading during initial treatment sessions. Load
can be increased in subsequent sessions until the
proper repetitions-pain balance (between 20 and
30 repetitions) is achieved. This usually takes no
more than two to three treatment sessions.
4. Repeat flexibility exercises (see step 2).
5. Apply ice. Ice is applied for 10 to 15 minutes to the
affected (painful to palpation) area. It is hoped that
this will help prevent any (hypothetical) inflamma-
tory response provoked by microscopic damage to
the tendon that might occur during the exercise. It
will also decrease pain.
Many clients with chronic tendinopathy are able to
participate in functional activity but find their participa-
tion painful (level 2/3) or their performance impaired
(level 4/5). Using the new International Classification
of Function, Health, and Disability (ICF) model of the
World Health Organization (WHO), these clients have
an impairment and a functional limitation, and they may
have a participation restriction.285 It is not essential for
clients to cease participating in activities while carrying
out the eccentric exercise program, unless they are unable
to perform their activities satisfactorily or their symptoms
are becoming worse. Ideally, nothing will change except
for the addition of the exercise program. This means
that only one variable has changed, allowing the effect
of treatment to be more accurately assessed. A decrease
in physical activity, changing a second variable, usually
will cause a parallel decrease in symptoms. This makes
it difficult to distinguish whether it is reduced activity
or the clinical intervention that is responsible for any
improvement. However, clients should not participate
in strenuous activities immediately before or after the
therapeutic exercise program (especially before), as this
may alter their pain response during the EEP. On the
other hand, clients who experience pain throughout an
activity should not force themselves to continue to par-
ticipate. Rather, these clients should reduce their func-
tional activity level until the point where they are able to
load the tendon moderately during the eccentric exercise
program. Usually this will mean a fairly rapid loading pat-
tern plus some external resistance. At that point, activi-
ties (e.g., running, jumping, fast walking, gripping) may
be reintroduced in a graded fashion by progressing the
time or intensity of participation.
Once the initial loading sequence is determined,
which usually takes two to three treatments, many clients
can be successfully treated with a home program (indeed,
this was a major impetus for the development of the
program). The EEP is easily performed and progressed
independently, and clients can check with the physical
therapist via telephone, e-mail, or visit. Most people will
become asymptomatic within 6 to 8 weeks, meaning they
will be able to participate in work or recreational activities
with no pain and no deficit in performance. If activity was
75
reduced earlier, involvement in activities can be increased
gradually (via time or intensity) as symptoms abate. This
activity progression will generally be slower if it was nec-
essary for the client to fully withdraw from activities at the
outset of treatment. Close supervision is recommended
in the early stages of the program until the level of load-
ing, rate of progression, compliance with instructions,
and response to treatment are well established.
The exercise program is performed daily, with contin-
uous progression, until symptoms are no longer present
during activity. The overall treatment period usually will
range from 6 to 12 weeks. Many clients will experience
a slight increase in symptoms for the first 2 weeks of the
program, then will begin to see progress (i.e., decreased
pain during functional activities) as the exercise program
moves forward.
Maximum strength testing should not be performed
until treatment is complete and the client is asymptom-
atic and has returned to activity, since the maximum
force levels generated during testing (especially eccentric
isokinetic testing) may damage the healing tendon. After
symptoms have resolved and functional activity is normal,
testing may be helpful to detect residual deficits or left-
right asymmetries. Strength deficits may persist even after
the symptoms of tendinopathy have reduced, suggesting
that testing may be beneficial in some cases to determine
whether strength training (progressive loading) should
be continued.286
It may be necessary to modify activity if symptoms are
more severe or are continually present. Most clients will
not seek help until function is affected, so many individu-
als may have already been forced to curtail their activity.
Level 5/6 symptoms (pain throughout activity or dur-
ing activities of daily living, see Table 3-7), especially, are
interpreted as reflecting a process of acute tendinopathy,
even though symptoms may be longstanding. Treatment
is commenced at a very low level—ice, gentle stretch-
ing, passive movement, modalities to stimulate collagen
synthesis, and medication if deemed necessary—until a
stable baseline is established. Treatment is progressed
as symptoms reduce, so that by 2 weeks more vigorous
exercise can usually be introduced. Continued progres-
sion as described in Figure 3-12 is usually then possible.
If the client has ceased participating in activities, the
stage between ending a rehabilitation program and resum-
ing full activity is the biggest challenge for both the injured
client and the clinician. However, when the client has
been able to continue activity in parallel with treatment,
this is not so great a problem. There are no strict rules
to guide reintroduction to activity after tendinopathy, but
it is recommended that nonathletic activities be pain free
and that the client be performing the appropriate eccen-
tric exercise rapidly. When the movement pattern (speed)
and load begin to reflect those that might occur during
activity, then it is probably appropriate for the client to
76 SECTION I • Scientific Foundations
begin participating in functional activities at a fairly low
intensity. It is safer and more satisfying for the client and
the clinician to start at a low level and progress rather than
try to resume participating at the preinjury level and find
this impossible to achieve. A too rapid return to preinjury
levels of involvement is probably the most common cause
of recurrence of tendon injuries. Clients can begin partici-
pating in functional activities at about 25% of the preinjury
level (duration or intensity, depending on the activity and
movement); initially they should participate on alternate
days to avoid muscle soreness and to evaluate the tendon’s
response to training. Assuming that few or no symptoms
are produced, progression can be made in approximately
10% increments until full training has been resumed. This
should take about 8 weeks. The entire treatment period
for tendinopathy therefore ranges from about 2 weeks for
mild cases with no interruption of activity, to 12 to 16
weeks for severe cases in which no activity was possible
until 4 to 6 weeks of treatment had been carried out.
Assessing Program Efficacy
Response to Treatment
Curwin and Stanish initially designed the eccentric exer-
cise program to treat the large numbers of clients with
chronic tendinopathy who were referred to them after
the failure of other forms of treatment. They designed
the program, created an estimate of severity, empirically
determined program progression, then gathered data on
200 clients with chronic tendinopathy. They reported
that 90% to 95% of 200 clients with longstanding chronic
tendon injuries achieved complete, or near-complete, res-
olution of symptoms within 6 to 8 weeks (Figure 3-13).
Most clients had minimal or no symptoms after 6 weeks.
Most of these clients (85%) began with moderate or
severe tendinopathy, and the duration of symptoms was 6
months to 10 years. All had been treated previously with
modality-based therapies, some several times.136,268,269
Although Curwin and Stanish demonstrated that
eccentric exercise could be used to treat resistant tendi-
nopathies,136 they did not use a control group or blinded
assessment, nor did they randomly assign clients to treat-
ment interventions. These design flaws made it difficult to
determine whether their success was truly due to the exer-
cise intervention. Since then, several groups have used the
eccentric exercise program successfully to treat patellar ten-
dinopathy, Achilles tendinopathy, and lateral epicondylalgia.
Though research design flaws exist in most of these studies
as well, all studies to date have shown eccentric exercise to
be superior to other treatment interventions.270–284
Outcome Measures
There is no generally accepted outcome measure for
chronic tendinopathy. In general, outcome measures
Patellar Tendinitis
80 Achilles Tendinitis
Tennis Elbow
60
WITH THIS DIAGNOSIS
% OF TOTAL
40
20
0
Complete
Relief
Marked
Decrease
No Change
Symptoms
Worse
LEVEL OF SYMPTOMS AFTER PROGRAM
Figure 3-13
Response to the eccentric exercise program. Approximately 90% to
95% of clients experienced complete or marked relief of symptoms
after 6 weeks of exercise. Some tennis elbow clients (20%) saw no
change in symptoms, perhaps reflecting the other possible etiologies
for this problem, while 5% of patellar tendinopathy clients experienced
an increase in symptoms. (From Curwin SL: Tendon injuries:
pathophysiology and treatment. In Zachazewski JE, Magee DJ, Quillen
SW, editors: Athletic injuries and rehabilitation, p 48, Philadelphia,
1996, WB Saunders. Data from Curwin SL, Stanish WD: Tendinitis: its
etiology and treatment, Lexington, Mass, 1984, DC Heath.)
can be divided into three categories: (1) those used to
measure overall outcome (e.g., excellent, good, fair,
or a visual analogue scale), (2) those used to measure
the severity of the tendinopathy (e.g., VISA, Level sys-
tem),287,288 and (3) standardized measures that can be
used for other disorders as well (e.g., DASH, PRFE).
Most researchers use a visual analogue or Likert scale
for pain intensity or have classified clients using a system
of “excellent-good-fair-poor” or a system of “gone-
improved-same-worse.”93,95,136,267,289 These classifications
are generally based on the overall impression of the client.
Curwin and Stanish developed an outcome mea-
surement system that incorporated both pain and func-
tion.136 Pain was defined by interference with activities
and duration once present. Other authors have used this
or similar classification systems.131 Questionnaires and
tests have been developed to assess the severity of patellar
and Achilles tendonitis and lateral epicondylalgia.287–290
The VISA questionnaires for patellar and Achilles ten-
dinopathy have been validated in the clinical setting,
 CHAPTER 3 • Tendon Pathology and Injuries: Pathophysiology, Healing, and Treatment Considerations
though further assessment of these tools is required.287,288
Standardized measures, such as the Disabilities of Arm
Shoulder and Hand (DASH), have been used infre-
quently in tendinopathy research.291,292
The measures used to date to assess the level of ten-
dinopathy have no known relationship to the structural
defects in chronic tendinopathy, and no data are available
on any correlation between scores on classification sys-
tems, imaging study findings, and the severity of symp-
toms or prognosis for recovery. Agreement on accepted
measures for evaluating the severity of chronic tendinop-
athy would greatly improve the ability to compare the
results of different studies.
Reasons for Success or Failure of the Program
Most clients (85% to 90%) using the eccentric exercise
program will probably experience marked or complete
relief of pain and dysfunction within 6 to 14 weeks.136
If the eccentric exercise is not successful in treating the
client’s tendinopathy, several explanations are possible:
Reasons for Unsuccessful Eccentric Exercise
Treatment for Tendinopathy
● Incorrect diagnosis
● Incorrect loading magnitude or progression
● Not paying attention to level of pain
● Noncompliance
● Unrecognized external factors
1. Incorrect loading magnitude or progression. A slight
increase in symptoms at the beginning of the pro-
gram is not unexpected and confirms that this is a
load-related problem. The increase should be tem-
porary and should plateau rather than continue.
Reduce slightly the magnitude of loading, ensure
the client avoids doing the exercise program imme-
diately before or after strenuous activity, and encour-
age the use of ice after both the EEP and activity. For
exercise treatment to be successful, symptoms must
be related to tensile loading, usually during eccen-
tric muscle activation (symptoms may not even be
provoked by concentric or isometric testing). The
most common reason for lack of success is incorrect
program progression (see Figure 3-10): the client is
either started at too high a level (and gets worse)
or is not progressed to the next level of intensity
(and stays the same). A progressive increase in symp-
toms indicates that an inappropriate level of loading
has been chosen, or the client is doing the exercise
incorrectly. Depending on the level of symptoms,
the tendinopathy may now need to be treated as an
77
acute injury. Usually little ground is lost if the cli-
ent understands the meaning of increased symptoms
or the clinician immediately adjusts the treatment
intensity.
2. Incorrect diagnosis. After the first 2 to 3 weeks on the
EEP, loading should progress rapidly and symptoms
during activity should begin to improve. Should 2
weeks of client-directed or one week of clinician-
directed (two to three treatments) activity pass with-
out the ability to progress the load on the tendon,
the clinician should thoroughly reevaluate the cli-
ent and reconsider his or her diagnosis. If he or she
remains convinced that tensile loading is the cause
(and the solution), the loading program will need
to be adjusted. It is possible that the client does not
have tendinopathy, or there may be unrecognized
external factors that are causing or perpetuating the
problem. A thorough check of spinal and peripheral
joint range of motion (active, passive, and acces-
sory), alignment, flexibility, and resisted movements
is required in a search to reproduce the client’s symp-
toms. As a rule, if abnormal joint signs are found,
these should be treated first. Readers are encouraged
to consult other sources for more information about
detailed examination and treatment of the spine and
extremities, as well as the differential diagnosis for
various chronic tendon disorders.293,294 Failure to
respond to treatment after elimination of possible
outside factors should make the clinician suspicious
about systemic disease, overtraining, or hormonal or
nutritional imbalance. These alternative explanations
for chronic tendon symptoms are not common but
should be considered.
3. Noncompliance. The client must be encouraged to
comply with the prescribed exercise program. The
clinician may discover, for example, that a client is
performing 300, rather than 30, repetitions of the
exercise program. More rarely, he or she is not per-
forming the exercises at all or is performing them
incorrectly. Clients should be monitored closely
for the first 2 weeks, after which supervision can be
reduced. Some groups have used >30 repetitions of
eccentric exercise and have achieved good results, so
some variability in repetitions may be possible, but
three sets of 10 or 20 repetitions should be more
than adequate if performed at the right loading
level.
4. Unrecognized external factor. The clinician has failed
to identify an external cause for the client’s symp-
toms. This could be footwear, training errors, or
some other factors. The EEP is not indicated for
all cases of chronic tendinopathy, only those clearly
related to tensile loading. Consider also other mecha-
nisms of tendinopathy (e.g., compression in patellar
tendinopathy).113
78 SECTION I • Scientific Foundations
Summary
Chronic tendinopathy remains a dilemma for many clini-
cians, and the best treatment is not always possible or
recognized. The general view today is that inflamma-
tion is not an important element in the treatment of
chronic tendinopathy, and the term tendinitis should be
avoided as it suggests a physiologic process that may lead
clinicians to treat clients inappropriately. The predomi-
nant view is that chronic tendinopathies are more likely
degenerative disorders better considered as a tendinosis.
Ideally, treatment should combine both resolution and
prevention of symptoms and should be based on good
science and common sense. The source of the symp-
toms in chronic tendinopathy is not known, although
neural factors are suspected to play a role. The use of
exercise to treat chronic tendinopathy relies on the sci-
ence related to tendon adaptation to increased stress,
the clinical evidence to date that suggests that eccentric
exercise is successful in treating chronic tendinopathy,
and the common sense of participation in activities based
on the client’s ability to perform. The evidence to date
suggests that eccentric exercise is the preferred treatment
for chronic tendinopathy, although research design prob-
lems exist in most studies.295,296 Some other treatments as
well as exercise have moderate evidence to support their
use in treating lateral epicondylalgia.250 The EEP is not
the only approach to consider in treating chronic tendi-
nopathy and should not be used in isolation if other fac-
tors are also involved, but a knowledge of the beneficial
effects of tensile loading on tendon can be used to induce
adaptation in injured tendons. Adoption of common
models for chronic tendon injuries and their evaluation
and treatment would foster the accumulation of further
evidence and perhaps lead to a common framework for
diagnosis, prognosis, and a widely accepted approach to
treating chronic tendinopathy.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 296 references for this chapter.
 4
C H A P T E R

A DAPTABILITY OF S KELETAL M USCLE :

R ESPONSES TO I NCREASED
AND D ECREASED U SE
William J. Kraemer, Barry A. Spiering, and Jason D. Vescovi

Introduction tissue, the perimysium, which allows neural and vascular

Skeletal muscle provides postural stability and imposes
forces on bones to create movement. Any alteration in
loading over a period of time will change the structure
and function of skeletal muscle. Understanding the
responses to increased or decreased use is therefore clini-
cally important when developing and implementing a
plan designed to improve human function. One of the
aims of this chapter is to describe the structural hierar-
chy of skeletal muscle by outlining the coupling between
chemical energy and mechanical work and discussing the
dependence of muscle function on the organization of
proteins within the sarcomere. The second purpose is to
provide an overview of the acute and chronic responses
of skeletal muscle to increased use (training) and disuse
(injury, immobilization). The basic and applied research
presented supplies the foundation of knowledge neces-
sary for advanced training and rehabilitation programs.
Structure of Skeletal Muscle
Ultra-Anatomy of Skeletal Muscle
The human body contains more than 600 hundred skel-
etal muscles,1 which are surrounded by a layer of con-
nective tissue called the epimysium. Each muscle belly
contains many muscle fibers arranged in parallel and
grouped together in bundles termed fascicles. The fas-
cicle is enclosed within another sheath of connective
access to the muscle. Examination of fascicles reveals it
is composed of multinucleated cells called muscle fibers,
or myofibrils. Muscle fibers are approximately 80 to
100 µm in diameter and can be up to several centime-
ters in length. Individual fibers are also surrounded by
connective tissue, the endomysium, which contains the
capillary bed. Each layer of connective tissue (the endo-
mysium, the perimysium, and the endomysium) is con-
tinuous with the tendons attached to bone, providing the
link between muscular actions and skeletal movement.
Figure 4-1 shows the hierarchical structure of skeletal
muscle.
The functional unit of the muscle fiber is the sarco-
mere. The characteristic striated appearance of skeletal
muscle is caused by alternating A (dark) bands and I
(light) bands. The A and I designations are derived from
anisotropic and isotropic, which refer to the appear-
ance of these bands when viewed under polarized light.
The dark and light bands result from the arrangement
of thick and thin filaments within the sarcomere (Figure
4-2). The cytoskeleton within each sarcomere connects
and arranges the thick and thin filaments, while provid-
ing structure, stability, and elasticity to muscle.
The A band consists of the thick filaments, which are
centered in the sarcomere on the M line. The M line is
a collection of protein filaments where the ends of two
separate thick filaments are joined together and act to
stabilize their position. By this connection, the cross

79
80 SECTION I • Scientific Foundations

Periosteum covering the bone

Fascia Skeletal muscle
Bone Blood vessel
Fasciculus
Sarcolemma
Sarcoplasm
Muscle fiber cell

Endomysium Filaments
Tendon Myofibrils
Figure 4-1 Perimysium
Hierarchy of skeletal muscle structure. Epimysium

Sarcolemma

Sarcoplasm

I A Z H
band band band band

Myofibril
Sarcomere
Z Z

Muscle
fiber

Z Z
A H

Sarcomere Z-line
nd
I-ba

nd
A-ba

Figure 4-2
Organization of skeletal muscle (gross to microscopic
level) including longitudinal arrangement of thick and thin
filaments within a sarcomere. A, Regions of the sarcomere. B,
Microscopic view of several muscle fibers. (B, Modified from
Fawcett DW: The cell, Philadelphia, 1981, WB Saunders.) B
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use 81

bridges and heads of the thick filaments face opposite
directions. This arrangement is functionally important
and is described in a later section. The I band contains
thin filaments and is the region between two adjacent A
bands. At either end of the sarcomere are dark Z discs.
The Z discs provide a direct anchor for the thin filaments
and an indirect anchor for the thick filaments. As such,
a sarcomere is defined as the region between two adja-
cent Z discs. Cross-sectional views of a sarcomere display
the geometrical relationship between the thick and thin
filaments. In the zone of overlap, six thin filaments are
associated with one thick filament (Figure 4-3).
Located just beneath the endomysium, muscle fibers
are surrounded by a plasma membrane called the sarco-
lemma. Somatic motor neurons terminate near the sar-
colemma at the neuromuscular, or myoneural junction.
Stimulation by a motor nerve causes a transient increase
in sarcoplasmic Ca+2 concentration, which is stored and
released from a membrane network called the sarcoplas-
mic reticulum. Most of the Ca+2 is stored in a specific
region of the sarcoplasmic reticulum known as terminal
cisternae. Terminal cisternae are separated by a system of
transverse tubules (T tubules) that are continuous with
the sarcolemma and propagate action potentials from
motor nerves into and throughout the muscle. Figure
4-4 shows the organizational relationship of these struc-
tures. The functional importance of these membranous
networks is described in a later section.
Key Points: Muscle
● Muscle groups are composed of many muscle cells, termed
myofibrils or muscle fibers.
● Muscle fibers consist of a series of sarcomeres, which are the
functional unit of a muscle fiber.
Microanatomy of Skeletal Muscle
A myofibril can contain several thousand sarcomeres joined
in series. As stated previously, sarcomeres are composed of

Sarcomere

Thick Thin
filament filament

Muscle Myofibril
fiber

M line
Zone of
Z line overlap
Connection
filaments
Titin
Attachment H zone
filament
of titin I band
Figure 4-3
Cross-sectional arrangement of thick and thin filaments within a sarcomere.
82 SECTION I • Scientific Foundations
Myofibrils
Triad of the
reticulum
Z line
A band
Figure 4-4
Organizational relationship of the I band
calcium storing/releasing network
within skeletal muscle. (From Guyton
AC: Textbook of medical physiology, ed
10, p 84, Philadelphia, 2000, Elsevier.
Redrawn from Bloom W, Fawcett
DW: A textbook of histology,
Philadelphia, 1986, WB Saunders.
Modified after Peachey LD: J Cell
Biol 25:209, 1965. Drawn by Sylvia
Colard Keene.)
thick and thin filaments. In addition, cytoskeletal and reg-
ulatory proteins exist that determine sarcomeric structure
and control actin-myosin interactions, respectively.
Thin filaments contain structural and regulatory pro-
teins (Figure 4-5). Actin is a globular protein (G-actin)
that when polymerized forms a double-stranded fila-
ment that is twisted into a helical formation (F-actin).
The active binding site for the thick filament cross bridge
is located on each G-actin. Nebulin is a large structural
protein (600 to 800 kDa) that serves as a guide wire for
F-actin formation and most likely standardizes thin fila-
ment length. Novel findings indicate nebulin may play
additional roles in signal transduction, contractile regula-
tion, and force generation.2 Tropomyosin is a rod-shaped
protein positioned in the groove between the F-actin coil.
Several tropomyosins are associated with each thin fila-
ment and span approximately six to seven G-actin units.
The placement of tropomyosin during resting conditions
is such that it physically blocks the binding site of actin
from the cross bridge. Because of the spatial relation-
ship between tropomyosin and actin, tropomyosin must
Sarcolemma
Terminal
cisternae
Transverse
tubule
Mitochondrion
Sarcoplasmic
reticulum
Transverse
tubule
Sarcotubules
be moved for muscular actions to occur; this process is
mediated by troponin, a regulatory protein attached to
tropomyosin and actin, which consists of three globu-
lar subunits. The main function of troponin is to bind
calcium ions, leading to a conformational change in the
troponin–tropomyosin complex and exposing actins
binding sites.
Thick filaments are approximately 1.5 to 1.6 µm in
length and are composed mainly of myosin molecules.
Myosin consists of three pairs of proteins: one pair of
heavy chains and two pairs of light chains. The heavy
chain tails have an alpha-helical structure, and two tails
twist around each other to form a coil. The other end
of the heavy chain is a globular subunit, the myosin
head (Figure 4-6A). Proteolytic degradation of myosin
cleaves the molecule into a long and short segment plus
the globular head. The two cleavage sites are where the
tail and head are permitted to flex. These flexion points
create projections, or cross bridges, and allow myosin
to interact with actin. The aggregation of myosin heavy
chain tails forms the thick filament. Their arrangement
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use
Troponin complex Tropomyosin
G-actin
Myosin molecule Tail
Heads
A
Crossbridges
Actin Myosin
B
Figure 4-6
Myosin filaments. A, The structure of the head and neck regions.
B, Myosin’s position within the sarcomere.
begins with tails being placed end to end at the M line.
Therefore, the cross bridges of each half project in oppo-
site directions. The central portion of thick filaments
does not contain cross bridges (Figure 4-6B).
Titin is the third most abundant protein in skeletal
muscle, behind actin and myosin.3 During myogenesis,
titin most likely acts as a template to standardize thick fila-
ment formation. It also contributes to the maintenance of
proper alignment between actin and myosin. Each titin
protein is bound on one end to the Z line and at the other
end to the M line, so for each thick filament there are two
associated titin proteins (Figure 4-7). It was originally
thought that this protein simply provided elasticity, pre-
venting excessive stretching and possible damage to the
sarcomere. Recent evidence indicates, however, that titin
has kinase domains and phosphorylation sites, pointing
to its possible signaling mechanisms and catalytic func-
tions..1 Therefore, this protein is an essential element for
the proper structure and function of skeletal muscle.
83
Figure 4-5
Structure of the thin filament.
(Redrawn from Fox SI: Human physiology, ed 8, p 336,
Boston, 2004, McGraw-Hill Higher Education.)
Muscle Contraction
● The primary contractile proteins within a sarcomere are actin and
myosin; however, a number of other cytoskeletal and regulatory
proteins exist as well.
● Specialized proteins (.e.g., troponin, tropomyosin) exist within the
sarcomere to regulate muscle contraction.
Function of Skeletal Muscle
Sliding Filament Theory
Filament Theory Muscle contractions are caused by
shortening of each myofibril and, more specifically, a
decrease in length of individual sarcomeres. Both thick
(A band) and thin filament lengths remain constant dur-
ing contractions; however, the I bands decrease in length.
Therefore, the Z discs are pulled closer together because
of the overlap of actin and myosin filaments (Figure 4-8).
The antiparallel arrangement of the myosin cross bridges
enables their action to cause each associated F-actin to
slide toward the center of the sarcomere (M line).
The globular head of a myosin molecule contains
binding sites for ATP and for actin. In addition, it also
has ATPase activity (myosin ATPase), which allows for
the hydrolysis of ATP to ADP and Pi. When a muscle
is at rest, ADP and Pi are bound to myosin, tropomyo-
sin is blocking the attachment site, and therefore cross
bridges are not in contact with actin. Sufficient stimu-
lation by a motor nerve allows the two filaments to form
an actomyosin complex (through processes that are dis-
cussed in the next section). At this time the myosin head
releases inorganic phosphate, initiating a power stroke
and pulling F-actin toward the center of the sarcomere.
Oftentimes it is illustrated that the two globular heads
of a myosin molecule performed a power stroke simul-
taneously; however, evidence suggests a hand-over-hand
motility pattern exists.4 Following the power stroke, ADP
is released and the myosin head binds with a molecule
of ATP, which significantly reduces the affinity between
actin and myosin. The energy released from hydrolysis of
84 SECTION I • Scientific Foundations
Figure 4-7
Cytoskeletal proteins within the sarcomere. (From McElhinny AS: The nebulous, multifunctional giant of striated muscle, Trends Cardiovasc
Med 13[5]:]196, 2003.)
I A I actomyosin complex. Electrical stimulation of an alpha
Z Z
Relaxed
I A I
Z Z
Contracted
Figure 4-8
The effects of muscle contraction on sarcomere length. (From Guyton
AC: Textbook of medical physiology, ed 10, p 70, Philadelphia, 2000,
Elsevier.)
ATP causes a conformational change in the cross bridge,
uncoupling the actomyosin complex as the head and arm
return to their original position. The cyclic pattern of
this process is shown in Figure 4-9. Cross bridge interac-
tions continue until neuronal stimulation ceases, Ca+2 is
removed from the myoplasm, ATP depletion occurs, or
the sarcomere can no longer shorten.
Regulation of Muscular Actions
Muscular contractions occur when myosin cross bridges
are allowed to attach to actin in a cyclic fashion. The
mechanical attachment, detachment, and reattachment
of this power stroke is due to chemical and enzymatic
actions of the regulatory and structural proteins. In the
resting state, tropomyosin covers the actin attachment
site and prevents myosin cross bridges from forming an
motor neuron causes the release of acetylcholine at the
neuromuscular junction. The action potential travels
throughout the muscle cell(s) via the T tubules. As a
consequence, the sarcoplasmic reticulum is depolarized,
causing the terminal cisternae to release Ca+2. There is a
sharp increase of the intracellular concentration of this
ion (Figure 4-10). Troponin cooperatively binds Ca+2
and in doing so induces a shift in tropomyosin, acting
like a switch and permitting cross bridge interaction with
actin. Upon termination of neural stimulation, calcium is
quickly removed from the myoplasm back into the termi-
nal cisternae, returning the muscle to the resting state.
Neuromuscular Control and Fiber Types
Skeletal muscle stimulation originates from upper
motor neurons located in the cerebral cortex of the
brain. Descending motor tracks synapse with lower
motor neurons in the ventral horn of the spinal cord,
exit via the ventral roots, and ultimately innervate skel-
etal muscle. The somatic neurons branch and innervate
multiple muscle fibers, terminating at the neuromus-
cular junction. Collectively, an individual motor neu-
ron and all of the muscle fibers it innervates are known
as a motor unit (Figure 4-11). The number of muscle
fibers a somatic neuron innervates is dictated by the
precision necessary to control a particular movement.
For example, the neuron to fiber ratio in ocular mus-
cles is approximately 1:10-20 because fine control is
required for movements of the eye. In contrast, the
innervation ratio for the gastrocnemius or quadriceps
can exceed 1:1000. These muscles rely more on gross
activation, and the precision of movement is somewhat
sacrificed.
The fiber type and motor unit composition of an
entire muscle is heterogeneous; however, the fiber
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use
(1) Resting fiber; cross bridge is
not attached to actin
(6) ATP is hydrolyzed, causing
cross bridge to return to
its original orientation
Myosin head
Thick filament
ATP
(5) A new ATP binds to
myosin head, allowing
it to release from actin
Figure 4-9
The role of adenine nucleotides in cross-bridge cycling. (Redrawn from Fox SI: Human physiology, ed 8, p 335, Boston, 2004, McGraw-Hill
Higher Education.)
type composition of an individual motor unit is
homogeneous. Motor units are classified as either type
I (slow oxidative) or type II (fast glycolytic); conse-
quently, these motor units, and they contain type I
or type II muscle fibers, respectively. In fact, it is the
neural innervation that ultimately determines fiber
type.
Motor units are specialized, and their recruitment
pattern depends on the gradation of force develop-
ment. Type I motor units have small neurons that are
easily activated because of their low threshold for exci-
tation. In addition, type I motor nerves contain only a
few terminal branches innervating a minimal amount
of muscle cells. Because type I motor unit activity is
typically sustained, they are characteristically resistant
to fatigue. So for prolonged, low-intensity activities
such as sitting or walking, type I motor units are the
primary motor units recruited. Type II motor units,
on the other hand, contain more neuronal terminal
branches and larger muscle fibers, which increase their
force-producing capability. Myosin ATPase activity is
85
Thin filament
ADP
Pi
Cross bridge
(2) Cross bridge binds
to actin
(3) Pi is released, causing conformational
change in myosin
(4) Power stroke causes
filaments to slide;
ADP is released
also greater in type II motor unit muscle fibers, there-
fore their contraction velocity is increased when appro-
priate stimulation is applied. Larger forces generated at
faster speeds require a greater amount of energy; there-
fore, fatigue occurs quickly because of type II motor
units.
The recruitment of motor units to complete a given
task follows the size principle. Smaller, type I motor
units are recruited first. Their activity can be maintained
for prolonged periods of time because of their slower
contraction velocity and their high mitochondrial con-
tent and oxidative capacity. When larger amounts of
force are necessary, type II (fast) motor units are sub-
sequently recruited. Therefore, when performing a par-
ticular task during unfatigued conditions, neural input
stimulates sufficient motor units to complete the task.
Initially, this is typically met by recruiting type I motor
units. However, as the force requirements of the task
increase, increasingly higher threshold motor units
are activated; this implies that type II motor units are
recruited.
86 SECTION I • Scientific Foundations

Motor neuron

Axon terminal

4
2 Electronic impulse

Sarcolemma
3
Acetylcholine
release Transverse T tubule
1 Ca2+

1 Acetylcholine released binds to Sarcoplasmic reticulum

nicotinic acetylcholine receptor
2 Release of acetylcholine produces
elcotyical impulse in muscle cell 4 Action potentials produced along 6 Sarcoplasmic reticulum calcium
plasm membrane sarcolemma into T tubule (Ca2+) release channel
3 Skeletal muscle voltage-gated 5 Transverse tubule voltage-gated 7 Ca2+ combines with troponin
sodium (Na+) channel calcium channel to stimulate contraction
Figure 4-10
Summary of muscle excitation. (Redrawn from Fox SI: Human physiology, ed 8, p 339, Boston, 2004, McGraw-Hill Higher Education.)

A practical example of the size principle is provided
by comparing endurance and resistance exercise.
Endurance exercise typically consists of prolonged
(>30 min) low-intensity exercise. Because the force
requirement of endurance exercise is low, primar-
ily type I motor units are recruited. This is advan-
tageous, as type I motor units are fatigue-resistant.
Alternately, resistance exercise is associated with brief
periods of very high-intensity exercise. Because the
force requirements are high, all motor units (type I
and type II) must be activated to achieve the force
requirements. The necessity of recruiting type II
motor units implies that fatigue will ensue relatively
quickly.
As one can see, skeletal muscle is a heterogeneous
mixture of several types of muscle fibers. Fibers types can
be classified based on structural, metabolic, functional
capacities and on neural recruitment strategies. General
characteristics of type I and type II fibers are summarized
in Table 4-1.
Muscle Contraction
● Regulatory proteins (.e.g., troponin, tropomyosin) prevent actin-
myosin cross bridges from forming in the absence of neural stimu-
lation; alternately, upon neural stimulation, calcium ion signaling
promotes conformational change in the troponin-tropomyosin
relationship to actin and allows cross bridge formation.
● ATP provides energy for muscle contraction. Energy is released
from ATP via the enzyme myosin ATPase.
● Muscle fibers are typically subdivided based on their structural,
functional, and metabolic properties into type I (“slow twitch”) or
type II (“fast twitch”).
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use 87

Motor unit 2

Motor neuron Motor unit 1 Neuromuscular

cell body junctions

Nuclei
Nerve
Muscle fibers
Spinal cord (cells)
Node of Ranvier
Motor neuron axon

Fascicle

Muscle

Tendon

Figure 4-11
Interrelationship between the nervous system and skeletal
Bone
muscle.

Table 4-1
General Characteristics of Type I and Type II Muscle Fibers
Type I Type IIa Type IIx

Structural
Myosin ATPase isoform Slow Fast Fastest
Sarcoplasmic reticulum Less quantity More quantity Most quantity
Metabolic
Glycolytic enzymes Low concentration High concentration High concentration
Oxidative enzymes High concentration Low concentration Lowest concentration
Mitochondrial content High Low Lowest
Functional
Peak tension Low High High
Contraction speed Slow Fast Fastest
Relaxation speed Slow Fast Fastest
Fatigability Low High Very high
Neural
Recruitment order Recruited first Recruited later Recruited last
Number of fibers Few Many Many
per motor unit

Adaptations to Increased Use increases in strength and changes in muscle cross-sec-

Anaerobic Training—Resistance Training
Neural Adaptations
Although strength can be dramatically improved within
a few weeks of training, weak relationships between
tional area,5 limb circumference,6,7 and muscle fiber
cross-sectional area5,8,9 indicate that other factors are
responsible for gains in strength (i.e., hypertrophy is
not the major adaptation early in a resistance training
program). Research clearly shows that early gains in
88 SECTION I • Scientific Foundations
strength (2 to 6 weeks) following resistance training
are primarily mediated via neural adaptations.10 For
example, one particular study showed that isometric
training produced a 92% increase in maximal static
strength but only a 23% increase in muscle cross-sectional
area.11,12 Neural factors affected by resistance training
include increased neural drive (i.e., recruitment and
rate of firing) to the muscle, increased synchronization
of the motor units, increased activation of agonists,
decreased activation of antagonists, coordination of all
motor units and muscle(s) involved in a movement,
and inhibition of the protective mechanisms of the
muscle (i.e., Golgi tendon organs).
It should be emphasized, however, that it is not just at
the beginning of a resistance training regimen that neural
factors are important. The neural component plays a
major role in mediating strength gains in advanced lifters
as well. In a study by Häkkinen et al.,12 the researchers
observed observed minimal changes in the muscle fiber
size of competitive Olympic weightlifters over 2 years;
however, strength and power increased significantly over
this time. Electromyography (EMG) analysis demon-
strated that increased voluntary activation of muscle was
an important factor in strength and power improvements.
Thus, even in advanced resistance-trained athletes, the
mechanisms of strength and power improvement may be
related to neural factors.
Mechanisms exist to protect muscles from self-
induced damage during intense muscular actions. The
Golgi tendon organ is a “tension sensor” that lies
within the tendon. If the threshold for musculo-ten-
don tension is exceeded, then inhibitory signals relax
the muscle and prevent potential damage. Resistance
exercise training is known to increase the threshold for
Golgi tendon organ activation. For example, during
hypnosis, Ikai and Steinhaus found that force devel-
oped during forearm flexion by non-resistance-trained
individuals increased 17%.13 However, in the same
study, force developed by highly resistance-trained
individuals under hypnosis was not significantly differ-
ent from force developed in the normal conscious state.
The researchers concluded that resistance training may
cause voluntary inhibition of these protective mecha-
nisms. These protective mechanisms appear to be espe-
cially active when large amounts of force are developed,
such as maximal force development at slow speeds of
movement.14,15
Information concerning protective mechanisms has
several practical applications. Many resistance training
exercises involve bilateral muscle actions (activating both
limbs at the same time). The force developed during bilat-
eral actions is less than the sum of the force developed by
each limb independently.16-18 This phenomenon is known
as “bilateral deficit.” Bilateral deficit is associated with
reduced motor unit stimulation of mostly fast-twitch
motor units.18 The reduced motor unit stimulation, and
thus less force production, could be due to inhibition
by the protective mechanisms such as the Golgi tendon
organ. Training with bilateral actions reduces bilateral
deficit,19 thus bringing bilateral force production closer
to, or even greater than, the sum of unilateral force
production; however, this should not undermine the
importance of unilateral training, as many sports require
force production in limbs working independently of one
another.
Knowledge of the neural protective mechanisms is
also useful in understanding the expression of maximal
strength. Neural protective mechanisms appear to have
their greatest effect in slow-velocity/high-resistance
movements.14,15,20 A resistance training program in
which the antagonists are activated immediately before
the exercise is performed is more effective in increas-
ing strength at low velocities than a program in which
precontraction of the antagonists is not performed.14
The precontraction in some way partially inhibits the
neural self-protective mechanisms, thus allowing a more
forceful action. Precontraction of the antagonists can
be used as a method both to enhance the training effect
and to inhibit the neural protective mechanisms dur-
ing a maximal lift. For example, immediately before a
maximal bench press, forceful actions of the arm flex-
ors and muscles that adduct the scapula (i.e., pull the
scapula toward the spine) should make a heavier maxi-
mal bench press possible than no precontraction of the
antagonists.
Neural Adaptation
● Initial strength gains are typically due to neural, as opposed to
hypertrophic, factors.
● The Golgi tendon organ acts as a “tension sensor” within skeletal
muscle. If tension increases above a specific threshold, the Golgi
tendon organ will inhibit further contraction to protect the muscle
from impending damage.
● Resistance training increases muscular coordination, which is
important for daily and recreational activities, and prevents falls
among the elderly.
Structural Adaptations
Muscle Size. As the duration of training increases
(>6 to 10 weeks), muscle hypertrophy eventually takes
place and contributes more than neural adaptations to
the strength and power gains observed. This growth
in muscle size has been thought to be primarily the
result of muscle fiber hypertrophy or an increase in
the size of the individual muscle fibers.21,22 However,
eventually muscle hypertrophy reaches a maximum
and plateaus.
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use
An increase in muscle size has been observed in both
animal and human studies. Increased muscle size in
strength-trained athletes has been attributed to hyper-
trophy of existing muscle fibers.23,24 This increase in the
cross-sectional area of existing muscle fibers is attributed
to the increased size and number of contractile proteins
(actin and myosin) and the addition of sarcomeres within
the fiber,25 although researchers have suggested that an
increase in noncontractile proteins may also occur.26 This
is reflected by an increase in myofibrillar volume follow-
ing resistance training.27
Not all muscle fibers undergo the same amount of
enlargement. Hypertrophy depends on the muscle fiber
type and the pattern of recruitment.22 Muscle fiber
hypertrophy has been demonstrated in both type I and
II fibers because of resistance training.28 However, stud-
ies in humans29 show greater hypertrophy of type II than
type I fibers.
Interestingly, research has indicated that it may be pos-
sible to selectively hypertrophy either the type II or the
type I muscle fibers depending on the training regimen.
Power lifters who train predominantly with high intensity
(i.e., heavy resistances) and low volume (i.e., small num-
ber of sets and repetitions) have been shown to have large
type II fibers (vastus lateralis mean fiber area of 79 mm2).
Conversely, body builders who train predominantly with
a lower intensity but a higher volume have been shown
to have type II fibers with a mean fiber area of 62 mm2.30
Additionally, body builders have been shown to possess a
lower total percentage of type II fiber area in the vastus
lateralis than Olympic lifters and power lifters (50% versus
69%, respectively).31
Muscle hypertrophy is the result of an increase in
protein synthesis, a decrease in protein degradation, or
a combination of both. When the amount of protein
synthesized exceeds that which is degraded, net protein
accretion is positive and hypertrophy occurs. Protein syn-
thesis is significantly elevated up to 48 hours postexer-
cise.21,32-34 Phillips et al.34 reported that protein synthesis
was elevated by 112%, 65%, and 34%, respectively at 3,
24, and 48 hours post resistance exercise. In addition,
protein breakdown rate was elevated by only 31%, 18%,
and 1% at these same time points indicating muscle pro-
tein balance was elevated 23% to 48% over the 48-hour
postexercise time period.
Training status of the individual plays a role in the
postresistance exercise change in protein synthesis. Phillips
et al. examined the fractional rate of protein synthesis and
breakdown in resistance-trained (at least 5 years of expe-
rience) and untrained men.26 Interestingly, they found
that the rate of protein synthesis 4 hours post exercise
was higher in untrained compared to trained individuals
(118% versus 48%, respectively). However, the rate of
breakdown was also higher in the untrained men, lead-
ing to a similar net protein balance of 37% and 34%,
89
respectively, for the untrained and trained men. It was
suggested that chronic resistance training reduces muscle
damage and consequently protein turnover.
Amino acid transport across the cell membrane and
consequent uptake by skeletal muscle is important
for enhancing protein synthesis. Biolo et al. reported
an increase in amino acid transport of 60% to 120%
(depending on the amino acid) in the 3 hours follow-
ing resistance exercise.35 Interestingly, arterial amino acid
concentrations did not change, but rather a 90% increase
in muscle blood flow accounted for much of the increase
in amino acid transport. There is growing evidence
showing the importance of blood flow in protein synthe-
sis and muscle hypertrophy. Studies that have restricted
blood flow and used light loading during resistance exer-
cise (thereby increasing the concentrations of metabolites
and the anaerobic nature of the exercise stimulus) have
shown prominent increases comparable to heavier load-
ing, demonstrating the importance of blood flow or
metabolite accumulation during resistance training to
bring about adaptations.36-38 This may, in part, explain
the efficacy of body building programs using moderate
loading and high volume with short rest intervals for
increasing muscle hypertrophy.
Muscle protein synthesis following resistance exer-
cise depends heavily on amino acid availability, timing of
protein intake, and insulin concentrations in addition to
other factors such as hormonal regulation (e.g., growth
hormone, testosterone, insulin-like growth factor-I, mech-
ano-growth factor), mechanical stress, and cellular hydra-
tion. The acute increases in protein synthesis appear to be
influenced by changes at the nuclear level and by posttran-
scriptional modifications (e.g., increase in protein synthesis
independent of changes in RNA) by enhancing transla-
tional efficiency or increasing the abundance/activation of
translation initiation factors.39,40
When insulin concentrations are elevated following
resistance exercise (either by glucose intake or insulin
infusion), the exercise-mediated acceleration of pro-
tein breakdown is reduced.41,42 Insulin concentration
increases after resistance training followed by postexer-
cise carbohydrate-protein supplementation.43 One study
has shown protein synthesis is greater when amino acids
are taken before a workout to optimize amino acid deliv-
ery and transport during the workout because of greater
blood flow.44 These results indicate a potential ergogenic
effect of glucose/amino acid intake before or directly fol-
lowing resistance exercise to maximize protein synthe-
sis and recovery. In our laboratory, we have found that
amino acid supplementation attenuates muscle damage
during the stressful early phases of overreaching (possibly
by reducing protein degradation and enhancing recov-
ery), which was crucial to maintaining muscle strength
and power (unpublished observations of Dr. Kraemer’s
laboratory). Based on the previous findings, Tipton and
90 SECTION I • Scientific Foundations
Wolfe proposed a model of protein metabolism during
resistance exercise:45 (1) resistance exercise stimulates
protein synthesis, (2) intracellular amino acid concen-
trations are reduced, (3) decreased amino acid concen-
trations stimulate protein breakdown and transport of
amino acids into the muscle cell, (4) the increased avail-
ability of amino acids further stimulates protein synthesis,
and (5) tissue remodeling occurs. Therefore, it appears
that optimal protein intake is crucial to optimizing recov-
ery and performance as well as subsequently adapting to
resistance training.
Muscle Hypertrophy
● Muscle fibers increase in size (hypertrophy) in response to resis-
tance exercise.
● Hypertrophy is primarily due to increased synthesis of contractile
proteins (actin and myosin).
● Hypertrophy is mediated by acute increases in anabolic hor-
mones (testosterone, growth hormone, IGF-1, insulin) following
resistance exercise.
● Those wishing to gain muscle size must adhere to a resistance
training program for at least 6 weeks for appreciable gains.
● Hypertrophy in response to resistance exercise results in
increased muscle mass.
● Increased muscle mass is associated with reduced risk for
certain metabolic diseases (e.g., diabetes).
Hyperplasia. Muscle fiber hyperplasia, an increase in
the number of muscle fibers, has also been one possible
mechanism for increasing the size of muscle. The concept
of hyperplasia following resistance training in humans
has not been directly proven because of methodological
difficulties (e.g., one cannot take out the whole muscle
for examination), but it has been shown in response
to various exercise protocols in birds and mammals.
(For review, see Antonio and Gonyea.46)
Several studies comparing body builders and power
lifters concluded that the cross-sectional area of the body
builders’ individual muscle fibers was not significantly
larger than that of power lifters; yet these athletes pos-
sessed larger muscles than normal.31 This indicates that
these athletes have a greater total number of muscle fibers,
and hyperplasia may account for this increase. However,
another study examining body builders concluded that
power lifters possess the same number of muscle fibers
as the control group, but possess much larger muscles.47
These results suggest that the large muscle size of body
builders is due to hypertrophy of existing muscle fibers
rather than hyperplasia.
McCall et al. used MRI and biopsy techniques to
examine hypertrophy and the possible increase in cell
number after a 12-week heavy resistance program.28
Results showed evidence for hyperplasia in the biceps
muscle; however, hypertrophy accounted for the great-
est portion of muscle enlargement. More recently, power
lifters have been shown to have higher numbers of myo-
nuclei, satellite cells, and small-diameter fibers expressing
markers for early myogenesis, thereby indicating hyper-
plasia.48 These effects appear to be enhanced by anabolic
steroid use,49 which potentially demonstrate an additional
mechanism (e.g., more myonuclei means greater number
of androgen receptors available for interaction) for ste-
roid-enhanced muscle growth.
Though limited data support hyperplasia in humans,
there are indications that hyperplasia can occur fol-
lowing resistance training. Because of these con-
flicting results, this topic remains controversial and
further research seems necessary. While hyperplasia in
humans may not be the primary adaptational response
of most muscle fibers, it might represent an adapta-
tion to resistance training that is possible when cer-
tain muscle fibers reach a theoretical “upper limit” in
cell size. It might be theorized that very intense long-
term training may make some type II muscle fibers
primary candidates for such an adaptational response.
If hyperplasia does occur, it likely only accounts for
a small portion (e.g., 5% to 10%) of the increase in
muscle size.
Muscle Hyperplasia
● Limited data support the occurrence of hyperplasia in humans in
response to resistance exercise.
● If hyperplasia does occur, it contributes little to the increase in
muscle size (i.e., hypertrophy is the primary mechanism).
Muscle Fiber Type Transition. Myosin proteins have
the capacity to change its phenotypic profile with resis-
tance training.50 Much of the resistance training research
focuses on the myosin molecule and examination of
fiber types based on the use of the histochemical myosin
adenosine triphosphatase (mATPase) staining activities
at different pHs. Changes in muscle mATPase also give
an indication of associated changes in the myosin heavy
chain (MHC) content.9 We now know that a continuum
of muscle fiber types exist, and transformation (e.g., type
IIX to type IIA) within a particular muscle fiber subtype
is a common adaptation to resistance training.22,51,52 It
appears that as soon as type IIX muscle fibers are stimu-
lated, they start a process of transformation toward the
type IIA profile by changing the quality of proteins and
expressing different types of mATPase.
In a study by Staron et al.,9 a high-intensity resistance
training protocol was performed by men and women
two times per week for 8 weeks. This protocol focused
on the thigh musculature (using squat, leg press, and
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use
knee extension exercises) with heavy, multiple sets and
adequate rest between sets (2 minutes) for recovery of
muscle function. Maximal dynamic strength increased
over the 8-week training period without any significant
changes in muscle fiber size or fat-free mass in the men or
the women (supporting the concept of neural adaptations
being the predominant mechanism in the early phase of
training). However, a significant decrease in the type IIX
percentage was observed in women after just 2 weeks of
training (4 workouts) and in the men after 4 weeks of
training (8 workouts). Over the 8-week training program
(16 workouts), the type IIX muscle fiber types decreased
from 21% to about 7% of the total muscle fibers in both
men and women. The alteration in the muscle fiber types
was supported by myosin heavy chain (MHC) analyses.
This study established the time course of specific muscu-
lar adaptations in the early phase of a resistance training
program for men and women.
Longer studies of heavy resistance training have exam-
ined changes in muscle fiber type and cross-sectional size
with training. Staron et al. examined changes in skeletal
muscle in women who trained for 20 weeks, detrained
for 2 weeks, and then retrained for 6 weeks.52 Increases
in muscle fiber cross-section were seen with training.
The percentage of type IIX fibers decreased from 16% to
0.9%. This study also demonstrated that short detrain-
ing periods result in muscle fibers starting to return to
pretraining values of cross-sectional area (especially type
II fibers) and a conversion of type IIA back to type IIX
fibers. This demonstrates that muscle fiber types return
to pretraining values during detraining. During retrain-
ing, a quicker change in muscle size and conversion to
type IIA fibers was demonstrated as compared to start-
ing in an untrained condition. Thus, the concept used
by athletes and coaches of “muscle memory” has some
validity in the retraining of an individual after a period of
detraining.
Changes in Muscle Fiber Type with Exercise
● Muscle fiber type transitions occur in response to exercise.
● The most frequently observed transition is from type IIX to type IIA.
● Fiber type transitions are a favorable adaptation because type IIA
fibers are more resistant to fatigue than type IIX.
Body Composition Changes. Body composition
changes do occur in short-term resistance training pro-
grams (6 to 24 weeks). The largest increases in fat-free
mass (FFM) consistently reported are a little greater than
3 kilograms (6.6 lb) in approximately 10 weeks of drug-
free training. This translates into an FFM increase of
0.66 pound per week. The maximal possible amount of
muscle mass gained in a given period of time should be
91
considered when coaches ask athletes to add body weight
during the off-season.
Other Structural Changes. Architectural characteris-
tics of muscle fibers following resistance training have been
investigated in a variety of studies. Despite the increase in
myofilament number, the myofibrillar packing distance
(e.g., the distance between myosin filaments) and the
length of the sarcomere appear to remain constant fol-
lowing 6 weeks to 6 months of resistance training.27,53 In
addition, the ratio of actin to myosin filaments does not
change following 6 weeks of resistance training.53 The
relative volume of the sarcoplasm, T tubules, and other
noncontractile tissue does not appear to change signifi-
cantly because of resistance training.23,27,47,54,55 Although
increases in myofilament number take place, it appears
that the spatial orientation of the sarcomere remains
intact following resistance training. Thus, sarcomeres are
added in parallel, contributing to the increase in muscle
cross-sectional area and fat-free mass observed during
resistance training.
Resistance training has been shown to increase the
number of capillaries in a muscle to help support metab-
olism by increasing the potential blood supply. With typi-
cal resistance training (three sets of 10 repetitions) over
12 weeks, McCall et al. observed significant increases
in numbers of capillaries per type I and type II fibers;28
however, because of fiber hypertrophy, no changes
in capillaries per fiber area or per area of muscle were
shown. Alternately, Hather et al. demonstrated that with
different types of training (i.e., combinations of concen-
tric and eccentric muscle actions), capillaries per unit area
and per fiber significantly increased in response to heavy
resistance training even with hypertrophy resulting in
increased fiber areas.57
The rate of change in capillary density may depend on
the volume and rest periods of resistance exercise train-
ing. Power lifters and weight lifters exhibit no change
in the number of capillaries per muscle fiber, primarily
because of muscle hypertrophy.30 On the other hand,
body builders, who typically employ high intensity, low
volume, and long rest intervals in their training proto-
cols, have shown increased capillarization.58 Therefore,
it can be hypothesized that high-intensity/low-volume
strength training actually decreases capillary density,
whereas low-intensity/high-volume strength training
has the opposite effect.
Increased capillary density may facilitate the perfor-
mance of low-intensity weight training by increasing the
blood supply to the active muscle. The short rest peri-
ods used by many body builders during their workouts
result in large increases in blood lactate concentrations
(i.e., greater than 20 mmol L−1).59 A higher capillary den-
sity may increase the ability to remove lactate from the
muscle to the blood, thereby allowing better tolerance to
training under such associated high acid-base disruptions.
92 SECTION I • Scientific Foundations
This idea is supported by data demonstrating that body
builders could use a heavier resistance under the same
acidic conditions as compared to power lifters.59
Few studies have examined the effect of resistance
training on mitochondrial density. Similar to capil-
lary density, mitochondrial density has been shown to
decrease with resistance training because of the dilution
effects of muscle fiber hypertrophy.27,60 The observation
of decreased mitochondrial density is consistent with the
minimal demands for oxidative metabolism placed on the
musculature during most resistance training programs.
Chilibeck et al.,61 using 12 weeks of resistance training,
found strength training resulted in significantly increased
type I and II muscle fiber cross-sectional areas of 26%
and 28%, respectively. Their analysis of mitochondria
demonstrated that strength training results in reduced
density of regionally distributed mitochondria (e.g., sub-
sarcolemmal and intermyofibrillar mitochondrial density
decreased similarly). The effect of resistance training on
mitochondrial number and density requires further study.
However, similar to enzyme activity and capillary density,
mitochondrial density appears to decrease in response to
resistance training because of a dilution effect because of
muscle fiber hypertrophy.
Other structural changes within skeletal muscle
take place during resistance training. For example, the
sodium-potassium ATPase pump activity (which main-
tains sodium and potassium ion gradients and membrane
potential) has been shown to increase by 16% following
11 weeks of resistance training.62 Some structural char-
acteristics do not appear to change during resistance
training in young men and women. However, resistance
training in the elderly appears to attenuate some of the
age-related declines in muscle morphology.
Hypertrophy and Muscle Changes
● Besides increased quantity of contractile proteins, skeletal muscle
undergoes other structural adaptations to support hypertrophy.
● Increased muscle volume, however, may lead to decreased
density of capillaries and mitochondria, which may decrease the
aerobic potential of the muscle fibers in the absence of concur-
rent endurance training.
● Resistance training improves the functional qualities of muscle
(i.e., it improves force production at any given velocity).
Functional Adaptations
As the concentric force requirements of a given task
increase, the maximal velocity of the movement decreases;
this is known as the force-velocity relationship (Figure
4-12). For example, if an athlete is asked to perform a
jump squat with his or her 1-RM, the weight will move
very slowly. If this load is reduced, to say 50% 1-RM,
Force
After training
Before training
Velocity
Figure 4-12
The force-velocity relationship before and after periodized resistance
training.
the velocity of the lift can increase accordingly. Maximal
velocity will continue to increase until the force is zero;
however, maximal mechanical power (force × velocity)
occurs at about 30% to 45% of 1-RM.63
The relationship between force and velocity is impor-
tant to consider when training a client whose activity
(work or leisure) relies on power. With resistance train-
ing, the force velocity curve moves up and to the right
(see Figure 4-12); however, this requires optimal train-
ing configuration (e.g., periodization) in order to achieve
changes in all phases of the force-velocity curve. Typically
periodized training strategies that address each of the
components of the power equation (i.e., force and veloc-
ity) are used to maximize strength and develop power.64
Power is a primary determinant of success in many sport-
ing events. Therefore, training to enhance muscle power
capabilities is obviously important for these popula-
tions. However, it should be noted that aging results in
reduced power capabilities, and this may be responsible
for impaired function.65
Muscle Power
● For athletes, increased power output would likely enhance
sport performance.
● For other populations, the ability to generate power improves
one’s performance of activities of daily living and reduces the
incidence of falls among the elderly.65
Anaerobic Training—Sprint and Interval Training
Adaptations to anaerobic activity depend on the intensity
and duration of the activity and the rest intervals between
each interval. Therefore, it is important to differentiate
between “quality” anaerobic training (long rest intervals
to achieve maximal speed) and “quantity” exercise con-
ditioning (short rest intervals to achieve speed endurance
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use
and improve of lactic acid buffering capacity). For exam-
ple, Shealy et al. trained athletes using high intensity/
short duration (45.7 to 91.4 m) sprints with long rest
intervals (90 seconds between reps, 3 minutes between
sets) for 8 weeks.66 Results showed that athletes increased
sprint speed; however, maximum oxygen consumption
did not change. Conversely, Kraemer et al. showed that
when multiple sprints were separated by short rest inter-
vals (60 seconds), significant increases in the maximal
oxygen consumption were observed by 8 weeks of a
10-week training program.67 Thus, the exercise-to-rest
ratio is a vital factor in determining the effects of exercise
intervals on increases in maximal oxygen consumption or
activity speed. Furthermore, the results of Kraemer et al.
show that traditional aerobic training is not requisite to
increase peak oxygen consumption, as this can be accom-
plished with intervals of activity when the exercise-to-rest
ratio is high.67
Muscle and Anaerobic Training
● Anaerobic training (e.g., sprinting) can be used to increase
running speed.
● In addition, combining anaerobic training with short rest intervals
can improve aerobic capacity.
Aerobic Training
Adaptations to aerobic (endurance) training have been
studied extensively. Historically, the most commonly
reported adaptation is an increase in maximal oxygen
consumption (VO2max). To summarize adaptations to
endurance exercise and to explain why there is an increase
in VO2max, it is best to begin with a mathematical
explanation:
VO2 = CO × avO2diff
VO2 = oxygen consumption
CO = cardiac output
avO2diff = arteriovenous oxygen difference
VO2max is limited by the ability to take in, transport,
and utilize oxygen. Although the ability to take in (ven-
tilate) oxygen does not change significantly following
endurance training, several adaptations work together to
increase oxygen transport and uptake. Following endur-
ance training, there is an increase in plasma volume,
which increases cardiac stroke volume at rest and dur-
ing exercise. Increased stroke volume, in turn, increases
cardiac output, thus providing one mechanism by which
endurance training increases maximal oxygen consump-
tion (i.e., increased transport of oxygen to muscle).
Enhanced oxygen uptake is reflected by increased
arteriovenous oxygen difference (which is the difference
93
between oxygen content of arterial and venous blood).
This adaptation is secondary to increased mitochondrial
and capillary density along with decreased fiber cross-sec-
tional area, which work together to decrease the diffusion
distance for oxygen and to facilitate uptake. Furthermore,
increased mitochondrial density also leads to increased
oxidative enzymes, thus enhancing the use of oxygen
upon arrival at the muscle. A summary of adaptations that
occur with endurance exercise is found in Table 4-2.
Muscle and Aerobic Training
● Aerobic training is associated with central (cardiovascular) and
peripheral (capillary and mitochondrial) adaptations that increase
oxygen consumption and improve endurance.
● Increased aerobic capacity improves performance during
sustained activities, increases recovery rate during and following
exercise, and is associated with a decreased incidence of certain
diseases (coronary artery disease, diabetes, etc.).
Compatibility of Training
As Table 4-3 shows, in many respects, that resistance
training and aerobic training seem to have opposing
effects on skeletal muscle. This topic of exercise com-
patibility was initially studied by Hickson,68 who dem-
onstrated that concomitant resistance and endurance
training compromised strength development; however,
aerobic capacity was not compromised when compared
to the aerobic-only training group. It should be noted
that neither the resistance nor endurance training regi-
mens used in this study were periodized; therefore, the
relatively high training volume may have resulted in
overtraining.
Using a more conventional frequency of training,
Dudley and Djamil found attentuated increases in angle-
specific peak torque only at fast velocities (160 to 278° s−1)
of movement in a group simultaneously trained for
strength and endurance as compared to a group trained
only for strength.69 No decrements in angle-specific peak
Table 4-2
Responses during Maximal Exercise after Endurance
Training
After Training
Heart rate No changes
Stroke volume Increases
Cardiac output Increases
Arterio-venous Increases
oxygen difference
Oxygen consumption Increases
94 SECTION I • Scientific Foundations
Table 4-3
Comparison of Muscular Responses to Resistance and Endurance Training
Resistance Training
Structural
Fiber size Increases
Capillary density No change or decreases
Mitochondrial density Decreases
Fiber type transition Type IIX to IIA
Metabolic
Oxidative enzymes No change
Glycolytic enzymes Increases
Functional
Peak tension Increases
Contraction speed No change
Fatigability No change
torque were observed at slow velocities (48 to 96° s−1)
of movement in the group that simultaneously trained
for strength and endurance. Again, aerobic power of the
combination training group was not compromised com-
pared to a group trained for endurance only. This study
was the first investigation to suggest that power is affected
first by concurrent training over a short period. In gen-
eral, studies investigating the compatibility of strength
and endurance training have shown similar results
(i.e., strength and power are compromised by endurance
training), while endurance is not mitigated by strength
training.70-72
Although endurance training may impact strength
development, the opposite does not appear to be true.
Studies have shown that resistance training can improve
endurance performance in trained athletes. Bastiaans
et al. replaced part of the conditioning program typically
dedicated to endurance training with explosive strength
training in cyclists and reported that endurance perfor-
mance was not compromised.73 Additionally, the inclu-
sion of explosive strength training negated a decrease in
30-second sprint ability shown with no explosive strength
training. Sprint performance is important to cyclists dur-
ing various parts of a race, such as the sprint at the end.
Paavolainen et al. equated training volume between two
groups of elite distance runners, but in one group 32%
of the total volume was dedicated to explosive strength
training and in the other only 3% was dedicated to explo-
sive strength training over a 9-week period.74 Only the
group who performed the additional explosive strength
training significantly reduced 5K run time with no change
in peak oxygen consumption. These studies indicate that
resistance training improved endurance performance
via neuromuscular mechanisms (e.g., enhanced stretch-
shortening cycle activity, reduced contact time with the
ground) independent of changes in aerobic capacity.
Endurance Training
Decreases
Increases
Increases
Type IIX to IIA
Increases
Variable
Decreases
Decreases
Decreases
Thus, resistance training programs that use moderate
intensities (5 to 15 RM) and emphasize injury prevention
are appropriate for endurance athletes, do not negatively
affect endurance performance, and may actually improve
performance.
Few cellular data are available to provide insights into
changes at the muscle fiber level with concurrent strength
and endurance training.71,75 The muscle fiber is faced with
the dilemma of trying to adapt to the oxidative stimulus
to improve its aerobic function and to the stimulus from
the heavy resistance training program to improve its force
production ability. Kraemer et al. examined changes in
muscle fiber morphology over a 3-month training pro-
gram in physically fit men.76 Both high-intensity strength
and endurance training programs were periodized to pre-
vent overtraining. Participants were grouped as follows:
the strength (S) group performed a total body strength
training program; the combined (C) group performed
the same total body strength training program but also
performed a high-intensity endurance training program;
the upper body (UB) group performed only an upper
body strength training program and the high-intensity
endurance training program; the endurance (E) group
performed only the high-intensity endurance training
program; and a control group performed no training. All
training groups had a shift of muscle fiber types from type
IIX to type IIA. The number of type IIX muscle fibers
was lower after high-intensity strength training (group S)
when compared to high-intensity endurance training
including interval training (group E). This may be due
to the greater recruitment of high-threshold motor units
with heavy resistance training.
From an aerobic perspective, it is interesting to note
the small but significant changes in the type IIC popula-
tion of muscle fibers. This change indicates that when two
high-intensity training programs are used (one focusing
 CHAPTER 4 • Adaptability of Skeletal Muscle: Responses to Increased and Decreased Use
on high-intensity endurance training and the other on
high-intensity strength training), the adaptive response at
the level of the muscle fiber is not the same as to a single
training mode. In this study, lower body power was com-
promised in the C group and the rate of strength devel-
opment demonstrated a trend toward a compromised
state in the C group as well. The response of the UB
group clearly indicated that upper body strength training
is not affected by lower body endurance training, indi-
cating that training two different muscle groups, one for
endurance and one for strength, can be done success-
fully. Consistent with several other studies, peak oxygen
consumption was not diminished by the performance
of both a high-intensity strength and an endurance
training program.69,72 Thus, the mechanisms of adapta-
tion to resistance exercise depend on the global exercise
stimuli presented to the activated musculature. In addi-
tion, concurrent training will begin to negatively impact
strength increases in 2 to 3 months. Thus, it appears that
at the cellular level a differential response to the simulta-
neous training occurred, and single training modes result
in different muscle fiber changes than are observed with
concurrent training.
Strength and Endurance Training
● Resistance and endurance exercises produce divergent
adaptations.
● Although combining resistance and endurance exercises may
mediate absolute gains in strength, it may be most beneficial for
overall muscle performance (increased strength and increased
endurance capacity).
Adaptations to Decreased Use
Detraining
A reduction or loss in the activation of motor units
results in detraining. The extent of such loss depends
on the type of events that stimulate detraining, such
as reduced physical activity, immobilization, or paraly-
sis. The greater the loss of neural stimulation to tissue,
the greater the extent of the impact on the physiologi-
cal mechanisms related to muscle actions. because of
structure-mechanisms. The level of performance dic-
tates the magnitude of initial reduction in performance,
making high-performance athletes or people working in
physically demanding jobs more sensitive to changes in
training stimuli than recreational athletes or those not
physically active. Thus, exercise detraining appears to be
mode specific and demonstrates a different time course,
which needs to be considered in typical training scenar-
ios related in the management of athletes’ training and
injury rehabilitation.
95
Early studies indicate that when training ceases com-
pletely or is drastically reduced, strength declines at a
slower rate than it was gained.77-80 In some cases, brief
periods of inactivity may actually increase performance.
For example, active men, after an initial period of train-
ing, showed a slight increase in isometric force during a
2-week detraining period. However, the magnitude of
early strength changes during a short detraining period
varies depending on a host of factors, such as training
status, competitive versus recreational athletes, and func-
tional level.
Longer periods of detraining (up to 30 weeks) also
result in a decreased strength; however, strength after the
detraining period is still greater than it was before begin-
ning resistance training. Relatively quick decreases in
strength during a detraining period followed by a slower
decline in strength have been shown.81 It has also been
reported that maximal isometric force declines (0.3% per
day) at the same rate at which it was gained during iso-
kinetic training.82
Collectively, the information available on both short
(2 to 4 weeks) and longer periods of detraining indicates
in general that strength decreases do occur, but the loss is
quite variable in magnitude and depends on prior train-
ing status, age, and strength measurement techniques
employed (e.g., concentric versus eccentric; isotonic
versus isokinetic) (for review, see Mujika and Padilla83).
The rate of strength loss may depend in part on the
length of the training period before detraining, the type
of strength test used (bench press, eccentric, concentric,
etc.), and the specific muscle group examined. These
studies indicate reduced training can maintain strength
levels in a variety of muscle groups if training intensity
is maintained at a high level, but no training at all does
result in a loss of strength during detraining.
Few studies have examined the effects of detraining
on cellular level variables. In general, during periods
of detraining, any adaptations that occurred because
of training regress toward the untrained or pretrained
state. During short periods (2 to 8 weeks) of detraining
in males, type I and type II fiber areas84,85 may decrease
compared to the trained state. However, no change has
also been reported.86,87 In men, the type I/type II fiber
area ratio has been reported to decrease during periods
of detraining,85,86 indicating a selective atrophy of type
II fibers, or remain unchanged compared to the trained
state.86 In women, small but nonsignificant decreases
in type I area accompanied by a significant decrease in
the combined areas of type IIAX and X fibers have been
shown.52 Collectively, this information indicates that
type II fibers may atrophy to a greater extent than type I
fibers during short periods of detraining in both men and
women. This, of course, can only occur if the training
induced an increase in fiber area.
96 SECTION I • Scientific Foundations
During short periods of detraining, lean body mass
and percentage of body fat show small, nonsignificant
changes.52,84,85 While the muscle cross-sectional area may
show significant decreases,82 the lack of a significant
change in lean body mass is probably caused by the gross
nature of measurements used and the short duration of
the detraining period.
The effect of detraining on motor performance has
received much less attention than the effect on strength.
After 24 weeks of heavy resistance training three times
per week, vertical jump ability increased 13%.88 Training
primarily consisted of squat type movements using 70 to
100 of 1 RM. Twelve weeks of detraining resulted in a
decrease in vertical jump ability, but it was still 2% above
the pretraining value. Another study showed that 24
weeks of stretch-shortening cycle type training increased
vertical jump ability 17%, and after 12 weeks of detrain-
ing vertical jump ability had decreased but was still 10%
above the pretraining value.89 Training consisted of vari-
ous jumps with and without added weight. During both
of the preceding studies, decreases in squat jump ability
(jump with no countermovement) during the detrain-
ing period also occurred. Two weeks of detraining in
strength-trained athletes (power lifters and football play-
ers) resulted in small, nonsignificant increases in vertical
jump (2.3%) and squat jump (3.6%) ability.87 It appears
that short-term detraining periods may not significantly
affect vertical jump ability; however, longer periods of
detraining are detrimental for vertical jump performance.
Electromyographic (EMG) changes during muscular
actions after training and detraining indicate changes
in motor unit firing rate and motor unit synchronization.
EMG changes have been followed during detraining peri-
ods ranging from 2 to 12 weeks in length. No changes in
EMG activity accompanied by decreases and no change
in strength/power measures during short periods of
detraining have been shown.87,88 Decreases in EMG activ-
ity because of short periods of detraining also occur.82,84
The decreases in EMG have shown significant correla-
tions with decreases in strength.84,89 However, decreases
in EMG activity of some muscles (vastus lateralis) but not
others (vastus medialis, rectus femoris) have also been
shown.84 This EMG information indicates that the initial
strength loss, when it does occur, during the first several
weeks of detraining is due to neural mechanisms, with
muscle atrophy contributing to further strength loss as
the detraining duration increases.90
Muscle and Disuse
● Aerobic de-conditioning occurs earlier than losses in strength in
response to decreased use.
● Strength losses are due to changes in neural activations initially,
followed by later decreases in muscle size.
● Although brief periods of inactivity (1 to 2 days) following
long-term activity may improve performance, extended periods
of disuse lead to a rapid decrease in endurance performance,
followed by decreased strength and loss of muscle mass.
Immobilization
Immobilization results in large and rapid changes in
size, strength, and functional capacity of skeletal mus-
cle. Hespel et al. showed that 14 days of immobilization
resulted in a ∼11% decrease in whole muscle size, accom-
panied by an 8% to 11% decrease in the area individual
muscle fiber types.91 As size and strength are closely cou-
pled, it is logical to assume that decrements in muscle
size produce falls in muscle strength. It has been shown
that just 9 days of immobilization decreased isometric
strength by 13%,92 while 14 days may decrease strength
by 22%.91 Strength decreases following immobilization
appear to be speed specific, as strength at slower angular
velocities falls more than at faster velocities.93
Muscle and Immobilization
● Immobilization produces similar responses as disuse; however,
at a much accelerated rate.
● Muscle power is quite sensitive to immobilization, as force
production at fast contraction speeds falls quite rapidly.
● Rehabilitation after periods of immobilization should focus on
restoring muscle power capacities as well as increasing overall
muscle size and strength.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 93 references for this chapter.

S KELETAL M USCLE : D EFORMATION ,
I NJURY , R EPAIR , AND T REATMENT
C ONSIDERATIONS
Elizabeth Matzkin, James E. Zachazewski, William E. Garrett, and Terry R. Malone
Introduction
As Americans continue to try to incorporate physical
activity and fitness programs into their daily lives, and
as these programs become more popular, the type and
number of activity-related injuries continue to increase.
With more than 60 million Americans involved in orga-
nized sports and with more than half of all Americans par-
ticipating in some form of regular exercise, our need to
understand muscle function, injury, and repair is becom-
ing more urgent.1,2 Reports state that 20 million people
a year sustain some type of muscular injury that results
in lost time from work.2 Work and recreational activities
require varying degrees of neuromuscular coordination,
cardiovascular and muscular endurance, speed, strength,
and flexibility. Acute traumatic injuries to the musculo-
tendinous unit are all too common, in athletes and in
the general population. These type of injuries account
for up to 50% of all injuries.3-10 One of the most common
injuries is muscle strain.
Our understanding of these injuries and the repair
process associated with them is still far from complete
but has improved significantly since the early 1990s.
Researchers continue to investigate methods to under-
stand the physiological, functional, and biomechanical
events that contribute to muscle strain, soreness, and
regeneration. The majority of basic science studies that
have explored muscle strain injury have used passive
stretch or lengthening of an electrically stimulated and
contracting muscle to induce these injuries. Clinically,
5
C H A P T E R
muscle strain injuries are associated most often with
muscle stretching with a simultaneous forceful eccentric
muscle action. Injury and damage predominantly in the
region of the musculotendinous junction are the result
and occur most often in two joint muscles such as the
hamstring complex, gastrocnemius, or rectus femoris.
Although the wealth of literature published on this
subject indicates that new scientific knowledge contin-
ues to be gained, many areas remain to be explored,
and questions must be answered by basic science and
applied clinical research. The purpose of this chapter is
to describe the anatomy and normal physiology associ-
ated with muscle deformation, the pathophysiology asso-
ciated with muscle strain injury, and the repair process.
Anatomy
Muscle is a unique structure with contractile proteins
(actin and myosin) and noncontractile viscoelastic collag-
enous elements. Muscle must be able to (1) shorten and
lengthen and (2) recover or return from shortened and
lengthened positions. Muscle must be able to be length-
ened to allow a single joint or a series of joints to move
through their full available range of motion. This char-
acteristic of muscle is often termed flexibility and is spe-
cific to the individual, the activity in which he or she is
involved, and the joint or joints involved in that particular
activity.11,12 The inability of muscle to be deformed and
lengthen readily may be described as stiffness, or resistance
to elongation. Historically, Stolov and Weilepp13 identified
97
98 SECTION I • Scientific Foundations
the following anatomical elements as possible contributors
to muscle stiffness: adhesion of one fibril to another, adhe-
sion between muscle and overlying subcutaneous tissue
(i.e., the epimysium, the perimysium and endomysium),
and contractile elements within the muscle fiber. More
recently, Garrett and various colleagues14-18 also have iden-
tified the myotendinous junction as an anatomical area
involved intimately with muscle deformation and patho-
physiological change as a result of injury.
Muscle Fibers
Anatomically, muscle is a complex arrangement of con-
tractile and noncontractile protein filaments. Muscles’
ability to contract and shorten, or to lengthen/deform
and recover from deformation, is dependent on this com-
plex arrangement.19,20 The limitation of muscles’ ability to
stretch is predominantly dependent on their noncontrac-
tile components. These noncontractile protein elements
are integrated into a viscoelastic network of connective
tissue. These collagenous elements, which make up the
series and parallel elastic components of muscle, provide
functional stiffness to enhance the transmission of ten-
sion. A large quantity of connective tissue is associated
with muscle (Figure 5-1). The majority of this connec-
tive tissue is composed of type I collagen. Types III and
IV collagen make up the rest of the connective tissue ele-
ment. The arrangement of the connective tissue allows
muscle to be divided into three different layers: the
endomysium, perimysium, and epimysium.
The endomysium is a delicate connective tissue sheath
that invests and separates each individual muscle fiber.
The endomysium provides for myocyte-to-myocyte con-
nectives, myocyte-to-capillary connectives, and a col-
lagenous weave associated with the basal laminae of the
Figure 5-1
Connective tissue of muscle. Cross-section through human sartorius
muscle showing the connective tissue of the epimysium surrounding
the entire muscle and the perimysium enclosing muscle fiber bundles
of various sizes. (From Fawcett DW: Bloom and Fawcett: Textbook of
histology, New York, 1986, Chapman & Hall.)
myocytes.17 External to the basal lamina and the sarco-
lemma, the endomysium is composed primarily of two
different-size collagenous filaments. Neither of these
filaments penetrates the basal lamina of the sarcolemma
(Figures 5-2A and 5-2B).21 Collagen fibers of the thicker
filament (50 µm in diameter) are arranged in a predomi-
nantly longitudinal direction. This orientation may reflect
the endomysium’s role in providing mechanical support
for the fibers’ surface and acting as an elastic device for
contraction-relaxation cycles. The thinner filaments rep-
resent immature forms of collagen and intermingle with
the thicker filaments. Figures 5-2C and 5-2D depict
the collagenous fibrils that make up the endomysium.
Although oriented predominantly parallel to the muscle
fiber, these collagen fibrils also run in a variety of direc-
tions, over and between the different muscle fibers. The
course and distance between the fibrils vary, depending on
the degree of stretch or contraction of the muscle. When
the muscle is contracted, the fibrils are close together and
at right angles to one another, and when the muscle is
stretched, they are parallel to the fibers. This arrange-
ment of the connective tissue permits easy displacement
of the muscle fibrils and offers increasing resistance to
deformation at extreme lengthened ranges.21,22 Arranged
as a weave network intimately associated with the basal
lamina, the endomysium is an important factor in the
passive series elastic component of muscle.
A thicker coating of connective tissue, the perimy-
sium, surrounds each group of 10 to 20 muscle fibrils,
which collectively form a fascicle. The perimysium may
be oriented in either a parallel or a circumferential direc-
tion to the fascicle. The perimysium is composed of vary-
ing amounts of collagenous, elastic, and reticular fibers
and fat cells.22 The collagen of the perimysium consists
of tightly woven bundles of fibers, 600 to 1800 µm in
diameter, which interconnect with the fascicles. During
passive stretch, the amount and arrangement of the con-
nective tissue in the perimysium may be more important
than those in the endomysium. Nagel, as summarized by
Borg and Caulfield,19 found that the perimysium, which is
arranged in a spiral fashion during relaxation of the mus-
cle, is wavy during muscle contraction, which indicates
little tension. This report allowed Borg and Caulfield to
conclude that the perimysium could be a major compo-
nent of the parallel elastic component of muscle, which
demonstrates the importance of maintenance of the
proper position of the muscle bundles and distribution
of the stress associated with passive stretch. The fascicles
of individual muscles are then grouped together and sur-
rounded by the epimysium.
The percentage of elastin and collagen in the connec-
tive tissue associated with muscle varies with the function
of the muscle. In the extremities, the elastic fibrils are
limited more exclusively to the septa between fasciculi in
the perimysium.
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations 99

Figure 5-2
A, Fibrous endomysium. Frog sartorius muscle fiber. Fiber surface is covered by a fibrous layer, through which cross striations are visible. B, Teased
preparation. Frog sartorius muscle (fixed with tannic acid–OsO4). Skeletal muscle fibers (M1, M2, M3) appear as cylindrical units aligned in parallel
bundles. Faint cross striations are visible along individual fibers. Coarse collagenous fibers of the endomysium run in various directions over and between
muscle fibers (arrows). C, Fibrous connective tissue of muscle. Fibrous layer on surface of frog sartorius muscle fiber. Collagenous fibrils cover muscle
fiber and take a predominantly longitudinal course. Cross striations can be seen through fibrous layer (arrowheads). D, Outer aspect of basal lamina of
frog sartorius muscle fiber by use of low-power SEM. Basal lamina is exposed where fibrous layer (CF) is stripped off. Cross striations (arrows) can be
seen more clearly through the lamina than through the fibrous layer. (From Ishikawa H, Sawada H, Yamada E: Surface and internal morphology of
skeletal muscle. In Peachey LD, Adrian RH, Geiger SR, editors: Skeletal muscle, Baltimore, 1983, American Physiological Society, pp 1–22.)

of the passive resting tension of a muscle may be due to

Contractile Elements and Muscle Stiffness
Muscle fibers can exist in three states: relaxed, activated,
and rigor.23 Each of these states is characterized by ten-
sion (of the contractile elements) and stiffness (the change
in force or tension produced by change in length). In
a relaxed state, muscle does not generate active force
and therefore does not possess a high degree of stiffness
in the range of muscle length where most physiologic
actions occur. With enough stretch, even relaxed muscle
is stiffer than activated muscle. However, in the physi-
ologic range, where the passive tension is not high, acti-
vation can significantly increase stiffness significantly.
Opinion varies regarding the exact contribution of
each of these elements to passive tension. A large portion
the connective tissue that lies parallel to the muscle fibers,
although some tension may be attributable to a small
proportion of cross-bridges between actin and myosin
filaments. These cross-bridges have been demonstrated
to resist deformation in skinned muscle fiber (muscle
fibers in which all connective tissue has been removed).
The amount of stiffness or resistance to deformation pro-
vided by the cross-bridges increases as the velocity of the
deforming force increases.24,25 According to Hill,26 these
cross-bridges are stable and may have a “long life.”
The exact contribution of each of the anatomic ele-
ments to muscle stiffness, or the resistance to deformation,
is unknown. The contribution of the contractile elements
appears to be related to the velocity of deformation. As
100 SECTION I • Scientific Foundations

muscle is deformed or stretched, the contribution to stiff-
ness from the noncontractile elements increases.
Myotendinous Junction
A working knowledge of the anatomy of the myotendi-
nous junction is important, because clinical and labora-
tory investigations of the morphology of muscle injury
resulting from deformation or strain indicate that injury
occurs at the myotendinous junction. This information
has been well summarized by Garrett and Lohnes,27
Garrett and Tidball,28 and Jarvinen et al.29
The musculotendinous junction occurs at the end of
each long, cylindrical muscle fiber. The location of this
junction, where myofibrils attach to the cell membrane,
supports its proposed function as the site of force trans-
mission between the contractile elements and noncon-
tractile collagenous tissue. Each muscle cell originates
and terminates with direct connections to the myotendi-
nous junction on which it acts (Figures 5-3A and 5-3B).

Figure 5-3
A, Light micrograph of longitudinal section through several frog semitendinosus muscle cells (M) attached to their tendon of insertion (T) at
myotendinous junctions (arrowheads) (×250). B, Two frog semitendinosus muscle cells terminating on tendon. Both bundles of collagen fibers
pass from tendon to ends of the cylindrical cells (SEM, ×600). C, Longitudinal section through myotendinous junction of frog semitendinosus
muscle cell. Note that the cell and surrounding connective tissue appear to interdigitate at the end of the cell. Also note that the dense, fibrillar
material extends from the terminal Z disc to the junctional plasma membrane (TEM, ×12,500). D, Single, digit-like process of skeletal muscle
at myotendinous junction in longitudinal section. Note that thin filaments run along the length of the process (IN). External to the process
(EX) the basement membrane (BM) is separated from the junctional membrane by the basal lucida (LL) (TEM, ×60,000). (A from Garrett WE,
Tidball J: Myotendinous junction: structure, function and failure. In Woo SL-Y, Buckwalter JA, editors: Injury and repair of the musculoskeletal
soft tissues, Park Ridge, 1988, American Academy of Orthopaedic Surgeons; B through D from Tidball JG: Myotendinous junction:
morphological changes and mechanical failure associated with muscle cell atrophy, Exp Mol Pathol 40:1–12, 1984.)
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations
This “connection” has to be able to withstand consider-
able tensile force of up to 1000 kg.30,31
For such high tensile strength to be available, specific
chains of molecules termed integrins and dystrophin-
glycoprotein complexes are contained within each myofi-
ber. It is the role of these integrins (a family of adhesion
receptors located on the cell membrane) and the dystro-
phin-glycoprotein complexes to connect the contractile
elements to the extracellular matrix through the sar-
colemma. The majority of integrins are located in the
muscle tendon junctions in a specific structure called
the integrin-associated complex. This is in contrast to the
distribution of dystrophin-glycoprotein complexes that
are relatively evenly distributed along the sarcolemma,
although they may be more abundant in the muscle
tendon and neuromuscular junctions (Figure 5-4).29
The cell membrane at the myotendinous junction is a
continuous interface between the intracellular and extra-
cellular compartments, possessing extensive folding so
that the cell and extracellular connective tissue appear to
interdigitate (Figure 5-3C). The external surface of the
myotendinous junction is covered by a basement mem-
brane, which is continuous and morphologically identi-
cal to basement membrane elsewhere on the cell. The
external region of the basement membrane, the reticular
lamina, provides structural connections to tendon colla-
gen fibers (Figure 5-3D). For successful transmission of
force across the muscle cell–tendon interface, the cell and
tendon must form an adhesive junction at these sites. The
load placed on the interface must not exceed the strength
of the interface under these loading conditions, and the
101
mechanical properties of the elastic and viscous elements
must permit some mechanical energy to be transmitted
at the junction. The role of the myotendinous junction
as a force-transmitting structure therefore appears to be
supported by its morphologic features.
The extensive folding at the myotendinous junction is
an important structural correlate to the magnitude of the
stress placed on the junction. This folding increases the
membrane surface contact area, which reduces stress on
the membrane when the junction is stressed by either con-
traction or deformation. Because muscle and the myoten-
dinous junction are viscoelastic structures, their behavior
under loading varies with the magnitude, frequency, dura-
tion, and rate of loading. Because of the effects of these
forces on viscoelastic structures, junction failure may occur
at different stresses during long-term loading and during
rapidly applied, short-duration loading.
Folding at the myotendinous junction places the
membrane at low angles relative to the force vectors
generated by muscle contraction or deformation. If the
membrane were not folded, load would occur in a ten-
sile manner at right angles. Because of the angle of the
folds, shear forces occur at the membrane. These folds
and shear forces allow the myotendinous junction to
behave like an adhesive joint. The strength of an adhe-
sive joint varies with the angle of the interface. The closer
the angle of the interface is to zero, which is the case at
the myotendinous junction, the stronger the junction.
Tidball and Daniel32 noted that disuse atrophy of muscle
results in an increase in the angle at the interface and
failure at the myotendinous junction (Figure 5-5). This
Figure 5-4
A schematic representation of myofiber-
extracellular matrix (ECM) adhesion. Each
myofiber contains specific chains of molecules
called the integrins and dystrophin, which
connect the contractile myofilament apparatus
to the ECM through the sarcolemma.
The majority of integrins are located in the
myotendinous junctions. The sarcomeric actin
binds via several subsacralemmally located
molecules in the β1 subunit of the muscle–
specific transmembrane integrin α7β1, which
binds the ECM proteins. The molecules of the
dystrophin-associated complex are relatively
evenly distributed along the entire sarcolemma,
although they are particularly abundant in the
myotendinous junctions and the neuromuscular
junctions. The contractile protein actin binds
to dystrophin, which is then associated with
three protein complexes: the dystroglycans,
the sarcoglycans, and the sytropihins. (From
Jarvinen TA, Jarvinen TL, Kaariainen M et al:
Muscle injuries: biology and treatment, Am J
Sports Med 33:746, 2005.)
102 SECTION I • Scientific Foundations

completely recovered (Figure 5-6A). Viscous properties

are characterized by time and rate change dependency.
The rate of deformation is directly proportional to the
applied force when considering the viscous property of
connective tissue (Figure 5-6B). The muscle-tendon unit
Figure 5-5
Diagram of a myotendinous junction. Muscle force is applied parallel combines both of these patterns, functioning as a visco-
to the longitudinal axis of the myofilaments and the collagen fibers. elastic structure (Figure 5-6C).36-38 Viscoelastic behav-
The junctional membrane lies at an angle relative to the myofilaments. iors explain many of the observed characteristics of the
(From Tidball JG: The geometry of actin filaments—membrane muscle-tendon unit.34,35
associations can modify the adhesive strength of the myotendinous
Intimately related to the viscoelastic properties of col-
junction, Cell Motil 3:439–447, 1983. Copyright 1983 John Wiley &
Sons, Inc. Reprinted by permission.) lagenous tissues are the physical properties of stress-relax-
ation, creep, and hysteresis. Stress-relaxation is exhibited
by a tissue if a decrease in force is required to maintain
the tissue, which has been stretched or deformed, at a
constant length over time; creep is characterized by a
increase in angulation may result in a decrease in strength
continuance in deformation in response to a maintained
or changes in the adhering surface at the myotendinous
load.35,36,38 The hysteresis response is the amount of
junction, but further research is needed to demonstrate
relaxation, or variation in the load-deformation relation-
any causal relationship.
ship, that takes place within a single cycle of loading and
Sarcomeres near the myotendinous junction tend to
unloading. During hysteresis, a greater amount of energy
be shorter than other sarcomeres within skeletal muscle.
is absorbed by the tissue during loading than is dissi-
Although these sarcomeres are not anatomically differ-
pated during unloading, which results in an increase in
ent, they must function in a different “environment.”
When functioning in this environment (the myotendi-
nous junction), their biomechanical properties may be
different from those of sarcomeres that are not adjacent
to the myotendinous junction. Shorter sarcomeres at the
myotendinous junction have a decreased force-generating
capacity, an increased rate of contraction, and a decreased
ability to change length (deform) compared with other
sarcomeres within the same muscle fiber. Fibers near-
est the distal myotendinous junction may undergo the
greatest strain during elongation.33 These physiologic
correlates suggest that the myotendinous junction is first
preloaded by forces generated by the terminal sarco-
meres and then subjected to further increases in tension
as other sarcomeres reach peak tension.28

Ability to Deform and Recover

Tissue Properties
Like any collagenous tissue, the musculotendinous unit
exhibits physical and mechanical properties when under-
going deformation. These properties give the tissue high
tensile stress, which allows it to respond to load and
deformation appropriately.
Mechanically, the muscle-tendon unit functions as
a composite viscoelastic structure.12,34,35 The viscoelas-
tic behavior of muscle is more complex because of the
contractile components found within muscle; however,
several of the noncontractile collagenous components
exhibit typical viscoelastic properties. The elastic prop-
erty implies that deformation of a change in length is
directly proportional to the load or the force applied.
When that load is removed, the change in length is
Figure 5-6
A, The hookean body. The perfect spring provides a model for
elastic behavior. Deformation is proportional to force. B, The
newtonian body. A model for viscous behavior is provided by a
dashpot or hydraulic cylinder containing viscous fluid. Velocity
of dashpot displacement is directly proportional to force. C, The
viscoelastic model. A spring and dashpot are combined in parallel
or series to exhibit viscoelastic behavior. (From Malone TR, Garrett
WE Jr, Zachazewski JE: Muscle: deformation, injury, repair. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p.76, Philadelphia, 1996 Saunders.)
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations
tissue temperature. Viscoelastic materials and tissues also
exhibit strain rate dependence, exhibiting higher tensile
stress at faster strain rates (Figure 5-7).35,39,40
The effect of each of these properties on muscle has
been illustrated by Taylor, Dalton, Seaber, and Garrett35
using an animal model. Controlled stretching of the
muscle-tendon units of the long extensor muscle of the
toes and the anterior tibial muscle was used in the rabbit
model. Figure 5-8A presents the data from 10 controlled
stretches of the long extensor muscle. Each stretch was
to 10% beyond resting length. The generated maximal
tension (resistance to deformation) was recorded and is
presented as a percentage of the initial stretch. The first
four curves or stretches show significant difference, but
no significant changes are seen beyond the fourth mea-
sure. Figure 5-8B presents the stress-relaxation sequence
and shows significant changes only through the initial
stretches. Figure 5-8C demonstrates that 80% of the
total change in length is accomplished in the first four
stretches of the long extensor muscle-tendon unit when
10 repeated stretches were applied at the same level of
tension; Figure 5-8D shows the hysteresis loops gener-
ated via loading-unloading at specific speeds. During
each stretch, different amounts of energy are absorbed
(during loading) and dissipated (during unloading), with
the difference resulting in ultrastructural change or heat
transfer. This process also may play a role in tissue tem-
perature response to exercise.41 Finally, a muscle strain
rate dependency and a viscoelastic response with greater
force (stiffer response) at higher velocity are demon-
strated in Figure 5-8E. The data presented by Taylor,
Dalton, Seaber, and Garrett35 demonstrate that the initial
cycles of cyclic stretching and deformation are the most
critical for causing change.
Figure 5-7
Physical properties of collagen. (From Butler DL, Grood ES, Noyes
FR et al: Biomechanics of ligaments and tendons, Exerc Sports Sci
Rev 6:126–282, 1979.)
103
Importance of Flexibility: Impact on Injury
Prevention
The notion that good flexibility is vital to health, efficient
physical function, and athletic performance is a widely
accepted belief. Historically, and traditionally, stretching
exercises have been part of warm-up and cool-down rou-
tines in athletics. According to the literature, good flex-
ibility has a number of benefits. Multiple reports in the
literature have stated that having good flexibility assists in
prevention of or decrease in the incidence of injury.10,42-
49
However, the attributes of good flexibility have been
difficult to demonstrate in clinical studies if these stud-
ies are subjected to rigid research criteria. A true cause-
effect relationship between flexibility and the incidence
of injury is difficult to establish if rigorous research cri-
teria are applied.50 The results of studies attempting to
demonstrate that good flexibility influences movement
efficiency and enhances athletic performance are also con-
flicting or inconclusive.51-55 Do the study design, meth-
odology, data collection, and statistical analysis support
the conclusions of the author(s)? Questions concerning
these factors and conclusions drawn have led to chal-
lenges of some of these traditional beliefs. These chal-
lenges have been best summed up by the meta-analysis
of publications from 1966 to 2002 by Thacker, Gilchrist,
Stroup et al56 and literature reviews by Shrier.57,58
The contradictions in the literature have caused
Witvrouw, Mahieu, Daniels et al59 to term the relationship
between stretching and injury prevention “an obscure
relationship.” In their review paper, the authors present
their discussion and argument that some of these contra-
dictions can be explained by considering the type of sport
that the individual is participating in. These authors pres-
ent a discussion of the literature that they feel supports
the positive benefits of stretching relative to injury pre-
vention for sports that require a high intensity of stretch
shortening cycles (bouncing and jumping activities
found in sports such as soccer or football) compared with
sports that have low intensity or limited stretch shorten-
ing cycles (such as jogging, cycling, and swimming). A
more robust discussion of this literature is presented in
Chapter 25, Joint Range of Motion and Flexibility. The
historical and current literature indicates that all ques-
tions regarding the value and importance of stretching,
real or perceived, have not yet been answered.
Types of Muscle Flexibility
Static and dynamic flexibility are required in athletics and
in all levels of physical activity and function. deVries has
defined static flexibility as the measured range of motion
available in a joint or a series of joints, and dynamic flex-
ibility as a measure of the resistance to active motion
about a joint or a series of joints.11 Resistance to tissue
104 SECTION I • Scientific Foundations

Figure 5-8
A, Tension curves of EDL muscle-tendon units repeatedly stretched to 10% beyond resting length. Each of the peak tensions for the first four
stretches showed a statistically significant (p < 0.05) difference from the other peak tensions. The overall tension decrease was 16.6%.
B, Relaxation curves for EDL muscle-tendon units stretched repeatedly to 78.4 N. The relaxation curves of the first two stretches demonstrated
statistically significant differences from the other curves. No significant differences exist in curves 4–10. C, Graphic representation of EDL
lengthening with repeated stretching to the same tension. Approximately 80% of the length increase occurred during the first four stretches.
D, Representative force-length relationships demonstrating the effect of stretch rate on a single TA muscle-tendon unit. E, Hysteresis loops
observed in TA muscle during loading and unloading at constant rates of 0.01, 0.1, 1, and 10 cm/sec. (From Taylor DC, Dalton JD, Seaber AV
et al: Viscoelastic properties of muscle-tendon units: the biomechanical effects of stretching, Am J Sports Med 18:300–309, 1990.)
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations
deformation (stiffness) decreases as dynamic flexibility
increases. As a rule, good static flexibility is a prereq-
uisite for good dynamic flexibility. Good static flexibil-
ity, however, does not ensure good dynamic flexibility.
Dynamic flexibility may be critical for maximizing human
performance and efficiency in addition to minimizing the
risk of injury, especially in high-velocity activities such as
gymnastics, hurdling, and sprinting, but further research
is required before a definitive statement can be made.
Periarticular connective tissue and muscle-tendon struc-
ture must be able to deform easily in the time required
to perform specific activities and minimize the chance of
injury. The importance of this is discussed in the review
of literature provided by Witvrouw, Mahieu, Danneels,
et al59 for sports that require high-intensity stretch short-
ening cycles such as are required in gymnastics. Dynamic
flexibility is limited by the ability of the connective tissue
to deform quickly and easily and by the integration of the
neuromuscular system (contractile elements of muscle
and its innervation).12
Influential Factors
Age
During the normal aging process, increased stability of
the collagen fibrils occurs as a result of changes within
the ground substance; an increase in the collagen fibril
diameter and the total collagen content of tendon, cap-
sule, and muscle; and the maturation and development
of complex intermolecular cross-links between tropocol-
lagen molecules.60-66 These changes can translate into
decreased joint range of motion and muscle flexibility
with aging. Clinically, this decrease has been reported
in the young as part of the maturation process67,68 and
throughout the life span.69-73
With aging, the cross-sectional area of muscle declines
and the number of muscle fibers decreases by about 39%
by age 80.74,75 Type I muscle fibers are not affected much
by aging, but type II fibers demonstrate a reduction in
cross-sectional area of 26% from age 20 to 80, most likely
a result of denervation.74 Aging thus leads to smaller
muscle mass, a higher proportion of type I fibers, and
less strength secondary to denervation of type II fibers.75
Both endurance and resistance training can affect the
losses and muscle adaptation in the elderly. Endurance
training enables type II fibers to become more aerobic,
whereas resistance training done consistently over time
shows improvement in mass and strength.75,76 Changes
in skeletal muscle from aging seem to be secondary to
the decline in demands on muscle and lack of physical
activity, and thus can be minimized or even reversed with
adequate training.73,75,77,78 All of these changes translate
into an increase in collagen and connective tissue content
in relation to actin-myosin complexes and force-generating
105
capacity. Greater possibility exists of muscle stiffness and
a loss of flexibility with less strength and subsequent
decrease in physical function.
Immobilization
The length of time and position of immobilization are
significant factors related to a muscle’s response and its
ability to recover its contractile characteristics and flex-
ibility. The effect of rigid immobilization on muscle has
been well detailed.79-83 The results of restricted motion,
in which joint and associated muscles are not allowed to
move through their complete range, have not been well
studied.
Stress-induced changes caused by immobilization tend
to occur at the myotendinous junction.28 An adjustment
in the number and length of sarcomeres occurs at the
myotendinous junction whether the imposed immobili-
zation takes place in a shortened or a lengthened posi-
tion. Sarcomeres are added when muscle is immobilized
in a lengthened position and lost when immobilized in a
shortened position.79-81,83,84 A change in sarcomere num-
ber begins within 12 to 24 hours and continues until
a normalization of tension occurs through regaining
motion. Changes also occur in the connective tissue.
Biological adaptation to muscle growth or muscle
immobilization in a stretch position occurs near the myo-
tendinous junction. When muscle is immobilized in a
shortened position, atrophy results in a loss of contractile
and noncontractile elements. Noncontractile elements
are lost at a slower rate than contractile elements, which
results in a relative increase in connective tissue and a
reduction in the extensibility of muscle. The thickness
of the endomysium and perimysium also may increase.66
These changes may result in an increase in the stiffness of
the muscle. Similar changes have also been demonstrated
in respiratory muscles that must function in chronically
shortened positions.85
Biomechanically, muscle immobilized in a short-
ened position develops less force and stretches to a
shorter length before injury than does nonimmobilized
muscle. Muscle immobilized in a lengthened posi-
tion responds differently; greater force and a greater
change in length are required to cause a tear than in
nonimmobilized muscle. In both cases, the tear occurs
at the myotendinous junction, which indicates an
alteration in the mechanical properties at the junction.
Clearly, a key factor in determining the nature of the
change at the myotendinous junction is the position of
immobilization.28
Temperature
Temperature has a profound effect on the physical
and mechanical properties of collagen (Figure 5-9).
106 SECTION I • Scientific Foundations
Figure 5-9
Effect of temperature on force relaxation response. (From Lehmann
JF, Masock AJ, Warren CG et al: Effect of therapeutic temperatures
on tendon extensibility, Arch Phys Med Rehab 51:481–487, 1970.)
Collagenous tissues have an inverse temperature–elastic
modulus relationship, especially at higher temperatures.86-91
Historically, numerous investigators have explored the
effects of therapeutic temperatures (which have an upper
limit of 45°C) and load on the extensibility of collagen,
using tendon as a model. All have demonstrated that
temperature elevation results in increased elasticity and
decreased stiffness when attempting to deform connec-
tive tissue.92-96
Studies on muscle demonstrate a similar relation-
ship using the anterior tibial muscle and long exten-
sor muscle of the toe in a rabbit model.97,98 Although
each study used a different testing temperature
(39°C versus 35°C92; 25°C versus 40°C 93), a signifi-
cant increase in length or deformation was attained
before failure by the warmer muscles in both of these
studies. The thermal effects in the study completed
by Noonan, Best, Seaber, and Garrett98 were depen-
dent on the loading rate and contractile state of the
muscle. Stiffness and energy absorbed to failure were
significantly higher in the colder muscles, which sug-
gests that warming a muscle may confer a protective
effect against muscle strain injury. Warm muscles
must undergo greater deformation before failure,
which is advantageous in the prevention of injury. A
warm muscle is less stiff than a cold muscle and develops
less force for a given deformation. Assuming that a
critical force must be reached in order for an injury
to occur, there may be some protection acquired by
a “warm” muscle and its ability to undergo greater
deformation (Figure 5-10). Still unclear, however, is
if the critical factor in the cause of injury is strain or
load. If the critical factor is strain, a warm muscle
may be prone to injury, because it undergoes greater
deformation to attain a given load. Further research
is needed in this area.
Figure 5-10
The biomechanical effects of warming a muscle. Warm muscle reaches
an arbitrary submaximal load at a greater length than cold muscle.
(From Noonan TJ, Best TM, Seaber AV et al: Thermal effects on skel-
etal muscle tensile behavior, Am J Sports Med 21:517–522, 1993.)
An increase in intramuscular temperature may be pro-
duced either by various means of external warming
(environmental factors or by using therapeutic modali-
ties)99 or through muscular contraction. Research shows
that exercise can increase intramuscular temperature100-102;
however, general exercise has not been shown to
increase the intramuscular temperature above 39°C
because of the body maintaining temperature equilib-
rium through normal head production and dissipation
mechanisms. Therefore exercise alone may not be suf-
ficient to increase the intramuscular temperature suf-
ficiently to influence viscoelastic behavior and passive
energy absorption. Despite this fact, Safran, Garrett,
Seaber et al41 were able to alter the amount of stretch
a muscle could withstand before failure in an in vitro
model by warming the muscle by 1°C and inducing a
single isometric contraction.
Contraction: Impact of Strength and Endurance
The strength of muscle is defined as its maximum ability
to produce contractive force. Muscle strength per se does
not limit flexibility or the ability of muscle to lengthen.
Strong muscle may provide a protective mechanism by
which to minimize the chance of muscle strain injury. An
appropriate balance of strength and flexibility must be
attained by an active individual for maximal protection.
Garrett and associates103 examined the biomechani-
cal properties of passive (relaxed) and active (stimulated)
muscle rapidly lengthened to failure in an animal model.
The parameters of force to failure, change in length to fail-
ure, site of failure, and energy absorbed before failure were
examined. With a rabbit model, the long extensor muscle
of the toe was pulled to failure either while being stimu-
lated electrically (tetanically or by wave summation [sub-
maximally]) or while in a relaxed or passive state. Stimulated
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations
muscle required a significantly greater force to cause failure
and absorbed more energy before failure than did nonstim-
ulated, passive muscle. All muscles were injured at the distal
myotendinous junction and demonstrated no difference in
the length to failure (Figure 5-11). Maximally stimulated
muscle absorbed more energy before failure than did sub-
maximally stimulated muscle. A muscle that can contract
strongly and effectively is well equipped to absorb energy.
A muscle that is developing more force is absorbing more
energy while stretching the same degree. This could be a
factor in prevention of muscle strain injury.103
If a strong muscle is able to absorb greater energy and
requires greater force to be imposed on it before failure,
apparently strength training and muscle endurance train-
ing have a role to play in muscle strain injury preven-
tion. Although a muscle that is stimulated submaximally
requires a greater force to failure and absorbs greater
energy than a relaxed muscle, its injury resistance capac-
ity is not as great as a tetanically stimulated muscle.104
Therefore the greater the strength and the fatigue resis-
tance capacity of the muscle, the less likely it is to be
injured. Reading the work of Hassleman, Best, Seaber,
and Garrett104 also may lead to the hypothesis that the
ability of muscle to undergo eccentric loading is a critical
factor in the ability to prevent partial muscle strain injury
that occurs within the available physiologic range. Based
on this hypothesis, incorporation of eccentric exercise
and strength training appears to be integral in the pre-
vention and treatment of muscle strain injuries.
Figure 5-11
Differences in relative energy absorbed to failure in stimulated versus
passive muscle shown schematically as the area under each length-
tension curve. (From Garrett WE, Safran MR, Seaber AV et al:
Biomechanical comparison of stimulated and nonstimulated skeletal
muscle pulled to failure, Am J Sports Med 15:448–454, 1987.)
107
Muscular strength does not limit muscle flexibility,
provided the athlete pursues an active flexibility pro-
gram. Changes in connective tissue strength resulting
from hypertrophy of collagen fibers do not decrease the
tissue’s ability to deform but do increase its stiffness and
resistance to deformation.
If injury has occurred, the clinician must remember
the physiologic and functional factors associated with the
injured tissue and the tissue’s tolerance for stress and strain.
Low-resistance exercise designed to prevent muscle atro-
phy and a loss of muscular endurance and gentle stretch-
ing exercises should be started 3 to 4 days after injury.
The clinician must remember that after injury, less force
and shorter stretch lengths are required to cause rein-
jury or complete rupture. Forces must be controlled and
progressively increased before the return to competition.
Controlled exercise and mobilization, after a minimal time
of rest and relative immobilization, have demonstrated
positive results in an animal model. These concepts are
discussed in greater depth later in this chapter.
Injury
Location and Pathophysiology
When a muscle strain injury occurs, it is because the ten-
sion generated exceeds the tensile capacity of the weak-
est structural element.105 These indirect muscle injuries,
caused by either stretching or a combination of muscle
activation and stretching, have been demonstrated to occur
near the region of the myotendinous junction15-18,105 and,
more recently, within random areas of the muscle belly.104
The most frequent muscle strain injuries occur to muscles
that cross two joints, muscles such as the gastrocnemius,
hamstring complex, gracilis, and rectus femoris.106,107
Although these in vitro studies used animal models,
subsequent computed tomography (CT) and magnetic
resonance imaging (MRI) studies demonstrated similar
results on more than 50 patients (Figure 5-12).108 MRI
demonstrated that high–signal-intensity fluid collected
at the site of the disruption (the myotendinous junc-
tion) and then dissected along the epimysium, at times
breaking through to the epimysium or subcuticular tis-
sues. Muscle tissue somewhat remote from the myo-
tendinous junction also demonstrated signal changes
consistent with edema and inflammation. These injuries
may result in a complete or incomplete tear.
Disruption of fibers occurs near the myotendinous
junction, not necessarily at the junction itself (Figure
5-13). The disruption usually occurs a short distance
from the tendon, ranging from 0.1 mm to several milli-
meters.27,28 The response to injury at the myotendinous
junction is limited to the area of injury and is usually
extremely focal in nature. The basic early structural
defect in this type of injury is thought to be a localized
108 SECTION I • Scientific Foundations

Figure 5-12
A, A T2-weighted coronal MR image (repetition time, 2000 msec; echo time, 70 msec) of a grade III distal adductor longus muscle strain with
proximal retraction (straight arrow). The normal contour of the adductor longus is shown by the curved arrow. Note the high signal within the
retracted muscle. B, A T2-weighted axial MR image (repetition time, 2200 msec; echo time, 70 msec) of a biceps femoris muscle strain (arrow).
Whole muscle involvement with edema and inflammation is present. The high-signal fluid has escaped the epimysium to abut adjacent structures.
The biceps femoris and semitendinosus muscles share a common tendon of origin situated between the two muscle bellies. The most intense
changes in the biceps femoris can be seen to occur near the tendon. (From Speer KP, Lohnes J, Garrett WE: Radiographic imaging of muscle
strain injury, Am J Sports Med 21:89–96, 1993.)

Figure 5-13
A, Gross appearance of tibialis anterior of rabbit after controlled strain injury. A small hemorrhage (arrow) is visible at the distal tip of injured
muscle at 24 hours. I, injured; C, control. B, Histological appearance of tibialis anterior immediately after strain injury showing limited rupture of
the most distal fibers near the musculotendinous junction along with hemorrhage. T, tendon; M, intact muscle fibers. Masson stain (×100).
C, Complete avulsion of muscle fibers from myotendinous junction. The tendon is at the lower margin. Approximately 2 mm of muscle
fiber remains attached to the tendon (bar gauge = 1 mm). (A and B from Nikolaou PK, MacDonald BL, Glisson RR et al: Biomechanics and
histological evaluation of muscle after controlled strain, Am J Sports Med 5:9–14, 1987; C from Garrett WE, Tidball J: Myotendinous junction:
structure, function and failure. In Woo SL-Y, Buckwalter JA, editors: Injury and repair of the musculoskeletal soft tissues, Park Ridge, 1988,
American Academy of Orthopaedic Surgeons.)
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations
disruption of the sarcolemma of the muscle fiber,
created by the force of stretching.109 Some current
research also suggests that after an acute muscle strain,
an intracellular barrier may effectively restrict the injury
response to less than 500 µm away from the initial site
of rupture.110, 111
After failure, muscle fibers may still be attached to the
tendon. It is not presently known how this may relate
to the membranous folding, angle of junctional load-
ing, or increase in terminal sarcomere stiffness at the
myotendinous junction. Although injury occurs within
this region of limited extensibility, and structural differ-
ences are noted, full detailed studies of this anatomical
area are lacking.
Threshold and Continuum
Hassleman, Best, Seaber, and Garrett104 have dem-
onstrated that a threshold and continuum for injury
induced by active stretch (lengthening of stimulated
and contracting muscle) in the animal model exist.
Fiber disruption occurs initially, and connective tissue
disruption results only with larger muscle deformation.
In rabbits, anterior tibial muscles and long muscles of
the toe were actively stretched at 10 cm per second to
60%, 70%, 80%, or 90% of the force required for passive
failure. The effects on maximal isometric contractile
force, tensile properties, and histological changes are
summarized in Table 5-1 and Figures 5-14, 5-15, and
5-16. This study, which induced partial injury, provides
evidence that injury with active stretch is selective,
with muscle fiber disruption occurring before connec-
Table 5-1
Continuum of Injury
Force for Passive Failure
Injury Parameter 60% 70%
Maximal isometric Unchanged Decreased 20%
contractile force
Failure properties Unchanged Unchanged
Histological Normal ■ Edema and bleeding
changes ■ Inflammatory cells
■ Focal myotendinous junction
fiber disruption
■ Normal muscle belly
From Hasselman CT, Best TM, Seaber AV et al: A threshold and continuum of injury during active stretch of rabbit skeletal muscle, Am J Sports
Med 23:65–73, 1995.
109
tive tissue damage. Injury occurs at the myotendinous
junction and within the muscle belly. A threshold for
injury with active stretch was demonstrated, and per-
haps more importantly, injury was produced within the
physiologic range of the muscles tested extensor digi-
torum longus (EDL). Injury was initially demonstrated
at the distal myotendinous junction and in distal fibers
near the junction. Muscle fiber damage progressed in
severity as force increased in the 70%, 80%, and 90%
groups. Muscle belly injury was associated with higher-
force injuries and also progressed in severity as the
force increased. Connective tissue disruption was dem-
onstrated only at the highest force (90%).
The mechanism of injury used in this study simulated
the most common mechanism seen clinically, the active
stretch, which does not usually result in complete rup-
ture of the muscle. The histological change seen at the
distal muscle fibers and the mid muscle belly may explain
why some athletes complain of diffuse muscle pain after
a muscle strain injury. The fact that the contractile ele-
ments were initially involved and injured, and that injury
to the connective tissue elements did not occur until the
highest forces were imposed on the muscles, may assist
in focusing prevention and rehabilitation efforts on the
appropriate structures.104
Repair and Regeneration
Incomplete muscle tears are more common than com-
plete tears.28 The process of injury and repair is similar to
that found in other collagenous tissues, with the excep-
tion of the activation of satellite cells.18,112-117 This process
80% 90%
Decreased 50% Decreased 80%
Unchanged Altered
■ Edema and bleeding ■ Edema and bleeding
■ Inflammatory cells ■ Inflammatory cells
■ Moderate myotendinous ■ Major myotendinous
junction fiber disruption junction fiber disruption
■ Random fiber disruption ■ Scattered fiber disruption
in muscle belly in muscle belly
■ Connective tissue
disruption
110 SECTION I • Scientific Foundations

Figure 5-14
Longitudinal light micrographs show the distal muscle-tendon junction for the different strain groups using trichrome stain. Both tibialis anterior
and extensor digitorum longus muscles had similar morphological features in each group. A, The 60% group showed normal findings. B, The
70% group showed hemorrhage, edema, inflammatory cells, and focal fiber disruption. C, The 80% group showed findings similar to the 70%
group, but damage was more widespread. D, The 90% group revealed connective tissue damage in addition to significant muscle fiber disruption.
(From Hassleman CT, Best TM, Seaber AV et al: A threshold and continuum of injury during active stretch of rabbit skeletal muscle, Am J Sports
Med 23:65–73, 1995.)

Figure 5-15
Longitudinal light micrographs show the distal muscle belly for the different strain groups using trichrome stain. The extensor digitorum longus
and tibialis anterior tendons were similar in morphology for the different groups. A, The 60% group showed normal findings. B, The 70% group
showed edema separating the muscle fibers. C, The 80% group showed random fiber disruption, edema, inflammatory cells, and hemorrhage.
D, The 90% group revealed connective tissue damage along with muscle fiber damage, edema, inflammatory cells, and hemorrhage. (From
Hassleman CT, Best TM, Seaber AV et al: A threshold and continuum of injury during active stretch of rabbit skeletal muscle, Am J Sports Med
23:65–73, 1995.)
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations 111

Figure 5-16
Cross-section light micrographs show the tibialis anterior middle muscle belly for the different strain groups using trichrome stain. A, Normal
anatomy was noted in the 60% group. B, Edema was noted in the 70% group. C, The 80% group showed hemorrhage, edema, and a number
of rounded, lightly staining cells that were two to three times the normal size. D, The 90% group was similar to the 80% group, except that
connective tissue damage was noted as well. (From Hassleman CT, Best TM, Seaber AV et al: A threshold and continuum of injury during active
stretch of rabbit skeletal muscle, Am J Sports Med 23:65–73, 1995.)

has been reviewed and summarized by Huard, Li and Fu 118
and most recently Jarvinen, Jarvinen, Kaarianen et al29
(Figures 5-17 and 5-18).
After injury the healing process sets up two competi-
tive events, the regeneration of muscle fibers and the
production of fibrous scar tissue (repair).113,114 During
this process three phases are present: destruction, repair,
and remodeling.
Muscle Healing Stages
● Destruction
● Repair/regeneration
● Remodeling
Destruction
Initially after rupture, hemorrhage and edema occur.
Soon after, degenerative change and necrosis are noted,
but these are confined to the site of the injury. Confining
the necrosis to the area of injury is a critical function of
cytoskeletal material that condenses into a contraction
band (Figure 5-19).110,111 An inflammatory reaction is
initiated as the necrotic area is then invaded by macro-
phages, to clear debris and T-lymphocytes, which secrete
cytokines and growth factors.118 The inflammatory
response is accelerated by adhesion molecules (P, L and
E-selectin) and cytokines (interleukins and tumor necro-
sis factor-alpha). Growth factors (insulin-like growth
factor (IGF-1), hepatocyte growth factor (HGF), epider-
mal growth factor (EGF), transforming growth factors
(TGF-A and TGF-B) and platelet-derived growth factors
(PDGF-AA and PGDF-BB) aid in regulation of myoblast
differentiation and proliferation to support muscle repair
and regeneration.118 Concurrently, satellite cells become
activated and are subsequently transformed into myo-
blastic cells, myotubes, and new muscle fibers (Figures
5-20 and Figure 5-21).
Healing and Remodeling
Once “destruction” has begun to subside, regeneration
and fibrosis (repair), two competing events begin at the
same time. These events must remain in balance for full
recovery to occur and are well summarized by Jarvinen,
Jarvinen, Kaariainen et al.29 A timetable for some of these
events and their impact on muscle contractile ability, peak
load, and elongation rupture is presented in Table 5-2.
Regeneration usually begins 3 to 6 days post injury
and peaks around 7 to 14 days. Myofiber regeneration is a
result of the intrinsic characteristics of the fiber itself, and
secondarily as the fiber having access to a pool of satellite
cells. These satellite cells are available to the myofiber
112 SECTION I • Scientific Foundations

Figure 5-17
A schematic illustration of the healing skeletal muscle. Day 2: necrotized parts of the transected myofibers are being removed by macrophages
while, concomitantly, the formation of the connective tissue scar by fibroblasts has begun in the central zone (CZ). Day 3: satellite cells have
become activated within the basal lamina cylinders in the regeneration zone (RZ). Day 5: myoblasts have fused into myotubes in the RZ, and the
connective tissue in the CZ has become denser. Day 7: the regenerating muscle cells have extended out of the old basal lamina cylinders into the
CZ and begin to pierce through the scar. Day 14: the scar of the CZ has further condensed and reduced in size, and the regenerating myofibers
close the CZ gap. Day 21: the interlacing myofibers are virtually fused with the intervening connective tissue (scar) in between. (From Jarvinen
TA, Jarvinen TL, Kaariainen M et al: Muscle injuries: biology and treatment, Am J Sports Med 33:747, 2005.)

Figure 5-18
A schematic presentation of a shearing injury of skeletal muscle. The ruptured myofibers contract and the gap between the stumps (Central
Zone [CZ]) becomes filled initially by a hematoma. Myofibers are necrotized within their basal lamina over a distance of 1 to 2 mm, within
which segment a complete regeneration usually takes place with time (Regeneration Zone [RZ]), whereas only reactive changes are seen in the
parts of the muscle surviving the trauma (Survival Zone [SZ]). Each myofiber is innervated at a single point of neuromuscular junction (NMJ;
black dots). Because the myofibers are usually ruptured on either side of the row of the NMJs of the adjacent fibers, the adjunctional stumps
of fibers 1 and 3 to 5 on the “ad” side (right) remain innervated, whereas the abjunctional stumps on the “ab” side (left) become denervated.
Even the adjunctional stump of fiber 3 has become denervated because its NMJ is located in the RZ. Reinnervation of the abjunctional stumps
occurs via penetration of new axon sprouts through the scar of the CZ and the formation of the new NMJs (shown here 1 sprout and NMJ
[white dot]). Fiber 3 becomes reinnervated when regeneration in the adjunctional RZ takes place. (From Jarvinen TA, Jarvinen TL, Kaariainen
M et al: Muscle injuries: biology and treatment, Am J Sports Med 33:748, 2005.)
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations 113

Figure 5-19
A semi-thin epon section of a ruptured muscle 2 days after a shearing
injury. The surviving parts of the four myofibers are demarcated
sharply from the necrotized segments, which have become
transformed in to basal lamia cylinders containing macrophages
(round cells) phagocytosing the necrotic debris. The contraction
band (thick arrow) that halts the propagation of necrosis is still clearly
visible in Fiber 1 but has disappeared in Fibers 2–4. The regeneration
process has already begun, as evidenced by the existence of myoblasts
within the basal lamina cylinders (thin arrows). Toludine blue. Bar
50µm. (From Jarvinen TA, Jarvinen TL, Kaariainen M et al: Muscle
injuries: biology and treatment, Am J Sports Med 33:748, 2005.)

from beneath the muscle fibers basil lamina in addition

to stem satellite cells. Cells proliferate and then differen-
tiate into myoblasts and ultimately form multinucleated
myotubes. This activation and regeneration of muscle
fibers occurs on both sides of the defect/injury. These
multinucleated myotubes then attempt to join the injured
myofiber on the opposite side of the injury to com-
plete the repair and allow function to be regained.117,119
Multiple branches are formed by surviving myofibrils
on either side of the injury defect and connective tissue
scar. These branches attempt to pierce the scar tissue that
separates them (Figure 5-22).111 Currently unknown is
whether the stumps of the transacted myotubes fuse with Figure 5-20
each other or through the formation of miniature mus- A, A myoblast (arrow) with desmin-positive sarcoplasma is already
visible within the basal lamina cylinder of the necrotized part of the
cle-tendon junctions with some type of connective tissue
sarcoplasm 21 hours after the injury, which indicates that it must
between them119,120 This attempt to regain strength and have differentiated from a committed satellite cell (antidesmin
integrity is reinforced laterally by adhesion of the regen- and hematoxylin counterstain). B, The first mitosis of the stem
erating parts of the myofibers to the extracellular matrix satellite cells (arrows) are seen approximately 24 hours after the
(Figure 5-23). This lateral reinforcement helps to pro- injury, visualized here by immunostaining for brinideixturidine
(a thymidine analoge) incorporated in nuclear DNA during the
tect the repair process and reduce the risk of rerupture
S-phase of the cell cycle (anitbromodeoxyuridine and hematoxylin
before the completion of the healing process. Some type counterstain; bar 30 µm). (From Jarvinen TA, Jarvinen TL,
of mechanical stress also may be required for this pro- Kaariainen M et al: Muscle injuries: biology and treatment, Am J
tective lateral adhesion to occur.29 Jarvinen, Aho, Lehto, Sports Med 33:750, 2005.)
114 SECTION I • Scientific Foundations

and Toivonen have noted that there is an overall decline

Figure 5-21
A schematic presentation of fetal development (A1-B1-C-D) and
regeneration of myofibers via the activation of satellite cells (A2-B2-
C-D or A3-B3-C-D). Satellite cells have been set aside underneath
the basal lamina during the fetal development (A2 and A3) to be used
in growth and repair. After injury, the committed satellite cells (csc)
immediately begin differentiation into myoblasts (mb) without prior
cell division (B2), while the stem satellite cesss (ssc) first divide, and
only then one of the daughter cells differentiates in to a myoblast
(B3), whereas the other replenishes the pool of satellite cells (B4).
Myoblasts fuse into myotubes (mt), which then grow and mature in
to myofibers, the sarcoplasm of which becomes filled with contractile
filamentous proteins organized as myofibrils and the myonuclei
located subsarcolemmally. mpc, myogenic precursor cell. (From
Jarvinen TA, Jarvinen TL, Kaariainen M et al: Muscle injuries: biology
and treatment, Am J Sports Med 33:749, 2005.)
in the regenerative capacity of aged muscle.121
During repair, the hematoma and resultant granula-
tion tissue that “fills the gap” between that is a result of
muscle strain injury provides wound tissue with the initial
strength to withstand contraction forces applied to it.29, 114
The integrity of the connective tissue framework begins
to be restored through fibroblastic proliferation and the
synthesis of proteins and proteoglycans. Some of these
initial proteins (fibronectin and tenascin-C [TN-C]) pos-
sess elastic properties that allow them to provide strength
and elasticity to the early granulation tissue formed. The
formation of type III collagen and type I collagen, only
a few days later, remains elevated for several weeks.29
Although Huard, Li, and Fu118 in a recent review propose
that general fibrosis occurs in healing muscle, Jarvinen
and Lehto122,123 and Lehto, Duance, and Restall114 have
presented evidence that intramuscular connective tissue
is not increased unless the muscle is immobilized for a
substantial period of time. Like any healing tissue, tensile
strength of healing tissue increases over time as type I
collagen comes into the area and matures. At approxi-
mately 10 days after trauma, the scar tissue has reached
a point where it is no longer the “weakest link” of the
injured muscle. If loaded to failure, rupture would occur
within the muscle tissue adjacent to the newly formed
mini musculotendinous junctions, between the regener-

Table 5-2
Muscle Repair and Regeneration
Time from Injury

16 to 24 3 to 6
Finding 15 Minutes 3 Hours 8 Hours Hours 48 Hours Days 7 Days

Hemorrhage115-117,131 + + + +
Pyknosis115-117,131 + +
Sarcolemma breakup115-117,131 + +
Mitochondrial disruption115-117,131 + +
Sarcoplasmic reticulum disruption115-117,131 + +
Interrupted sarcolemma115-117,131 + +
Phagocytosis115-117,131 + +
Satellite cell activation115-117,131 + + +
Myotubes evident115-117,131 +
Scarring and fibrosis18 +
Contractile ability (% of control)18,132 67–80% 51.1% 74.5% 92.5%
Peak load (% of control)132 63%
Elongation to rupture (% of control)132 79%

Updated and revised from Malone TR, Garrett WE Jr, Zachazewski JE: Muscle: deformation, injury, repair. In Zachazewski JE, Magee DJ,
Quillen WS, editors: Athletic injuries and rehabilitation, Philadelphia, 1996, Saunders, p 85.
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations
Figure 5-22
A, Seven days after a contusion injury, the tips of the regenerating
muscle cells extend out of the orifices of the old basal lamina tubes
and begin to penetrate into the scar tissue in the central zone
(anitdesmin and hematoxylin counterstain; bar 100 µm).
B, This penetration is soon halted by the formation of new mini-
myotendinous junctions at the tips of the myofibers, whereby
the adhesion of myofibers to the extracellular matrix becomes
reestablished. These new myotendinous junctions appear as
accentuated immunostaining with antibody to the muscle-specific α7
chain of the adhesion molecule integrin α7β1 (arrows) (anti-integrin
α7 and hematoxylin counterstain; bar 30 µm). CZ, central zone; RZ,
regeneration zone. (From Jarvinen TA, Jarvinen TL, Kaariainen M
et al: Muscle injuries: biology and treatment, Am J Sports Med
33:751, 2005.)
ated myofibers and the scar tissue.29 More time is needed,
however, for full recovery to occur.
Although in most cases muscle strain injury heals with-
out the formation of excessive scar tissue, the formation
of scar tissue sometimes can be excessive, which results in
a dense fibrous scar. This can occur with large ruptures,
reruptures, or chronicity, which create a mechanical bar-
rier that affects the regeneration of myofibers across the
site of the injury. This may leave scar tissue as the final
result of the biological muscle repair process.118 Complete
regeneration of muscle tissue does not occur. The devel-
opment of methods to enhance muscle regeneration
while preventing fibrosis is being investigated currently
and will be discussed briefly below.
115
Figure 5-23
A, In the beginning of the healing process of the injured skeletal
muscle, the expression of cell adhesion molecule integrin (α7β1) is
enriched at the end of the regenerating part of the injured muscle
fibers, whereas only minor amounts are present on the lateral aspects
of the myofiber. B, A dramatic increase in the expression of the α7β1
integrin takes place along the lateral aspect of the plasma membrane
in the intact and regeneration parts of the injured myofibers when
the regenerating muscle fibers pierce into wound tissue. Thus the
α7β1 provides stability for the regenerating muscle fibers that lack
adhesion at their ends. C, The expression of the α7β1 integrin
returns to normal level on the lateral sarcolemma with simultaneous
redistribution of α7β1 integrin to the ends of the regenerating
myofibers when they form new myotendinous junctions and adhere to
the scar. (From Jarvinen TA, Jarvinen TL, Kaariainen M et al: Muscle
injuries: biology and treatment. Am J Sports Med 33:753, 2005.)
The inflammatory process described above is a vital
part of initiating tissue repair. Clinicians often seek to con-
trol the inflammatory process by limiting the amount of
hemorrhage and edema. This is usually accomplished by
the use of rest, ice, compression, and early mobilization.
Nonsteroidal anti-inflammatory drugs (NSAIDs) often
are given in an attempt to control pain and inflammation.
Short-term use decreases the inflammatory cell reaction
and has not been demonstrated to have any adverse impact
on healing, tensile strength, or muscle function124-126; or
116 SECTION I • Scientific Foundations
the ability of the muscle to regenerate.127 The effect of the
NSAID piroxicam (Feldene, Pfizer Inc., Groton, CT) on
the histological, biomechanical, tensile, and contractile
characteristics of rat and rabbit muscle strained to fail-
ure has been investigated by Almekinders and Gilbert125
and Obremsky, Seaber, Ribbeck, and Garrett126 from 1
to 7 days and 1 to 11 days after injury, respectively. In
the study by Almekinders and Gilbert, the animal’s test
limb was immobilized after injury, whereas the animals
in the study by Obremsky and colleagues were allowed
free cage activity. The inflammatory response in the ani-
mal group receiving piroxicam was delayed in both stud-
ies. Tensile strength of the muscle was not significantly
different in either study, but there was a trend toward
decreased tensile strength. Although no significant del-
eterious effects on tensile strength of muscle or contrac-
tile ability are apparent, dose response studies appear to
still be lacking. An interesting note is that muscles of the
sham control animals in the study by Almekinders and
Gilbert125 demonstrated a progressive decrease in ten-
sile strength with immobilization alone over an 11-day
period. Mishra, Friden, Schmitz, and Lieber128 also using
a rabbit muscle injury model, showed that an NSAID-
treated group demonstrated initial benefit with remark-
able recovery but showed a significant decline in torque
generation after 28 days. In summary, the early use of
NSAIDs offers some initial benefits of analgesia and
reduction of inflammation without an adverse effect on
healing. However, long-term use may be somewhat det-
rimental to skeletal muscle regeneration in some injury
strain models.128-130
Injections of corticosteroids have been used in
major college and professional athletics in an effort
to return injured players to competition sooner. The
effect of corticosteroid injections has been studied
and reported in the literature using animal models.
Although these drugs may block pain and result in
an increase in the ability to generate muscle force in
the short term, the muscle may be subjected more
easily to tensile forces above the threshold for com-
plete rupture or rerupture, resulting in reinjury.125,131-133
Research regarding the effects of suppression on the
inflammatory process after muscle injury still needs to
be further elucidated.
Multiple research avenues have been explored to find
ways to improve muscle regeneration and prevent muscle
fibrosis. Growth factors are thought to play an impor-
tant role in muscle regeneration, especially IGF-1, which
is particularly mitogenic for myoblasts.118,134 IGF-1 has
been shown to prevent loss of muscle mass in healthy
older men,135 exhibit muscle hypertrophy in transgenic
mice,136 and block the age-related loss of muscle mass
and function in mice after gene transfer of IGF-1 via
an adeno-associated viral vector.137 The use of IGF-1 in
conjunction with basic fibroblast growth factor (bFGF)
and nerve growth factor (NGF) in a mouse model has
demonstrated accelerated regeneration in injured mus-
cle.138,139 Fifteen days after injection, the mice demon-
strated improvement in overall strength (tetanic and fast
twitch strength) likely because of the increased numbers
and diameter of regenerated myofibers compared with
controls.138,139
Although growth factors can potentially improve
muscle healing, the ability to administer them to the
injured muscle and in effective concentrations is criti-
cal. Gene therapy is being investigated as a method to
deliver stable high concentrations of growth factors safely
to injured muscles.118 Most of this research has focused
on adenoviral vectors for growth factor delivery vehicles.
An adenovirus carrying IGF-1 has been developed, but
studies thus far have failed to demonstrate an improve-
ment in muscle function, although they do demonstrate
improvements in the healing process.118,140
Improvement of the healing process and inhibi-
tion of fibrosis are necessary. Research has focused
on operative intervention or antifibrotic therapy by
blocking the overexpression of TGF-B. Menetrey,
Kasemkijwattana, Fu et al141 investigated the effects
of surgical repair with suturing compared with immo-
bilization after muscle laceration in a mouse model.
This study suggested that immobilization led to slower
muscle regeneration and a large amount of deep and
superficial scar tissue within the muscle. Surgical inter-
vention with suturing of the lacerated muscle appeared
to promote healing and prevented the development of
deep scar, although it did not eliminate the develop-
ment of superficial scar. TGF-B1 has been found to
be expressed in high levels when muscle injury and
skeletal muscle fibrosis are present.118 Antagonization
of TGF-B1 or any other part of the fibrotic cascade
are current targets of research in the prevention of scar
formation. Other antifibrosis agents such as decorin,
gamma-interferon, and suramin are also under investi-
gation for scar tissue prevention and elimination within
healing skeletal muscle.
Contractile and Tensile Strength after Injury
Tensile strength of the healing tissue increases over
time. Normal intramuscular collagenous tissue has a
greater proportion of type I collagen than type III col-
lagen.112-114 After injury, type III collagen demonstrates
a significant increase over type I collagen in the area of
repair as a function of the granulation response. As the
tissue matures, collagen cross-links stabilize and gain
strength. The proportion of type I to type III collagen
returns to normal. The response to healing and tissue
maturation takes time. Although the active contractile
tension that an injured muscle is able to generate from
the remaining intact muscle fibers increases rapidly
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations 117

after muscle strain injury, the tissue maturation and simultaneous eccentric contraction (intrinsic force) may
collagenous strength do not increase as rapidly. The fail because of excessive load being applied while at a
process by which collagenous strength is regained may point of extreme deformation.
take weeks. Factors that contribute to muscle strain injury—inad-
Nikolaou, Macdonald, Glisson et al18 and Taylor, equate flexibility, inadequate strength or endurance, dys-
Dalton, Seaber, and Garrett132 examined the structural synergistic muscle contraction, insufficient warm-up, or
and functional strength of muscle immediately after an inadequate rehabilitation from previous injury—have
experimentally created strain injury using the long exten- been well reviewed and summarized.50,143,144 Based on
sor muscles of the toe and the anterior tibial muscles in these factors, Worrell and Perrin50 proposed a multiple-
a rabbit model. A nondisruptive strain injury was cre- factor hamstring injury model (Figure 5-24). This model
ated by stretching the experimental muscle just short of appears to be supported by the studies and information
complete rupture. All failures occurred in the area of the presented earlier. A compromise of one or more of these
myotendinous junction. Immediately after injury, the factors could predispose an athlete to injury or increase
contractile ability of the muscles was 20% to 33% of con- the chance of injury.
trol in the experiment conducted by Taylor and 70.5%
of control in the data presented by Nikolaou. Nikolaou
continued to test contractile ability up to 7 days after
Clinical Implications
injury, which demonstrates a further decrease to 51.1% Diagnosis of Muscle Strain Injury
at 24 hours, followed by a progressive return to 74.5%
Symptoms of muscle strain injuries are pain on contrac-
at 48 hours and 92.5% days after injury (see Table 5-2).
tion and stretch, in addition to the possible development
Immediately after injury, the peak load was 63% of con-
of ecchymosis and swelling with large or complete tears.
trol and elongation to rupture was 79% of control in the
Sometimes, a palpable defect when swelling has resolved
experiment conducted by Taylor.
in the presence of large or complete tears or if the injury
Although contractile strength may demonstrate fairly
is palpated soon after occurring. Various imaging modal-
rapid increases in a short period of time after injury in
ities such as ultrasound, CT scanning, and MRI also
the animal model, tissue maturation and integrity do not
can be used in the diagnostic work of these injuries to
occur in this short time span. Controlled mobility and
visualize accurately the extent of the pathology and/or
stress are key considerations in the post-injury period.
the amount of residual scarring that may be present in
Scar formation, muscle regeneration, orientation of
the case of chronic repetitive muscle strain injuries (see
new muscle fibers, and tensile properties of muscle have
Figure 5-12). The anatomical, physiological, and biome-
been demonstrated to be enhanced in an animal model
chanical factors presented from the animal model studies
when subjected to controlled mobilization or move-
discussed earlier in this chapter, in addition to each of the
ment compared with immobilization.141 This fact must
causative factors presented by Worrell and Perrin,50 must
be considered relative to the results of the immobilized
be addressed in any flexibility program. These consider-
sham group from the study by Almekinders and Gilbert
ations hold true if the program is prophylactic in nature,
discussed above.125
Clinically, scarring and fibrosis, with their inability to
tolerate the tension that uninjured contractile elements
may generate, may explain the frequent recurrence of
injury to strained muscles if excessive load or deforma-
tion is placed on the healing tissues too early.18,132 The
findings presented imply that, even in severely injured
muscle, enough structural strength remains so that mus-
cle may undergo functional rehabilitation in the form of
low-force exercise designed to prevent muscle atrophy
and to maintain muscle tone. Gentle stretching allows
maintenance of range of motion and muscle flexibility. A
treatment regimen of complete rest and immobilization
may be too conservative, prolonging recovery.132,142

Mechanism of Injury
Muscle strain injury is an indirect injury caused by exces-
sive intrinsic force production, excessive extrinsic stretch,
or both. Muscle undergoing an extrinsic stretch with a
Figure 5-24
Multiple factor hamstring injury model. (From Worrell TW, Perrin
DH: Hamstring muscle injury: the influence of strength, flexibility,
warm-up and fatigue, J Orthop Sports Phys Ther 16:12–18, 1992.)
118 SECTION I • Scientific Foundations
intended to improve flexibility and prevent injury, or if an
injury has occurred and the program is designed to return
the individual to function. If injury has occurred, the cli-
nician must also take into consideration the time frame
required for tissue repair and regeneration. The greater
the severity of injury, the longer the time for full recovery
and return of full, pre-injury function. This is based on the
magnitude of the injury and amount of damage because
all injuries, regardless of severity, must go through the
same healing phases.
Principles of Rehabilitation and Intervention
The following principles should serve as a guide for clini-
cians caring for patients who have suffered from some
type of muscle strain injury or tear. These principles are
developed based upon knowledge of the physiology,
pathophysiology, healing, and repair process associated
with muscle strain injury.
Principles of Rehabilitation
● Prevention is easier than treatment
● Intervention depends on stage of healing
● Controlled mobility and activity are best
● Medications and modalities are important adjuncts to care
● Develop strong, flexible tissue
● SAID principle is vital
● Pain is the guiding factor
● No “quick fix” is possible
Prevention Is Easier than Treatment
One of the primary roles any clinician assumes is that of
educator. Stress should be placed on teaching the patient
and/or athlete the best possible injury prevention tech-
niques and strategies. This includes instruction in the
most appropriate warm-up and stretching exercises, and
the development of conditioning programs and strategies
to increase the strength and endurance for specific mus-
cle groups at risk. The maintenance of strong, flexible
muscle with good endurance characteristics is the best
prevention to injury.
Intervention Depends upon the Stage of Healing
Muscle, like any structure that contains connective tissue,
goes through four basic phases of healing.18,112,115,116,122
These phases are summarized in Table 5-3. The length
of time for each phase varies with the severity of injury.
The following offers a rough guideline for intervention
techniques and considerations for third-degree strains or
muscle tears:
Phase I: 1 to 3 days
Phase II: 3 to 6 days
Phase III: 6 to 18 days
Phase IV: 18 days onward
The time required for each phase is the same regardless
of the severity of the strain; however. the amount of dam-
age is less. Return to activity should be based on healing
stages in addition to symptoms, risk of re-injury, and abil-
ity to protect the injured muscle. Recommended inter-
vention considerations are summarized in Table 5-4.
Controlled Mobility and Activity versus Immobility
and Rest
Collagen formation is perhaps the best illustration of
Wolff ’s Law, and this is certainly true for muscle strain
injury. Controlled mobility is a key consideration for the
treatment of muscle strain injury. Considerable evidence
exists to support its use based on the work of Jarvinen
and others beginning as early as 1975.114,123,141,145-151
These changes positively affect scar formation, revas-
cularization, muscle regeneration, metabolic processes,
the orientation of muscle fibers, and their ability to gen-
erate tension and tolerate tensile stress. The clinician
must apply these stresses judiciously, however. During
this period injured fibrils begin to acquire the strength
to tolerate contractile and tensile forces. Too much
motion and/or too much stress applied too early may
result in an excessive amount of scar formation (which
results in difficulty for muscle fibers to penetrate the
scar tissue formed), or re-rupture. Controlled mobil-
ity and motion within the pain free range, rather than
absolute rest and immobilization, are therefore key con-
siderations in the first few days (1 to 3 days) after acute
muscle strain injury. Ice and compression also should be
used during this time period to minimize swelling and
pain. Limiting weight bearing should be used if neces-
sary with lower extremity muscle strain injury to make
sure that pain and excessive stress are avoided, while
maintaining mobility.
After the first few days of controlled mobility and
activity, flexibility and strength should start to be
addressed. The limits of the pain free range should be
addressed progressively and pain free resistive exercise
may be initiated. This assists in promotion of the pene-
tration of muscle fibrils through scar laid down during
the initial post-injury time period. Strength and flex-
ibility training should progress based on tissue healing
and under the guidance of the clinician. By 7 to 10
days post injury, muscle has regained much of its con-
tractile ability.18,132 Results of experiments have shown
that by 10 days after injury, muscle again stressed to
failure demonstrated injury in the intact portion of the
muscle, not the recently injured area.152 All activity
within this period (Phase II: 4 to 6+ days post injury)
should be pain free. Therapeutic modalities (e.g., heat,
ice, or ultrasound) may be used to assist in preparation
of the tissue for stress to be imposed on it, to control
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations 119

Table 5-3
Stages of Healing
Stage Description

I. Inflammatory Response
II. Ground Substance Proliferation
III. Collagen Protein Formation
IV. Final Organization
Characterized by hemorrhage and hematoma formation, pyknosis (with third-degree
strains), and phagocytosis. This response initiates the repair process.
Fibroblasts begin to produce gel-like matrix that surrounds collagen fibrils. Phagocytosis
continues but at a slower rate. An attempt to limit the inflammatory process should
be made if it appears to continue out of control. The length of time devoted to repair
and rehabilitation may be somewhat contingent upon the extent of the inflammatory
process.
Collagen is produced by fibroblasts in the area. Initially a high proportion of collagen
is soluble or immature because of the lack of cross-links between collagen molecules.
The inflammatory process must be halted by this stage because the soluble collagen
may be susceptible to enzymatic breakdown.
Collagen fibrils begin their maturation process. Motion is important as these fibrils
react as stated in Wolff’s law and orient themselves in accordance with the tension
placed upon them.

pain, for patient comfort, and to minimize any inflam-
matory response. Proper exercise warm-up should be
used to obtain its maximal benefit.
Medications and Modalities: Important Adjuncts
to Care
The use of NSAIDs has been discussed in depth earlier
in this chapter. Their use should be considered early in
the post-injury period for control of pain and discom-
fort. They then should be discontinued to minimize their
chance of disrupting the healing process. Although their
use later in the healing process and through long-term
use may be detrimental to the healing process, it does not
appear that a true dose-response relationship is known at
this time. Topical steroid administration may be consid-
ered through the use of phonophoresis or iontophoresis.

Table 5-4
Muscle Strain Intervention
Phase of Healing
Treatment Considerations I - Day 1-3 II - Day 4-6 III - Day 6-18 IV - Day 18+

Rest/“immobilization”
Controlled X
Progressive X X
Modalities
Cryotherapy X X A A
Thermotherapy B B B
Ultrasound P P C C
Electrical stimulation X X
Medication
NSAIDs X X
Phonophoresis/iontophoresis X X
Exercise
Maintenance X
Stretching X X
Strengthening X X
External supports X X X X

A, After treatment; prophylactic. B, Before treatment to increase tissue temperature. P, Pulsed ultrasound. C, Continuous ultrasound.
Modified from Zachazewski JE: Flexibility for sports. In Sanders B, editor: Sports physical therapy, Norwalk, 1990, Appleton and Lange.
120 SECTION I • Scientific Foundations
Although these modalities have demonstrated effective-
ness for the treatment of acute superficial inflammatory
conditions such as patella, Achilles, or lateral/medial
epicondylar tendonitis153,154, the clinician must consider
the depth of penetration necessary for the most com-
mon muscle strain injuries (hamstrings, adductors, rectus
femoris) and the ability of these modalities to drive effec-
tively the compound to this depth. No research has been
completed to address these issues in muscle strain injury.
Nonetheless, these modalities may prove beneficial in a
limited patient population.
Ultrasound has historically been, and continues to be,
widely used clinically for the management of muscle strain
injury in all phases of healing. In early stages, it has been
proposed that ultrasound could aid in the initial stage of
muscle regeneration; however, this has been difficult to dem-
onstrate from a research perspective for muscle injury.155,156
Experimental evidence exists, however, that this does occur
in tendon.157-161 Pulsed ultrasound also has a micro massage
effect that may assist with resolution of soft tissue swelling in
the early phases. In later phases, continuous ultrasound may
be used to assist in elevating tissue temperature, approach-
ing the therapeutic threshold (103°F) that may allow for
easier tissue deformation and stretching. The impact of
increasing the temperature of the musculotendinous junc-
tion also may have a positive impact on the sensitivity of the
Golgi tendon organ to tension.162
Cold therapy, or cryotherapy, should be used initially
after injury to limit pain, inflammation, swelling, and
hematoma formation. In the later phases of rehabilita-
tion, ice may be used in a prophylactic manner to pre-
vent inflammation that may be caused by microtrauma.
Cold may reduce the sensitivity of the muscle spindle to
stretch162 and decrease spasm associated with pain.
Electrical stimulation has also been demonstrated to
be effective in the reduction of swelling and edema, espe-
cially with combined with compression. Studies demon-
strating this, however, typically have studied the effect of
electrical stimulation on joint injuries.163-165
Strong Flexible Tissue
A strong tissue exhibits greater strength to failure and
an increased stiffness.166 A strong tissue exhibits greater
strength to failure and an increased stiffness. As long as
a muscle’s flexibility/range of motion/deformation is
maintained, there will not be a change in the elongation
to failure of that muscle. The beneficial effects of main-
tenance of muscle strength and flexibility (ROM) thru
exercise have been well documented.
There will be no change in the elongation to failure
provided the ROM is also maintained. The beneficial
effects of exercise on connective tissue have been well
documented. Strengthening should be initiated in a
pain-free manner as soon as possible (phase II). Emphasis
should be on endurance initially with progressive empha-
sis placed on strength. Endurance should be a key con-
sideration so that strong contractile capacity remains
throughout any activity. This may assist in the prevention
of muscle strain injury. This may be especially important
in the prevention and management of athletic injuries.
The potential protective effects of muscle activation and
strength have been demonstrated by Garrett, Safran,
Seaber et al.103
A flexible tissue has an increased elongation to failure
and decreased stiffness. No loss of tissue strength takes
place.166 This is critical in muscle that must undergo a
large range of deformation (two-joint muscles) and high-
velocity changes (dynamic flexibility) imposed by ballistic
athletic type activities.59
SAID Principle
The SAID Principle (Specific Adaptation to Imposed
Demands) is vital for any activity, especially athletics. Just
as specific training programs must be designed to assist the
athlete to meet the demands of his or her sport, specific
flexibility programs must be designed to assist in meet-
ing the flexibility requirements of sports or other physical
activities. Considerations of static or ballistic flexibility
demands must be taken into account. Specific stretch-
ing programs and exercises must take this into account.
These considerations are discussed in detail in Chapter
25, Joint Range of Motion and Flexibility. Although basic
principles and concepts are constant, treatment programs
from the onset of injury to the return to activity should
be individualized in all cases.
Pain: A Guiding Factor
The clinician should make every attempt to use the
most up-to-date knowledge provided by basic science to
design the most appropriate treatment and intervention
programs. However, patients and their subjective feed-
back must always be the guiding factors when dealing
with muscle strain injury.
No Quick Fix
Immature collagen and healing tissue cannot tolerate
excessive stress and strain. Clinicians are responsible
for designing the most appropriate rehabilitation pro-
gram possible given their knowledge of the normal and
pathophysiology of muscle strain injury and healing. If
progressed too quickly, the injury may become chronic,
prolonging recovery time. The greater the severity of
injury, the longer the expected recovery time.
Other Considerations
Hyperbaric Oxygen Therapy
The use of this modality/equipment has been proposed
and studied; one study demonstrated its ability to assist in
the regeneration of injured skeletal muscle.167 However,
 CHAPTER 5 • Skeletal Muscle: Deformation, Injury, Repair, and Treatment Considerations
based on the authors’ comments and comments from the
AOSSM Research Committee,168 caution has been urged
in extrapolation of these experimental findings into clini-
cal practice. To date, no clinical studies have been pub-
lished regarding the efficacy of this type of therapy.29
Surgical Intervention
Jarvinen and colleagues29 urge extreme caution regard-
ing the consideration of surgical intervention for muscle
strain injuries based on the fact that most muscle injuries
of this type heal conservatively. Indications for surgical
consideration include large intramuscular hematoma,
complete strain or rupture of a muscle that has few or
no agonists, or if greater than 50% of the muscle belly is
torn.107,169 Surgical intervention is easier if the injury has
taken place close to the musculotendinous junction rather
than in the middle of the muscle belly. Attempts to reat-
tach ruptured stumps of torn muscle cannot be accom-
plished unless these sutures can be placed through the
fascia overlying the muscle. This technical difficulty may
affect the results seen in experimental models.170 Studies
by Almekinders169 and Menetrey, Kasemkijwattana, Fu
et al141 have demonstrated somewhat conflicting results
regarding whether surgical repair is better than conserva-
tive intervention when completed in the animal model.
Applicability to clinical situations is unknown. All aspects
of the hematoma and necrotic tissue should be removed
carefully. Postoperatively, a compression wrap and “rela-
tive” immobilization in a neutral (nonstressful) position
should be used. A splint or orthosis should be applied
that prevents load from being applied to the repaired
muscle. The duration of immobilization depends upon
the extent and severity of the tear and repair. Patients
who have undergone repair of a weight-bearing muscle
(e.g., the gastrocnemius or rectus femoris) should not
be allowed to bear weight for 4 weeks. At 2 weeks, how-
ever, gentle ROM and stretching within pain limits may
be initiated. After 4 weeks, weight bearing is progressed
and all restrictions in weight bearing are removed after
approximately 6 weeks.
121
Summary
This chapter provides the basic science background of
muscle deformation, injury, and repair and the possible
clinical application of this information. It appears that
most muscle strain injuries occur in the area of the muscle-
tendon junction and involve strong eccentric muscle
activation with stretching. Less severe partial strain inju-
ries may involve predominantly the contractile elements;
more severe injuries and complete muscle tears also
cause injury to the associated connective tissue struc-
tures. Significant alterations in extensibility of the mus-
culotendinous unit can be provided through changes in
temperature and the level of activation (contraction) in
addition to speed of applied load or force. Resistance
to stretch is multifactorial, coming from the neural
mechanisms, contractile elements, and connective tissue
resistance. Strength, fatigue, warm-up, and flexibility
are critical factors associated with muscle strain injury.
Clinicians should focus on injury prevention through
the increase in flexibility and increases in strength,
particularly emphasizing the eccentric pattern of muscle
utilization. Imperative is recognition that muscle typi-
cally functions as an energy absorption system in which
the highest tensile loads and demands are greatest. Clinical
studies have documented the usefulness of specific inter-
ventions, but further basic and applied clinical research
is needed. Knowledge of what happens from a physi-
ological perspective will guide the clinician in the appro-
priate management of muscle strain injury. Information
presented in this chapter is meant to complement the
information presented in Chapter 25, Joint Range of
Motion and Flexibility.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever pos-
sible. There are a total of 170 references for this chapter.

122 SECTION I • Scientific Foundations
B ONE B IOLOGY AND M ECHANICS
Barbara J. Loitz-Ramage and Ronald F. Zernicke
Introduction
Although apparently inert macroscopically, bone is a
dynamic structure that perpetually remodels in response
to alterations in mechanical loads, systemic hormones,
and serum calcium levels. Bone’s dynamic structure-
function relation, Wolff’s law, makes it a prime focus for
exercise and rehabilitation specialists interested in physi-
cally active individuals who place heightened mechanical
and systemic demands on their skeleton. Maintaining a
positive balance between adaptive and maladaptive skel-
etal responses is vital if participation, performance, and
healing are to be optimized.
Here, after providing an overview of bone structure,
the authors emphasize bone structure-function relations
in addition to what exercise- and disuse-related changes
in bone dynamics reveal about underlying mechanisms
of bone remodeling. The truncated discussion of bone’s
other functions reflects only the need to focus this
chapter and does not connote a hierarchy of functional
importance.
The skeleton provides levers from which muscles con-
trol movements, protects vital organs, serves as a min-
eral storehouse, and houses bone marrow hematopoietic
cells.1 Each of these functions is interrelated synergisti-
cally; that is, the specific anatomy of a bone reflects the
specific function of that bone. For example, in the slen-
der trabeculae of cancellous bone, osteocytes are located
close to vascular channels, which suggests that cancellous
bone contributes effectively to mineral mobilization.
Function of Bone
● Provides levers for movement
● Protects vital organs
● Serves as mineral storehouse
● Contains hematopoietic cells
122
6
C H A P T E R
Skeletal Organization
Bone is described as an organ, as a tissue, or in terms of
its cells, and it is important to appreciate that bone is a
functional entity at each of these organizational levels.
As an organ, bone encompasses a substantial percent-
age of total body mass. A distinction is not made here
regarding bone size, shape, or developmental origin,
but it is as an organ that bone metabolic processes (e.g.,
hematopoiesis) can be described. Bone tissue can be
classified as either cortical or cancellous. Although cor-
tical and cancellous bone comprise the same cells, the
mechanical behavior and adaptive responses differ. Many
types of cells are native to bone tissue, and these cells
function interactively to maintain bone as a tissue and
as an organ.
Development of Bone
Skeletal development is an intricate, highly refined pro-
cess, the full details of which are beyond the scope of
this chapter. Nonetheless, in a clinically relevant context,
the general milestones and terminology associated with
bony development are introduced, with examples of the
developmental phases that, if modified, can produce
skeletal dysplasia (abnormal growth or development).
Particular note is made of the role of mechanical stress
in the development of the skeleton. For an in-depth dis-
course on skeletal development, several excellent reviews
are available.2,3
Skeletal development begins when mesenchymal
cells derived from the primary germ layers (mesoder-
mal cells) condense. In a few bones (cranium and facial
bones and, in part, the ribs, clavicle, and mandible),
the cellular condensations form fibrous matrices that
subsequently ossify directly (intramembranous ossifica-
tion). In this process, mesenchymal cells differentiate
and begin producing the enzyme alkaline phosphatase.
 CHAPTER 6 • Bone Biology and Mechanics 123

Soon thereafter, calcification and ossification of the
fibrous matrix occur, which forms individual bony tra-
beculae that together constitute a primary ossific cen-
ter. Bone deposition continues in a centrifugal direction
from the primary center until a bony island is formed.
As centrifugal expansion slows, the periosteum thickens
and develops mature osteoblasts on its deepest layer.
The deep periosteal layer then becomes the primary site
of continued bone growth.
In appendicular and axial bones, mesenchymal con-
densations form a cartilaginous model (anlage) of the
bones rather than proceeding directly to calcification
and ossification. The cartilage cells within the anlage
are organized in five distinct zones that correspond his-
tologically to the cartilage layers of the growth plate.2
At the ends of the cartilage model, the cells of zone
1 are tightly packed with little extracellular matrix.
Cells of zone 2 are flattened with their cellular axes
oriented transverse to the anlage longitudinal axis. This
orientation reflects the diametric growth that occurs
in the cartilage anlage, in contrast to the longitudi-
nal growth that predominates in the growing bone.
Zone 3 cells are cuboidal in shape and begin to show
vacuoles, indicative of active synthesis of matrix com-
ponents. The neighboring cells of zone 4 are the larg-
est of the chondrocytes. These cells actively produce
extracellular matrix components. At the central mid-
shaft level of the anlage, the cells of zone 5 are rap-
idly involuting or dying, leaving large empty spaces, or
lacunae. Initial deposition of osteoid tissue occurs in
this region. Circumferentially, the perichondrium sur-
rounding zone 5 thickens and lays down a thin layer
of osteoid tissue, which subsequently mineralizes and
forms a bony collar at the midshaft level. Vascular chan-
nels penetrate the central region and bony collar, ulti-
mately forming the primary ossific center. Ossification
proceeds quickly toward the ends to form the bone
diaphysis and metaphysis (Figure 6-1).

Bone collar of calcified cartilage E Cartilage

covered by periosteum
D
C Metaphysis
A B Primary ossification center
Bone

Cartilage
anlage
Primary
(diaphyseal)
ossification center

Secondary ossification I Articular

center (epiphysis) H cartilage
G
Cancellous
F bone
Artery

Physis Cortical
Primary or bone
ossification center growth Bone marrow
plate (medullary cavity)
Bone
Bone covered
by periosteum

Figure 6-1
Development of a typical long bone in longitudinal sections. A, Mesenchymal condensation—the basic anlage. B, Precartilaginous model.
C, Cartilage model with bone collar. D, Fibrovascular tissue penetrates primary osseous collar. E, Central replacement of cartilage by bone,
with extension of bone longitudinally forming the primary ossification center, which will become the diaphysis and metaphysis. F, Vascular
tissue enters distal epiphyseal cartilage. G, Epiphyseal (secondary) ossification center develops and grows larger (primarily a postnatal process).
H, Second epiphyseal ossification center develops. (Note the difference in growth rate of the two ends. Each long bone has a “growing
end” that allows more growth to occur at that end.) I, As epiphyseal cartilage disappears bone ceases to grow in length and bone marrow cavity
becomes continuous throughout length of bone.
124 SECTION I • Scientific Foundations

In the epiphyseal regions, the vascular channels layers of chondrocytes. An important anatomical region
directly invade the cartilage, which subsequently ossi- within the developing long bone is the zone of Ranvier,
fies and forms secondary ossific centers (see Figure 6-1). found at the cortical margins of the growth plate toward
Vascular ingrowth is a mandatory step in the formation the primary ossific center.2 The zone of Ranvier contains
of the primary and secondary centers because the blood the periosteal collar of bone that is advancing from the
supply ensures the arrival and subsequent differentiation bony shaft toward the epiphysis, a region of undifferen-
of osteogenic precursor cells.4 tiated mesenchymal cells that gives rise to chondrocytes
Between the bone formed by the primary and sec- along its deepest surface, in addition to the junction
ondary ossific centers, the cartilage anlage persists as the between the periosteum, which covers the bony shaft, and
epiphyseal (growth) plates between the shaft (diaphysis) the perichondrium, which covers the epiphyseal cartilage.
and ends (epiphyses) of the long bone (Figure 6-2). The This complex zone is important because it is here that the
growth plate results from a compaction of the cellular increase in metaphyseal diameter occurs during growth.
zones of the cartilage anlage and thus contains analogous Therefore trauma that damages the zone of Ranvier may
disrupt the normal circumferential growth of the long
Epiphysis or
bone metaphysis.
Joint capsule
secondary Longitudinal bone growth occurs through activity
Articular
cartilage
growth center of the chondrocytes within three functionally distinct
regions of the growth plate: the regions of growth, matu-
ration, and transformation (Figures 6-3 and 6-4A). The
region of growth contains two subpopulations of chon-
Epiphyseal
plate or drocytes. Resting cells lie close to the secondary ossific
physis center. These cells are associated with the small arterioles
Cancellous and capillaries from the epiphyseal vessels. The vessels are
(spongy) bone
important in transporting undifferentiated cells to add
to the pool of resting cells. Away from the resting cells
Artery to is an area of active cell division. In this area, the cells are
periosteum
organized in longitudinal columns, and during a period
Periosteum
of rapid growth, the columns may account for over half
the height of the growth plate.3
Marrow cavity The region of maturation is composed of chondro-
Cortical cytes that actively synthesize and secrete cartilaginous
(compact)
bone extracellular matrix. Adjacent to the region of growth,
the cells are large and actively produce matrix compo-
Nutrient artery
Diaphysis
nents, whereas the cells near the ossific front become
trapped in the rapidly calcifying matrix and therefore are
not as active in matrix production.
Periosteum The third zone is characterized as an area of transfor-
mation where the cartilage matrix becomes increasingly
calcified and is invaded by metaphyseal blood vessels.
The encroaching vessels bring the osteoblasts necessary
for the formation of bone osteoid. The osteoid is rapidly
mineralized to form true bony tissue.
Eventually, chondrocyte differentiation and prolif-
eration slow in the regions of growth and maturation,
Metaphysis
which allows the bone mineralization, encroaching from
the diaphyseal edge of the plate, to catch up. This brings
Level of together the bone formed initially by the primary and
epiphysial
plate secondary centers and marks the culmination of long
Epiphysis bone growth.
In most long bones, primary growth plates are found
at each end of the bone and are loaded in compression
Figure 6-2 (Figure 6-5), as loads are transmitted across the plate
Schematic diagram of a long bone and its blood supply showing
the different parts of bone. (Modified from Gardner E, Gray
between the bone diaphysis and epiphysis. In the larger
DJ, O’Rahilly R: Anatomy: a regional study of human structure, bones, such as the tibia and femur, small growth plates
Philadelphia, 1975, WB Saunders, p 9.) also exist between the bone diaphysis and the large bony
 CHAPTER 6 • Bone Biology and Mechanics 125

Second
ossification
center
(epiphysis)

Perichondrial
ring
Resting
zone
Growth
Proliferative
zone

Zone of Ranvier Secretory

zone
Maturation
Zone of
hypertrophy
Cutback zone Zone of
provisional
calcification
Transformation
Primary
trabeculum

Figure 6-3
End of long bone showing growth at the distal growth center. (Modified from Bogumill GP, Schwamm HA: Orthopedic pathology, Philadelphia,
1984, WB Saunders, p 17.)

processes, such as the greater trochanter or tibial tuber-
osity, where the large muscles insert. These “apophyseal”
growth plates allow for continued growth of the process,
independent of the longitudinal growth of the bone.
Apophyseal plates are histologically similar to the pri-
mary epiphyseal plates, although they resist tensile loads
rather than compression. Mechanically, epiphyseal carti-
lage, and ultimately the articular cartilage that remains at
the joint surfaces of the long bones, is well suited to sus-
tain compressive loads. The apophyseal plates, however,
are mechanically weaker when loaded in tension. This is
clinically relevant when a particularly active child presents
with localized pain. Radiological examination may reveal
a fracture of the apophyseal plate caused by excessively
large musculotendinous forces that the plate cannot
tolerate. This is seen most often at the tibial tuberosity,
for example, in a teenager who participates in jumping
sports, such as volleyball, in which large forces from the
quadriceps muscles are transmitted through the patellar
tendon into the tibial tuberosity (Osgood-Schlatter dis-
ease). In most cases, activity modification and rest are
prescribed until apophyseal plate closure occurs and the
tuberosity becomes continuous with the bone diaphysis.
Types of Secondary Growth Plates
● Pressure epiphysis
● Traction epiphysis (apophysis)
● Atavistic
A somewhat unusual but clinically relevant example
of another type of epiphyseal plate is an atavistic plate.
Atavism, derived from the Latin term for grandfa-
ther, refers to an evolutionary remnant that reappears
126 SECTION I • Scientific Foundations

A B
Figure 6-4
A, Histological section of the growth plate of a rabbit acetabulum. Note the areas of proliferating (open arrow) and hypertrophied (solid arrow)
chondrocytes. Trabeculae of the newly deposited woven bone (double arrow) surround small areas of cartilage matrix (curved arrow). Paraffin-
embedded section, stained with safranin O and light green; original magnification = 10×. B, Primary osteons (double arrowheads) are replacing
woven bone. Osteocytes are embedded in the bony matrix that is deposited by osteoblasts within the vascular channels. Paraffin-embedded
section, stained with safranin O and light green; original magnification = 25×. (Modified from Loitz-Ramage BJ, Zernicke RF: Bone biology and
mechanics. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and rehabilitation, Philadelphia, 1996, WB Saunders, p 101.)

most common site of an atavistic plate is at the base of

Cancellous bone the fifth metatarsal in the foot.

Types of Developmental Ossification

● Intramembranous
Traction ● Endochondral
epiphysis

Both intramembranous and endochondral ossification

Pressure
Cortical
epiphysis
bone
Medullary
cavity
Figure 6-5
Upper femur showing types of growth plates.
generations after it apparently disappeared. In this case,
it represents the reappearance of an extra bone or bony
prominence that is not typically seen. Although not con-
sidered to be pathological, atavistic plates are important
clinically when a patient presents with localized pain
and x-ray reveals what appears to be a fracture. In fact,
closer examination may reveal that the radiolucent line is
an atavistic plate connecting a bony end and diaphysis.
Atavistic plates may persist throughout life, which pro-
vides a further clinical challenge in examining an adult in
whom one would not expect to see growth plates. The
can occur in the same bone. The shaft of the clavicle, for
example, is formed by intramembranous ossification, but
a secondary ossific center develops within a cartilaginous
epiphysis to form the sternal end of the bone. The pri-
mary ossific center is present in most bones at birth, but
the secondary ossific center of the distal femur is the only
secondary center present at birth and often is used as a
landmark to identify a full-term fetus. Both endochondral
and intramembranous ossification persist postnatally dur-
ing fracture repair (endochondral) and periosteal bone
deposition (intramembranous), which occurs during an
increase in the midshaft diameter of a long bone.
The initial condensation of mesodermal cells appears
to be directed by a genetic message. Epigenetic factors,
such as mechanical stress, are unable to influence the devel-
oping structure until after the fundamental three-dimensional
form is complete. After the initial form is present, how-
ever, specific changes occur, such as enlarged tuberosities
or muscle insertion sites. The distinction between these
processes is relevant in a discussion of the origins of skel-
etal abnormalities. If a genomic disturbance is present,
the fundamental form of the bone may be altered, and a
 CHAPTER 6 • Bone Biology and Mechanics 127

specific skeletal dysplasia may result. In contrast, although may be greater depending on which physis is affected (Table
the fundamental form of the bone may be intact because 6-1). Angular deformities may result if only one portion
of a competent genetic message, epigenetic factors can of the growth plate sustains damage, with normal growth
influence the functional, mature form. Achondroplasia is occurring in the remaining portion of the growth plate.
a good example of both processes. The decreased bone Development of the muscular, vascular, neural, and
length seen in this condition reflects a genetic defect articular anatomy happens at the same time as skeletal
that influences the fundamental form of the developing development and growth. Although understanding the
cartilage anlage. A varus deformity, often present in an developmental specifics of these other systems is not vital
achondroplastic adult, results from the forces acting on in the present context, recognition of the complexity of
the bone after the genetic defect is expressed. Thus the the interactive musculoskeletal development is impor-
bony deformity present in the adult reflects combined tant, particularly for clinicians treating musculoskeletal
genetic and epigenetic influences. injuries of children.
Mechanobiological principles have been developed
to describe the interactions between external forces and
biological response during bony development. Shefelbine
Anatomy of Osseous Tissue
and Carter5 studied development of the femoral head Microscopic
in healthy children and in children with cerebral palsy in
Cellular Components
whom the forces sustained by the proximal femur were
Osteoblasts and osteocytes are responsible for bone forma-
abnormal because of muscle spasticity. Using finite element
tion. These two cell types are distinguished primarily by
modeling, the researchers tested a previous hypothesis
their location and only secondarily by their structure or
that octahedral shear stress (stresses pulling away from
function.11 The osteoblast is the primary bone-forming cell
the bone surface) increases growth and ossification rate,
located on the bony surface. It becomes an osteocyte when
whereas hydrostatic stress (stresses pushing toward the
it has produced sufficient mineralized matrix to completely
bone surface) tends to decrease growth.66,7 The model
surround itself. Cells intermediate in the changeover from
results agreed well with previously documented abnor-
osteoblast to osteocyte have been identified (osteoid osteo-
malities in the anteversion angle between the femoral
cyte, osteocytic osteoblast),12 but demonstrable differences
neck and shaft often seen in children with cerebral palsy.
in function are yet to be found. The distinctions, then,
Overall, the findings illustrated how mechanical stimuli
among osteoblast, osteocyte, and the intermediate cells are
influence the final skeletal form and provide evidence
related more to their differing developmental stages rather
linking mechanical forces at the tissue level to specific
than to differing cell phenotypes.
biochemical responses at the cellular level.
Extrinsic factors, such as hormones, also influence
the rate and extent of long bone growth. The growth Bone-Forming Cells
cartilage is stimulated by thyroxine, growth hormone,
and testosterone. Estrogen exerts a greater stimulatory ● Osteoblasts
influence on the bony tissue while suppressing cartilage ● Osteocytes
growth. Such distinct influences of testosterone versus
estrogen may account for the differences in the timing of
physeal closure between boys and girls.8
Normal skeletal growth can be interrupted by trauma Table 6-1
or fracture. Physeal injuries account for approximately 15% Contribution of Each Physeal Center to Growth
of all fractures in children.8 Girls are more prone to phy- of Long Bones
seal injury from 9 to 12 years of age, and boys are more Upper Limb Lower Limb
prone between the ages of 12 and 15 years.8 The periods
of increased incidence parallel the times of rapid growth Humerus Femur
during which hormone-mediated changes in the growth Upper physis 80% Upper physis 30%
plate cartilage may alter its response to mechanical stress.9 Lower physis 20% Lower physis 70%
Most pediatric fractures are classified according to a system Radius Tibia
developed by Salter.10 The classification system considers, Upper physis 25% Upper physis 55%
Lower physis 75% Lower physis 45%
generally, the location of the fracture, whether the fracture
Ulna Fibula
disrupts the growth plate, and, if present, the extent of Upper physis 60% Upper physis 20%
growth plate damage. Growth disturbances may result if Lower physis 80% Lower physis 40%
the fracture and subsequent callus formation stimulate the
premature closure of the growth plate, which prevents the From Connolly JF: DePalma’s The management of fractures and
normal longitudinal growth of the bone. This disturbance dislocations—an atlas, p 149, Philadelphia, 1981, WB Saunders.
128 SECTION I • Scientific Foundations
Scanning electron micrographs of growing bone
reveal active osteoblasts covering most of the bony sur-
face. The more active the cells, the more closely packed
they are. Osteoblasts assemble along surfaces created
by active resorption of existing bone, which creates
a spatial and temporal coupling between resorption
and deposition. Osteoblasts identified in the growing,
immature skeleton have a different origin from those
identified in the remodeling, adult skeleton; however,
in the present context, subtle differences between
these can be blurred without a loss of basic under-
standing. Active osteoblasts are plump, rounded cells
with abundant cytoplasm filled with rough endoplas-
mic reticulum, mitochondria, and Golgi membranes,
indicative of the active protein and polysaccharide
synthesis being undertaken by the cell. The cells stain
intensely with a basic stain, which indicates the pres-
ence of large quantities of RNA.11 When osteoblasts
are not actively producing matrix (resting osteoblasts),
their size decreases, and spaces exist between adjacent
cells. Most of the decreased size can be attributed to
a decrease in cytoplasmic volume, with a concomitant
decrease in the number of cellular organelles. When the
active osteoblast begins the transition to osteocyte, cell
volume decreases by 30% initially, and as the metabolic
activity of the osteocyte gradually decreases, cell vol-
ume continues to decrease. The osteocyte slowly fills in
its surrounding lacuna with matrix, and thus both cell
and lacunar size decrease.
Neighboring osteocytes communicate with one
another, and the deeper osteocytes communicate with
the surface-covering osteoblasts by interconnecting pro-
cesses housed within channels (canaliculi) in the extracel-
lular matrix. Connections between adjacent processes are
gap junctions, which allow for cell-cell communication
by permitting ions and small molecules to move between
the cells. The presence of gap junctions between bone
cells suggests that the osteoblasts, osteocytes, and bone-
lining cells form a functional syncytium that may play
an integral role in many physiological functions, includ-
ing the conversion of mechanical signals into remodel-
ing activity and mineral movement into and out of the
bone.13
Osteoclasts are easily identified using light microscopy
because they are large (two to three times larger than
osteoblasts), multinucleated cells with many cytoplasmic
extensions that hint of cell mobility. Indeed, time-lapse
microscopy reveals that the cells move along the surface
and leave behind a trail of resorbed bone that has the
appearance of an etched surface. The multiple nuclei
reflect the osteoclast’s origin as a union of several mono-
nuclear cells. Osteoclast cytoplasm appears “foamy”
because of multiple intracellular vacuoles and the lysing
function of the cell. The most distinguishing feature of
the osteoclast is the extensive infoldings of the cell plasma
membrane that give rise to a “ruffled border.” This
border has important functional significance, because it
greatly increases the surface area along which the cell can
interact with the surrounding bony matrix. Adjacent to
the ruffled border is an area of cytoplasm with a smooth
plasma membrane and no cellular organelles. This “clear
zone” always accompanies osteoclasts and may be an area
where the cell attaches to the bone surface undergoing
resorption. In this way, the cell can adhere to the surface
while the highly motile ruffled border resorbs the tar-
geted bone. Without the clear zone, the cell could not
remain anchored to the surface long enough for resorp-
tion to occur.11
Because bone resorption and deposition typically are
tightly coupled, osteoclasts and osteoblasts often are
found in close proximity to one another. Theories state
that, during remodeling, osteoblasts initiate the signal to
the osteoclasts to begin resorption.11 In contrast, dur-
ing modeling, one cortical surface undergoes resorption
while the opposing surface is deposited (cortical drift,
medullary expansion), and osteoclasts and osteoblasts are
not in close proximity.
Extracellular Matrix
Bone matrix comprises three elements (Figure 6-6):
organic, mineral, and fluid. Organic components consti-
tute 39% of the total bone volume, which contains 95%
type I collagen and 5% proteoglycans. Minerals include
primarily calcium hydroxyapatite crystals and contrib-
ute about half of total bone volume. Fluid-filled vascu-
lar channels and cellular spaces constitute the remaining
volume.14 Bone mechanical behavior reflects a balance
between the mineral and organic phases, with mineral
contributing stiffness and the organic matrix adding to
bone strength.
Vascular channels
Pg's
Minerals
Proteins
Figure 6-6
Relative amounts of the constituents of bone extracellular matrix (Pg’s =
proteoglycans; proteins include collagen and noncollagenous proteins).
(From Loitz-Ramage BJ, Zernicke RF: Bone biology and mechanics. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, Philadelphia, 1996, WB Saunders, p 103.)

Collagen deserves special attention because it provides
the major structural support of all connective tissues and
because, in a clinical context, collagen abnormalities can
have far-reaching effects on the skeleton’s ability to resist
mechanical stresses. Collagen derives its tensile strength
from polypeptides arranged in α chains. Each α chain is
composed of amino acids; glycine, proline, and lysine are
prominent. Three α chains coil together to form a triple
helix called procollagen. Osteoblasts secrete procollagen
into the surrounding matrix, where the terminal pep-
tide of each α chain is cleaved, which allows procollagen
bundles to link together. The linked procollagen bundles
form tropocollagen. The tensile strength of collagen
relies on cross-links between the hydroxylysine molecules
of the procollagen. The degree of cross-linking changes
with age and between types of collagen, with more cross-
links producing a stiffer tissue.
Collagen orientation in immature (growing) and
mature bone has been linked to the mechanical behavior
of individual layers of bone (lamellae), individual osteons,
and cortical sections of whole bone.15,16 The question
that should, perhaps, be addressed first is, how does the
collagen become organized initially during bone devel-
opment? Stopak, Wessells, and Harris17 injected collagen
into the limb buds of developing chicks and saw collagen
orientation change within 24 hours and persist for up to
9 days after the injection. They concluded that, even in
this early developmental phase, traction forces exerted by
the proliferating cells were sufficient to “organize” col-
lagen fibrils in a systematic pattern. The relevance of this
work to the present context is to illustrate that, although
mechanical influences are predominantly generated by
loads applied to the structure, forces within the structure
also may affect the final form of the tissue.
More than 200 noncollagenous proteins also are
found within bone’s extracellular matrix,18 although in
terms of concentration, collagen occupies the greatest
portion of the matrix. Among the noncollagen proteins
are osteonectin, osteocalcin, and bone sialoproteins I and
II. The noncollagen proteins may facilitate cell differen-
tiation and growth, cell adhesion, and organization of
the matrix and also may modulate resorptive processes
related to maintaining calcium homeostasis. Therefore
the abundance of these proteins may be important diag-
nostically in metabolic bone dysfunctions and disease.18
Mineral content distinguishes bone from other con-
nective tissues, provides bone with its characteristic stiff-
ness, and provides a mineral storehouse. The mechanism
responsible for calcification of the extracellular matrix of
bone and not of other connective tissues is not completely
understood, but apparently, the ability to bind mineral
crystallites is unique to type I collagen. Neither type II
nor type III collagen can bind to minerals. This is a sig-
nificant and active area of basic research, because if the
process of calcification is revealed, clinical interventions
CHAPTER 6 • Bone Biology and Mechanics 129
to enhance or slow mineral deposition may be useful in
the management of certain skeletal dysplasias.
Macrostructure
Despite differences in size and mechanical properties,
bone tissue is similar in all bones. Macrostructural dif-
ferences therefore account in part for the functional dif-
ferences between bones. At a tissue level, bone may be
divided into woven, primary, and secondary bone. Woven
bone is laid down rapidly as a disorganized arrangement
of collagen fibers and osteocytes. Although the mineral
content of woven bone may be similar to that of lamel-
lar bone, the disorganized pattern and generally lower
proportions of noncollagenous proteins (osteonectin
and osteocalcin)18 decrease the mechanical strength of
woven bone compared with that of primary or secondary
bone.19 Developmentally, woven bone is unique because
it can be deposited de novo, without a previous hard or
cartilaginous model.1 The cell-to-bone volume ratio is
high in woven bone, which confirms its role in providing
temporary, rapid mechanical support, such as after trau-
matic injury. In the healthy adult skeleton, woven bone is
not typically present but can be found in a fracture callus,
areas undergoing active endochondral ossification, and
some skeletal pathologies. During maturation, primary
bone systematically replaces woven bone, which provides
the mature skeleton with the appropriate functional
stiffness.14
Types of Bone
● Woven (immature)
● Lamellar (primary)
● Cancellous (trabecular)
● Cortical (compact)
● Lamellar (secondary)
Primary bone comprises several types of bone, each
with unique morphology and function. A common fac-
tor among the types of primary bone, however, is that,
unlike woven bone, primary bone must replace a pre-
existing structure, either a cartilaginous model or previ-
ously deposited woven bone. Primary lamellar bone is
composed of layers of bone matrix and cells organized
circumferentially around the endosteal or periosteal sur-
face of a whole bone. Vascular channels are infrequent in
primary lamellar bone, so it can be very dense. Cancellous
bone found in the vertebral bodies and in long bone
epiphyses is primary lamellar bone. In this case, although
vascular channels are not enclosed within the lamellar
structure, the individual struts or trabeculae of cancellous
bone are in intimate contact with a rich vascular supply.
Because of this close proximity, cancellous bone assumes
130 SECTION I • Scientific Foundations
an important role in mineral homeostasis; calcium stores
can be mobilized quickly in response to decreased serum
calcium. Primary lamellae formed around individual
vascular channels (rather than around the whole bone
circumference) are called concentric lamellae (Figure
6-4B). The concentric lamellae that surround a common
vascular channel, or haversian canal, constitute a primary
osteon. In this case, individual lamellae are arranged in
concentric rings that are 5 mm thick.20 Developmentally,
primary osteons are considered modified vascular chan-
nels, where sequential layers were deposited within exist-
ing vascular channels.
Secondary bone is deposited only during remodel-
ing and replaces primary bone. Differences between the
developmental process of primary and secondary bone
imply that a different controlling mechanism may be
responsible for the endosteal or periosteal deposition of
primary bone versus the intracortical deposition of sec-
ondary bone during remodeling. Toward this end, the
deposition of secondary osteons must be linked tem-
porally and spatially to the resorption of existing bone
by active osteoclasts. Histologically, secondary osteons
can be distinguished from primary osteons because the
secondary units are larger, with larger haversian canals,
and secondary osteons are surrounded by a cement line
between the osteon and the surrounding interosteonal
bone matrix (Figure 6-7). The cement line marks the
Figure 6-7
A longitudinal and transverse section through secondary Haversian bone.
Note the orientation of the vascular channels (Haversian and Volkmann
canals) relative to the secondary osteons. Cement lines demarcate the
boundary of each secondary osteon. (From Ham AW: Bone. In Ham
AW, editor: Histology, ed 7, Philadelphia, 1974, JB Lippincott.)
reversal phase of osteonal remodeling, as resorption
ceases and deposition begins.21
Each primary or secondary lamella contains osteocytes
housed in lacunae and surrounded by extracellular matrix.
Collagen orientation within each lamella is controversial;
some investigators suggest that all fibrils within a lamella
assume the same orientation.15 Others suggest that
although parallel-fibered bundles do exist, the bundles
themselves do not necessarily lie in parallel.22 Similarly,
collagen orientation within the interlamellar spaces may
differ between adjacent lamellae and adjacent osteons.
These disparate views may reflect sampling artifacts that
occur during tissue processing.23 Collagen orientation is
measured as the brightness of polarized images of the
structure: collagen fibers that lie orthogonal to the direc-
tion of the polarized light appear dark, and fibers oriented
longitudinally appear light. Sampling artifacts may result
if the sections being compared were not oriented simi-
larly when cut or if the orientation of individual osteons
differs between samples. From a functional perspective,
this controversy is not trivial, because collagen orienta-
tion can influence the ability of the lamellae and osteons
to resist mechanical loads.
Riggs and colleagues16,24 examined the relations among
interosteonal collagen orientation, mechanical behavior,
and in vivo strain patterns. Strain gauge data collected
on the equine radius during walking revealed that the
cranial cortex sustained tensile loads, whereas the caudal
cortex was loaded in compression. Samples from each
cortex were tested mechanically in compression and ten-
sion, and collagen orientation was measured from circu-
larly polarized light (CPL) images of each sample. Their
results revealed a high positive correlation between col-
lagen orientation (as measured by CPL) and the radius
cortical strength and stiffness. Collagen within the cau-
dal cortex, loaded in compression in vivo, oriented more
obliquely or transversely (relative to the longitudinal axis
of the bone), whereas the collagen within the cranial cor-
tex oriented more nearly parallel to the bone’s long axis.
Samples from the cranial cortex were stiffer but absorbed
less energy during loading than did the caudal samples.
These findings provided important support for a strong
relation between the functional loads sustained by a
bone and its architecture. These data also strengthened
a structure-function argument that microscopic architec-
ture reflects the mechanical environment present during
skeletal growth or remodeling.
Blood Supply
All elements of bone, including the marrow, periosteum,
metaphysis, diaphysis, and epiphysis, are richly supplied
with blood. Gross and associates25 estimated that, in dogs
at rest, 11% of the cardiac output was sent to the skel-
eton. Blood reaches each area of the bone via extensive

arterial anastomoses that feed a network of sinusoids. The
sinusoids, in turn, empty into central venous channels
deep within the medullary canal in long bones or a cen-
tral canal in flat bones. The primary nutrient vessel enters
the medullary canal via an obliquely oriented nutrient
foramen. Once within the bone endosteum, the artery
divides into longitudinal branches that course along the
bone’s length and then reenter the cortical bone. This
vascular distribution is consistent with reports by Singh
and coworkers26 that most of the blood flow in long bone
is in a centrifugal (from endosteum to periosteum) rather
than centripetal direction. In the epiphyses, the longi-
tudinal vessels branch into extensive arcades that supply
the bony ends. Medullary vessels pierce through the cor-
tex and anastomose with periosteal vessels to supply the
outer surfaces of the cortex.
Within the compact bone, primary arteries and veins
travel parallel to the osteonal longitudinal axes within the
haversian canals. Transversely oriented vessels are con-
tained within the Volkmann canals, but apparently no
branches are distributed from the arteries at this point.
Blood flow in bone has been quantified in animal
models of disuse and joint injury. Gross and colleagues27
reported that hyperemia precedes loss of cortical bone
in an avian model of disuse, suggesting a probable link
between bone cell behavior and vasoregulation. That is,
the absence of mechanical stimuli of the bone apparently
elicited a vascular change that increased local blood flow.
Changes in blood flow also have been reported in the
distal femur of rabbits after anterior cruciate ligament
transection.28 The increased flow was highly correlated to
a decrease in bone mineral density, which again suggests
a link between the bone’s mechanical milieu and blood
flow. Although these invasive studies can be completed
only in animal models, improved technology in the
research laboratory has allowed quantification of blood
flow in bone without destruction of the tissue. For exam-
ple, laser Doppler imaging can reliably measure perfusion
in bone29,30 and shows promise in allowing researchers to
study noninvasively blood flow changes in human exer-
cise and injury models.
Fracture Healing
Fracture healing can be divided into three phases: inflam-
mation, initial union of the bony ends, and remodeling
of the callus. Of clinical importance are the findings that
the timing and strength of the initial union can be influ-
enced by the mechanical stability across the fracture site,
which gives the impetus for internal fracture fixation.
The advantage of an internal fixator is that less external
splintage is necessary, which thereby decreases the mor-
bidity related to immobilization (e.g., joint contracture
and loss of strength). Internal fixation with compression
across the fracture line results in an insignificant external
CHAPTER 6 • Bone Biology and Mechanics 131
callus, but when the fracture is mechanically unstable,
micromotion across the gap results in the formation of a
large external callus.
Phases of Fracture Healing
● Inflammation
● Initial union
● Remodeling of callus
Immediately after injury, a hematoma develops around
the fracture site. Within 3 days, mesenchymal cells arrive
in the area and produce a fibrous tissue that envelops the
fractured bone ends. The outer layer of the fibrous mate-
rial begins to form the new periosteum. Until this point,
stable and unstable fractures react similarly, but between
days 3 and 5 after a fracture, the degree of stability influ-
ences subsequent healing steps. Microscopic examination
of the fibrous tissue reveals that in a stable fracture, the
tissue is well vascularized, but in an unstable fracture, the
fibrous tissue contains no vessels. Where the fibrous tis-
sue meets the original bony cortex–in both stable and
unstable fractures–new bony trabeculae are formed by
osteoblasts lying on the old bone surface. In a stable frac-
ture, new bone forms along the periosteal surface of the
fibrous layer and bridges the fracture site. In an unstable
fracture, new bone also forms along the periosteal surface
of the fibrous material but does not bridge the fracture
line. In rabbits, this union occurs 9 days after injury, but
in humans, minimal periosteal bone formation is present
at this point in healing, and periosteal union is further
delayed. This difference, however, may be a consequence
of damage to the periosteum and the resulting stim-
ulation of osteoblasts in the rabbit fracture model,
rather than resulting from damage to only the bone. 31
As bony trabeculae continue to form, the bony collar
becomes more compact, and the periosteum increases
in thickness.
In the gap between the bony ends (rather than along
the periosteal surface), the first cells to invade after injury
(approximately day 9) are macrophages, followed by
fibroblasts and capillaries. Macrophages scavenge cell
and matrix debris, and fibroblasts produce the struc-
tural foundation for cells and vessels. Osteoblasts begin
bone deposition by 2 weeks after a fracture, and bony
union across the fractured ends is established (ideally) by
3 weeks. If bone adjacent to the fracture site dies sec-
ondary to disruption of its blood supply at the time of
fracture, osteoclasts may be present to resorb the dead
material. Otherwise, contrary to previous reports, osteo-
clasts are not routinely present in all fractures.32 In small
gaps (<10 mm) or where fracture ends contact, healing
is via direct haversian remodeling: osteoclasts resorb a
cone of bone, osteoblasts deposit new haversian bone,
132 SECTION I • Scientific Foundations

and osteocytes maintain the new bone after mineraliza-

tion. In 10-mm to 30-mm gaps (too large for haversian
remodeling, but too small for cells to move), osteo-
clasts may resorb the bone to increase the gap width.
Osteoblasts subsequently arrive to lay down disorganized
lamellae across the gap. The disorganized bone is then
remodeled.
In an unstable fracture, periosteal bone formation
continues from the old bone ends toward the fracture
line, but across the fracture line (where the fibrous mate-
rial is avascular), chondrocytes proliferate and lay down a
cartilage matrix. At the intersection of the cartilage-bone
layers, a matrix forms with types I and II collagen. In
10 days (in rabbit), cartilage formation is completed and
forms a V over the fracture site (Figure 6-8).
The fracture site, now with some stability, is called clin-
ical union. In a sequence identical to that which occurs
during endochondral ossification of long bones, the car-
tilage bridging the fracture ends gradually is replaced by
bone. In the rabbit, by 3 to 4 weeks after a fracture, bone
has replaced most of the cartilage, and the bony callus
offers stability across the fracture site. In humans, this
process takes slightly longer, with good stability generally
achieved by 6 weeks. With the improved stability, blood
vessels and fibroblasts proliferate in the fracture gap. The
important milestones of fracture healing are summarized
in Figure 6-9.
The formation of cartilage in an unstable fracture may
arise because the mobility across the fracture site inhibits Figure 6-9
Milestones of fracture healing, distinguishing how the process
differs between stable and unstable fractures. (From Loitz-Ramage
BJ, Zernicke RF: Bone biology and mechanics. In Zachazewski JE,
Magee DJ, Quillen WS, editors: Athletic injuries and rehabilitation,
p 107, Philadelphia, 1996, WB Saunders.)

angiogenesis (blood vessel formation). Mathematical mod-

Figure 6-8
Fracture callus of a rabbit rib 14 days after fracture. The bony callus
has bridged the fracture. Osteoblasts covering the surfaces of the
spicules of woven bone are depositing new bone. In addition, bone is
replacing cartilage via endochondral ossification. A hematoma persists
between the bone ends.(From Loitz-Ramage BJ, Zernicke RF: Bone
biology and mechanics. In Zachazewski JE, Magee DJ, Quillen WS,
editors: Athletic injuries and rehabilitation, Philadelphia, 1996, WB
Saunders, p 106. Modified from Ham AW, Harris WR: Repair and
transplantation of bone. In Bourne GH, editor: The biochemistry and
physiology of bone, ed 2, vol III, New York, 1971, Academic Press.)
els predict where stresses will be high in fracture calluses,
and such areas correspond with the regions where carti-
lage develops.33 This association suggests that high stresses
limit vascularization and subsequent bone deposition.
Remodeling of the fracture callus begins as soon as
the fracture site regains stability. The dynamics of this remod-
eling are similar to those that occur in haversian remodeling,
in that the old bone is resorbed by osteoclasts, and new
bone is deposited by osteoblasts. The process is vigorous
in the area where the periosteal callus meets the surface
of the old bone. Before remodeling, this line is clearly vis-
ible, but after remodeling, the junction between the old
bone and the callus is indistinguishable.
Factors contributing to fracture nonunion are poorly
understood, but instability is thought to result in persis-
tence of the fibrous material and type III collagen, both
of which suggest that the fracture healing sequence has
been altered. Type III collagen is typically present only

during early healing and is indicative of immature cal-
lus. Its persistence suggests that the subsequent steps to
replace the early tissue are altered. Also, type III colla-
gen may be unable to bind minerals; thus, by persisting,
type III collagen may block the mineralization of a newly
formed matrix.
Mechanical Behavior of Bone
Cortical Bone
The mechanical behavior of any structure can be assessed
in a variety of ways, with each method yielding useful
details about bone as a structure. Ostensibly, the method
of testing is chosen to assess most closely the loading situ-
ation that the structure encounters in vivo. Because bone
experiences multiaxial loads, however, it is difficult to test
each direction in which a bone is loaded. Cortical bone
frequently is treated as an elastic beam of uniform dimen-
sion and tested in three- or four-point bending, or a piece
of bone of known dimension is machined out of a larger
piece and tested in uniaxial tension or compression.
In three-point bending tests, a long bone shaft or a cor-
tical strip of bone rests on two supporting points, while
a load from above is applied at the midpoint; this creates
three points of contact (Figure 6-10). Alternatively, the
load from above can be applied at two contact points to
produce four-point bending. As the load is applied, the
bone sample bends with a compressive strain in the superior
surface (concave) and a tension strain in the inferior sur-
face (convex). During bending tests, the distance between
the contact points should be maximized so that the loads
bend the bone sample rather than crush it. In a typical
bending test (see Figure 6-10A), when the bone is first
loaded, the load-deformation curve is concave toward
the load axis (see Figure 6-10B). As load application
Figure 6-10
A structure is loaded in three-point bending (A), generating the load-
deformation curve (B). (From Loitz-Ramage BJ, Zernicke RF: Bone
biology and mechanics. In Zachazewski JE, Magee DJ, Quillen WS,
editors: Athletic injuries and rehabilitation, Philadelphia, 1996, WB
Saunders, p 107.)
CHAPTER 6 • Bone Biology and Mechanics 133
continues, load and deformation increase linearly (obey-
ing Hooke’s law). The slope of this linear region repre-
sents the bone’s flexural rigidity (a measure of stiffness).
The proportional limit indicates the end of the linear
region, beyond which small increases in the applied load
easily deform the sample. After this area of nonlinear
deformation, the sample either reaches its maximal load
and fails abruptly or reaches its maximal load and then
decreases slightly before catastrophic failure. The area
under the load-deformation curve quantifies the energy
absorbed by the sample during loading. Each of these
measures (stiffness, loads and energy at the proportional
limit, and maximum and failure points) constitutes a
structural property of the bone. If the geometry of the
tested bone sample is known, the structural properties
can be “normalized” (e.g., force per unit area) to bet-
ter understand the behavior of the bone material itself.
Elastic moduli and stresses at the proportional limit and
at maximum and failure points are examples of a bone’s
material properties. For comparative purposes, stresses
at the proportional limits and elastic moduli of differ-
ent materials and bones from a variety of species are pre-
sented in Table 6-2.
Data recorded from isolated mechanical tests can be
“translated” into terms that are relevant to the clinician.
During normal daily activities, bones sustain loads well
within the linear region of the load-deformation curve,
with the odd event placing high (but not catastrophic)
loads on the bone. When loaded within the linear region,
the bone bends but does not sustain permanent deforma-
tion. However, even within this region, if low loads are
sustained repetitively over a short period of time, such as
during long-distance running, fatigue-related damage to
the bone may result. That is, although each loading cycle
alone is not sufficient to cause damage, the cumulative
effect of the loading events may result in failure, such as a
stress fracture. When loads or stresses exceed the propor-
tional limit, the bone sustains permanent deformation
because of substantial microarchitectural damage. The
bone elastic modulus is a measure of the resistance of the
bone material to being deformed; a more highly mineral-
ized matrix possesses a higher elastic modulus. An opti-
mal mechanical balance is created by varying the relative
amounts of the various matrix components. Bone with a
low elastic modulus deforms easily at relatively low loads
and may result in permanent skeletal deformity, such as
occurs with rickets. Conversely, bone that possesses a
high elastic modulus may be too stiff to “give” with the
daily loads placed on the skeleton, which increases the
risk of fracture.
Bone geometry influences its mechanical behavior.
During bending, for example, the distribution of bone
about the bending axis (second moment of area equals I)
and the distance from the centroid to the tensile surface
134 SECTION I • Scientific Foundations
Table 6-2
Elastic Modulus and Stress at the Proportional Limit for Various Bones and Other Materials
Elastic Modulus
Material Tested (GPa)
20-yr-old human femur* 17.0
70-yr-old human femur* 16.3
20-yr-old human tibia* 18.9
70-yr-old human tibia* 19.9
8-wk-old chick TMT – 113
Adult rooster TMT 12.8
16-wk-old canine femur 7.1
Adult canine femur 15.6
18-wk-old rat tibia 11.4
Stainless steel 190.0
Wood 12.5
TMT, tarsometatarsus.
*Machined samples, tested in tension.
From Loitz-Ramage BJ, Zernicke RF: Bone biology and mechanics. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 108, Philadelphia, 1996, WB Saunders.
are pertinent. For example, assume that two bone sam-
ples with identical cortical cross-sectional areas are tested
(Figure 6-11). One is a perfect circle (hollow, thick-walled
cylinder) with its mass distributed uniformly around a
constant radius. The other is an oval sample of the same
total mass but with its mass distributed around a major
axis that is twice as long as the minor axis. Even though
the masses of the two samples are the same, their struc-
tural behavior is different. But how do the data collected
from each test differ? When the oval sample is tested with
the bending about the major axis (smaller I), the bone
sample is less stiff and carries less load than the circular
sample, or even the oval sample when tested in bending
about the minor axis (larger I) (see Figure 6-11).
To illustrate further how mass distribution (I) affects
a structure’s response during bending, consider the fol-
lowing. Imagine that you are standing, midlength, on
a wooden plank (2 meters long by 4 cm thick by 30 cm
wide) that is supported only at its two ends; the plank
will be much stiffer and carry greater load when you
stand (albeit precariously) on the plank’s edge (4 cm sur-
face down) than if the 30 cm side is placed down. In a
comparable fashion, the redistribution of cortical bone
after remodeling is significant because of the influence
that geometry has on the bone’s mechanical behavior.
Tensile tests of machined cortical samples also produce
data for the same mechanical variables as the bending test.
The advantage of working with machined samples is that
the structural variables can be compared directly between
samples because the geometry of each sample is identical.
The disadvantage of machined samples is that, although
great effort may be made to ensure that the machining
does not damage the sample, any change or surface crack
Stress at Proportional
Limit (MPa) Author
120 Burstein et al34
111 Burstein et al34
126 Burstein et al34
120 Burstein et al34
Matsuda et al35
153 Loitz and Zernicke36
60 Torzilli et al37
123 Torzilli et al37
146 Li et al38
500 Beer and Johnson39
– Beer and Johnson39
that happens as a result of heating of the sample or from a
dull or imperfect cutting edge will affect the outcome.
Cancellous Bone
The mechanical behavior of trabecular bone and how its
behavior changes during aging and disease are of para-
mount importance to health care practitioners. In the
United States, for example, more than 500,000 verte-
bral fractures, 250,000 hip fractures, and 200,000 dis-
tal radius fractures occur annually. Hip fractures can be
fatal in up to 20% of these cases.40 These statistics add an
urgent tone to the efforts directed toward understanding
trabecular bone mechanics and physiology.
Cancellous bone samples generally are tested in compres-
sion. Usually, a sample of trabecular bone is cored from a
larger sample and then compressed. The variables measured
are similar to those measured in cortical bone tests. The
challenge in testing cancellous bone comes in identification
of the effects of the trabecular pattern on the mechanical
behaviors. The greatest problem comes from the anisotropic
nature of cancellous bone, which means that the mechani-
cal behavior of an anisotropic structure differs in different
direction or among various parts of the structure. Trabecular
pattern reflects the in vivo loading pattern sustained by the
tissue and results in anisotropic mechanical behaviors. For
example, if trabeculae are oriented predominantly parallel to
the bone’s longitudinal axis, a sample tested by loading in
a transverse direction will have a very different mechanical
response from a sample tested longitudinally.
Cancellous bone also can be tested in a whole bone
preparation, such as may be performed on vertebrae or
on the femoral neck. In these cases, the contribution of

Figure 6-11
The hypothetical load-deformation curves that might result from
loading a cylinder with uniform mass distribution (A) and a cylinder of
nonuniform mass distribution bending about its major axis (B). Note
the differences in maximal load and flexural rigidity between the two
structures. Second moment of area (I)—distribution of cortical mass
relative to the bending axis—is significantly greater in A because the
distance between the bending axis and the cortical surface is much
greater in A. (From Loitz-Ramage BJ, Zernicke RF: Bone biology and
mechanics. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic
injuries and rehabilitation, Philadelphia, 1996, WB Saunders, p 108.)
the cortical shell versus the cancellous bone can be quan-
tified by digitizing photographic images of each bone
cross section. This approach may be more relevant clini-
cally, because the behavior of the integrated cortical and
cancellous structure can be assessed. This approach is of
limited use, however, if the contribution of the cancel-
lous bone alone is of interest.
Recently, the architecture of cancellous bone has been
quantified with microcomputed tomography (microCT)
CHAPTER 6 • Bone Biology and Mechanics 135
to distinguish changes in bone structure from changes in
bone material.41 After anterior cruciate ligament transec-
tion, the microCT demonstrated increased perforations
in the bony plate as early as 3 weeks after transection,
which indicates that architectural adaptation predomi-
nated over tissue modulus (material) changes. The tech-
nique and the findings are important in understanding
the role of cancellous bone structure and material in
providing bony support to articular cartilage.
Remodeling of Bone
Adaptation prompted by changes in the mechanical stress
state, such as prolonged bed rest, spaceflight, or exercise,
forms the basis for much of the research being done in
bone physiology and mechanics, with the premise being
that if function is altered, the resulting change in struc-
ture can be examined. As with most connective tissues,
bone possesses strong structure-function interactions.
Cellular Events
The remodeling process, by definition, is the resorption
and replacement of existing bone. The sequence of events
can be remembered as ARF: activation, resorption, forma-
tion (Table 6-3). The first step in remodeling is activation
of osteoclasts to resorb existing bone. A line of osteoclasts
(osteoclastic front) cuts a longitudinal cone through the
bone by secreting acid phosphatase, collagenase, and other
proteolytic enzymes.42 The “cutting cone” resorbs approxi-
mately three times its volume and, when completed, leaves
a resorptive channel 1 to 10 mm deep.19
New bone is deposited by osteoblasts that follow the
resorptive front. Mineralized matrix is first laid down
around the walls of the resorptive channel, which forms
the cement line. Osteoblasts fill the remaining volume
that was eroded by the osteoclasts. Deposition of new
bone is a much slower process than resorption. It takes
three times longer, despite the fact that osteoblasts can
outnumber osteoclasts by more than 200 to 1.43 The dis-
tance between the osteoclasts and osteoblasts translates
into the time lapse between resorption and formation.
Generally, this latent period is about 1 week.19 Initially,
osteoblasts deposit a nonmineralized matrix that calcifies
8 to 10 days later. In so doing, the osteoblasts trap them-
selves within the matrix and become osteocytes.
Generally, skeletal remodeling is triggered in three
circumstances: to release mineral stored in the bone in
response to a low serum calcium level, to repair skeletal
microdamage, and to balance the mechanical and mass
needs of the skeleton.44 Although each circumstance can
explain the remodeling stimulus, experimental evidence
describing the actual controlling mechanism in each case
is lacking. It is difficult to conceive how the body’s need
136 SECTION I • Scientific Foundations
Table 6-3
Summary of Modeling-Remodeling Differences
Factor
Timing
Resorption and formation surfaces
Surfaces affected
Activation
Balance
Coupling of formation and resorption
ARF, Activation-resorption-formation.
From Loitz-Ramage BJ, Zernicke RF: Bone biology and mechanics. In Zachazewski JE, Magee DJ,
Quillen WS, editors: Athletic injuries and rehabilitation, Philadelphia, 1996, WB Saunders p 110.
Modified from Parfitt AM: The cellular basis of bone remodeling: the quantum concept reexamined in
light of recent advances in the cell biology of bone, Calcif Tissue Int 36:S37-45, 1984.
for calcium, for example, could result in the site-specific,
reproducible pattern of bone resorption that is seen.
Triggers for Bone Remodeling
● Low serum calcium level
● Skeletal microdamage
● Mechanical stimulus
● Mass needs of skeleton
Most commonly, in true remodeling, bone resorption
and deposition are sequential events, and the responsible
cells (osteoclasts and osteoblasts) are located within the
same functional framework, the basic multicellular unit
(BMU).45 This “functional unit” reinforces the concept
of the tightly coupled interaction between resorption
and deposition, and current theory suggests that resting
osteoblasts (bone-lining cells) are responsible for initiat-
ing the remodeling process and recruiting the osteoclasts
to begin resorption.21 In another example of coupled
osteoclast-osteoblast activity, the respective cells are not
active along the same surface. In modeling (change in
bone architecture when bone deposition does not fol-
low bone resorption), resorption occurs along one cor-
tex, and deposition occurs along another (see Table 6-3).
Because osteoclasts and osteoblasts do not populate the
same bony areas, the stimulus that initiates this process
is unclear.
Several observations support the role of mechanical
stimuli in bone remodeling, including the following: (1)
bone is lost when mechanical stimuli are greatly reduced
or eliminated (i.e., stress magnitude is decreased); (2) a
change in the distribution of stresses on the bone stimu-
lates adaptive remodeling; and (3) although the quan-
tity of bone at various sites may be altered by varying
mechanical stimuli, the quality of the bone matrix being
Modeling Remodeling
Continuous Cyclical (ARF)
Different Same
100% 20%
Not required Required
Net gain Net loss
Systemic ? (no ARF) Loss
deposited generally remains similar for all sites. That is,
in response to mechanical stimuli, the body changes the
quantity of bone but not its composition.
One of the prevailing theories of bone remodeling
is the “mechanostat hypothesis” postulated by Frost46
and recently updated.47 Frost suggests that as a biologi-
cal system, mammalian bone develops and adapts during
the postnatal period to make load bearing bones strong
enough to prevent fracture during voluntary activities
(i.e., nontraumatic). He proposes that the ability to
withstand typical daily loads could be labeled a bone’s
“mechanical bone competence,” or MBC, and that the
MBC could define a bone’s health in functional terms,
rather than terms such as bone mass or bone mineral
density, the functional significance of which are often ill
defined. The MBC can be achieved by balancing bone
deposition and resorption as determined by the daily
loads experienced by the bone. The hypothesis allows, for
example, the inclusion of a disuse-mode bone modeling
unit,48 wherein bone resorption exceeds bone deposition
during periods of disuse (e.g., bed rest or spaceflight),
and for strain-dependent signals to translate mechanical
deformation with cellular response.49
In a similar vein, Lanyon50 described functional
remodeling as an “interpretation and purposeful reac-
tion” to a bone’s strain state, which allows for adaptation
to increased and decreased strains. “Functional strains
are both the objective and the stimulus for the process
of adaptive modeling and remodeling.”50 Rubin and
Lanyon51 hypothesized that if functional strains were too
high, the incidence of damage and probability of failure
increased. If strains were too low, the metabolic cost of
maintaining unnecessary bone mass was too high. Thus
functional strain appeared to be a relevant parameter to
control. The question remains, however, which attribute
of strain (i.e., magnitude, rate of application, frequency,
distribution, or gradient) has the greatest sensitivity.

Another remodeling theory related to mechanical use
of the bone suggests that remodeling is stimulated by
fatigue damage that occurs during physical activity. In an
engineering sense, “fatigue” is the loss of strength and
stiffness that occurs in materials subjected to repeated
cyclic loads. In bone, fatigue has been attributed to the
microscopic cracks that develop within and between
the osteons.1 In healthy bone, if damage is not exces-
sive, remodeling resorbs the material around the crack,
and new bone is deposited. If the damage is excessive
and the normal remodeling process cannot keep up with
the repair, macroscopic failure and fracture may result.
Clinically, the accumulation of fatigue microdamage may
result in a stress fracture, an injury common to athletes
participating in activities that place highly repetitive,
cyclic loads on the weight-bearing bones, such as ballet
dancers, gymnasts, and long-distance runners.
The mechanism linking microcracks to cellular acti-
vation and remodeling remains controversial. Martin
and Burr1 suggest that when a crack propagates along a
cement line, the osteon surrounded by the cement line
becomes isolated from mechanical stresses. The resulting
lack of mechanical stimuli may be likened to that which
occurs during bed rest, immobilization, or spaceflight.
A cutting cone would be initiated within the osteon, and
new bone would be deposited. In contrast, Frost52 argues
that cracks disrupt the canalicular network and trigger
a cellular membrane response. The osteocytes then ini-
tiate the signal to begin remodeling of the damaged
matrix. Evidence exists in support of both postulates, and
research is proceeding toward resolving this question.
Clinical evidence suggests that electrical phenom-
ena alter remodeling and fracture repair and supports
the premise that electrical effects may be important in
the information transfer between mechanical deforma-
tion and cellular response. Although the mechanisms
responsible for the production of electrical potentials are
unknown, two possible sources of electrical phenomena
exist: piezoelectricity and streaming potentials.
During deformation, crystals with a lattice structure
and no central symmetry develop a net charge between
the anions and cations. This charge separation causes a
potential difference to develop between opposite ends
of the crystal. Wet collagen within bone can act like a
crystalline lattice when deformed, thus generating piezo-
electric potentials in bone. The marked directionality of
the piezoelectric potential is consistent with the different
potentials generated in bone during compression versus
tension.
Streaming potentials are generated when an ionized
fluid flows through channels in a solid that carries a sur-
face charge. As the fluid flows, ions from the fluid are
attracted to the oppositely charged surface and form a
charged layer along the surface. The remaining ions in
the fluid create a charge of opposite polarity, and as the
CHAPTER 6 • Bone Biology and Mechanics 137
fluid flows, a current is generated. For example, if the
surface charge along the walls of a channel is negative,
positive ions will be attracted from the fluid and cre-
ate a slow-moving, positively charged layer along the
outer edges of the channel. The negative ions remaining
in the fluid will accumulate in the middle of the chan-
nel, thereby creating a negatively charged current in the
channel. Extracellular fluid in bone is charged and tends
to move during deformation, which results in the devel-
opment of streaming potentials.
Lanyon and Hartman53 noted that when bending a
sample of wet bone, the tensile surface developed a net
positive charge, and the compressive surface carried a
negative charge. The difference between the surface
charges was dependent on both the rate and the mag-
nitude of deformation. When the same magnitude load
was applied statically rather than cyclically, the poten-
tial decayed to zero within a few seconds.54 Eriksson55
postulated that the polarization created during bending
was a result of the decrease in fluid channel diameters
on the compressive side, forcing the charged extracellular
fluid to flow toward the open, tensile surface channels.
This explanation is consistent with earlier data that static
bending does not generate potentials and with the dif-
ferential sensitivities to strain rate and magnitude.
Rubi, McLeod, and Lanyon56 examined the effective-
ness of pulsed electromagnetic fields in preventing dis-
use osteoporosis. When the midshaft of a turkey ulna
was stress-shielded by isolating it from the bony ends,
cortical mass decreased 13% in 8 weeks. However, if the
experimental stress-shielded limb was exposed to a daily
1-hour dose of electromagnetic current, the ulna mass
increased 23% over the same time interval. The investiga-
tors suggested that electrical potentials generated by the
electromagnetic current may have influenced cell activity,
similar to the influences created by strain-related poten-
tials generated during bending. This was the first pub-
lished study of a dose-response relationship describing
electrically induced osteogenesis.
After fracture, the developing callus becomes electro-
negative with respect to the ends, which suggests that
electrical currents may be used to enhance fracture heal-
ing.57 The first reported use of electrical current in the
management of nonunion was reported by Brighton,
Friedenberg, Mitchell, and Booth in 1977.58 In this study,
they reported an 84% success rate among 164 patients
with 171 fractures. Since this early report, several stud-
ies have been conducted with reported success rates of
greater than 50%.59,60 In each study, the osteogenic range
for stimulation has consistently been 1 to 10 mV/cm and
10 to 20 mA/cm2. Currently, ongoing studies focus on
the mechanism responsible for enhanced healing and on
whether electromagnetic fields can be used to enhance
healing in fresh fractures in addition to those in which
healing is delayed.50
138 SECTION I • Scientific Foundations
Exercise-Induced Changes in Bone
Exercise-related increases in cortical thickness61,62 and
bone mineral content63 suggest that exercise can be a
potent stimulus for bone remodeling. Over the past sev-
eral years, exercise models have become a more common
means for studying the influence of mechanical overload
on bone remodeling. Interestingly, many studies sug-
gest that the responses to similar exercise protocols differ
between mature and immature (open physes) animals.
In growing chicks, 9 weeks of moderately strenuous
exercise increased the cortical cross-sectional area of a
weight-bearing bone (the tarsometatarsus, or TMT)
but did not increase maximal bone strength.35 In addi-
tion, the exercise apparently delayed longitudinal bone
growth, as the TMTs of the exercised chicks were sig-
nificantly shorter than those of the age-matched, seden-
tary controls. Forwood and Parker64 described similar
findings in growing rats. After a 1-month training pro-
gram, tibial and femoral lengths were significantly less
for the exercised animals compared with the sedentary
controls. Also, the proximal epiphyseal cartilage in the
tibia was thinner in the exercised rats, and the bones
absorbed less energy to failure. These studies suggest
that in growing animals, “competition” between exer-
cise- and growth-related stimuli may alter the normal
rate of calcification and longitudinal growth; in these
animal models, growing bone did not benefit from
strenuous exercise.
Bone’s differential sensitivity to strain rate also may
be a factor in exercise-induced adaptation. Judex and
Zernicke65 investigated whether high-impact drop jumps
could increase mid-diaphyseal bone formation in the tar-
sometatarsus of growing roosters. In vivo strain measure-
ments revealed a large (740%) increase in peak strain rate
with only a moderate (30%) increase in strain magnitude
and no difference in strain distribution. After an exer-
cise program of 200 drop jumps per day for 3 weeks,
the exercise animals had a significant increase in bone
formation rates at the periosteal (40%) and endocortical
(370%) surfaces. Strain rate correlated significantly with
bone formation rate at the endocortical sites but not at
the periosteal surfaces. Their data support a conclusion
that growing bone is sensitive to high strain rates. In
cancellous bone, Hou, Salem, Zernicke, and Barnard66
examined the effects of strenuous exercise on the femo-
ral neck and L-6 vertebral body in rats. After 10 weeks
of training at 75% to 80% of maximum aerobic capac-
ity, the material properties of the femoral neck were sig-
nificantly diminished compared with sedentary controls.
An increase in the percentage of trabecular bone, with a
concomitant decrease in the cortical shell in the exercised
femoral necks, apparently contributed to the detrimental
changes. In contrast, no exercise-related changes in the
lumbar vertebrae were noted.
Thus strenuous endurance exercise can affect
adversely the mechanical integrity of immature bone, but
it is unclear whether a more moderate exercise regimen
would have a positive effect. Lucas, Lucas, Vogel et al67
examined the effects of moderate exercise on bone min-
eral density, body lean versus fat mass, and menarchal age
in 42 adolescent girls. The authors focused specifically on
whether moderately strenuous exercise delayed puberty
and therefore detrimentally affected bone by delay-
ing the estrogen-related bone deposition that typically
occurs during the peripubertal years. The results dem-
onstrated that body composition, physical activity, and
sexual maturity were significant determinants of bone
density during adolescence. Runners had lower body
fat than non-runners, but this did not upset hormonal
cycles, which suggests that the exercise did not negatively
affect bone density. The authors concluded that moder-
ate exercise had no negative effect on bone mass accrual
in adolescent females.
In a longitudinal study, Slemenda, Miller, Hui et al68
enrolled 59 pairs of twins (5.3 to 14 years of age) and
obtained self-reports and reports from the mothers
regarding the youngsters’ activity patterns. Bone mineral
densities of the distal radius, proximal femur, and lumbar
spine were assessed with single- and dual-photon absorp-
tiometry. These authors reported a high positive correla-
tion between the hours spent in weight-bearing activities
and the density of the femur and radius. Vertebral density
also correlated to activity, but the relationship was not as
strong. Slemenda, Miller, Hui et al68 concluded that (pg.
1232) “more active children may emerge from adoles-
cence with 5% to 10% greater bone mass, depending on
skeletal site. This may represent an important advantage
in terms of peak skeletal mass, and this advantage may
persist throughout adult life.”
Lloyd, Petit, Lin et al69 followed females over a 10-
year interval to examine the relative contributions of
calcium intake, oral contraceptive use, and exercise on
bone mass (measured with dual energy x-ray absorpti-
ometry) and strength (estimated from proximal femur
section modulus). Calcium intake was quantified from
45 days of prospective food records at regular intervals
during the time when the subjects were 12 to 22 years
of age. Oral contraceptive use and activity were moni-
tored over the same time frame with questionnaires. The
authors reported no association between bone mass and
either calcium intake or contraceptive use but found a
strong relationship between bone mass and exercise dur-
ing adolescence. The data support the positive influence
of moderate exercise (none of the subjects participated
in long-term strenuous exercise) during growth on the
mass and strength of mature bone.
The effects of strenuous exercise on mature bone (ceased
longitudinal growth) are different from those on growing
bone. In a follow-up to an earlier study that examined the

effects of strenuous exercise on growing chick bone,62 we
examined the effects of a similar strenuous training pro-
gram on the tarsometatarsus (TMT) of mature roosters.36
The exercised birds ran a total of more than 150 km over
the 9-week training program. When compared with those
of age-matched, sedentary control birds, the exercised
TMTs had similar cortical areas, but the medial and ante-
rior cortices were thicker than those of the controls. None
of the mechanical properties differed significantly between
the exercise and sedentary groups. During treadmill walk-
ing, however, the in vivo strains recorded along the TMT
anterior cortex were significantly greater (13%) in the
exercised birds than in the sedentary roosters, which sug-
gests that strain may not be the primary objective for bone
remodeling. Although remodeling may have been driven
by the need to maintain strain within an optimal range, the
maximal amount of bone tissue that could be deposited
to accomplish that goal may have been tempered by the
need to minimize metabolic cost. Because exercise was the
remodeling stimulus in this study, energy expenditure dur-
ing running was a relevant parameter for the bird to mini-
mize. If no limit was placed on the mass of the bone, the
exercised birds may have developed thick-walled, heavy
bones in an effort to decrease strain. Metabolically, this
solution would not be optimal. Therefore the resulting
adaptation may have represented a compromise between
the desire to maintain optimal strains and the need to
minimize energy expenditure.
Jee, Li, and Schaffler70 undertook a comprehensive
study examining the effects of overload on the rat tibia.
One hind limb of each rat (9 months old) was taped to
the animal’s abdomen so that the limb could not be used
for weight bearing, and the contralateral hind limb was
forced to sustain all the loads normally shared between the
hind limbs. The geometry, mass distribution, and remod-
eling dynamics of the overloaded tibia were assessed after
2, 10, 18, and 26 weeks. Over these intervals, cortical
area increased gradually in the overloaded bones, with a
significant increase (10%) after 26 weeks. In the sedentary
controls, endosteal resorption resulted in a significant
increase in the bone endosteal diameter at each interval.
This normal, age-related remodeling was altered in the
overloaded bones, with the endosteal diameter remaining
similar to the baseline throughout the entire 26 weeks.
A comparison of the relative positions and amount of flu-
orochrome labels incorporated into the bone, the degree
of subperiosteal remodeling was also quantified. Their
analysis revealed that the overload stimulus slowed the
remodeling of existing bone and increased the rate of
new bone deposition, which resulted in a net increase
in subperiosteal bone. The authors suggested that their
data supported the mechanostat hypothesis of Frost46:
the increased mechanical use of the limb slowed age-
related bone loss and increased the deposition of new
bone around the periosteal surface.
CHAPTER 6 • Bone Biology and Mechanics 139
Stress Fractures
Although bone requires mechanical loads to maintain its
mineral mass and strength, repetitive loading may result in
structural failure, despite the magnitude of each loading
cycle being within the physiological range. Historically,
march fracture has been used to describe bone failure
resulting from repetitive loading cycles.71 This term
identifies the high incidence of fracture among military
recruits who spend many hours marching on hard sur-
faces without resilient footwear.72,73 More recently, two
terms have been used to describe distinct phases of this
overuse injury. “Stress reaction” describes the series of
pathophysiological changes that occur with repetitive
loading, and “stress fracture” is the structural failure of
bone that may follow a stress reaction and results in a
radiographically evident fracture line.74
The American College of Sports Medicine has issued
a position paper describing the Female Athlete Triad,75
a syndrome that occurs in physically active girls and
women. Pressure placed on young women to achieve or
maintain unrealistically low body weight underlies devel-
opment of the syndrome that includes components of
disordered eating, amenorrhea, and osteoporosis. The
combination of these systemic, hormonal, and emotional
factors with strenuous weight-bearing training may pre-
dispose a female athlete to sustain a musculoskeletal
injury, such as a stress fracture. In these cases, the lack of
a single causative factor makes it difficult to prospectively
identify athletes at risk. Additionally, many of the indi-
viduals prone to fracture are highly trained elite athletes
or highly motivated military personnel who may tend to
“run through the pain,” which thereby prevents the med-
ical team from management of the symptoms of a stress
reaction before a frank stress fracture develops.
Jones, Harris, Vinh, and Rubin74 proposed a grading
system to assist in the accurate diagnosis of stress reaction
and stress fracture. By standardizing the terminology,
they also sought to facilitate identification of the actual
incidence of such injuries among athletes. In this schema
(Table 6-4), several clinical tools are used in forming a
diagnosis: bone scan, plane x-ray, clinical symptoms (pain
and tenderness, palpable mass), and history of recent
increase in activity intensity or duration. Recently, Aoki,
Yasuda, Tohyama, and Ito76 reported that MRI can differ-
entiate stress fracture and shin splints before radiographs
show a detectable periosteal reaction in the tibia. Earlier
diagnosis is clearly an advantage to allow earlier clinical
intervention and activity modification, which therefore
increases the lost training or competition time.
Treatment of a stress fracture generally follows two
phases. Phase I consists primarily of therapeutic modali-
ties aimed at pain reduction (e.g., ice and nonsteroidal
anti-inflammatory medications) and reduced weight-
bearing aerobic activities, such as swimming and running
140 SECTION I • Scientific Foundations
Table 6-4
Classification Scheme for Diagnosis of Stress Reaction and Stress Fracture
Grade 0 Grade 1
Normal remodeling Mild stress reaction
Detectable by bone scan Positive bone scan;
undetectable on plane
x-ray
No structural
compromise
Asymptomatic Local pain during
activity; no pain at
rest
From Loitz-Ramage BJ, Zernicke RF: Bone biology and mechanics. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, Philadelphia, 1996, WB Saunders, p 114. Modified from Jones BH, Harris JM, Vinh TN et al: Exercise-induced stress fractures
and stress reactions of bone: epidemiology, etiology, and classifications, Exerc Sport Sci Rev 17:379-422, 1989; and Grimston SK, Zernicke RF:
Exercise-related stress responses in bone, J Appl Biomech 9:2-14, 1993.
in water. After 3 weeks of pain-free participation in phase
I activities, the individual begins phase II by gradually
increasing weight-bearing activities and continues the
modalities for pain management. Matheson, McKenzie,
Taunton et al77 reported that among 320 athletes with
stress fractures, average rehabilitation time was 13 weeks
from diagnosis to resumption of full activities. Whitelaw,
Wetzler, Levy et al78 suggest that the rehabilitation time
can be reduced significantly to 3.6 weeks with the use
of pneumatic leg braces during weight-bearing activities.
The brace appears to act as a dynamic splint that provides
enough support to the injured extremity to allow healing
without substantial curtailment of weight-bearing activi-
ties. Multicenter studies examining the use of pneumatic
braces are ongoing.
Disuse-Related Changes in Bone
Disuse-related changes in bone commonly are associated
with bed rest, immobilization, or spaceflight. Animal
studies examining disuse changes in bone suggest that
lack of regular load bearing prompts remodeling in a
variety of ways. Loads can be diminished through neu-
rectomy, tenotomy, or cast or pinned-joint immobiliza-
tion. Regardless of the specific methodology, however,
the effects of disuse are profound. Disuse results in a sub-
stantially increased resorption and decreased deposition.
Weinreb, Rodan, and Thompson79 reported that bone
resorption in a rat model increased dramatically within
30 hours after tenotomy or neurectomy because of a sig-
nificant increase in the number of osteoclasts per mil-
limeter of bone surface. A sustained decrease in the rates
of bone formation and mineral apposition contributed to
Grade 2 Grade 3 Grade 4
Moderate stress Severe stress reaction Stress fracture
reaction
Positive bone scan; Positive bone scan; Positive bone
minimal change on positive plane x-ray scan; positive
plane x-ray Structural changes plane x-ray
No structural evident Structural failure
compromise
Local pain during Significant pain Extreme pain with
activity; tender to does not abate after weight bearing
palpation cessation of activity;
palpable mass
a marked decrease in trabecular bone volume and bone
mineral content at the end of the 42-day experiment.
Because disuse changes are comparatively clear-cut
and immobilization may be unavoidable in certain cir-
cumstances, of greater clinical relevance is whether dis-
use-related changes can be reversed by remobilization.
Using a rat tibia and femur, Tuukkanen, Wallmark,
Jalovaara et al80 examined the effects of 1 or 3 weeks of
immobilization followed by 3 weeks of remobilization.
After 3 weeks of immobilization, tibial and femoral ash
weights decreased (9% to 12%) compared with nonimmo-
bilized controls, with the tibia and femur demonstrating
similar losses. After remobilization, the tibia recovered
62% of its mineral mass, and the femur regained only
38%. The shorter immobilization period resulted in an
improved recovery of mineral mass, although full return
was not demonstrated. These data suggest that mineral
loss prompted by immobilization can be reversed to
some extent, although recovery does not occur rapidly.
The degree of recovery is related to the duration of the
immobilization. Clinically, the impact of these data is
reflected, to some degree, in the surge in the use of frac-
ture braces and early mobilization in the management of
orthopedic trauma.
Spaceflight induces similar dramatic changes in both
cortical and trabecular bone. Interesting, too, are the sug-
gestions that weight-bearing bones may be more sensitive
to decreased mechanical usage than non–weight-bearing
or axial bones. Three-point bending tests of the tibia and
humerus from rats after a 1-week spaceflight revealed a
decrease in bone stiffness and strength, with the tibial
changes more dramatic than those of the humerus.81
In addition, the animals used in this study were rapidly

growing, and the absence of mechanical loads appeared
to delay the maturation of the humerus but not the tibia.
These findings support the theory that the mechanical
threshold that triggers remodeling may be bone specific,
a premise supported by the extensive work of Biewener,
Swartz, and Bertram,82 who demonstrated site-specific
optimal strains in growing chicks.
Trabecular bone appears to react to spaceflight with
decreased stiffness and strength, as noted in rat lumbar
vertebrae after 12.5 days in space.83 The concentration
of mature collagen cross-links was also diminished in the
spaceflight rats compared with the earth-reared controls,
which indicates that bone maturation may have slowed
during the flight. Similar to the above-noted relevance of
remobilization, the pertinent question is whether these
marked detrimental changes can be minimized during
flight. This question continues to be investigated.
Disease-Related Changes in Bone
Diabetes
In clinical studies with humans84-89 and in experimental
studies with animals,90-95 diabetic osteopathy has been
reported, with diabetes-related effects being more pro-
nounced in patients with insulin-dependent (type I)
diabetes. Patients with non–insulin-dependent (type
II) diabetes have more variable results.86,96 Mechanical
deterioration of diabetic bone has been reported for
the femoral shaft91,97 and femoral neck,92 but the spe-
cific relation between severity of diabetes and extent
of osteopathy remains equivocal. McNair, Madsbad,
Christiansen et al98 found a correlation between osteo-
penia and blood glucose level, but other clinical stud-
ies did not find such a relation.99,100 Schwartz, Ornoy,
and Soskolne101 indicated that bone growth, formation,
and calcification decreased with glucose concentrations
higher than 200 mg/dL, but the changes gradually
reached a steady state. Those mixed findings may, in
part, be a consequence of the different severities and
durations used in studies and the difficulties in establish-
ment of an adequate clinical control group, because dia-
betic patients vary widely in diets, treatment regimens,
environment, and physical activity levels. Detrimental
effects of diabetes on bone are particularly important
to health care providers caring for persons at risk of fall-
ing.102 If diabetes increases fracture risk, education of
diabetic individuals and their caregivers is important to
decrease the likelihood of falling.
Animal studies indicate that severe diabetes can
retard bone growth and development,103 and the serum
from diabetic rats with high glucose levels can retard
the growth of rat fetuses in culture.104 One study92
demonstrated that moderate type I diabetes can del-
eteriously affect rat femoral neck mechanical prop-
CHAPTER 6 • Bone Biology and Mechanics 141
erties. Insulinopenia may account for these growth
retardation effects97,105,106; recent studies have shown
that the potent effects of growth factors in bone (e.g.,
insulin-like growth factors I and II) are highly similar
to insulin.107,108 Indeed, with moderately diabetic rats,
insulin therapy ameliorated growth-retardation effects
on bone.92
We investigated the relation between the severity of
diabetes and degree of osteopenia in rats.93 The interac-
tive effects were studied of diabetes and insulin therapy
on the geometrical, biomechanical, and histomorpho-
logical characteristics of the femoral neck in strepto-
zotocin-induced insulin-dependent (type I) diabetic
rats. Female Sprague-Dawley rats (8 weeks old) were
randomly assigned to one of three groups: control (C),
severe diabetes (SDM), and severe diabetes with insu-
lin treatment (SDI). Rats with severe insulin-dependent
diabetes had significantly lower total body mass than
controls, in addition to significantly less femur mass,
femur length, total bone cross-sectional area, and cor-
tical shell cross-sectional area. Insulin therapy amelio-
rated some, but not all, of the detrimental effects of
diabetes on femoral neck geometry. Compared with C
and SDI rats, SDM rats had lower femoral neck struc-
tural properties. SDM rats had significantly greater
porosity in the femoral neck cortex than control rats.
Decrements in material properties of the rat femo-
ral neck were linearly correlated with diabetic severity
(blood glucose level), and insulin therapy mitigated
diabetic osteopathy (Figure 6-12). The data suggest
that there are clear severity-related changes in diabetic
bone; the material properties were the most directly and
adversely affected.92,93
Figure 6-12
Relation between the normal stress of the femoral neck at the
proportional limit and maximum, and blood glucose levels. Values are
means ± SD. (From Hou JC-H, Zernicke RF, Barnard J: Effects of
severe diabetes and insulin on the femoral neck of the immature rat,
J Orthop Res 11:263, 1993.)
142 SECTION I • Scientific Foundations
Osteoporosis
Aging alone causes changes in the intracortical bones of
people.1 Most of these changes are associated with the
BMU remodeling system, and their effects are found in the
age-dependent alterations in bone geometry, size, and num-
ber of osteons.1 As indicated earlier, bone at the tissue level
undergoes remodeling; bone is continually resorbed and re-
formed.109 A negative balance between bone resorption and
formation (in many cases related to excessive resorption) is
the basic mechanism associated with many bone diseases.109
Generally, increased age is associated with increased bone
porosity. Increased porosity can be associated with increased
numbers of haversian canals, more resorption spaces and
incomplete refilling of osteons, and larger haversian canals.1
Furthermore, cortical bone typically becomes weaker and
slightly more brittle with increasing age.1
Osteoporosis is a disease characterized by reduced
bone mineral mass and changes in bone structural geom-
etry. After peak bone mass is achieved by the third decade,
men and women experience an age-related bone loss of
approximately 0.7% to 1% annually.110 Between the teen-
age years and the eighth or ninth decade, women lose
42% of their spinal and 58% of their femoral neck bone
mass.110 This loss is strongly associated with an increased
probability of fractures, primarily of the hip, spine, and
wrist.111 Although osteoporosis is recognized as widely
prevalent, the incidence of the disease is not well docu-
mented.112 Praemer, Furner, and Rice111 indicate that part
of the difficulty associated with determining the preva-
lence of osteoporosis is that (1) some progressive loss of
bone mass is a function of the normal aging process, (2)
loss of bone can be caused by other disease processes, and
(3) the amount of bone mass at one site is not necessar-
ily correlated with bone mass at other sites in the body.
Currently, no internationally recognized survey data use
objective diagnostic criteria for osteoporosis.
A large prospective study of bone mineral density and
fracture incidence recently completed in the Netherlands
examined bone mineral density and fracture incidence
in 7800 adults over age 55.113 Fracture rate was tabu-
lated from follow-up data collected for an average of 6.8
years. Two primary findings pertinent to osteoporosis
incidence and research emerged from the study. Firstly,
hip, wrist, and upper humeral fractures were the most
frequent fractures in men and women, with an overall
incidence rate of 9.6 and 18.9 per 1000 person years for
men and women, respectively. Secondly, only 44% of all
nonvertebral fractures occurred in women identified as
osteoporotic, with a BMD T-score below the −2.5 cut-
off. Among men, 18% of the subjects who sustained a
nonvertebral fracture had a normal BMD. The results
identified a clear need to develop more sensitive risk
assessment techniques that incorporate clinical measures
other than bone mineral density.
Although standard radiographic techniques can be
used to assess the degree of osteoporotic bone loss quali-
tatively, quantification of bone mineral content and the
subsequent prediction of fracture risk that result from
osteoporosis require the use of quantitative computed
tomography (QCT).114 QCT provides a measure of the
trabecular bone mass of the vertebrae or other sites with
predominantly trabecular bone.
The mean normal vertebral mineral mass for young
males and females is 175 mg/cm3. By age 75, men have
lost an average of 40% of that mineral mass (110 mg/
cm3); at the same age, women have lost 50% (approxi-
mately 90 mg/cm3).111 The fracture threshold has been
estimated to be 110 mg/cm3, with the fracture risk being
low for individuals with mineral mass greater than the
threshold. Although this is only an estimation and con-
siderable overlap exists in vertebral mineral mass between
normal women and those who have sustained atraumatic
(non–accident-related) fracture, it can be used as a general
guideline to assess fracture risk. QCT also has been useful
in studies that compare vertebral mineral mass between
amenorrheic elite athletes and cohorts with normal men-
strual function.115 The amenorrheic athletes were found
to have 20% to 25% less mineral mass than the normal
women, which suggests that estrogen deprivation has a
powerful effect on trabecular mineral mass.
Hip fractures resulting from osteoporosis have sig-
nificant social impact in terms of disability, medical costs,
and mortality.111-116 An estimated 250,000 hip fractures
occur each year in the United States alone.111,116 Because
the frequency of hip fractures is increasing rapidly among
the population, it is becoming a greater public health
concern.111 In addition to substantial contributions to
morbidity and disability within the older population, hip
fractures are associated with increased mortality for years
after the fracture.112 After the age of 50, the incidence
of hip fractures increases almost exponentially, with an
approximate doubling of the incidence of fracture for
every 5- to 6-year increase in age.111,117 Of those who
survive hip fractures, up to 50% may spend time in a
long-term care setting.111,112 Of those individuals who
were living at home and independently before the frac-
ture, approximately 20% remained in long-term institu-
tions for at least a year after the fracture. Those people
who sustained hip fractures had approximately a 15%
higher mortality rate in the first year after the fracture
compared with people of comparable ages, and most of
those deaths occurred within the first 4 months after the
fracture.111,112
Men and women experience some loss of bone mass
during normal aging, but osteoporosis progresses much
more rapidly in postmenopausal women.118 After 30
years of age, men typically lose bone mass at approxi-
mately the same rate for the remainder of their lives. In
women, however, the loss of bone increases significantly

for about 5 years after menopause and then slows to a
more gradual loss.118 Just after menopause, the rate of
bone mass loss is up to 10 times faster in women than in
men of the same age.118 To retard the rapid loss of bone
in postmenopausal women, therapeutic interventions
and exercise have been proposed. In premenopausal
adult women, the rates of bone formation and bone
resorption are approximately equal, calcium balance is
maintained, and no effective loss of bone mass occurs.119
After menopause, however, bone formation and resorp-
tion rates increase, but the rate of bone resorption
increases more rapidly and produces a calcium imbal-
ance and a net loss of bone.118 One of the goals of osteo-
porosis prevention is to restore bone resorption and
formation rates to premenopausal levels.
Frost120 discussed the pathogenesis of osteoporo-
sis in terms of mechanical usage. Frost suggested that
decreased mechanical usage stops the deposition of bone
by modeling and increases the removal of endosteal bone
by remodeling. More data are becoming available that
indicate that regular exercise may have a positive impact
on bone mass and that increased trabecular bone density
may be increased as a result of exercise that specifically
loads the affected bones in postmenopausal women.121
Snow-Harter and Marcus122 wrote an extensive paper
reviewing the relations among exercise, bone mineral
density, and osteoporosis. Among the numerous issues
presented, they summarized information about physical
activity and bone mass from cross-sectional and inter-
ventional studies. Cross-sectional studies usually involve
an assessment of an active versus a sedentary group of
people at a single point in time. Generally, cross-sectional
data reveal a positive correlation between activity level
and bone mineral density,123,124 although the duration,
frequency, and intensity of the exercise regimen often are
not detailed, and many confounding factors are associated
with the differences that are reported.
Interventional studies are prospective studies that assess
the effect of an exercise program on bone mineral density.
Snow-Harter and Marcus,122 after reviewing a wide range
of studies, concluded that generally there is a good indi-
cation that bone mineral density is enhanced as a result
of an exercise program, but the effects are “site specific.”
Furthermore, it is still unknown which exercise best pro-
motes bone density.122 Running, jogging, and walking
are usually the types of exercise prescribed to ameliorate
bone loss related to menopause, but Snow-Harter and
Marcus122 suggest that exercise with higher loads at spe-
cific sites may provide a greater osteogenic response.
With physical training, muscle mass and strength can
increase. Discovering the interrelation between muscle
strength and bone mineral density has become a target
of more recent research.34,123 Although a site specificity
CHAPTER 6 • Bone Biology and Mechanics 143
between muscle strength and bone mineral density seems
apparent, in some cases, postural and axial muscles appar-
ently exert beneficial forces on bones.122
Snow-Harter and Marcus122 state that the efficacy of
exercise in prevention and treatment of osteoporosis is
unknown. They summarize the known information,
however, by answering the following questions: (1) Can
exercise maximize peak bone mass? (2) Can exercise fore-
stall or reduce age-related bone losses? (3) Does exer-
cise enhance bone mineral density in those people with
existing osteoporosis? (4) Can exercise replace estrogen
replacement therapy during the postmenopausal years?
Given reasonable caveats, the answer is positive to the
first three questions. The answer to the fourth question,
however, is no. To date, no basis exists for the statement
that exercise alone is superior to estrogen replacement
for maintaining bone mass and reducing the fracture risk
for postmenopausal women.122
Summary
Skeletal biology is the focus of substantial ongoing
research, and it is impossible to summarize the essence of
the field in a single chapter. However, within the context
of sports medicine and rehabilitation, we selected specific
topics that are both pertinent and of interest to clini-
cians and rehabilitation specialists. Briefly, the material
presented here can be summarized as follows. Bone is a
dynamic and highly complex organ that plays an inte-
gral role in many of the normal metabolic processes of
the body. The close coupling that exists between bone
and the external mechanical environment dictates that
change in one will influence the other; a bone fracture
changes the response of the tissue to mechanical load,
and, conversely, change in the mechanical environment
stimulates adaptation. Such interaction is particularly rel-
evant clinically, because it is toward this that many thera-
peutic interventions are directed.
The goal of this chapter is to provide the clinician with
information to which he or she can refer when reviewing
research studies that describe bone adaptation or heal-
ing. In addition, the material will help the clinician tie his
or her clinical knowledge and skills to the ongoing basic
research being done in this area. The materials referenced
in the chapter are current and provide a good base to
which the reader can turn if additional, in-depth study
is desired.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever pos-
sible.There are a total of 124 references for this chapter.

144 SECTION I • Scientific Foundations
C ARTILAGE OF H UMAN J OINTS
AND R ELATED S TRUCTURES
Katie Lundon and Joan M. Walker
Introduction
This chapter describes the morphology and physiology
of articular cartilage and its associated subchondral bone
tissue, fibrocartilage, and synovial tissues and fluid. It
considers innervation, nutrition, lubrication, age-related
changes, response to loading, breakdown, repair, tissue
engineering, and the implications for rehabilitation. The
hyaline articular cartilage (HAC) that covers synovial joint
surfaces cannot be considered by itself. HAC is part of
the load-bearing unit that consists of the HAC layer and
the subchondral bone; it has important interactions with
synovial fluid and associations with other joint structures
such as the menisci of the knee joint. The joint’s static
and dynamic stability is heavily dependent on the contour
of the joint surfaces created by HAC in partnership with
subchondral bone as well as the supporting structures—
capsule, tendons, ligaments, and muscles—that surround
the joint; these structures are detailed in other chapters.
The specialized HAC has many functions: to provide
a viscoelastic structure that can distribute and transmit
loads and shear forces to the underlying bone, to protect
the underlying subchondral bone, and to permit diar-
throdial (synovial) joints to have a wide range of almost
frictionless movement. HAC is aneural, largely avascular
and acellular, and has a water content of up to 80%.1
The collagenous HAC matrix is targeted in destructive
processes in arthritic and degenerative diseases of the
joint. Current therapeutic efforts aim to develop colla-
gen tissue engineered scaffolds that will act as vehicles
for cell and growth factor transport therapy at sites of
subchondral bone/cartilage damage. Such lesions have
been notoriously difficult or impossible to heal with
previous modalities or surgical approaches.
144
7
C H A P T E R
Function of Articular Cartilage
● Distributes and transmits loads and shear forces to
underlying bone
● Allows almost frictionless movement
● Permits synovial joint to have specific, functional ROM
Composition of Cartilage:
Cells and Matrix
All connective tissues are made up of cells and extra-
cellular matrix. The cellular elements are chondroblasts,
chondrocytes, fibroblasts, and fibrocytes (chondrocyte-
like cells). Chondrocytes (2% to 5% of cartilage volume)
are responsible for the synthesis of proteoglycans, growth
factors, and cytokines, as well as collagen fibers, all of
which constitute the principal elements of the cartilage
matrix (95% cartilage volume). Chondrocytes are central
to the maintenance of the extracellular matrix (ECM) in
which they are embedded. Chondrocytes have both ana-
bolic activity, which contributes to balanced matrix turn-
over of their surrounding ECM, and catabolic activity
secreting matrix-degrading molecules including mem-
bers of the family of matrix metalloproteinases (MMPs),
such as collagenases and stromelysin. Chondrocytes are
the source of several cytokines and growth factors that
act in either a paracrine or autocrine manner by switch-
ing these anabolic and catabolic processes on and off.2
Cartilage cells are embedded in a finely textured matrix,
in small zones that conform to the cell shape. The thin
pericellular matrix that surrounds the chondrocytes is up
to 2 µm thick and contains a few well-defined collagen
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
fibers. The chondrocyte and its pericellular matrix have
been termed a “chondron.” In contrast, cartilage cells
in fibrocartilage are squashed between the thick bands
of collagen fibers and thus appear elongated without
any significant pericellular matrix surrounding them,
except close to the osseous junction. The young cell, or
chondroblast, is small and often flattened with a regular
contour and many surface projections.
The main morphological features of chondrocytes are
that they are normally rounded or polygonal except at
tissue boundaries where they may be flattened or dis-
coid such as at the articular surface of joints.3 Nuclei are
round or oval. Multinucleated cells are common. The
chondrocyte shows typical features of a metabolically
active cell that has to synthesize and turn over a large
matrix volume. Its cell cytoplasm contains the Golgi
apparatus, mitochondria, the granular endoplastic reticu-
lum, a few fat goblets, pigment granules, and glycogen
deposits. In immature cartilage, both the Golgi apparatus
and the granular reticulum are particularly prominent.4
Every chondrocyte has a monocilium,5 and these may
have a mechanotransductory function, detecting changes
caused by mechanical effects in the cell’s environment
and enabling it to respond.
“Cell density is at its highest at the articular sur-
face and is progressively reduced in the mid- and deep
zones to about one-half to one-third that of the superfi-
cial layer.”6 Cell density is also at its highest in fetal and
newborn cartilages and decreases with increasing age.
Cell density is relatively low in HAC, and the decreased
number of cells caused by aging and by the move from
superficial to deep greatly reduces the repair capacity of
HAC. Nutrient/waste exchange occurs through diffu-
sion. Chondrocytes have a unique ability to exist in a low
oxygen tension environment.
Cartilage cells are capable of changing their shape. The
isolated living chondrocyte constantly changes its shape,
putting out and withdrawing pseudopodic processes. If
in vitro cells from the superficial layer are transplanted to
a deeper layer, they change their shape and become more
rounded.7
Chondrocyte proliferation, differentiation, and homeo-
stasis are not only governed by soluble mediators in inter-
action with the genetic makeup of these cells, but also the
ECM itself provides important signals for interpretation
by the chondrocytes. This interaction between chondro-
cytes and the matrix is partly mediated by the integrins,
a family of transmembrane receptors composed of α and
β subunits.8
In the developing embryo, chondroblasts and mature
chondrocytes are derived from progenitor mesenchy-
mal cells. After the embryonic period, prechondrogenic
mesenchyme forms cartilage even when transplanted
to other sites.9 The chondroblasts that will mature into
the chondrocytes of HAC are similar in origin to the
145
chondroblasts of fracture callus and growth plates. The
latter develop into hypertrophic chondrocytes and have
the capacity to form calcified cartilage, which acts as a
scaffold for osteoblasts to deposit osteoid.10 Differences
in chondrocyte function according to location may be
related to the presence or absence of a receptor for the
basic fibroblastic growth factor (bFGF), which all chon-
droblasts possess.6 Whereas the chondrocyte of HAC
retains a receptor for bFGF, the hypertrophic chondro-
cyte found in the growth plate or in fracture callus has
no bFGF receptor. The factors that regulate the com-
mitment of chondroblasts to develop into hypertrophic
chondrocytes or chondrocytes of HAC are not yet fully
established.6 Chondrocyte death in the conversion of
surrounding matrix from cartilage to bone occurs either
by apoptosis, or it transdifferentiates or metaplases into
an osteoblast, with the determining factor remaining
unknown.11 A further distinction between chondrocytes
in the epiphyseal growth plate and those in HAC is that
blood vessels are usually found in close proximity to
the growth plate and fracture callus. Poole commented
that “for cartilage to calcify during endochondral ossifi-
cation [and in fracture repair], angiogenesis appears to
be required, which can be induced by chondrocytes.”6
Since HAC is avascular even in development, angiogen-
esis apparently is not induced by HAC chondrocytes.
Obviously, calcification of HAC is detrimental to its nor-
mal function. This is evident in aging cartilage, in which
there is expansion of the deep calcified layer.
Angiogenesis is always present in developing growth
plates and fracture sites, and hypertrophy of chondro-
cytes precedes this vessel ingrowth in those situations.
In contrast, although the deepest zone of HAC contains
hypertrophic chondrocytes, vascular invasion of the cal-
cified zone is limited or not present at all. The absence
of vascularity is a critical factor in HAC’s inability to
respond to injury with the typical stages of inflammation
and seriously impairs its repair capacity.
Cells of fibrocartilaginous structures, such as menisci
and the anulus fibrosus of the intervertebral disc, are a
chondrocytic type of cell (mature cells are termed fibro-
cytes) that synthesizes and secretes type I rather than
type II collagen, which is synthesized and secreted by
HAC-like cells. Where these structures carry significant
loads, the cells synthesize proteoglycan aggrecan, which
increases the stiffness of the fibrocartilage.6
Extracellular Matrix (ECM)
Both the articular cartilage and the nucleus pulposus of
the intervertebral disc (IVD) are specialized connective
tissues in which resident cells are relatively sparsely distrib-
uted within the matrix that surrounds them. The ECM
of HAC and the IVD is a resilient gel with a complex
macromolecular organization. It is this largely avascular,
146 SECTION I • Scientific Foundations

aneural, and alymphatic matrix that confers to the tissue

its specialized loading and biomechanical properties,
such as the ability to withstand both static and dynamic
loading stresses. The extracellular matrix is composed of
fibrous collagens (mainly type II collagen), a nonfibrous
component or ground substance (proteoglycans, non-
collagenous protein [NCPs]), and water. Large protein
aggregates (LPAs) are formed by variably associated pro-
teoglycans (PGs) and glycosaminoglycans (GAGs). The
water content of ECM (65% to 80%) is greater in the
superficial layers than in the deeper layers.12

Proteoglycans
The PGs and GAGs in articular cartilage account for
about 35% dry weight in articular cartilage (HAC). In
HAC, proteoglycans exist as PG monomers or PG aggre-
gates. These hydrophilic (water-loving) polyaminos play
an important role in regulating the movement of water
in the matrix and thereby greatly influence the mechani-
cal and lubrication properties of cartilage.13 By binding
with water, the high proteoglycan content gives cartilage
a low hydraulic permeability, which limits fluid loss when
it is loaded in compression. Cartilage deforms revers-
ibly, loses water to the joint space when loaded, and
imbibes water when the load is released. Contributing to
this mechanism is the LPA, an elastic molecule that can Figure 7-1
A, Diagrammatic model of the cartilage proteoglycan aggregate.
expand in solution and resist compression in a small vol-
The filamentous backbone of the aggregate is hyaluronate.
ume.14 It is this constraint of the proteoglycan aggregates Proteoglycan monomers (aggrecan molecules) of variable length arise
and the dense network of collagen fibers that gives some at regular intervals from the opposite sides of the hyaluronate chain.
remarkable mechanical properties (resistance to com- Proteoglycan monomer core protein contains three globular domains
pressive load, elasticity, and self-lubrication) to articular designated G1, G2, and G3; G1 is located at the NH2-terminus and
contains the hyaluronate acid binding region. Link protein binds
cartilage.
simultaneously to hyaluronate and G1 and stabilizes the aggregate
against association. (From Walker JM: Cartilage of human joints and
related structures. In Zachazewski JE, Magee DJ, Quillen WS, editors:
Mechanical Properties of Articular Cartilage Athletic injuries and rehabilitation, p 122, Philadelphia, 1996, WB
Saunders.) B, Diagrammatic model of the structure of the cartilage
● Resistance to compressive loads proteoglycan monomer (aggrecan). (From Rosenberg L: Structure
● Elasticity and function of cartilage proteoglycans. In McCarty DJ, Koopman
● Self-lubricating WJ, editors: Arthritis and allied conditions, ed 12, vol 1,
p 230, Philadelphia, 1993, Lea & Febiger.)

The HAC has three major PG families. The first con-

sists of LPAs that form a “noncovalent” association of
collagen protein monomers referred to as aggrecan,
which comprises 50% to 58% of the total amount of PGs
found in HAC. Nonaggregating PGs present as 40% of
the total PG content of HAC.15 Aggrecan is bound at
intervals with a single central filament of hyaluronate and
is stabilized with link proteins (Figure 7-1). Aggrecans
have three globular domains known as G1, G2, and G3.
The major component of proteoglycans consists of GAG
side chains of chondroitin sulphate (CS), which exist
as either CS-6 or CS-4. Regions that are rich in kera-
tan sulfate (KS) lie between domains G2 and G3.14 CS
and KS are linear polymers consisting of sugar residues,
representing 87% and 6%, respectively, of the group of
polysaccharides called GAGs found in the ground sub-
stance of several connective tissues including HAC. An
entire aggrecan molecule has a molecular weight of 2 to
3 million (an aggrecan molecular protein core is about
220,000; CS chains are about 20,000 to 30,000; and
KS chains are about 5000 to 10,000).14 An important
feature of CS and KS is that the repeating units of GAGs
contain closely packed, negatively charged groups, so
that when these chains are linked to the aggrecan core
protein (ACP), they stand out like bristles on a brush.
This concentration of negative charge is referred to as
fixed charge density (FCD).
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
The strongly repelling forces of the thousands of
negatively charged groups mean that the protein aggre-
gate (PA) would occupy a greater volume of solution
in vitro, but in vivo, the PAs are constrained by the
collagen network. It is this feature that gives articular
cartilage its elastic properties. The elastic forces of PAs
are balanced by the tensile forces of the collagen net-
work. When cartilage is compressed, water (interstitial
fluid) is extruded from the cartilage, and the aggregate
is confined to a smaller area. With relief of pressure, the
aggregate expands until limited by the collagen fiber
network; simultaneously, cartilage imbibes water and
the volume of cartilage increases. This characteristic is
vital to cartilage’s ability to deform yet withstand loading
and thus protect the underlying subchondral bone from
damage. The link protein (see Figure 7-1) stabilizes the
aggregate against dissociation by binding with hyaluro-
nate and to the G1 globular domain of the ACP. This
arrangement is unstable at a low pH and will dissociate
at pH 4.14 Therefore, a greater amount of aggregate is
present when the pH is about 7.
The second group of PGs are a family of leucine-rich,
structurally related PGs including biglycan, decorin, and
fibromodulin that have one to two GAG chains. These
PGs bind to matrix components, specifically to collagen
fibrils, and thus regulate fibrillogenesis, matrix assembly,
and stabilization in cartilage.16,17 These small PGs also
interact with TGF-β and modulate its bioavailability and
stability.16 Specifically, biglycan and decorin inhibit the
processes involved in tissue development and repair. They
have been shown to bind to the surface of collagen fibers,
inhibiting collagen fibrillogenesis, and to bind to fibro-
nectin, thus inhibiting cell adhesion and thrombin activity
in clot formation. Their activity could explain why lesions
of articular cartilage do not heal well or repair spontane-
ously.14 Mature articular cartilage contains biglycan and
decorin in roughly equal amounts, “and they tend to be
most concentrated near the articular surface and least in
the deep zone.”6 The significance of this distribution is
yet to be determined.
The third family of PGs in HAC is made up of the
cell-surface PGs. These molecules interact with various
components of the cellular environment including growth
factors, proteases, and matrix components. An alteration
in the expression of these PGs occurs during degenera-
tive pathologies and ultimately may lead to a change in
functional properties of HAC, as well as growth factor
bioavailability.16 Therefore, in addition to their impor-
tant role in maintaining HAC tissue structure, some PGs
operate in molecular signaling as reservoirs and receptors
for growth factors.18
Matrix Metalloproteinases (MMPs) and Tissue
Inhibitors of Matrix Metalloproteinases (TIMPs).
MMPs are a group of enzymes that digest ECM in both
normal and degenerative articular cartilages; they are
147
activated through signaling pathways and target specific
components of the matrix. Chondrocytes produce a
significant proportion of the catabolic matrix-degrading
molecules, including members of the MMPs such as
collagenases and stromelysins.2 Collagen, aggrecan,
fibronectin, laminin, and elastin are degraded by colla-
genases (MMPs-1, -8, and -13), gelatinases (MMPs-2
and -9) and stromelysins (MMP-3 and -10). The MMPs
contain a Zn2+ ion at their active site and are stabilized
by Ca2+ ions.19,20 Their activity is inhibited by a group
known as tissue inhibitors of matrix metalloprotein-
ases (TIMPs). Elevated levels of MMPs and TIMPs are
observed in patients with osteoarthritis and rheumatoid
arthritis.19,20
Signaling Molecules in Articular Cartilage:
Growth Factors and Cytokines. Several growth
factors and inflammatory cytokines interact to regulate
cellular function and maintenance of healthy cartilage.
A disruption in the homeostasis of these molecular
signals manifests in cartilage pathologies.21 The inter-
play of these signaling pathways is important for the
development of new drug therapies aimed at imped-
ing damage to articular cartilage.22 The major growth
factors include the transforming growth factor family
(TGF-βs: TGF-β1s, -β2s, and -β3s) that regulate cell
growth and differentiation and are involved in wound
healing.23 Bone morphogenetic proteins (BMPs) are
a subfamily of the TGF superfamily and induce bone
and cartilage formation.23 BMP-7 or osteogenic pro-
tein (OP-1) demonstrates strong anabolic activity,24
uniquely only stimulating the synthesis of the majority
of cartilage ECM proteins as well as the expression of
TIMPs. The ability to induce cell proliferation might
have both positive and negative effects as BMPs were
initially found in the bone matrix; however, BMP-2, -7,
and TGF-β all appear to induce and increase PG synthe-
sis and accumulation. There are contradictory records
of catabolic events (cell proliferation and osteophyte
production) stimulated by the administration of BMP-
2 and TGF-β in adult articular cartilage.24 Insulin-like
growth factors (IGF-1 and IGF-2) act in an anabolic
manner to increase PG and type II collagen synthe-
sis.25 Fibroblast-derived growth factor (FGF) is stored
by heparin sulphate in the ECM of HAC. FGF is criti-
cal in attracting cells of mesodermal origin and plays a
role in angiogenesis.26 In addition, FGF has been shown
to inhibit type II collagen-PG synthesis27 and induce
synthesis of MMPs.28 Platelet-derived growth factor
(PDGF), epidermal growth factor (EGF), and vascular
endothelial growth factor (VEGF) also are important to
cartilage in health and injury. PDGF stimulates macro-
phages and fibroblasts in wound healing processes23 and
has a role in mesenchymal stem cell differentiation,29
ossification,30 and MMP expression.28 EGF stimulates
the proliferation of chondrocytes31 and a decrease
148 SECTION I • Scientific Foundations
in type II collagen expression.32 VEGF is detected in
elevated levels in osteoarthritic cartilage33 and is needed
in endochondral bone formation.34
The interleukins (Ils) are secreted by chondrocytes,
fibroblasts, macrophages, and synovial cells and are
important players in articular cartilage repair as they
interact with several growth factors during inflammation
and wound-healing processes.35 For example, IL-1 plays
a critical role in cartilage degeneration, with IL-1β acting
to suppress the expression of PGs, type II collagen, and
TIMP-1 in human HAC chondrocyte cultures.36 TNF-α,
a member of a cytokine group, is known for its differ-
ential cytotoxic and stimulatory effects, is expressed in
osteoarthritic cartilage but not in normal articular carti-
lage,37 and can suppress PG synthesis, stimulate collagen
degradation, and induce MMP expression.28,38
Collagen
The collagen superfamily now includes more than 20 col-
lagen types with at least 38 distinct polypeptide classes and
more than 15 additional proteins that have collagen-like
domains.39 Collagen serves two important roles in HAC,
being both mechanical and responsible for directing the
binding and release of cellular growth mediators. Type II
collagen is the predominant and fibrillar form found in
HAC, and it accounts for 50% to 90% dry weight of HAC
(Table 7-1). The various types of collagen are strands of
α chains that are composed of amino acids. Each fibrillar
Table 7-1
Collagen Types in Joint Tissue6,40,41,43–45
Type Distribution
I Bone, ligament, tendon, fibrocartilage, capsule,
synovial lining tissues, skin
II Cartilage, fibrocartilage
III Blood vessels, synovial lining tissues, skin
IV Basement membranes
V Pericellular region of articular cartilage when
present,* bone, blood vessels
VI Nucleus pulposus, articular cartilage, ligament
VII Anchoring fibers of various tissues
VIII Endothelial cells
IX Cartilage matrix*
X Hypertrophic zone cartilage* and calcified cartilage*
XI Cartilage matrix*
XII Tendon, ligament, perichondrium, and articular
surface periosteum
XIII Skin, tendon
XIV Associated with collagen fibers throughout HAC
From Walker JM: Cartilage of human joints and related structures. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 123, Philadelphia, 1996, WB Saunders.
*Small amounts (<20%).
collagen is composed of three polypeptides forming a
triple-helical structure. Fibrils, several thousand molecules
in diameter, are packed in bundles to form large fibers.
HAC also contains fiber-associated type IX (5% to 20%),
type XI, and two types of nonfibrillar collagens: type X,
and short-chained type VI collagen, which is also found
in ligaments. Type X collagen (1% of collagen in HAC)
is principally found in the hypertrophic and calcified car-
tilage and is considered important in the development of
the growth plate.40 Collagen forms about 55 g per 100 g
of HAC’s dry weight, whereas proteoglycans form about
25 g per 100 g dry weight.41 A high degree of cross-linking
stabilizes the tightly wound triple helices that constitute
the fibrillar collagen fibers. This network gives tensile
strength to HAC within the collagen network and resists
the swelling pressure of the proteoglycans, enabling HAC
to withstand compressive loads.
The metabolic turnover of collagen is continuous
through growth to maturity, when the collagen fibers
become more metabolically stable and have half-lives
of weeks or months.41 Collagen turnover increases in
conditions of malnutrition, starvation, Paget’s disease,
hypoparathyroidism, and metastatic diseases of bone.41
The degradation of collagen under these conditions or
diseases provides the body with a source of amino acids.
Researchers hypothesize that, in these conditions, HAC
is more vulnerable and should not be subjected to heavy
loading stresses. It is suspected that mechanical forces, or
degradative enzymes secreted by the chondrocytes them-
selves such as collagenase and other metalloproteinases
including stromelysin, may degrade the “glue” that binds
the collagen fibers into a network and be a contributing
factor in the pathogenesis of osteoarthritis.42
Table 7-2 summarizes the intracellular and extracellu-
lar events in the synthesis of collagen. Collagen maturity
is achieved in the extracellular matrix.
Elastin Fibers
In contrast to the collagen fibers of HAC, fibroblasts
are thought to be responsible for formation of the pro-
tein elastin, of which elastin fibers are chiefly composed.
Elastin fibers are yellowish, tend to branch freely, and are
usually thinner than collagen fibers. They stretch easily,
although they may show some calcification and reduced
elasticity with advancing age.4 Although Buckwalter and
associates demonstrated elastin fibers in human interverte-
bral discs,47 to date, there is still controversy as to whether
elastin fibers are found in HAC. Elastin fibers are found in
the fibrous layer of the perichondrium. Cotta-Pereira and
colleagues used ultrastructural studies to demonstrate the
presence of elaunin and oxytalan fibers in rat HAC, but
not elastin fibers.48 Location of these elastic-related fibers
suggests a modulation of elasticity from the perichon-
drium to HAC and may reflect resistance requirements
of these tissues to mechanical stress. Surrounding soft
 CHAPTER 7 • Cartilage of Human Joints and Related Structures 149

Table 7-2
Multistep Process in Collagen Synthesis
Intracellular Events

• Synthesis of mRNA specific for collagen

• Formation of polyribosomal clusters
• Association of polyribosomal and endoplasmic reticulum
• Formation of an alignment segment of the polypeptide
chains
• Hydroxylation of specific proline and lysine residues
• Glycosylation of selected hydroxylysine residues
• Conversion of procollagen to collagen by procollagen
peptidase and extrusion of tropocollagen into the
extracellular milieu
Extracellular Events

• Formation of peptide-bound aldehydes as specific lysine and

hydroxylysine
• Formation of intramolecular cross-links by an aldol
condensation reaction
• Formation of intermolecular cross-links, peptide-bound
aldehydes, and unmodified amino groups of lysine or Superficial
hydroxylysine residues as Schiff bases lamina
• Aggregation of collagen fibers in the extracellular matrix Middle lamina
to reflect the specific structural characteristics of a given
tissue46
Deep lamina
From Castor CW: Regulation of connective tissue metabolism.
In McCarty DJ, Koopman WJ, editors: Arthritis and allied conditions, Tidemark
ed 12, vol 1, p 246, Philadelphia, Lea and Febiger, 1993.
Calcified
cartilage

tissues (capsule, ligaments, aponeurosis) also blend with

the perichondrium and periosteum. The presence of elas-
tic-like fibers should facilitate stretching at the extremes
of range, recoil on return to neutral range, and enlarge-
ment of the joint space in the effused joint.
The Tissues
The two major subtypes of cartilage in synovial joints—
hyaline cartilage and fibrocartilage—as well as the synovial
lining tissues and the subchondral bone are considered in
the following section.
Hyaline Articular Cartilage
B
Figure 7-2
A, Light microscopy view of the articular cartilage: uc = uncalcified
layer; c = calcified layer; sb = subchondral bone; arrow indicates the
tidemark. (From Walker JM: Cartilage of human joints and related
structures. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic
injuries and rehabilitation, p 124, Philadelphia, 1996, WB Saunders.)
B, Ultrasound backscatter micrograph of porcine articular cartilage
with the use of a 50-MHz transducer: location of various laminae
and the hyperechoic subchondral bone surface. (From Gahunia H:
The nature of the dense connective tissues of the musculoskeletal
system: structure, function, and biomechanics of articular cartilage and
meniscus. In Lundon K: Orthopaedic rehabilitation science: principles
for clinical management of nonmineralized connective tissue, p 76,
Boston, 2003, Butterworth-Heinemann.)

HAC is a specialized type of hyaline cartilage that covers
the joint surfaces, except for those of the sternoclavicular
and temporomandibular joints, which ossify in membrane.
These joints, along with the sacroiliac joint, have at least
one fibrocartilaginous surface.4,49,50 Figure 7-2 shows the
typical two-layered arrangement of HAC. The superfi-
cial layer is uncalcified cartilage, and the deeper calcified
cartilage layer is integrally bound to and merges with the
subchondral bone. The tidemark forms the boundary
between these two layers. Three zones, or laminae, are
distinguished within the uncalcified cartilage: a superficial
(tangential or gliding) zone, a mid or transitional zone, and
a deep or radial zone (Figure 7-3; see Figure 7-2). Each
zone is unique with regard to cell number and distribution,
cell shape, orientation, collagenous fiber arrangement, PG
composition, and concentration and nutrition. Cartilage
is classified for convenience by the type of matrix. Three
varieties are described: hyaline, fibro-, and elastic.4
150 SECTION I • Scientific Foundations
Lamina
splendens
Tangential zone
C
Transitional
zone
L Figure 7-3). A superficial layer called “lamina splendens”
Radial zone
Calcified zone
Figure 7-3
Diagram of the fibrous architecture of human articular cartilage.
The lamina splendens is the very thin layer that covers the articular
surface. Beneath this layer lies the tangential zone. Below that zone
is the transitional zone. The deepest layer of the uncalcified cartilage
is the radial zone. The calcified zone is the basal layer of the articular
cartilage. See the text for further detail on these layers. (From Lane
JM, Weiss C: Current comment: review of articular cartilage collagen
research, Arthritis Rheum 18:558, 1975.)
Tensile strength comes from the collagen network,
which limits the expansion of the viscoelastic aggrecan com-
ponent and provides compressive stiffness. The aggrecan
hyaluronan aggregates bind high amounts of intercellular
water attributed to their fixed negative charges and are in
turn responsible for the elasticity of HAC.
Tidemark
The tidemark is a boundary in a metabolically active zone
between the noncalcified and calcified articular cartilage
(see Figure 7-2).51,52 Noncalcified preparations of human
femoral heads have been shown to have three structural
components to the tidemark: (1) a PAS-positive, pro-
teoglycan-containing tidemark line adjacent to the basal
cartilage; (2) a subliminal light-colored zone; and (3) a
demarcation line to the calcified cartilage.52 In life, there
is calcifying activity in the tidemark region, so that the
tidemark slowly advances in the direction of the noncalci-
fied cartilage.51 Variations in the subchondral bone vol-
ume are thought to influence the tidemark region and
the changes in cartilage that lead to osteoarthrosis.52 The
number of tidemarks increases significantly after age 60.53
This increase relates to the continuous remodeling that
appears to occur with age and to changes that are related
to endocartilaginous ossification affecting the calcified
zone. The latter becomes thinner with age.
HAC Organization
In light microscopy studies, some investigators have
described HAC as having four zones or strata, whereas
others described the two layers (as noted previously) with
three zones or laminae within the uncalcified cartilage (see
has been described on the surface of the superficial layer,
being a layer of fine fibers (4 to 10 mm) that can be peeled
off with forceps and shear types of trauma.54,55 Other
investigators did not distinguish the “lamina splendens”
from the superficial zone, which is thin and exhibits the
largest amount of collagen and the lowest concentration
of PGs.56 Cells in the superficial zone are small ellipsoid
chondrocytes that are oriented with their long axes paral-
lel to the surface.57 In the transitional zone, the cells are
either rounded or oval.57,58 In the radial zone, the cells are
larger and rounded and may be paired in irregular col-
umns numbering four to eight. Variation in descriptions
of the cell shapes in HAC may be related to methods of
tissue preparation and the plane of sectioning. Cell den-
sity decreases from the superficial to the deep layer.59 Cells
in the calcified zone are heavily encrusted with hydroxy-
apatite (crystals of calcium salts) and are surrounded
with calcified matrix in mature cartilage. These cells are
considered to be relatively metabolically inactive.60
While the HAC matrix can be subdivided according
to different cartilaginous zones based on the arrange-
ment of cells and matrix fibrils, the cartilage matrix can
also be divided into compartments depending on its
relationship to the cells. Ultrastructural studies reveal a
thin layer of pericellular matrix immediately surround-
ing the chondrocyte, a unit referred to as a chondron.61
The chondron is considered the microanatomical, micro-
mechanical, and metabolically active functional unit of
HAC.62 Surrounding the pericellular matrix is a wider
layer of lighter-staining interterritorial matrix referred to
as the glycocalyx, which is predominantly type VI col-
lagen63 and enclosed by a collagenous fibrillar capsule.
Adjacent to and outside the interterritorial matrix is the
territorial matrix58 (Figure 7-4), which is defined as the
cell-associated matrix located in between the pericellular
and interterritorial components. The interterritorial matrix
is made up of two basic components: larger-diameter,
more closely packed collagen fibers and an extrafibrillar
matrix, which consists largely of highly sulphated aggre-
can monomers as well as small nonaggregating PGs such
as decorin, biglycan, and fibromodulin. It is also stiffer
because of a high concentration of keratan sulfate.64 The
KS concentration may enable the interterritorial matrix
to better resist compressive deformation.58 Abnormal KS
concentration (decreased with immobilization, increased
 CHAPTER 7 • Cartilage of Human Joints and Related Structures 151

stresses, providing a tight framework to contain matrix

Articular surface components and, in the deep layers, giving a tight bond-
Superficial ing to subchondral bone. Thicker fibers may be more
zone stable with a slow rate of turnover.
Pericellular
region
The closely packed fibrils in the superficial zone make a
Middle less permeable layer than is present in the underlying zones
zone and that this may function as a “skin” for the hydrated
cartilage.61 The calcified layer possesses antiangiogenic
Territorial molecules, which appear to confer an ability to inhibit the
region vascular invasion that would bring about ossification, similar
to that in the growth plate.72 Thus, calcified cartilage can
Interterritorial persist and be a buffer zone between the uncalcified articu-
Deep region lar cartilage and subchondral bone.6 Figure 7-5 shows the
zone

Tide mark
Calcified
zone Hypertrophic
chondrocyte
Subchondral
bone

Figure 7-4
Regional organization of articular cartilage based on studies in
adult cattle and humans. The pericellular region contains a high
concentration of aggrecan, the proteoglycan decorin, and type VI
collagen. The superficial zone contains thin collagen fibrils arranged
parallel with the articular surfaces. The partially calcified cartilage of the
calcified zone is indicated. The interterritorial zone is first recognizable
at about 17 years of age in humans, based on changes in distribution
of aggrecan and link protein. (From Poole AR: Cartilage in health and
disease. In McCarty DJ, Koopman WJ, editors: Arthritis and allied
conditions, ed 12, vol 1, p 282, Philadelphia, 1993, Lea & Febiger.)

with aging) may contribute to cartilage pathology, because

changes in matrix stiffness impact load bearing and dissi-
pation of forces through cartilage.
The superficial zone of the uncalcified cartilage has
been described as fibrillar,65 hyaline like,66 and membrane
like;67 as a dense, unfibrillated layer;68 as a random
fibrillated layer;69 and as a biomechanical protecting
membrane.70 There is agreement that the bundles of
fibers in the superficial zone lie in layers parallel to the
joint cavity (see Figure 7-3). In the transitional zone, the
fibers are more randomly dispersed. Fibers in the super-
ficial zone have a diameter of about 35 nm; the fibers in
the transitional zone are slightly bigger (about 60 nm).
In the radial zone, the fibers have an arcade-type pat- Figure 7-5
A, Normal smooth cartilage surface covering the femoral condyles
tern, with radial rows in the deepest regions. These fibers of the rhesus macaque. (From Gahunia H: The nature of the dense
are coarser, about 80 nm in diameter.70 The fibers in the connective tissues of the musculoskeletal system: structure, function,
calcified zone are greater than 100 nm in diameter and are and biomechanics of articular cartilage and meniscus. In Lundon K:
oriented perpendicular to the surface.55 The collagen fiber Orthopaedic rehabilitation science: principles for clinical management
pattern in the deeper zones is similar to that described by of nonmineralized connective tissue, p 72, Boston, 2003, Butterworth-
Heinemann.) B, Normal adult rabbit articular cartilage showing
Benninghoff.71 The implications of the variation in fiber numerous pits on the surface (× 400). (From Ghadially FN, Oryschak
size are not fully known. Size appears to be related to AF, Yong NK: Experimental production of ridges on rabbit articular
structural stability and the ability to withstand horizontal cartilage: a scanning electron microscope study, J Anat 121:121, 1976.)
152 SECTION I • Scientific Foundations
gross and ultrastructural features of articular cartilage as it
covers the femoral condylar regions.
Subchondral Bone
The role of the subchondral bone in the pathogenesis
of cartilage damage and progression of osteoarthritis
is still debated but has likely been previously underes-
timated. Research now clearly recognizes that cartilage,
subchondral bone, and underlying cancellous bone work
in functional biomechanical unity.73 The importance of
the interrelationship between the subchondral bone and
HAC becomes evident based on the results of several
studies74–76 of the pathogenesis of osteoarthritis, leaving
in question whether changes in this area occur prior to
cartilage deterioration or subsequent to these changes.77
Furthermore, the importance of the subchondral bone
to the health of the articular cartilage is clear when one
considers that more than 50% of the glucose, oxygen,
and water requirements of cartilage are acquired via ter-
minal subchondral blood vessels, which have, in part,
direct contact with the deepest HAC layer.78 Some stud-
ies support the theory that subchondral bone changes
are not etiological for osteoarthritis but are perhaps sec-
ondary to the loss of HAC that precedes subchondral
sclerosis characteristic of this condition.79 Other research
supports the idea that changes in the relative density and
architecture of the underlying subchondral bone may
have a profound effect on both the initiation and pro-
gression of cartilage damage.73 Compositional analysis of
the mineralized plate beneath the articular cartilage in
nonhuman primates with osteoarthritis identified thick-
ened overmineralized calcified cartilage or subchondral
bone, possibly by a process of reactivated endochondral
ossification, which may lead to a cycle of added mechani-
cal stress on the joint and further the progression of
osteoarthritis.80
Aging Changes of HAC
Gross changes in HAC with aging include increased con-
gruity of the articular surfaces and a variable fibrillation
or fraying of the surfaces. Goodfellow and Bullough81
related the latter more to joint type (multiaxial or uni-
axial) and to underlying bone and joint mechanics where
there is an increased load on formerly unloaded carti-
lage82 than to aging. The appearance of HAC changes
from a transparent bluish to an opaque yellow. The func-
tional significance of the pigment change is not known.
With light microscopy and histochemical staining,
a number of changes have been revealed in HAC, such
as an increased grainy or fibrillar appearance, thought to
be caused by the unmasking of collagen fibers. Fatigue
of collagen bundles with depletion of surface GAGs also
may contribute to splitting and fraying of the superficial
layers.83 The number of tidemarks increases,53 and the
overall thickness decreases,84 confirmed by MRI studies.85
With advancing age, there may be an imbalance between
the extension of the calcified zone into the noncalcified
area of the HAC and replacement of new bone through
endochondral ossification at the bone-cartilage junc-
tion.86 These changes make articular cartilage susceptible
to ossification and eventual osteoclastic resorption. Knets
commented that the “intensity of this process decreased
with age,”70 which is fortunate, since these changes not
only impair normal load bearing but also may contribute
to the development of osteoarthritis.
Intercellular components may display more aging
changes.87 Although the total content of collagen may
not change,88 older collagen remains in the extended
state longer than younger collagen as it loses its ability
to return to the resting state. Verzar demonstrated an
increased formation of cross-bridges, which give altered
solubility to collagen.89 The increased cross-bridges
involve both inter- and intramolecular cross-linking90 and
result in increased stiffness. With thicker and less resil-
ient collagen fibers, and the calcification in the deeper
zones, load-bearing properties of cartilage are affected.
Theoretically, there is impairment of the chondrocytes’
nutrition, which contributes to further deterioration.
With histochemistry, the loss of proteoglycans is
demonstrated with a decrease in the articular cartilage’s
reaction to alcian blue staining and an increased reaction
to Schiff reagent.49 Several studies of aging have reported
a decrease in GAGs,91,92 a decrease in CS-4, an increase in
CS-6, and an increase in the small molecular KS. However,
there is variability in the reports as to whether these com-
ponents—as well as cell frequencies, lipids,93 and water
content—actually increase or decrease.59,84,94–97 Livne
and associates demonstrated in mice that the number of
cells decreased and that the interstitial growth was very
limited.98 The synthetic ability of chondrocytes decreases,
as well as their responsiveness to anabolic growth factors.83
The size and aggregation of matrix aggrecan decrease, and
fewer functional link proteins are synthesized. Ziv and
coworkers demonstrated in aging human facet cartilage
that there was a high hydration,99 which increased from
the fourth decade and was indicative of collagen damage
and cartilage degeneration.
The impact of these changes, indicating imbalance
between synthesis and degradation of matrix compo-
nents, is a decreased ability of cartilage to withstand shear
forces and impulsive loading, and increased susceptibil-
ity to trauma. Cartilage is both softer and, in its deeper
layers, stiffer; microfractures of subchondral bone may
occur because of the reduced dispersion of loads.
Although some investigators consider degenerative
changes to typify the aging process,98 it should be noted
that it is difficult to distinguish among natural aging
changes, functional adaptive changes, and degenerative
changes that result from micro- or macrotrauma or dis-
ease.96 Magnetic resonance imaging (MRI) has made it
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
possible to accurately and precisely measure HAC volume
and thickness, and the development of semiautomatic
techniques will enable large-scale studies.100 Laasanen
and associates have shown that acoustic parameters from
ultrasound measurements can be used to analyze the
mechanical properties of HAC.101 A quantitative electri-
cal impedance device has been used in vitro to map focal
lesions of the HAC.102 These new techniques will enable
clinicians to assess disease progression and may clarify the
interface between aging changes and disease affecting
articular cartilage.
Fibrocartilage
Intra-Articular Discs, Menisci, and Labra
Intra-articular discs, menisci, and labra are found in certain
joints in all species. In humans, these may take the form
of the complete disc that subdivides the cavity into two
separate compartments, as in the temporomandibular and
sternoclavicular joints, or they may be incomplete struc-
tures, such as the menisci in the knee. These structures
increase the congruity of the articulating surfaces. They
may assist in joint lubrication and protect the edges of the
joints; in the knee joint, menisci function as shock absorb-
ers103 and bear loads.104 Whereas articular discs tend to be
overall circular structures, possibly with a central perfora-
tion,105 the menisci are semilunar or C-shaped structures
with an inferior flat surface and a superior concave surface.
The degree of fixation of articular discs and menisci varies
between species and joints (see Van Sickle and Kincaid106
for a comparative arthrology review).
Function of Intra-Articular Fibrocartilage (Disc [e.g.,
Temporomandibular, Sternoclavicular], Meniscus,
Labrum)
● Increases joint congruity
● Assists joint lubrication
● Protects edges of joint
● Acts as shock absorbers
● Acts as load bearers (transmit loads)
Similar to the intervertebral disc, the meniscus is
a complex structure that consists of several “zones”
related to the distance from the attachment to the joint
capsule, with cells displaying significantly different phe-
notypes ranging from a more chondrocytic phenotype in
the inner region to a more fibroblastic one in the outer
region. Although menisci, labra, and articular discs are
often termed “fibrocartilages,” many have little or no
fibrocartilage present but are principally composed of
153
collagenous connective tissue.106 Specifically, in the highly
loaded, avascular inner region of the wedge-shaped
meniscus the phenotype of the tissue is fibrocartilage-like
and in the peripheral, vascularized region of the meniscus
where the meniscus connects to the internal surface of
the joint capsule, the cells and matrix have a fibrous phe-
notype.107 The histological appearance of these structures
is a dominance of circumferential collagenous fibers.
Poole defined fibrocartilage as being “characterized
by the presence of chondrocytic cells that synthesize
and secrete type I rather than type II collagen.”6 On
gross and light microscopic examination, the matrix of
HAC appears translucent, homogeneous, and apparently
structureless. White fibrocartilage, however, is character-
ized by collagen fibers arranged in abundant bundles of
dense, white, fibrous tissue.4 Scattered groups of cells
with ovoid-shaped nuclei lie between the fiber bundles.
The amount of visible matrix varies considerably between
different structures and with age. Detail of the so-called
fibrocartilaginous structures follows.
“Fibrocartilaginous” structures exhibit both territo-
rial (former “lacunae” zone around the cells) and inter-
territorial (general) matrix. The latter is composed of
sheets of collagen fibrils and fibers in a sparse interfibril-
lary matrix. Some radial and oblique fibers are seen, and
these are thought to bind the dominant circumferential
fibers. The primary circumferential orientation of the
meniscal collagenous fibers may function to counteract
the tensile forces to which the meniscus is exposed.108
Both meniscal and articular discs have tensile strength
that is similar to that of HAC.108 In comparison with
HAC, the collagen is predominantly type I (2α1, 1α2),
which forms some 60% to 90% of organic solids in
the menisci with variable amounts of collagen II, III,
V, and VI.57,109 Water composes some 70% to 78% of
menisci, and proteoglycans are less than 10% of the dry
weight and are mainly chondroitin sulfates and derma-
tan sulfate, with very little keratan sulphate and traces
of heparin sulphate (HS) and hyaluronic acid (HA).57
Differences between the structure and composition of
discs and cartilage probably reflect the primary functions
to resist tensile stresses and act as efficient shock absorb-
ers. Variation in fiber thickness and orientation allows
these structures to respond to a wide range of vibrations
created by compressive forces.
Articular discs and menisci are largely aneural and
devoid of lymphatics, but they do have a vascular sup-
ply, which tends to be rich at the periphery where
there is a bony attachment. Although the inner por-
tion of menisci is avascular, vessels may penetrate the
distal one third.106,110,111 Nerves appear to be associated
in the meniscus only with the vessels at the periphery.65
Proinflammatory cytokines can modulate the response of
meniscal cells to mechanical signals, suggesting that both
biomechanical and inflammatory factors could contribute
154 SECTION I • Scientific Foundations
to the progression of joint disease in response to altered
loading of the meniscus.112
Labra, which Van Sickle and Kincaid termed “marginal
fibrocartilages,”106 are located in the glenohumeral and
hip joints. These structures deepen the socket and assist
in joint lubrication, and they may protect the joint edges.
In the developing hip, the histological structure resem-
bles that of a ligament with no apparent matrix. Labra are
covered on both surfaces by synovial lining tissues.4 In
contrast, the load-bearing surfaces of the menisci are not
covered with synovial lining tissues. A vascular synovial
fringe, however, is adherent to the surfaces and extends
1 to 3 mm over the superior and inferior margins.113
Mikic showed in human radioulnar discs that central
perforations increased with age.114 The discs between
the sternum and first costal cartilage and between the
manubrium and the sternal body (manubriosternum
joint [MSJ]) have been observed to ossify with age. The
central portion of the MSJ disc in some 30% of people
may be absorbed, converting the symphysis into more
of a synovial-type joint.4 A similar change may occur in
the symphysis pubis, where the fibrocartilaginous disc is
covered with a hyaline cartilage layer and is firmly united
to the bone. A cavity is not seen before the 10th year, and
it is not lined by synovial lining tissues.4
The thickness of articular discs varies among joints
and is related to the joint contour. For example, the disc
of the temporomandibular joint is thickest near the cen-
ter, where it lies in the deepest part of the mandibu-
lar fossa.4 In contrast, both labra and knee menisci are
thicker on the periphery. Tears usually occur in the inner
avascular part of the meniscus and consequently do not
heal spontaneously.107 Larger, more complex tears show
limited potential for repair. Removal of the meniscus is
now broadly accepted as leading to severe joint degen-
eration,115 and the current aim is to preserve as much of
the tissue as possible (e.g., partial meniscectomy). Partial
regeneration occurs from the vascular fibroareolar tissue
around the meniscal periphery and is thought to be of
a fibrous variety. The periphery is probably chondro-
cytic “in origin and type.”57 After injury, the vascular
periphery permits healing within this zone, which is
similar to that of other tissues and involves formation of
a fibrin clot. Fibrous scar tissue forms within 10 weeks,
but modulation into fibrocartilage-like tissue may take
several months.113,116,117 These time periods for regenera-
tion of tissues should be considered in planning reha-
bilitation programs and return to participation in serious
training and sports activities (see also Repair of Articular
Cartilage, presented later in this chapter). Meniscal
allograft transplantation118 and tissue engineering—a
combination of cells, growth factors, and scaffolds—is
one approach that aims to regenerate meniscal lesions
or to potentially replace the degenerated part of the
meniscus.107
Intervertebral Discs (IVDs)
With the exception of the first two cervical levels, the
opposing surfaces of free vertebra are separated by inter-
vertebral discs, which form between one fifth and one
third of the total length of the spine. Intervertebral discs,
often described as fibrocartilaginous structures4 that are
part of a trijoint complex (intervertebral disc and physi-
cal [facet] joints), are composed of an inner nucleus
pulposus (NP), an outer anulus fibrosus (AF) and the
vertebral end plate, a cartilaginous layer, which covers
the superior and inferior surfaces of the IVD proper. The
IVD is the largest avascular structure in the body, and
it relies on diffusion across the vertebral end plate for
its nutritional supply.119 Discs occupy a greater propor-
tion of the length of the cervical and lumbar regions
in comparison with the thoracic region; thus, they con-
fer greater motion to the cervical and lumbar regions.
The intervertebral discs are firmly attached by connec-
tions with the anterior and posterior longitudinal liga-
ments and, in the thoracic region, by the intra-articular
ligaments. The shape dimensions of the discs reflect the
region in which they are situated.
Discs are thicker in the cervical and lumbar regions
than in the thoracic region and contribute to the con-
vex forward alignment of those regions; they are thinnest
in the upper thoracic region and thickest in the lumbar
region.4 For further details, refer to Holm and Urban,120
Happey,121 and Lundon and Bolton.122 The functions of
the disc are to transmit loads through the vertebral col-
umn, act as impact or shock absorbers, sustain shearing
forces, and resist wear. The AF, in particular, absorbs nat-
ural forces by resisting and modifying pressures through
the stretching of its collagenous framework.
Anulus Fibrosus (AF)
The AF is the outer laminated layer that contains the
inner NP. It consists of a series of concentric laminae that
are visible to the naked eye in horizontal sections. The
outer zone is chiefly collagenous fibers (mainly type I),
and the wider inner zone is fibrocartilaginous; there are
also minor amounts of collagen types III, V, IX, X,123
XI, XII, and XIV.124 Laminar bundles form collars within
which most of the collagen fibers lie in parallel. Laminae
are convex from superior to inferior and pass obliquely
between two adjacent vertebrae, subscribing an angle
of between 40 and 70 degrees with the vertebrae.121,125
Strong fibrous bands connect the concentric laminae.
Between the contiguous bundles, fibers lie at obtuse
angles and pass in different directions.4,125 Electron
microscopy studies have revealed the highly specialized
organization of these collagenous fibers.125 There are 15
to 20 concentric laminae in the parallel bundles that aver-
age 10 to 50 µm in size. Each bundle has fine fibrils that
vary between 0.1 and 0.2 mm in diameter. Laminae can
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
vary between 200 and 400 mm in width, with the outer
laminae being the thickest. In comparison, the collag-
enous fibers in the inner NP are finer (20 to 50 mm in
diameter) and have a loose, irregular network.125 The AF
is anchored firmly to the cartilaginous end plates, with
the fibers in the medial half anchored more deeply than
those in the lateral half.126 Up to 10% of fibers in the AF
of human lumbar discs are of the elastic variety.127
Nucleus Pulposus (NP)
The NP is encased by the AP. It is demarcated by a tran-
sitional zone and lies slightly more posteriorly within the
disc. This structure demonstrates significant developmen-
tal and aging changes. The young nucleus is described
as being semifluid, soft, and gelatinous. It consists of
mucoid material with a few notochordal cells present; the
latter disappear by the end of the first decade.4 Gradually,
the mucoid material is replaced by fibrocartilage, which
appears to be derived from the cells in the AF or the con-
tiguous vertebral end plates. The NP is united to the AF
by fibers that connect to the AF inner zone; this transi-
tion zone is gradual. Compared with articular cartilage,
the NP is soft, more compressible and deformable, and
capable of considerable changes in its volume and shape
with spinal motion. Aging changes, possibly as early as
the fourth decade, gradually reduce this capacity. The
consequence of these changes is decreased dissipation of
forces from the nucleus to the AF, thereby concentrat-
ing forces transmitted to the vertebrae, with potential for
microfractures of vertebral trabeculae.
With the exception of the inner NP, the cell ele-
ments of the disc and vertebral end plates are formed
from embryonic mesoderm in early prenatal life, and
the central portion of the NP is derived from the
notochord. As in articular cartilage, the disc matrix is
155
produced and maintained by cells of the disc, which
are either chondrocytes or chondrocyte-like cells. They
are rounded in the NP and more elongated in the AF.
Hence, there is a predominance of type II collagen in
the NP. The discs are relatively acellular, with similar
cell density between human AF and NP (4.3 cells/mm2
in NP; 5.0 in AF).128 Investigators have reported that in
both humans and animals, the young anulus does not
contain cartilage cells; only fibroblasts are observed.129,130
Chondroid-like cells, however, are frequently seen in
the older AF.
Vertebral End Plate
The vertebral end plate (Figure 7-6) is an integral part
of the disc’s structure and contributes to disc function in
that it is important in the metabolism of the otherwise
avascular IVD in adults.131,132 The cartilaginous end plate
serves as an anchor for the finer NP fibers and the coarser
AF fibers.
Disc Composition
Water constitutes about 90% of the total disc content.
Although water content decreases with age, it still remains
high.120 The AF is about 60% to 70% water, whereas the
NP is between 90% and 70% water (from younger to
older). The collagen content is higher in the AF, being
50% to 55% dry weight; in the NP, it is between 20%
and 30% dry weight.133,134 The collagen in the AF is pre-
dominantly type I; that in the NP is almost all type II.
The proportion of type I collagen fibers decreases from
the outer part of the AF, and the proportion of type II
increases toward the center of the NP. The vertebral
end plate contains interstitial collagens types II and IX
but never type I, regardless of degenerative changes.123
Collagen and proteoglycans are the major structural
Figure 7-6
Schematic diagram of the
nutritional routes into the
intervertebral disc and an
enlarged view of the area
underneath the hyaline cartilage.
(From Holm S, Maroudas A,
Urban JPG et al: Nutrition of the
individual disc: solute transport
and metabolism, Connect Tissue
Res 8:117, 1981.)
156 SECTION I • Scientific Foundations
macromolecules in the disc. There are some minor
amounts of other glycoproteins, elastin, and some serum
proteins.134 The major GAGs (part of proteoglycans) are
CS and KS. Compared with HAC, proteoglycans of the
disc are smaller and richer in KS.134 With aging or degen-
eration, there is a greater loss of the small proteoglycans,
so that the larger ones remain. In the intracellular matrix,
collagen content is higher in the outer anulus, and it
decreases inward to the nucleus, whereas the values for
proteoglycans are the reverse.134
Nutrition
The level of hydration confers the mechanical proper-
ties to the disc, and changes in the fluid content affect
these properties. The creep or loss of disc height (1
to 2 cm between morning and night) relates to fluid
loss.135 Changes in the microcirculation affect fluid
flow patterns in the disc and its nutrition.134 Since
the cellularity of the disc is low, much of the water is
interfibrillar and freely exchangeable. Proteoglycans
maintain disc hydration by controlling osmotic pres-
sure and the resistance of the tissue to fluid loss. The
proteoglycan concentration in the collagen network
determines the pore size of the matrix and thus the rate
of fluid flow. Because of the avascularity of the disc,
nutrients are derived by transport of solutes through
the disc from the surrounding blood vessels, including,
for the nucleus, vessels close to the central portion of
the vertebral end plate.
The main mechanism for metabolite transport is dif-
fusion, and the main route for supply of nutrients into
the nucleus is via the end plate (see Figure 7-6).131,132,136
Holm and associates demonstrated that the periphery of
the vertebral end plate is practically impermeable.136 In
the region of the NP, however, numerous blood vessels
are in contact with the bony end plate and may be the
sole source through which the NP is nourished. Only
a small amount of glucose is predicted to be supplied
by convection transport, as most solutes are transported
by diffusion. Diffusion distances in humans can be large,
and for about 16 hours of the day while the individual is
upright, the overall direction of fluid flow is outward.120
Oxygen retention is consistent through the AF but is
much higher in the central portion of the NP.136 This
finding supports the theory of impermeability of the
outer end plate and implies that the AF must derive its
nutrition almost solely from the surrounding vasculature
and not through the vertebral end plate.
Innervation
In a disc, only the outer third of the AF is innervated.137
Bogduk and colleagues found that nerves penetrated up
to one third of the total thickness of the AF of lumbar
discs.138 Most of these nerves were remote from blood
vessels; were of large diameter; and were derived from
the lumbar sinuvertebral nerves, the ventral primary
rami, and the gray rami communicans to innervate the
posterior, posterolateral, and lateral aspects of the discs.
Although most investigators have reported finding only
free nerve endings,139–142 Malinsky described the presence
of both encapsulated and nonencapsulated nerve endings
on the lateral surface of the AF.143
Age Changes
With aging, the NP is less distinguished from the anulus.
It becomes amorphous—a firm fibrous plate demon-
strating decreased elasticity and water-binding ability.
A progressive degeneration of the laminae in the AF
from middle age onward,129 as well as in the inner fibers
in particular, has been observed.144 Chondroid mate-
rial may be deposited, and the collagen fibers became
frayed and split and decreased in number. In the anuli of
persons more than 70 years old, few laminae remained
intact and discernible129 and the boundary between the
AF and NP ultimately becomes indistinguishable.145
The fibers of the inner AF expand at the expense of the
NP, while the size of the outer anulus remains approxi-
mately unchanged.144 Clefts and fissures are visible after
the third decade.120 Additionally, with aging, vertebral
cartilage end plates become calcified, which leads to
resorption and replacement by bone.129,146 There is also
an apparent weakening of the anchoring of the AF to the
bony end plate, since the collagenous fibers are embed-
ded only superficially into the end plate.129 Lesions asso-
ciated with age changes in the AF have been thought to
predispose the individual to disc protrusions as a result
of rim or peripheral,147 circumferential,145 and radial147
tears. Aging changes are largely detrimental to the inter-
vertebral disc’s function, suggesting that heavy-impact
loading and the abrupt application of torques should be
reduced as an individual ages.
Fibrous Capsule
The joint cavity is lined by synovial tissues that cover all
but the articulating surfaces of the joint and the contact
surfaces of any intra-articular structure, such as menisci.
Synovial tissues are intimately bound externally with the
fibrous capsule, which is mostly type I collagen (2α1,
1α2).57 This type I collagen is similar but not identical
to that in the dermis. It is hyperhydrated, with a water
content estimated at about 70%. There is variability in
the thickness and attachment of the capsule.4 It may be
thin and redundant, as in the shoulder joint, or thick and
dense, as in the hip and the knee. Fiber diameter varies
between 150 and 1500 nm, and fibers are organized in
chiefly parallel bundles. Articular ligaments reinforce and
may form the majority of the capsule. It is unique com-
pared with other connective tissues involved in human
articulations.
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
The extent of redundancy in the fibrous capsule, or
lack thereof, has important consequences to the mobility
of the joint (compare that of the hip and glenohumeral
joints). Following injury, the unique characteristics of the
specific joint must be restored. An inflamed capsule has
a high potential for adhesion formation between redun-
dant folds, indicating a need for early mobilization to
prevent this occurrence.
It should be remembered that joint pathology and
trauma invariably involve inflammation of synovial lining
tissues. The fibroplasia phase may convert the prolifera-
tive fibro-fatty connective tissue formed in inflamma-
tion into adhesions, which, particularly when the part is
immobilized, mature into strong scars. In small joints,
where soft tissues are in close proximity, and in joints
such as the shoulder, where redundant capsular folds
may be present, this process can have profound effects
on mobility and function.
When a joint is deprived of mechanical stimuli, there
is decreased concentration of GAG content and water.148
The loss of the gel structure compromises connective
tissue. Fiber-fiber distances and the lubrication between
fibers that facilitates normal gliding decrease, and adhe-
sion formation and cross-linking between fibers are
enhanced. The collagen arrangement is more random;
fibers may be thicker as new fibers are laid down without
regard to mechanical requirements. It is vital to control
the inflammatory process and to guide the fibroblastic
(proliferative) phases of healing with appropriate mobi-
lization. Therapy should limit further aggravation until
this is achieved, but there is considerable evidence that
early motion should be encouraged. Continuous or
intermittent passive motion, although less commonly
used today, has been demonstrated to be effective in the
maintenance of mobility and the restoration of more
normal tissue structure and function.149,150
Innervation
Articular cartilage is aneural; however, chondrocytes
detect and respond to mechanical stress. Our knowledge
of the mechanoreceptor mechanism in HAC is slowly
growing.83,151,152 Researchers have demonstrated that
mechanical loading is needed to maintain the cell cyto-
skeleton and may have a protective anabolic response via
the cell to influence HAC structure.153,154 How mechani-
cal stress is transformed into a chemical response is still
unclear. Each chondrocyte has at least one nonmotile
monocilia that may have a mechanotransduction func-
tion,5 or the many cell processes that have connec-
tions with the collagen framework may be involved.7
Alternatively, mechanical stress may provide a pressure
wave that perturbs the cell membrane.155 Lammi consid-
ers the integen-interleukin-4 route the best investigated
mechanotransduction pathway activated in chondrocytes
157
by loading.156 Also involved is substance P, which is asso-
ciated with glutamate, an excitatory transmitter in both
the CNS and PNS,154 and a series of events that in normal
HAC influence synthesis of mRNA.
Although HAC is aneural, joint connective tissues
(ligament, capsule, etc.) are well innervated with myelin-
ated and unmyelinated fibers. Most nerve endings are
located in the fibrous portion of the capsule and not in
the synovial lining tissues, except for those accompany-
ing vessels.139,157–159 Mapp has shown that the synovium is
richly innervated by fine, unmyelinated fibers that lack spe-
cialized endings, are slow conducting, and may transmit
diffuse pain sensation.160 Sympathetic nerve fibers accom-
pany blood vessels and contain and release classic neu-
rotransmitters, such as Substance P. There is variability in
location within and between joints and among species.139
Refer to review papers on arthokinetic reflexes.161–164
Synovial Lining Tissues
The synovial lining tissue (synovium) is the soft con-
nective tissue that borders the joint cavity and covers all
intra-articular structures except for the central load-bear-
ing portions of menisci and articular cartilage. Synovial
intima is the layer of lining cells that is in contact with
the joint cavity. Beneath the intima is a supporting layer
of sparsely cellular subintimal tissue that merges on its
external surface with the fibrous capsule of the joint or
the fibrous outer coating of the tendon sheath or bursa.
Synovium is a type of mesothelium that is derived from
the original skeletoblastoma.165
Synovial lining tissues have been described in a num-
ber of articles.166–168 The synovial intima layer consists of a
layer of cells 1 to 3 deep and set in a matrix (Figure 7-7).
Since this is not a continuous layer, both the synoviocytes
and the matrix can come in contact with the joint fluid.
Between the cells in the intimal layer, there are collagen
fibers and some electron-dense, amorphous material that
includes hyaluronate. Because a clearly defined basement
membrane is lacking, the term synovial membrane is inap-
propriate.169,170 Cell processes—thin branching filaments—
appear to provide a supportive membrane for the cells.
Functions of the Synovial Lining Tissues168,170,171
● Maintain an intact nonadherent tissue surface
● Synthesize biological lubricants and lubricate articular cartilage
● Control synovial fluid volume and composition
● Supply nutrition to chondrocytes within joints
● Remove metabolic waste
● Contribute to joint stability and health
● Assist in regulation of intra-articular temperature
● May have an antimicrobial effect
158 SECTION I • Scientific Foundations

Joint cavity

Blood Synovial
capillary intima
zPc

Subintimal
tissue
Lymphatic
capillary

Compliant
Mast extra synovial
cell Macrophage sink

Fibroblast
Figure 7-8
Diagram showing pathways for fluid exchange across the synovium.
Adipocyte (From Levick JR: Synovial fluid dynamics. In Maroudes A, Holborow
GJ, editors: Studies in joint disease, vol 2, p 165, London, 1983,
Pitman.)

Figure 7-7
Normal synovium. The intimal layer consists of types A and B cells.
The subintimal layer shows the vascular structures and various cell
types seen normally. The arrow indicates the path taken by synovial
fluid as it filters through the subintimal capillary and extracellular
matrix on its way to the interior of the joint. (From Rodosky MW, Fu
FH: Induction of synovial inflammation by matrix molecules, implant
particles and chemical agents. In Leadbetter WB, Buckwalter JA,
Gordon SL, editors: Sports-induced inflammation, p 359, Park Ridge,
Ill, 1990, American Academy of Orthopaedic Surgeons.)

The subsynovial layer is a vascular connective tissue

framework composed of fibrous, areolar, and fatty tis-
sues (the predominance of these tissues varies by site and
within the joint), with some elements of the endothelial
and lymphatic systems.172 Where fibrous tissue predomi-
nates, there is little difference between the amount of
collagen fibers in the intima and that in the subsynovial
tissues. In fatty or areolar varieties, however, few collagen
fibers are seen in the intima.170,171 Reticular fibers may be
seen between the lining cells, and elastin fibers are found
in the deep layer associated with capillaries. Synovial lin-
ing tissues are endowed with a rich plexus of blood ves-
sels and lymphatics in the subsynovial layer responsible
for the transfer of nutrients into the joint cavity and the
formation of synovial fluid (Figure 7-8).
Intimal capillaries are fenestrated (contain small pores cov-
ered with a thin membrane), which facilitates movement of
water and solutes into the tissues (Figure 7-9).172 Vascularity
varies both between joints and within a joint.173,174 Capillary
density is low in fibrous subsynovial tissues and greatest
where these tissues are areolar or adipose.175 Whereas capil- Figure 7-9
laries reach the intimal surface, blood sacs from the deeper Synovial membrane of rabbit showing a large capillary (C) lying under
a type A (A) synovial cell. An endothelial cell nucleus (N) is seen on
lymphatic plexuses penetrate the intima but do not reach
the deep aspect of the capillary. Fenestra (arrowheads) are evident in
the surface. Arteriovenous anastomoses are present and the endothelial lining. Joint space (J) (× 28,000). (From Ghadially
may play an important role in articular blood flow, as well FN: Fine structure of joints. In Sokoloff L, editor: The joints and
as functioning in regional hemodynamic regulation.175 synovial fluid, p 148, London, 1978, Academic Press.)
 CHAPTER 7 • Cartilage of Human Joints and Related Structures 159

Although there are no free nerve endings in the
subsynovial tissues, there are many autonomic fibers in the
adventitia of blood vessels. Pacinian corpuscles are pres-
ent at the border of the capsule and the synovial lining tis-
sues.176 Although the precise way in which pain is sensed
from synovial lining tissues has not yet been elucidated,
the surrounding tissues that are affected in synovitis are
well innervated by pain fibers.177 The sensation of pain
may be derived from pressure transmitted by the myelin-
ated and nonmyelinated C fibers and free nerve endings
close to blood vessels within the subsynovial fluid.177,178
Joints exist to provide motion within the constraints
of the surrounding soft tissues. The synovial lining must
adapt to a wide range of positions without being pinched.
An effective lubrication system is vital. The synovial lining
must be able to expand and contract with joint motion,
a process of folding, unfolding, and elastic stretching of
the tissue.
Synovial Lining Cells
Synovial lining cells (SLCs), also known as synoviocytes,
form the intimal layer. Morphologically, two types can
be distinguished, A and B. Transitional cells (type C
or AB) are quite common and may be A and B cells in
transition. Macrophage-derived type A cells have promi-
nent Gogli complexes, many vacuoles, vesicles, filopo-
dia, and mitochondria. Fibroblast-derived type B cells
have prominent nucleoli, few vacuoles, and long cyto-
plasmic processes.170,179 This initial classification based
on morphology is now considered of limited value since
cytochemistry is now the tool for cell identification.168
Herein, SLCs will be referred to according to their main
function, as macrophages or as fibroblasts.
Research suggests that synovial intimal macrophages
(SIMs) are true macrophages derived from bone mar-
row via circulating monocytes but initial fibroblasts (SIF)
are locally derived from mesenchymal cells.179 Fibroblast-
like cells (SIF) express a vascular cell adhesion molecule
(VCAM-1), a complement decaying factor (DAF),
and enzymes of hyaluronan synthesis.179 SIF cells have
abundant rough endoplastic reticulum and are prob-
ably responsible for protein and polypeptide secretion
into the joint fluid, as well as secreting enzymes capable
of degrading HAC.168,177 These cells may be primarily
involved in the synthesis and secretion of substances that
can degrade cartilage: neutrophils, neutral proteinases,
collagenase, gelatin, and stromelysin.180
Intimal macrophage-like cells (SIMs) are, in healthy
conditions, in the minority. These cells release cytokines,
such as interleukin-1 and prostaglandin E2. Cytokines play
a major role in perpetuation of synovitis.181 Interleukin-1
is an inflammatory mediator that provokes chondrocytes
to decrease matrix synthesis and to resorb their surround-
ing matrix. SIM cells also influence the immune response
by expressing high levels of the immunoglobin receptor
Fc(Rilla) and play a role in regulation of leukocyte
movement into the tissues.168
With the demonstration that SIF cells express enzymes
of hyaluronan synthesis,179 it seems apparent that both
cell types are involved in synthesis of hyaluronan that
critically functions in the fluid-film lubricating model and
contributes the visco-elasticity of synovial fluid. SIF cells
seem responsible for synthesis of a surface-active phos-
pholipid lubricating factor (initially termed lubricin)182
and secrete this into the joint cavity.183 SAPF appears to
be the lubricant functioning in the boundary lubrication
model. Macrophage cells remove debris, such as artificial
ligament wear fragments or gold deposits, and thus clear
the joint cavity.177
Synovial Fluid
Synovial fluid (SF) has a concentration of electrolytes and
small molecules roughly the same as that of plasma.184
However, it is not a dialysate of blood plasma, since syno-
vial fluid contains molecules filtered through from plasma
and synoviocytes secrete various substances into SF, such
as hyaluronate, a glycoprotein. It is important to realize
that there are only small amounts (a few drops) of free
fluid in human joints and only a thin film of fluid cov-
ers the articulating structures within the joint. There are
still no good methods to measure SF volume in healthy
human joints, and values are reported only for the knee
(0.5 to 4 mL).185 Larger volumes than those found in
the knee are reported in the shoulder or ankle, depend-
ing on the species studied. The joint cavity is a potential
space, not a real space, as is often depicted diagrammati-
cally. The thickness of SF between opposing articular
surfaces has been shown to be about 26 µm.186 A gross
analysis of normal joint fluid is given in Table 7-3.187 SF
Table 7-3
Gross Analysis of Joint Fluid
Parameter Normal Finding
Volume (human knee) <4 mL
Color Clear to pale yellow
Clarity Transparent
Viscosity Very high
Mucin clot Good
Spontaneous clot None
Parameter Range Mean
pH 7.2–7.43 7.38
White blood cells/mm2 13–180 63
Total protein (g/dL) 1.2–3.0 1.8
Hyaluronate (g/dL) – 0.3
From Walker JM: Cartilage of human joints and related structures. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 134, Philadelphia, WB Saunders, 1996.
160 SECTION I • Scientific Foundations
has no tensile force. The solute pressure (that exerted
by dissolved substances, e.g., crystalloids) is balanced
by extrinsic forces (i.e., plasma hydrostatic) and osmotic
forces (exerted by proteins that are normally higher in
plasma than in SF). Equilibrium between these forces
is important in the control of fluid exchange between
the joint space and synovial vessels; effusion is a result of
imbalance.
SF volume is dependent on conditions in the lining
interstitium, the forces acting on it, and the permeabil-
ity of the tissue surface to water and solutes. SF con-
tains hyaluronic acid, a nonsulfated GAG, in higher
concentration than that found in other connective tissue
interstitial fluids. Hyaluronic acid is present in fluid as a
complex with protein. There is evidence that the cells,
specifically the fibroblast-like cells, synthesize hyaluronic
acid.183
SF is low in protein and has a high viscosity. It has a
number of molecules with lubricating properties, mainly
glycoproteins, and its clearance rates depend on the
molecular size. The glycoprotein-1 (termed “lubricin”)
is believed to be responsible for the lubricating abil-
ity of SF.182 Although normal SF is mainly acellular, 185
differential white blood cell analysis shows, in decreas-
ing values, monocytes, lymphocytes, plasmacytes, and
polynuclear and synovial lining cells.169 Protein is com-
posed of approximately 60% of the small molecule albu-
min and 40% of the larger molecule globulin.169 The
albumin concentration is responsible for SF’s colloid
osmotic pressure. As SF does not contain fibrinogen
or any clotting factors, it does not clot. Hyaluronate
is responsible for the viscosity. Small molecules, such
as lactose, carbon dioxide, and inorganic pyrophos-
phate, are produced by the joint tissues and diffused
into the SF; glucose enters the SF by a facilitated diffu-
sion. Despite the large amount of fat in synovium, little
lipid is present in SF.169 All plasma proteins can cross
the vascular endothelium, traverse the synovial intersti-
tium, and enter SF (see Figure 7-8). The major mecha-
nism is a size-selective process of passive diffusion; small
molecules such as albumin enter easily, whereas larger
molecules such as fibrinogen are largely excluded.183
The interstitium or tissue space of the synovial lining
appears to be an important factor in the trans-synovial
exchange of small molecules into SF.
In summary, joint fluid is the vehicle for transport-
ing nutrients, solutes, and waste products between the
synovial lining tissues and HAC. Joint fluid also acts as a
lubricant and enables fluid-film models of lubrication to
act under most conditions. It decreases the coefficient
of resistance in low-impact movements and promotes
adherence of joint surfaces that improves joint stabil-
ity and tracking of one surface on another. Hyaluronate
assists in joint surface adherence during distractive forces,
along with the subatmospheric intracavity pressure.185,187
Intra-Articular Pressure
The intra-articular pressure (IAP) of healthy joints is
subatmospheric with a range of −3 to −6 cm Hg reported
both at rest and during exercise.188 In active exercise, the
hydrostatic pressure may decrease further, with values
reported of −25 to −102 mg Hg in human knees during
simple isometric exercise.189 With passive joint motion,
IAP does not change.190 When low pressure exists, dis-
solved gases may come out of solution and cause the
“knuckle crack” on sudden distraction of joint surfaces
often associated with but not a necessary occurrence for
manipulation.191
The IAP maintains joint surface alignment and con-
gruency, facilitates transfer of nutrients between the
synovial lining tissues and HAC, and decreases strain on
supporting structures such as ligaments. In the presence
of effusion, the IAP may become positive (Figure 7-10).
Neither muscle contraction nor the pumping action of
lymphatics is thought to play a role in maintenance of
IAP.171 Clinicians should recognize that positive IAP
compromises joint stability and interrupts synovial blood
flow, as well as blood flow to the subchondral plate. This
effect is greater during exercise in joints with chronic but
not acute traumatic inflammation.192,193
Intra-Articular Temperature (IAT)
The joint intra-articular temperature (IAT) is normally
lower than body temperature, and variation between the
two depends on the location of the joint. Deeply located
joints such as the hip are cooler than superficial joints
such as hand joints. Non-weight-bearing exercise may
raise the IAT as much as one degree, probably because of
increased blood flow.45,152
Figure 7-10
Pressure-volume relation in a diarthrodial joint when increasing
the intra-articular volume. (Modified after Levick JR: Synovial fluid
dynamics. In Maroudes A, Holborow GJ, editors: Studies in joint
disease, vol 2, p 165, London, 1983, Pitman). (From Geborek P,
Wollheim FA: Synovial fluid. In Wright V, Radin E, editors: Mechanics
of human joints, p 118, New York, 1993, Marcel Dekker. Reprinted
by courtesy of Marcel Dekker, Inc.)
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
Cartilage Nutrition
Cartilage nutrition is believed to be derived from three
sources: from the vascular net in the perichondrium and
the synovial tissue near its periphery, from the synovial
fluid, and from blood vessels in the underlying marrow
cavity. The importance of these sources is disputed.4
Ekholm concluded in 1951, from studies using radioac-
tive gold on rabbit joint cartilage, that cartilage nutrition
was probably partly from synovial fluid and partly from
direct contacts between the epiphyseal marrow spaces
and basal layers of cartilage.194 Later studies substantiated
that immature articular cartilage received some nutrition
via the subchondral route.95,195,196
Mow and colleagues noted that even though HAC is
very hydrated (about 75% water) its pores are of a molec-
ular size.197 This indicates that macromolecules that con-
stitute the solid matrix, collagens, proteoglycans, and
other glycoproteins are highly dispersed in the interstitial
fluid. These authors proposed that the motion and defor-
mation behavior of the tissues must be described by a
genuinely valid and “finite deformation nonlinearly per-
meable biphasic theory.”197 The rate of loading on this
porous, free-draining surface or tissue causes a variable
rate of fluid efflux at the loading surface or, at least, at the
edges of the contact zones. Although fluid flow in carti-
lage and intervertebral discs is influenced by loading, the
bulk of fluid flow in these tissues is largely passive.
The pore size depends on proteoglycan concentra-
tion. Pore size controls the rate at which water can flow
through articular cartilage or the intervertebral disc, and
it also controls the distribution of large solutes in the tis-
sues. Small solutes, such as simple ions, can fit through all
pores, but as the molecular size of the solutes increases,
the ability to fit through the pores decreases. If there is a
loss of proteoglycan in hyaline cartilage, the larger proteins
can enter with increasing concentrations. The proteogly-
can content is responsible for the osmotic pressure. The
hydraulic permeability coefficient is also sensitive to the
proteoglycan content. Osmotic pressure depends more
on the charge concentration than on the proteoglycan size
or degree of aggregation. Fixed negative charges exclude
anions such as Cl− and SO4, and cations such as Na+, Ca2+,
Mg2+, and K+ have a higher concentration.
The subsynovial microvasculature and lymphatics
obviously play a large role in cartilage nutrition because
they are the source of nutrients and the normal clearance
mechanism, respectively. Imbalance between microvas-
cular permeability, especially to proteins, and the normal
clearance mechanism of the lymphatic outflow occurs in
effusions. It is reflected by an increased protein concen-
tration in synovial fluid. Regular motion may adequately
clear the leaking protein, but rest, sleep, or immobili-
zation allows the synovial lining tissues to become
edematous; the individual experiences pain and stiffness.
161
This indicates the importance of even once-daily move-
ment through available range in effused joints.
Clinicians should be aware of the positive correlation
between effective synovial plasma flow and intra-articu-
lar temperature.198 Cooler, low-flow effusions are more
likely to have metabolic evidence of ischemia and of low-
glucose, pH, and lactate.199 This finding suggests that
moderate heat modalities should be more effective in pro-
moting clearance than cold therapy. In effused joints—
either hot or cold—clinicians should be concerned not
only with pain relief but also with achieving the primary
goal of inflammation control and effusion reduction.
Production of the matrix is the responsibility of chon-
drocytes and more specifically the chondron, and cell
health depends on an adequate supply of nutrients and
the efficient removal of metabolic waste products; solute
diffusivity is important to this process. There is a negative
correlation between oxygen concentration in the NP as
a function of distance from the vertebral end plate.136 Since
the end plate is almost totally impermeable, any solutes
entering the NP must enter the blood vessels that surround
the anulus on the periphery.136 Thus, oxygen concentra-
tions vary with the position in the intervertebral disc and
are highest at the periphery and lowest at the center of the
nucleus. This is similar in HAC, where the oxygen con-
centrations are highest at the surface closest to the synovial
fluid, the source of diffusing oxygen from the blood supply
within the synovial lining tissues, and lowest in the calcified
zone of the cartilage adjacent to the subchondral plate.
Joint Lubrication
Healthy human synovial joints have a remarkable ability to
permit reciprocal movements within a wide range of loads
and speeds while maintaining stability. Like engineering
bearings, human joints should function with very low fric-
tion and wear, regardless of the loading conditions. The
type of loading is an important factor in the mechanism
of human joint lubrication. Human joints are subjected to
steady (static or constant) loading (as in standing still) and
dynamic (cyclic) loading (as in jumping or in gait). Loading
can vary from very light loads, such as in the swing phase of
gait (< 500 N), to three to five times body weight, such as at
heel contact in the stance phase of gait when hip and knee
forces are about 1500 N (40 lbs = 177 N).200 High loads
tend to occur for only brief periods (0.01 to 0.15 second),
whereas low loads occur for longer periods (> 5 seconds).
Human joints are theorized to have two basic catego-
ries of lubrication: fluid film and boundary.201 A mixed
model is also described (Table 7-4). The successful oper-
ation of these models depends on certain critical variables
listed in Table 7-5.
Surface compliance or elasticity is important as the
harder the surface, the higher the friction; healthy joints
have very low friction. Under conditions of no load or
162 SECTION I • Scientific Foundations

Table 7-4
Models for Lubrication of Human Joints
Mechanism Author Year Definition

Hydrodynamic MacConnaill208 1932 UL, wedgelike fluid film present to separate surfaces in
unidirectional motion
Mixed (fluid film Jones209,210 1934, H/C, rough points in contact but fluid present in “dips” to
and boundary) 1936 provide fluid film at those sites
Linn211 1968
Hydrostatic McCutchen212 1959 High loads, cartilage compression, fluid extruded ahead of the
Mow and 1977 loaded areas and in dips in rough surface
Mansour204
Boundary Charnley213 1959 Low loads, thin layer of large molecules absorbed on the surface,
forming a gel to protect rough points in contact; inadequate
compression for fluid extrusion from HAC
Weeping McCutchen212 1959 H/C, surfaces kept apart owing to impervious subchondral bone,
which causes fluid outflow during the creep phase of cartilage
deformation
Elastohydrodynamic Dintenfass214 1963 UL-L, wedge-film, model recognizes pliability of HAC to
reduce friction
Squeeze film Fein215 1966–67 L, pliability deformability of HAC reduces peak pressures and
spreads load when loads are maintained after motion ceases
Boosted Walker et al.206 1968 H/C porosity of cartilage allows fluid efflux to augment fluid
film between surfaces
Micro- Dowson and Jin216 1986 L, local pressures on high spots, given HAC deformability
elastohydrodynamic smooths surface, allows fluid film to exist

From Walker JM: Cartilage of human joints and related structures. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 136, Philadelphia, WB Saunders, 1996.
H/C = high and/or constant loading; L = brief loading, no motion; UL = unloaded; UI-L = unloaded, free swinging (swing phase gait).

Table 7-5
Critical Variables in Joint Lubrication Mechanisms
Variable Effect of Change from Normal Values*

Surface compliance
(elasticity)
Surface roughness
Low coefficient of friction
Rolling and sliding
velocities
Synovial fluid viscosity
Synovial fluid protein
lubricants
Surface permeability
Joint surface contour
When ↓ dispersion load, focal concentration of forces leading to microfracture of SCB,
↓ adjustment of surface to loads; therefore, EHD or M-EHD less effective, vulnerable
to long-term, high-stress, cyclic loading
When ↑ there is ↑ contact stresses and friction, ↓ potential for fluid film
↑ force required to move joint under load; boundary lubrication more likely to exist than
fluid film
Normally sustain HDL and fluid film; absence ↑ contact, therefore, boundary lubrication,
↑ friction and wear
Owing to hyaluronate, NB lubricant of synovium, not cartilage, gives thixotrophy to SF
(slower the flow, more viscous it becomes); inadequate lubrication of SLT where contact occurs
If ↓ loss of boundary lubricants, ↓ defense against distraction and ↓ joint stability, ↑ friction,
↑ slippage under load; inadequate lubrication in low-load states
If ↑ larger molecules can penetrate, ↓ ability to have boundary lubrication conditions,
therefore, ↑ wear; if ↓ impairs cartilage nutrition and removal of waste products,
↓ stiffness, inadequate protection of SCB from peak forces
Incongruity of unloaded joint permits deformation of SCB under loads; loss of normal
variability in HAC across surfaces means > area in initial contact, ↓ load dispersion,
more boundary lubrication conditions, ↑ wear

From Walker JM: Cartilage of human joints and related structures. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 138, Philadelphia, WB Saunders, 1996.
EHD = elastohydrodynamic lubrication; HAC = hyaline articular cartilage; HDL = hydrodynamic lubrication; M-EHD = micro-EHD;
SCB = subchondrial bone; SF = synovial fluid; SLT = synovial lining tissue.
*Variables are not acting alone to determine lubrication type and ease of motion.
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
low load, as in pendular motion, joint surfaces are incon-
gruent. Because of surface compliance, under high loads,
surfaces are more congruent, a greater area is potentially
in contact, and joint stability increases.
Surface roughness, shown by all types of microscopy
(see Figure 7-5B), allows pools of fluid to be trapped
between contact areas under load. Since synovial fluid is
thixotrophic—that is, the viscosity changes with change
in velocity—a thinner lubricating fluid film can occur as
required, at very low velocities.202 Full contact between
opposing contact areas is prevented by a surface active
phospholipid factor (SAPF) in synovial fluid (lubricin),
which adheres to the joint surfaces—hence bound-
ary lubrication.183 Boundary lubrication may work best
under low-load conditions182 when inadequate compres-
sion fluid replenishment cannot be relied on.
The remarkable slipperiness of human joints is mea-
sured by the coefficient of friction (COF). The COF is the
shear force needed to make one surface slide on another,
divided by the force pressing them together. The lower the
COF, the lower the resistance to sliding. A skate on ice has
a COF of 0.03; the theorized COF for cartilage on carti-
lage is between 0.02 and 0.001.203 More force is needed
to produce motion when the COF is high. In the fluid
film model, the COF is about 0.01, with the joint layers
separated by a thin film of pressurized fluid. The COF is
higher in boundary lubrication, 0.1 to 0.5, independent
of the speed of sliding or load.200 In this model, the SAPF
and macromolecules too large to penetrate cartilage form a
thin layer adsorbed onto the surface. In disease states, with
fibrillated surfaces, boundary lubrication is compromised
since larger molecules can enter cartilage under load.
The hydrostatic mechanism is best at generating a fluid
film under high loads when cartilage is compressed and fluid
is extruded on the surfaces, especially ahead of the load.204
Researchers theorize that a fluid film mechanism can operate
in healthy human joints under most conditions. In the mixed
lubrication model, transitional phases involve the weeping205
and boosted206 models. Cartilage weeps in noncontact areas
ahead of the load, and macromolecules, such as hyaluronic
acid protein, cannot penetrate HAC and remain on the sur-
face. These mechanisms may not be mutually exclusive. The
boundary lubricant reduces friction and wear when motion
recommences and a fluid film is restored.200
Research suggests that during loading a plateau of
fluid loss may be reached after which no further decrease
in cartilage thickness occurs (revealed by MRI).207 More
data are needed to determine if this effect, observed in
young men, occurs at other ages, especially in old age.
Compressive forces that are highest at the surface of
HAC, and other restrictions to fluid flow, maintain a
pressurized layer of fluid at the surface and reduce the
stress on the solid matrix, as well as wear of HAC.
Figure 7-11 shows the theorized loading-lubricating
mechanisms for the hip joint during the dynamic motion
163
of the gait cycle.200,217,218 In the swing phase, there is a
light load, and a fluid film separates the two surfaces. At
heel contact, the load is very high, with a low entraining
velocity, and the fluid film, though reduced, still separates
the joint surfaces. In midstance, the load is decreased,
the entraining velocity is increased, and there is elas-
tic deformation of the surface; the mechanism is one of
elastohydrodynamic (EHD) lubrication (a rolling or slid-
ing motion that pressurizes the viscous joint fluid and
squashes cartilage, which changes the pressures generated
in the fluid), which maintains a small fluid film. At toe-
off, once again there is a very high load and a very low
entraining velocity. Researchers theorize, however, that
with high loads, the squeeze film mechanism (compliant,
deformable surface and incompressible fluid) can main-
tain a small fluid film between the two surfaces for a few
seconds. Therefore, because there are transient applica-
tions of variable loads, a fluid film mechanism can operate
in a healthy human joint throughout the gait cycle.
Glucoproteins and surface active phospholipids are
more important when joint fluid viscosity is reduced
through injury or disease, and in aging when a decrease
in deformability of HAC under loading increases con-
gruity. The latter compromises maintenance of a fluid
film via the micro-elastohydrodynamic mechanism.
Lubrication and Exercise
The greater focus of research into all aspects of cartilage
should yield data clinicians can use to plan therapy pro-
grams that provide and maintain fluid film conditions
during exercise. Data still do not exist to prescribe ideal
exercise programs that will maintain fluid film conditions
and avoid HAC damage. However, prudence suggests that,
in the presence of joint pathology, trauma, or effusion, pas-
sive motion should be accompanied by gentle traction to
avoid compression of softened cartilage and overstretch-
ing of vulnerable soft tissues such as ligaments.
Factors Clinicians Should Consider When Planning
Therapy in Patients with Known or Suspected
Articular Cartilage Damage
● The manner (type) of loading is more important than the actual
load.
● The potential for wear increases when the joint goes from static
loading to high loads.
● Joint fluid volume and lymphatic clearance increase with exercise.
● Friction is inversely related to the predicted thickness of the
fluid film.
● Cartilage deteriorates in the unloaded state.
● Repetitive impulsive loading (RIL)—such as typing, skipping,
and the use of a pneumatic drill—is detrimental to both articular
cartilage and the subchondral bone plate.
164 SECTION I • Scientific Foundations
Figure 7-11
Lubrication mechanisms for the right hip joint. (From Unsworth A: Lubrication of human joints. In Wright V, Radin E, editors: Mechanics of
human joints, p 158, New York, 1993, Marcel Dekker. Reprinted by courtesy of Marcel Dekker, Inc.)
Pendular-type movements provide a fluid film and min-
imal or no wear. Static loading and isometric exercise, if
used, should be brief (a few seconds), as these conditions
favor a mixed model of lubrication with boundary friction
predominating. High loading should be either brief or
avoided. High loading is possibly least harmful following
low-load, high-velocity motion, since the latter encour-
ages the presence of a fluid film region. If high loads are
sustained for less than 0.5 second, a squeeze film mecha-
nism should ensure that a fluid film exists. If resistance is
applied in any form, the individual should work through
the range, and holding periods at the end range (e.g.,
knee extension) should be very brief. Controlled eccentric
loading creates large compressive (loading) forces; these
should be avoided where cartilage damage may exist.
Research suggests that cartilage has such a low perme-
ability that any fluid outflow from cartilage to contribute
to lubrication of joint surfaces is negligible. Therefore,
clinicians cannot predict that load-bearing exercises will
provide an adequate fluid film by promoting fluid efflux
from cartilage. However, load bearing will promote fluid
influx into cartilage and facilitate cartilage nutrition. It
is hoped that further research will elucidate this area for
which minimal “hard” evidence still exists.
Mechanisms of Cartilage
Breakdown
Since cartilage is avascular, it cannot demonstrate an
inflammatory process, a normal response to injury and
an important component of repair. Conditions in which
breakdown of cartilage occurs are generally classified as
inflammatory (e.g., rheumatoid arthritis) or noninflam-
matory (e.g., chondromalacia [nonprogressive], osteoar-
throsis [progressive, leading to osteoarthritis]). Multiple
factors are involved in cartilage breakdown, the imbal-
ance between extracellular matrix synthesis, and degra-
dation. Repetitive impulsive loading may be the major
factor in cartilage breakdown leading to osteoarthrosis
and osteoarthritis.219 Other factors are stress depriva-
tion (immobilization, bed rest, weightlessness), excessive
loading (body weight), developmental etiologies leading
to abnormal force transmission (e.g., developmental hip
dysplasia, coxa valga, genu valgum), joint surface incon-
gruity, and joint instability (generalized ligamentous
laxity and cruciate ligament damage). In rheumatoid
arthritis (RA), free radicals, cytokines (especially TNF-α
and IL-1β), neutral proteinases, and catabolic enzymes
(which may be derived from synoviocytes, chondrocytes,
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
or polymorphonuclear leukocytes) play a primary role;
they are also a factor in osteoarthritic cartilage break-
down.6,19,84,105,220–228 Regardless of the cause of exudation,
proliferation, or infiltration, the highly vascular synovial
lining tissues can respond with an inflammatory process.
This produces variable joint effusion and potentially
eventual fibrosis and thickening, which may adversely
affect synovial fluid production, cartilage nutrition, and
joint space clearance. The inflamed synovial lining tis-
sues secrete enzymes and neutral proteinases, such as
cholinase, as well as release neutral proteoglycans, which
decrease cartilage matrix synthesis, break down and
absorb matrix, degrade the collagenous matrix, and may
play a role in maintenance of synovitis.6,199,224
The body’s response to articular cartilage defects
resulting from trauma upon impact of loading depends
on the lesion depth.22 The typical response to partial
thickness lesions of HAC leads to an intrinsic response
and includes chondrocyte proliferation and clustering
near the injured site soon after joint trauma.22 The intrin-
sic response is limited by the constraints of an avascu-
lar ECM, and an attempt at repair results in failure to
integrate with remaining cartilage. This ultimately leads
to further wearing of the HAC surface during loading
and eventual effect on subchondral bone.229 Full thick-
ness lesions are cartilage defects that penetrate the sub-
chondral bone and can undergo spontaneous repair
through the formation of a fibrous or cartilaginous tis-
sue mediated primarily by mesenchymal cells from the
bone marrow. An extrinsic response with the develop-
ment of a fibrin clot is generated within two days of
trauma with full thickness lesions.230 This response entails
the penetration of mesenchymal stem cells to the fibrin
clot, chondrocyte differentiation, and synthesis of PGs
and type II (and because of angiogenesis, type I) col-
lagen, which ultimately develops into mechanically infe-
rior fibrocartilage tissue. Unfortunately the repair tissue
initiated in the fibrous tissue that forms at the articular
surface degrades over time.231
The chondrocyte is at particular risk because of its
location in avascular cartilage and the long transit route
of its nutrition from subsynovial capillaries through syno-
vial lining tissues, synovial fluid, and cartilage matrix.
Therefore, if a lesion of articular cartilage is a partial
defect that by definition does not penetrate the under-
lying subchondral bone (chondral lesion), the bioactive
molecules and cells that reside in the bone marrow are not
disrupted and an intrinsic response occurs in an attempt
to regenerate new tissue. These lesions do not heal spon-
taneously. With a full thickness defect of HAC, contact
is made with bone marrow (osteochondral defect) via
penetration of the vascularized subchondral bone leading
to an extrinsic response and release of mesenchymal stem
cells, fibroblasts, and inflammatory cells to the injured or
165
exposed site leading to full thickness defects, repair, and
formation of fibrous tissue.230
Radin proposed that repetitive impulsive loading
is the principal mechanism of cartilage breakdown
in osteoarthrosis.225 He theorized that repetitive
impulse loading leads to microfractures of subchon-
dral bone and activation of the secondary center of
ossification, which causes the tidemark to advance and
duplicate and the noncalcified cartilage layer to thin,
perhaps totally. This process increases shear forces
in the deeper layers, decreases dispersion of stresses
within HAC, and leads to deep horizontal and vertical
splitting, with surface fibrillation, as cartilage deterio-
rates. Proteoglycan loss occurs. Articular detritus is
present in synovial fluid. This may perpetuate syno-
vial effusion, leading to synovial tissues producing and
releasing more cartilage-degrading substances into
synovial fluid.
Osteoarthritic cartilage is characterized by hypertro-
phic chondrocytes and clustering of cells. This reflects
an attempt by the cells to increase matrix synthesis.
With the loss of proteoglycans, there is an unmasking
of collagen fibers within the cartilage matrix. In osteo-
arthritis, extensive damage to type II collagen fibers
occurs, with eventual unwinding of the triple helix and
the appearance of crimping of collagen fibrils. This pro-
cess commences in the superficial layers and progresses
to involve deeper layers.6,41 As collagen fibers become
exposed on the surface, normal joint motion gradually
produces a roughened surface, encouraging splitting,
cartilage detachment, and potentially complete cartilage
abrasion. Since cartilage cannot regenerate, its destruc-
tion causes a reaction by subchondral bone consisting
of osteosclerosis and osteophytes. Bone may become
eburnated. Joint fluid detritus may lodge in the exposed
medullary spaces, producing cysts. This end process
is similar in both osteo- and rheumatoid arthritis. All
phagocytosed structural elements, including bone cal-
cium apatite crystals, contribute to joint space detritus,
which provokes synovitis (secondary in osteoarthritis)
or perpetuates it in RA-like conditions. Fassbender,
however, emphasized that the synovial tissue in second-
ary synovitis of osteoarthrosis or osteoarthritis does
not destroy HAC as it does in RA.232 Exposure of sub-
chondral bone provides blood vessels to the area as well
as collagen fibers, enabling a scar pannus to form to
provide a measure of repair.
In RA, there is proliferation of the synovial lining tis-
sues. Mesenchymal cells migrate over the joint surface—
a process thought to be facilitated by fibronectin—and
eventually form a fibrous pannus.181 This may lead to
fibrous ankylosis. Obviously and fortunately, not all indi-
viduals demonstrate the total degradation of cartilage
described here.
166 SECTION I • Scientific Foundations
Monitoring Changes in Cartilage Breakdown
and Repair
Conventional radiography allows for two-dimensional but
indirect imaging of HAC as reflected through joint space
narrowing, subchondral sclerosis or cysts, and the pres-
ence of osteophytes.233 Ultrasound—a relatively inex-
pensive, noninvasive, and fast technique—is employed
to determine articular cartilage thickness but is limited
by a lack of reproducibility and insufficient accuracy and
is applicable to joint surfaces only in superficial loca-
tions.234 The use of computed tomography arthrog-
raphy is limited by its invasive nature as it requires a
contrast agent to be injected into the joint. For the
purpose of evaluating the surface of articular cartilage,
diagnostic arthroscopy is considered the gold standard;
however, it is an invasive procedure.235 The most accu-
rate noninvasive imaging technique for visualizing the
entire articular cartilage surface of a joint is magnetic
resonance imaging (MRI). Sectional images with high
soft tissue contrast currently allow for the evaluation of
cartilage macromorphology, bone-cartilage interface,
and articular cartilage surface, making MRI useful for
detecting early degenerative changes in HAC and the
subchondral bone.207,236 For instance, one MRI study
observed that alignment of the knee caused by cartilage
degeneration is associated with bone formation in the
diseased condyle and bone resorption in the opposite
compartment.237
Repair of Articular Cartilage
Potential
It is well established that articular cartilage has a low
potential for repair, for both the cellular and the matrix
components.6,84,238,239 When trauma or disease occurs, a
tissue must have regenerative capacity for the repair pro-
cess to result in the presence of tissue that is identical
to the original tissue. This repair process is well known
and involves an inflammatory reaction and formation of
a fibrin clot, which provides the scaffold for new cells to
come in and reconstitute the tissue. Sledge noted that
repair of articular cartilage is not intrinsically well pro-
grammed; the emphasis is on protection from damage.240
With either partial thickness or full thickness articular
cartilage lesions, in spite of poor intrinsic or extrinsic
responses to injury, incomplete tissue regeneration and
subsequent tissue degeneration will ultimately occur at
a lesion site.
The constraints on repair of articular cartilage are low
cellularity, which limits its intrinsic healing response,
lack of a primitive cell population with chondrogenic
potential within mature tissue, avascularity of the tis-
sue, and great distance of cells from their nutritional
sources.232 The healing of articular cartilage appears to
depend on whether the defect penetrates the subchon-
dral plate. When subchondral plate penetration occurs,
as in deeper injuries, there is extensive fibroblastic pro-
liferation from cells in the adjacent bone, but “seldom
is true hyaline cartilage produced.”240 Landells noted
that essentially no repair was evident by surviving or
remaining cells when the cleft involved only the articu-
lar cartilage.241
A few authors have reported the existence of mitotic
activity. Havdrup and Telhag demonstrated mitosis in
unoperated and sham-operated rabbits with traumatized
cartilage.242 It was unknown whether the mitotic activity
was caused by a decrease in cell inhibitors or an increase
in stimulation factors. Evidence of mitotic activity was
also reported in rabbits that had been subjected to sus-
tained pressure by clamping the limb in an abnormal
position of full extension.243
Several investigators noted that in the presence of
degeneration, as is characteristic in osteoarthritis, the
HAC chondrocytes appear to recover their ability to
undergo division.242 The ability of chondrocytes in osteo-
arthritis to replicate their DNA appears to be an ability
that cells of healthy HAC either suppress or lose.244 It
was also demonstrated that cartilage can undergo mito-
sis when grown in culture.245 Poole noted that in both
in vivo and in vitro studies of adult periosteum, it was
demonstrated that the bone morphogenetic molecules
such as osteogenin can cause cartilage to form; adult
periosteum appears to remain chondrogenic.6,246,247 The
latter is reflected in osteophyte formation at the perios-
teal-cartilage junction in osteoarthrosis. Cultured articu-
lar cartilage appears to have properties more like those
of fibrocartilage than of articular cartilage.245 There are
species differences in the growth and behavior of mam-
malian chondrocytes. Articular cartilage, when repaired,
has been reported in a number of studies to be similar
to hyaline cartilage, particularly when examined with
light microscopy. Biochemical and biomechanical stud-
ies, however, have clearly demonstrated that the carti-
lage formed in the repair process has characteristics that
are more like those of fibrocartilage. There is a higher
portion of type I collagen in repaired articular cartilage
than in HAC.
Repair is controlled by numerous factors, mainly
hormonal, synovial, and cartilage-derived chemical
mediators, as well as mechanical stimuli. Knowledge of
the factors governing the anabolic and catabolic pro-
cesses that are crucial to the repair potential of cartilage
is critical to understanding HAC’s responsiveness to
injury. Akeson and colleagues150 stressed that a number
of studies over the years—first by Convery and associ-
ates248 and later by Salter and colleagues149—have amply
demonstrated that healing by HAC occurs only in small
defects (about one eighth of an inch in diameter) and
does not occur in large or full-thickness defects, with or
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
without motion. This finding has been demonstrated
by histological, biochemical, and biomechanical studies
of the replacement tissue. It demonstrates that physical
stimuli, such as motion and load, are critical to the repair
of HAC and may either stimulate or inhibit the repair
capacity. The collagen network may provide the sub-
stratum used by mesenchymal cells to migrate over the
surface of cartilage defects.14 The reviews by Buckwalter
and coworkers,226 Caterson and Buckwalter,249 Byers
and Brown,250 Akeson and associates,150 Buckwalter and
Mow,239 Salter,149 Risbud and Sittinger,251 and Holland
and Mikos22 offer descriptions and discussions of studies
of articular cartilage injury and methods of facilitating
repair of articular cartilage. A brief description of these
approaches is given here.
Approaches to Facilitate Repair
Current practice in severe joint damage is the surgi-
cal replacement of the joint by an artificial prosthesis.
Joint replacement devices have a limited tolerance for
heavy loading and vigorous wear. Particularly in younger
patients, in whom implanted devices may work loose with
growth, arthroplasties and arthrodeses do not provide
satisfactory simulations of natural joints. Investigators
continue to search for methods to stimulate repair of
damaged cartilage and provide a near normal articulat-
ing surface. If techniques can be employed to simulate
the coverage of load-bearing surfaces with tissue that
has loading characteristics that permit functioning simi-
lar to that of natural HAC, in younger patients, joint
replacement procedures can be deferred until after
maturity. Methods explored to improve repair continue
to encompass improved drug delivery strategies, biome-
chanical, biophysical, alterations to subchondral bone,
grafting, surgical implantation, genetic engineering, and
various combinations of these methods. One focus is on
tissue engineering approaches to facilitate HAC repair
with the aim of restoring pathologically altered tissues
using transplanted viable cells associated with supportive
matrices and biomolecules.
Drug Delivery Strategies
In the quest to enhance the quality of repair of HAC,
an active area of research lies in the advancement of
drug therapies that target and localize the effects of
these agents to these tissues.22 The aim of delivery of
pharmacological agents is to regulate the inflammation-
triggering cytokines, regulate matrix degradation, and
regulate chondrocyte metabolism. In this way, strategies
have concentrated on the means to regulate the destruc-
tive effects of IL-1, to prevent loss of important matrix
molecules, and to promote chondrocyte proliferation in
articular cartilage defects.22 Challenges to these strate-
gies include pathological side effects associated with
167
growth factors/cytokines, ensuring safe methods of sus-
tained localized delivery, and an increased understand-
ing of therapeutic dosages and release kinetics of these
agents.
Biomechanical
Biomechanical approaches that have shown variable suc-
cess involve the following:
1. Using osteotomies to alter the distribution of the load
and improve the congruity or alignment of the joint
surfaces
2. Performing tendon transplants or muscle releases,252
which alter the forces acting over the joint
3. Decreasing the load through the weight-bearing sur-
faces by the use of different ambulatory aids (e.g.,
canes, crutches)
4. Using continuous or intermittent passive motion
(CPM or IPM)
The biomechanical approach of CPM has shown
a degree of success, as reported mainly by Salter and
associates.253 CPM may be delivered either continuously
or cyclically. In adolescent rabbits, Salter and cowork-
ers demonstrated the healing of full-thickness drill hole
defects by hyaline cartilage within 4 weeks, with a signifi-
cant difference in the animals that had been treated by
CPM.254 The percentage of HAC in the three experimen-
tal groups of rabbits was as follows: immobilized, 8%;
free motion, 9%; CPM, 52%. O’Driscoll and Salter had
similar results using free intra-articular periosteal grafts.255
These results were less impressive in mature rabbits. It
was not established how the newly synthesized HAC
responded to normal loading over time. Both of these
studies showed a combination of approaches—CPM
and involvement of the subchondral bone with the use
of full-thickness drill holes or periosteal grafts. Refer to
Salter149 and Akeson and colleagues150 for more detailed
descriptions and discussions of the use of passive motion
to promote healing of cartilage.
Coutts and associates demonstrated in the medio-
femoral condyles of adult rabbits with full-thickness
defects and rib perichondrial grafts that nearly normal
HAC was present in 55% of animals at 6 weeks; at 1 year,
82% demonstrated type II collagen.256 The shear moduli
did not differ between the two groups (those exposed
to cage activity alone and those having passive motion
followed by cage activity). This study showed that HAC
with biomechanical properties would develop and not
degrade within 1 year after the full-thickness defects had
been created. Also, the percentage of type II collagen
may increase over time.257 Moran and colleagues, using
rabbits with full-thickness defects and autogenous peri-
osteal grafts, utilized either CPM or IPM.258 The tissue
was examined with a variety of microscopy approaches
and histochemistry, but no biomechanical tests were
done. They demonstrated healing by hyaline cartilage
168 SECTION I • Scientific Foundations
that contained type II collagen, but with an irregular
organization. This result was better in the animals that
had been grafted and better in animals that had CPM
rather than IPM.
In vitro or in vivo studies to simulate, induce, or
improve repair of articular cartilage should include
biomechanical testing of the functional behavior of the
tissues. Several studies using microscopy have shown
that the repair tissue may have the appearance of hyaline
cartilage, but it fails to perform like articular cartilage,
especially over time. This suggests that a return to
activity with repetitive impulsive loading (e.g., hurdling,
running, ice skating with jumps) is probably ill advised.
Since it is shown in animals that type II collagen takes a
year or more to develop, a very gradual return to high
loading conditions would be prudent.
Biophysical
Variable effects of electromagnetic fields on cartilage
and chondrocytes have been demonstrated. No effect
of pulsed electromagnetic fields on extracellular matrix
synthesis of chondrocytes in high-density cultures has
been observed.259 However, increased proteoglycan
and DNA synthesis occurred with chondrocytes grown
in cultures with constant direct current.260 Other stud-
ies revealed a stimulating effect of electromagnetic fields
on chondrocyte activity.261–263 Two studies demonstrated
enhanced healing of osteochondral defects in rabbits,
with the animals showing repair tissue resembling hyaline
cartilage.264,265 The long-term results and biomechanical
characteristics of the repair tissue are not known, but it is
reasonable that electromagnetic fields should have a bio-
logical effect. Current intensity may be a critical factor.
On growth plate chondrocytes grown in electrical fields,
Armstrong and coworkers showed inhibited growth with
strong electrical fields but enhancement of proliferation
with weaker electrical fields.266
Subchondral Bone
Surgical methods that involve the penetration of sub-
chondral bone are designed to disrupt the vascularity and
promote fibrin clot formation as well as provide a source
of new cells and contact with bioactive molecules from
the bone marrow. Subchondral bone may be involved by
some form of penetration or microfracturing, such as drill
holes, or by resection of the cartilage through to the can-
cellous bone, a procedure called spongilization.267 The
latter procedure involves excising the damaged cartilage
to below the subchondral plate to promote the growth
of fibrocartilage. This technique can provide a biologi-
cal resurfacing, particularly where the joint congruence is
good and the load is well distributed over a large area.267
Unfortunately these techniques do not restore the native
structure of cartilage and ultimately lead to further tissue
loss.230,268,269
Grafting
Approaches employing grafting have used periosteal,258
perichondrial,256 or osteochondral270 grafts. Grafts pro-
vide cells that have the potential to synthesize matrix, but
osteochondral grafts (allo-, auto-, and xenogenic) tend
to produce a severe immunological rejection reaction.270
Generally, however, the graft tends to degenerate within
1 to 2 years, resulting in fibrillation and breakdown of
the surfaces.271
Cartilage Tissue Engineering and Surgical
Implantation
Conventional surgical procedures involving autologous
chondrocyte joint resurfacing (abrasion, drilling, debride-
ment, microfracture techniques, or arthroscopic shaving)
or biological autografts result in insufficient repair and
formation of mechanically inadequate fibrocartilage.251
The recurring problem in tissue transplantation thera-
pies for articular cartilage defects has been the lack of
integration between the implant and the host cartilage
leading to the current therapeutic strategies targeting
both the extracellular components and the cellular bio-
synthetic activities of implants and host cartilage.272 Cell
therapy involves enzymatically isolating chondrocytes
from a biopsy of healthy articular cartilage from a minor
weight-bearing area (for example, from a non-weight-
bearing portion of the articular cartilage from the knee
joint), which are then expanded in monolayer culture and
reinjected under an autologous periosteal flap, sutured on
the cartilage defect.273 Surgical implantation is designed
to provide a new cell population and may involve the use
of cultured or harvested chondrocytes,270 mesenchymal
cells,274 a fibrin clot,275 or an artificial synthetic matrix.276
Tissue engineering, however, is a field that focuses on
the delivery or in situ mobilization of competent cells
to restore pathologically morphological and functional
characteristics of HAC and holds great promise in the
biomedical sciences, merging advances in cellular and
molecular biology and chemical and mechanical engi-
neering fields.251 Current bioregenerative approaches
now prevail that focus on reconstituting tissue struc-
ture by restoring impaired articular cartilage based on
the transplantation of cells in concert with supportive
matrices and biomolecules that have been developed in
vitro.251 Cartilage tissue engineering now embraces three
critical components: the delivery and integration of func-
tionally active and responsive cells, a carrier system com-
prised of a supportive matrix, and bioactive molecules
that are known to promote cell differentiation and tis-
sue regeneration. The development of new cell culture
systems consisting of 3D cell cultures in gels (e.g., colla-
gen, agarose, alginate, and fibrin)277 or degradable poly-
mer scaffolds within specific bioreactor modules allows
for a closely simulated in vivo cellular microenvironment
(Figure 7-12). These “vital transplants” allow for critical
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
Figure 7-12
Schematic drawing showing the strategy of developing tissue-
engineered cartilage constructs using fibers and embedding
substances. Embedding substances offer 3D immobilization and
uniform distribution of cells in the fiber mesh. (From Risbud MV,
Sittinger M: Tissue engineering: advances in in vitro cartilage
generation, Trends Biotech 20(8):351-356, 2002.)
cell-cell and cell-extracellular matrix interaction, and thus
cell signaling via cell adhesion molecules including integ-
rins and adherens,278 previously not achieved by conven-
tional monolayer cell culture systems. These therapeutic
efforts are based on the knowledge of the critical interde-
pendence of the ECM and chondrocytes within articular
cartilage.8
Cartilage Tissue Engineering. Autologous car-
tilage cells are retrieved using biopsies from healthy
joint cartilage tissue sites typically contralateral to the
affected side; however, these cells may have limited abil-
ity to proliferate and differentiate. Research is intent on
determining the precursor (uncommitted mesenchy-
mal progenitor or multipotential stem cells), enabling
tissue regeneration. There is evidence that already
differentiated tissues contain populations of undif-
ferentiated pluripotential cells that retain the capacity
to regenerate tissue after trauma, disease, or aging.279
The challenge of tissue-engineered cartilage remains
in determining the ultimate mechanical stability, graft
fixation, and overcoming immunological aspects of
HAC.280 Differences remain in the histology of regener-
ated cartilage between native and transplanted cartilage,
questionable water binding capacity, and fixation of the
cartilage transplant to the subchondral bone in the
joint.251 Much attention has been paid to the retrieval
of adult mesenchymal stem cells from the bone marrow
where they reside as both a resource for hematopoiesis
and as a potential reservoir and pool of regenerative
cells for mesenchymal-based tissues281 including HAC
when they are embedded in an appropriate carrier sys-
tem. Cells with chondro-osteoprogenitor features have
been isolated from several tissues, including periosteum,
169
bone marrow, spleen, thymus, skeletal muscle, adipose
tissue, skin, and retina.282–285 In addition, gene silenc-
ing approaches, such as RNA interference, may be used
to block expression of genes that produce inhibitors of
chondrogenesis.286 Because of the continued failure to
generate tissue architecturally identical to HAC, tissue
engineering efforts are currently directed at recreating
the zonal arrangement in HAC in order to reproduce the
function with specific subpopulations of chondrocytes
used to replicate each zone.287
Scaffolding. The second key component underly-
ing the engineering of HAC is the manufacturing of
bioresorbable scaffolds—such as fibrin, hyaluronic acid,
collagen, and alginate288,289—that guide the shape and
give the template for in vitro and in vivo HAC tissue
development.290
Bioreactors. While the scaffolding allows for 3D
immobilization of differentiated chondrocytes, a more
solid bioresorbable scaffold (e.g., poly α-hydroxy ester
compound) is required to offset the mechanical defi-
ciencies.291 It is also necessary to culture artificial tissue
constructs in rotating bioreactor vessels or perfusion cul-
ture systems in order to simulate a natural environment
characteristic of HAC that will avoid contamination.292
Clinicians should be aware that “the available
evidence indicates that, at a minimum, repair tissue
generated from any therapeutic effort must have ini-
tial protection from loading, followed by a regimen
of loading and motion that promotes remodelling,293
but thus far experimental studies have not defined this
optimal sequence of changes in the mechanical environ-
ment.”226 Clearly, it is not yet possible to give defini-
tive direction to clinicians regarding progression of a
rehabilitative program. However, repetitive high loads,
as in long-distance running or high-impact loading (as
in sports involving jumping motion such as ice skating,
long jumps, and skiing) should be avoided for perhaps
a year, and when they are experienced, they should be
applied briefly.
Response to Mechanical Stimuli
Since the 1990s, a number of histological, biochemical,
and biomechanical studies, as well as analytic models,
have documented the biological response of articular
cartilage or chondrocytes, both in vitro and in vivo,
to mechanical stimuli. Using a finite element analysis,
Wilson et al. determined that local stresses and strains
in HAC appear to be influenced by the local morphol-
ogy of the collagen fibril network.294 Microfilaments
and possibly intermediate filaments within the cytoskel-
eton of the chondrocyte may provide the viscoelastic
properties of the chondrocytes, thereby influencing the
mechanical interaction between the chondrocyte and
surrounding tissue matrix.295 Chondrocytes in loaded
170 SECTION I • Scientific Foundations
joints experience hydrostatic compressive, tensile, and
shear forces,296 and it is now known that the appropriate
application of these forces is necessary for the pheno-
typic expression of the chondrocyte and the production
of matrix.297–299 Specifically, intermittent hydrostatic
pressure is believed to maintain healthy cartilage in con-
trast to shear stresses, prolonged static loading, or the
absence of loading, which lead to cartilage destruction
and ossification.144 Loads may influence cells “indirectly”
(systemic, regional, and pericellular) and “directly” (cell
related).300 Studies show chondrocytes undergo specific
changes in shape and volume and ultimately gene expres-
sion and protein synthesis in a coordinated manner in
response to load-induced deformation of the matrix.301
The matrix changes that are effected by alterations in
hydrostatic pressure, ionic (pericellular pH values) and
osmotic composition, interstitial fluid, and streaming
potentials are detected by the chondrocytes.301 The
chondron (the chondrocyte and its pericellular matrix
[PCM]) has a role as a mechanical transducer poten-
tially through an interaction of type VI collagen with
cell surface integrins or hyaluronan.278 Changes in the
properties of the PCM with osteoarthritis may have an
important influence on the biomechanical environment
of the chondrocyte.302 Chondrocytes are now known
to respond to their local stress-strain environment in a
temporal and spatially dependent way. Specifically, static
and oscillatory mechanical compression and oscillatory
tissue shear can enhance or inhibit extracellular matrix
synthesis and gene expression in chondrocytes.296
Application of oscillatory tension in a fibrin construct
culture system influenced proliferation and matrix
production in both chondrocyte and fibrochondrocyte
biosynthesis.303
Reduced Loading
The suggestion that chondrocytes are sensitive to
mechanical stimuli is supported by studies of denervated
and immobilized joints.7 In disuse atrophy (paraple-
gia, poliomyelitis)304–306 and denervation,307 researchers
observed that chondrocytes increased their synthetic
activity with mechanical stress, whereas their activity was
lowered with decreased compression on the loading sur-
faces. The decrease in the thickness of articular cartilage
(atrophy) and in CS observed in these conditions was also
observed in studies using animal models and hind paw
amputations.308,309 Compared with disuse atrophy condi-
tions, partial amputation of a limb decreases compression
but still allows motion in the remaining joints. Under
these conditions, adult rabbits may show changes within
1 week. In dogs, similar changes may take 11 weeks to be
detectable.310,311 Some of the problems in the use of ani-
mal models for these studies are related to different ages
and species. Another problem is variability in methods,
such as the position of immobilization, the degree of
compression of the joint surfaces, and the extent to which
motion is limited. Reduced loading studies support the
view that maintenance of healthy joint surfaces requires a
regular program of loading. Encouraging seniors to walk
regularly should be beneficial.
Immobilization
Immobilization prevents motion, and, depending on the
position, it may or may not provide an increase or decrease
in loading to the contact area of the joint surfaces. This
limitation in motion results in degenerative changes that
are similar to those seen in osteoarthritis and may result
in cell necrosis.309,311–315
Investigators have used clamps to induce immobiliza-
tion, mostly of the knee joint in small animals, and inten-
tionally or unintentionally they may have compressed
the articular cartilage.316–320 Cell death occurs with such
rigid sustained pressure at focal points of the articular
cartilage. This is presumably because of interference with
nutrition to cells, which is dependent on the cyclic com-
pression and expansion of articular cartilage that occurs
with normal intermittent loading.7 Tomlinson321 and
Maroudas322 considered that simple diffusion of small
solutes was unaffected by cyclic loading. They suggested
that changes such as decreased articular cartilage amount
were caused by the absence of mechanical stimuli to be
sensed by the chondrocytes. Permeability of the cartilage
did decrease with compression.197 Maroudas indirectly
demonstrated that permeability of cartilage correlated
inversely with hydration.322 Large deformation of carti-
lage regulates the manner and rate of fluid transport; the
more rapid the applied load, the more rapid the efflux at
the loading surface.
Simple immobilization without compression
(“unweighting”) also causes atrophy and apparent thin-
ning of the articular cartilage.323,324 Under these condi-
tions, a 41% increase in thickness of the calcified layer
was reported, whereas the actual thickness of the non-
calcified layer decreased.325 In this study, however, there
were no changes in calcified and uncalcified thickness
of HAC in rats with their joints unweighted by tail sus-
pension without cast immobilization. Unweighting a
mobile joint appears to accelerate the advancement of
the tidemark as opposed to restriction of motion that
activates resorption at the chondroosseous interface
only.306 The effect on HAC of unweighting a mobile
joint therefore differs from unweighted joint immobili-
zation. Other changes include a decrease in GAGs and
CS compared with the nonoperated or nonimmobilized
side,326 whereas intermittent compression of articular
cartilage causes the reverse.327–329 With the atrophy of
articular cartilage that has been observed in immobiliza-
tion, there is also an enhancement in collagen synthesis
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
but not in the total amount of collagen. Tammi and
coworkers used splints to immobilize dogs and showed
a 53% increase in collagen production.330 In compari-
son, there was only an 11% to 13% increase in the dogs
that ran on a treadmill for 15 weeks. While no changes
in quantity of collagen were reported, immobilization
reduced the amount of collagen cross-links following an
11-week period of rigid immobilization in dog femora,
a condition that reversed itself upon remobilization.331
While this may be a transient loss in HAC integrity as
the tissue is vulnerable to relatively abnormally high
stresses following a period of immobilization, results
support introduction of gradual loading following this
condition. When immobilization is an essential com-
ponent of, for example, fracture management or fol-
lowing surgery, clinicians should devise exercises that
provide loading to immobilized joint surfaces to best
maintain chondroosseous/subchondral bone integrity.
Unfortunately as there is a lack of accurate, reproduc-
ible, and noninvasive methods to characterize articu-
lar cartilage, especially in vivo, quantitative data about
changes in human HAC after a set period of immobili-
zation are not yet available.306
Rehabilitation Following Cartilage Repair
● High-impact loading should be avoided.
● Immobilized joints should go through cyclic loading.
● Controlled loading should occur through range of motion.
● Sufficient rest periods should be allowed between loading sessions.
● In the early rehabilitation phase, unloaded quick movements
should be used.
● Longer, low-stress exercise is better than shorter, high-stress
exercise.
● Dynamic loading is better than static loading.
● Gentle graduated weight bearing should be used.
●
Unloaded period should be minimized.
● In summary, always consider the type, role, and quantity of the
loading according to the underlying condition of the joint.
Excessive Loading
There have been a number of experiments in which the
joint surfaces have been abnormally loaded. This may be
done by having one non-weight-bearing limb, thereby
creating an increased and altered load on the weight-
bearing side. Alternatively, putting backpacks on the
animal or simulating weight gain could lead to abnor-
mal loading.332 Severe excessive loading experiments
have employed the “drop tower” procedure to subject
articular cartilage to high stress levels. These studies
have shown that chondrocytes can survive up to a 30%
171
compressive strain, but if the stress exceeds 25 MN/m2
and produces a strain that is greater than 40%, tissue
death results.333 This type of impact loading results in a
loss of proteoglycans, fibrillation of the surfaces, and cell
death.227 Load-induced chondrocyte death was related
to load duration and magnitude, with chondrocytes
in the superficial tangential zone more vulnerable to
load-induced injury than those in the middle and deep
zones.334 When loaded tissue extrudes interstitial fluid, it
becomes less hydrated, which causes an increase in pro-
teoglycan concentration.7 That in itself inhibits synthe-
sis of proteoglycans. Parkkinen and colleagues observed
during in vitro studies that “static compressive pressures
consistently inhibit PG [proteoglycan] synthesis in car-
tilage.” The response to cyclic compressive loading is
more variable.
Excessive loading may occur in certain individuals
such as ice skaters who repetitively jump and land on a
hard surface in both practice and performance. Studies
suggest that activities such as jumps should be inter-
spersed with much longer periods of nonimpulsive load-
ing to allow the cartilage to reconstruct following severe
compression.
Effect of Exercise
Exercise or motion in animals and humans has been
shown to cause a swelling of articular cartilage.
Prolonged exercise in animals was observed to pro-
duce hypertrophy of chondrocytes, an increase in the
pericellular matrix, and an increase in the number of
cells per chondron, particularly in the radial and tran-
sitional zones.336 In rabbits, the superficial cells became
more spherical for a transient period after brief exer-
cise. This resulted in an overall change in the size of
the cells.194 Long-term exercise or loading produces
more lasting enlargement. There was an increase in
the volume of the nucleus but not in the overall size
of the cells in the superficial layers. There also was an
increase in the quantity of endoplasmic reticulum and
other cytoplasmic organelles.337 These changes were
observed in young rabbits given a nonstrenuous tread-
mill exercise program for 8 weeks. An increase in the
size of chondrocytes in guinea pigs who did a running
exercise has been reported.338 Helminen and associates
observed an increase in the number but a decrease in
both the volume and the volume density of chondro-
cytes after “strenuous” running in beagles.339 Following
moderate running in young beagles, this Finnish group
has also shown a positive change in articular cartilage
proteoglycans340 and no degeneration of the surface
after a 15-week period.341,342 Eckstein and colleagues
have demonstrated with MRI that thickness of HAC
decreases after physical exercise: 2.8% after 30 knee
bends and 4.9% after squatting with knee at 90 degrees
172 SECTION I • Scientific Foundations
for 20 secs.343 This group also showed that post exercise
HAC imbibes fluid and full recovery may be obtained,
but this can take 90 minutes.343–345 Such studies provide
guidance for therapy programming.
Other investigators have shown marked “wear and
tear” type changes following exercise.342–346 There were
more degenerative surface changes in the femoral heads
of rabbits with sudden maximal exercise compared with
submaximal running.346 Several in vitro studies have
shown that the chondrocytic response to loading, par-
ticularly cyclic stresses, may vary with the length of the
treatment. Palmoski and coworkers subjected cartilage
plugs to static and cyclic stresses that were equivalent to
about 1.5 times body weight.347 They demonstrated a
38% increase in synthesis of GAGs with a cycle of 4 sec-
onds on/11 seconds off but a decrease with a cycle of
60 seconds on/60 seconds off.329 This varied response
has been shown both in cell cultures and in chondrocyte
cultures.337 The response varied with the frequency of
the pressure, the duration of the application, and the
state of the cells. Application for 1.5 hours produced
a strong inhibitory reaction, whereas 20-hour expo-
sure produced stimulation of sulfate incorporation.335
Response variability may relate to the observation that
“complete aggrecan molecule synthesis takes about
1.5–2 hours.”335
When cartilage explants were exposed to two different
cycles of high frequency (2 seconds on/2 seconds off)
and low frequency (60 seconds on/60 seconds off),
there was a decrease in protein and proteoglycan syn-
thesis with low frequency and static loading, whereas
during the high-frequency cycle, there was a stimula-
tory effect on protein and proteoglycan synthesis.348
Unloading restored the synthesis to the preloaded lev-
els. Results of these studies suggest that in the early
stages of rehabilitation, unloaded, quicker movements
should be used. When static loading is introduced, time
in unloaded conditions should follow and be of a longer
interval. Research is needed to determine how differ-
ent exercise regimens affect in vivo cartilage. Following
a review of in vivo and in vitro studies, van Kampen
and van de Stadt concluded that “nutrition of the tissue
plays only a minor role in the processes” involved in
articular cartilage’s adaptation and response to under-
or overloading.327
Note that in vitro studies expose the tissues to only
one type of stress, with forces that are mostly lower than
the physiological levels experienced in vivo, such as at
heel contact and toe-off in the gait cycle. Human hip
and knee forces may reach 4 to 7 times body weight
during gait.349,350 Quantitatively, contraction of mus-
cles may result in greater forces across articular carti-
lage than does normal weight bearing.224 For instance,
although forces of 4 to 5 times body weight may be
transmitted through the knee in walking, the force may
be as much as 10 times body weight in squatting.351 The
compressive ankle joint reaction forces during running
reach 9 times body weight.352 Similar reaction forces are
estimated to occur in gymnastics (straight arm swing on
rings: shoulder, 6.5 to 9.2 times body weight; takeoff
vertical forces, 3.4 to 5.6 times body weight).352 High
transarticular forces can be predicted for all jumping
activities. Studies show that joint surfaces can tolerate
higher dynamic forces than static forces. Equipment can
play a major role in damping joint forces. A new mat in
gymnastics reduced tibia accelerations from 50 to 10 g
and hip accelerations from 20 to 8 g.353 Radin and col-
leagues demonstrated negative effects on articular car-
tilage in weight-bearing joints in sheep that walked for
long distances on concrete floors.354 Those that walked
on wood chips did not show similar effects. It can be
predicted that repetitive forces are considerably greater
when a parachutist lands or when an ice skater lands
following a triple axle. If practice and performance
jumping times are summed, these result in high repeti-
tive impulsive loading to joint surfaces. Microtrauma is
cumulative.
If cartilage is exposed to unloading and is then
loaded, there may be “gross functional failure of
matrix.”347 A reduction in amount of collagen cross-
links following 11 weeks of rigid immobilization in
the femur of dogs331 pointed to a reduced ability of
the PGs of the HAC matrix to cope with compressive
stresses, making the cartilage vulnerable to injuries
of heavy loading. These results suggest that there is
a need for programs of graduated weight bearing and
activity after extended periods of non–weight bearing
or casting. Tammi and associates reviewed studies of
various animal species involving “enhanced loading,”
which produced mixed results as to whether running
exercise injures or does not injure articular cartilage.355
They suggested that one factor in the variability of
results may be the rate at which the program com-
mences. A conditioning period seems to be important.
The Finnish group has conducted many studies on
articular cartilage both in vitro and in vivo, including
immobilization, reloading, and moderate and strenu-
ous exercise. The researchers concluded that the detri-
mental effects of unloading (loss of stiffness, atrophy)
can be reversed with a gentle, graduated program, but
complete restoration was uncertain.156,355 Enhanced
loading in the form of moderate running has positive
effects on articular cartilage, but these are reversed by
strenuous running. It is not yet demonstrated whether
the response to nonstrenuous exercising in human ath-
letes is similar to that of animals. The limits of the
“physiological range” need to be determined, as well
as how mature articular cartilage responds in vivo
(Figure 7-13). Studies suggest that exercise involving
loading should be done gradually.
 CHAPTER 7 • Cartilage of Human Joints and Related Structures
Figure 7-13
Hypothesis of the effect of intermittent physical stress on the
biological properties of articular cartilage. Tammi et al. suggested that
atrophy or injury occurs in articular cartilage because of suboptimal
physical stresses, whereas stresses within physiological limits stimulate
the tissue to develop improved biological properties. Increasing
the stress beyond this physiological boundary causes progressive
deterioration of its biological properties. (From Tammi M, Paukkonen
K, Kiviranta I et al: Joint loading-induced alterations in articular
cartilage. In Helminen HJ, Kiviranta I, Tammi M et al, editors: Joint
loading, p 82, Bristol, 1987, Wright.)
The knowledge of the response of articular cartilage
to loading and to mechanical stimuli is growing. The
results of studies completed since the 1980s appear to
challenge the ancient dogma of “rest,” since in unloaded
joints, rest has proved to be detrimental to the health of
articular cartilage. Researchers have hypothesized that
one of the objectives of physical therapy, particularly
in mature clients who have been confined to bed for
lengthy periods, such as in conservative treatment of a
fractured femur, should be to provide loading experi-
ences for the unaffected leg to maintain the health of
articular cartilage. This could be as simple as a regimen
of leg pushes against rubber bands or springs and bent
leg and resisted pelvic raises. It may well be that all
health care professionals should aim to minimize the
unloaded period and, whenever possible, to allow at
least partial weight bearing to provide some mechani-
cal stimuli to the articular cartilage. Additionally, clini-
cians must recognize that there is an unknown critical
upper limit to the load that cartilage can bear without
adverse effects. Following injury and periods of immo-
bility, cartilage is less stiff and less capable of tolerating
high loads.
Summary
HAC is part of the load-bearing unit that consists
of the HAC layer and the subchondral bone; it has
important interactions with synovial fluid. Nutrients to
chondrocytes must traverse a long route from vessels
173
in the subsynovial tissues, such as the supporting sub-
chondral bone, through the joint space to cartilage.
The vascular synovial lining tissues also play a large role
in the health of the joint and articular cartilage. These
tissues can also release, secrete, or allow passage of
many substances with the capacity to degrade cartilage.
A sparse single population of chondrocytes is respon-
sible for maintaining the extracellular matrix (ECM) of
this tissue through a balance of anabolic and catabolic
activities.
HAC distributes and transmits loads to the
subchondral bone, which also undergoes significant
deformation under loading. Both the collagen frame-
work and the proteoglycan matrix are essential to the
normal function of HAC. Tensile strength comes from
the collagen network, which limits the expansion of the
viscoelastic aggrecan component and provides compres-
sive stiffness. The aggrecan/hyaluronan aggregates bind
high amounts of intercellular water attributed to their
fixed negative charges and are in turn responsible for
the elasticity of HAC. The mechanical environment of
chondrocytes and their strong interrelationship with the
ECM in conjunction with biochemical factors (growth
factors and cytokines) contributes largely to carti-
lage homeostasis. Researchers theorize that repetitive
impulsive loading plays a major role in the degradation
of HAC, producing microtrauma that is cumulative.
Conditions of stress deprivation to HAC demonstrate
an alteration in morphological, biochemical, and bio-
mechanical characteristics of both HAC and underlying
subchondral bone.
Because it is avascular, healing is imperfect unless the
defect involves the vascular subchondral bone. Healing
times for restoration of HAC’s normal structure are
lengthy and are not well defined in humans. Chondrocytes
have a limited ability to reconstitute the tissue once it is
injured. Both natural and surgical repair efforts to replace
the highly ordered ECM of native HAC ultimately result
in mechanically inferior fibrous tissue. The developing
science of tissue engineering may improve the repair and
regeneration of cartilage via in situ delivery of enough
chondrogenic cells in a medium that supports maximal
differentiation and deposition of appropriate ECM for
further cartilage regeneration. Clinical success of such
therapy is of great research interest and is measured by
the quality of integration into the surrounding surface,
biomechanical properties of the tissue, and durability
of the engineered tissue, biocompatibility, and eventual
outcome of proper alignment with the surface of the
adjacent tissues.
Advances in imaging technology, such as MRI, are start-
ing to provide qualitative evaluation of HAC’s response
to loading, critical to the continued health of HAC and
its recovery following inactivity or immobilization. This
174 SECTION I • Scientific Foundations
technology should allow for a more evidence-based
approach to the design of optimal rehabilitation pro-
grams and management of cases involving prolonged
movement restriction, immobilization and weightless-
ness, and under conditions in which there is reintroduc-
tion of movement postimmobilization and postsurgery
in humans. High loads and static loading are less well
tolerated and can be detrimental; microtrauma is cumu-
lative. Clinicians must consider the type, role, and quan-
tity of load in treatment programs.
References
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been incorporated into a CD-ROM that is provided with this text. The
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possible.There are a total of 355 references for this chapter.

P ERIPHERAL N ERVE : S TRUCTURE ,
F UNCTION , AND P HYSIOLOGY
David S. Butler and John P. Tomberlin
Introduction
The health status of neural tissue will always be a con-
sideration in the management of any injury or disease.
This chapter focuses on the peripheral nervous sys-
tem by describing the physiology and dynamics, the
pathophysiology and pathodynamics, and the clinical
sequelae that may follow nerve injury. The incidence
of peripheral nerve injuries and their clinical impact
may well be underestimated, as many authors have
argued.1–4 Increases in the prevalence of diabetic neu-
ropathy and that associated with HIV/AIDS surely
contribute. In addition to motor and sensory conse-
quences of nerve injury, further pathobiological pro-
cesses such as neurogenic inflammation, dorsal root
ganglia upregulation, central sensitization, immune
activation and pain construction—all of which may be
initially adaptive—may ultimately become damaging.
This chapter also presents the case for the minor nerve
injuries that clinicians are likely to encounter and that
may be evident with physical diagnostic testing, as
outlined elsewhere.4
Nerve Fibers
The functional unit of the nervous system is the neu-
ron. A neuron consists of a cell body and outgrowths,
the Schwann cell–enveloped axon, and dendrites, which
together are referred to as a nerve fiber. The neurons
contributing to the peripheral nervous system exist in
the cranial and spinal nerves, linking the brain and spinal
cord to peripheral tissues.
8
C H A P T E R
Parts of the Nerve Fiber
● Cell body
● Axon
● Dendrites
There are three functional types of nerve fibers in the
major nerve trunks: afferent (sensory), autonomic (vis-
ceral efferent), and motor (somatic efferent). These fibers
exist in varying quantities depending on the particular
nerve. Alphabetical and numerical classifications exist and,
unfortunately, do not always overlap. Commonly used
classifications and the functions of the various types of
fibers in peripheral nerve are presented in Table 8-1. Care
should be taken when classifying nerve fibers because of
functional overlap.
Types of Nerve Fibers
● Afferent (sensory)
● Motor (somatic efferent)
● Autonomic (visceral efferent)
The faster nerve fibers such as A delta fibers are more
concerned with speed and quality of human movement.
C fibers conduct far more slowly and are more involved
with nociception and, via the compounds they release,
the health of surrounding tissue. In myelinated fibers,
there is a direct proportional relationship between fiber
175
176 SECTION I • Scientific Foundations

Table 8-1
Type, Function, and Speed of Peripheral Nerve Fibers
Diameter Speed Speed
Type Function (µ m) (m/sec) (mph)

Afferents
DEEP
I Input from muscle and tendon 12–20 70–120 160–272
receptors
II Afferents from muscle spindles 6–12 30–70 68–160
III Pressure/nociceptive 2–612–30 27–68
afferents from joints and <20.5–2 1–4
aponeuroses
IV Pain
CUTANEOUS
Aα,β Tactile receptors 6–12 30–70 68–160
Aδ Cold; “fast” nociception 2–6 12–30 27–68
C Warm; “tissue damage” nociception 0.5–1.0 0.5–1.0 1.0–2.5
Efferents
α Extrafusal muscle fibers 12–20 60–100 135–225
γ Intrafusal muscle fibers 2–8 10–30 23–68
B Preganglionic autonomic <3 3–30 6–68
C Postganglionic autonomic <1 0.5–2.0 1–4

Modified from Butler D: Nerve: structure, function, and physiology. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 171, Philadelphia, 1996, WB Saunders.

diameter and conduction velocity. Myelinated axons, such Axon

as the alpha-motor and the large-diameter sensory neu-
rons, possess unmyelinated gaps (1 to 2 mm apart) that
are full of ion channels in the axolemma, called nodes of Schwann cell
Ranvier. These allow fast conduction because depolariza-
tion at one node can “jump” and initiate a depolariza-
tion at the next node without activation of the internodal
Endoneurium
membrane. Impulse conduction in myelinated fibers can
be six to eight times faster than in nonmyelinated fibers.
Myelination is often altered in diseases and injury to
peripheral nerves, either from mechanical distortion such Myelin
as overstretch or compression, loss of metabolic support, sheath
or the presence of various inflammatory compounds. Basement
A key element of a nerve fiber is the Schwann cell membrane
(Figure 8-1). Schwann cells are responsible for laying
down myelin and “wrapping” it around axons. They
are also a source of immune compounds, which may be
proinflammatory (e.g., interleukins) and relate to nerve Node of
Ranvier
regeneration but also inflammation and pain.5,6 Where
axons are unmyelinated, such as in the case of C fibers,
a Schwann cell will wrap around a single axon or a num-
ber of axons; this unit is known as a Remak bundle. A
bilaminar plasma membrane, the axolemma or axon
membrane, lies on the innermost aspect of the Schwann
cell. This membrane ultimately surrounds the cytoplasm
Figure 8-1
or axoplasm of the neuron. Diagrammatic myelinated peripheral nerve fiber. (From Sunderland
Sodium channels are “pores or passages” in mem- S: Nerves and nerve injuries, ed 2, Edinburgh, 1978, Churchill
brane bound protein complexes (receptors) that allow Livingstone.)
 CHAPTER 8 • Peripheral Nerve: Structure, Function, and Physiology
ions to transfer across the axolemma and give the
neuron the property of excitability. The channels are
“gated” and can be opened or closed in response to
various stimuli (electrical, chemical, mechanical, or
changes in temperature) to allow passage or blockage of
ions (Figure 8-2).7,8 Channels have a half-life of only a
few days,9 suggesting that the peripheral nervous system
is highly self-regulatory. Sodium channel expression
alters during nerve injury, creating a different reper-
toire of channels in the dorsal root ganglion (DRG)
or at injury sites.3,10,11 The axons and Schwann cells
are enclosed in a basement membrane (see Figure 8-
2) and then surrounded by a connective tissue sheath,
discussed later.
The Peripheral Nerve Trunk
The nerve fibers, blood vessels, and various connective
tissues sheaths constitute the nerve trunk. The connec-
tive tissues are quite specialized (Figure 8-3). Around
the basement membrane of each myelinated nerve
fiber or group of unmyelinated fibers is an endoneurial
tubule. Bundles of tubules are surrounded by layered
perineurium to form fascicles, and these fascicles are
held within an internal epineurium and surrounded by
external epineurium. A thin connective tissue mem-
brane, the mesoneurium, then surrounds the nerve
trunk. This tissue helps nerve trunks to slide next to
adjacent tissues.12 This gliding is likely to be inhibited
if the tissues are scarred from injury or in the presence
of inflammation. The epineurium, perineurium, and
endoneurium provide a tough supporting framework
for the contained nerve fibers. Collagen and a few elas-
tin fibers are part of the framework and interlace in all
directions to form an irregular lattice pattern. The peri-
neurial layer is quite specialized. Perineurial cells are
layered, which allows the perineurium to exert some
influence over the tiny vessels that pass through it,
forming a blood-nerve barrier (Figure 8-4). The endo-
neurium provides the intrafascicular packing and, by
the tubular arrangement, also helps maintain the neuro-
nal environment including an appropriate endoneurial
fluid pressure.1,2,13
A B C D
Neurotransmitter Neurotransmitter
-- --
++ ++
Magnesium ion Cytoskeleton G-protein
177
Perineurium
Axon
Blood vessel
Internal
epineurium
Endoneurium
External
epineurium
Mesoneurium
Figure 8-3
The peripheral nerve trunk. (From Butler DS: Mobilisation of the
nervous system, Melbourne, 1991, Churchill Livingstone.)
Structural Variations in the Peripheral Nerve
Complex
Nerves are not homogeneous structures. Approximately
50% of a peripheral nerve is connective tissue, although
this amount varies depending on the nerve and the level,
from 80% (as in the sciatic nerve in the gluteal region) to
as little as 22% (the ulnar nerve at the elbow).14 In addi-
tion to these variations, the fascicular arrangement differs.
Fascicles spiral and form multiple links, allowing variable
contributions of sympathetic, motor, and sensory fibers
to branch off the parent nerve. The maximum length of
a segment of nerve with a consistent fascicular pattern is
15 mm,1 although distal segments of the nerve have fewer
internal interconnections.15 The fascicular patterns can
Figure 8-2
Four different kinds of open ion channels.
A, Electrically gated channel. B, Ligand
Outside cell membrane gated channel. Neurotransmitters dock
into the protein, opening or closing the
gate. C, Mechanically gated channel. The
cytoskeleton may pull the channel open.
D, Metabotrophic channel of G-protein
Inside cell membrane
gated channel. The receptor is separated
Metabotrophic from the ion channel, and G-protein
receptor activation is required to open the channel.
178 SECTION I • Scientific Foundations
Endoneurium
Epineurium
Perineurium
Feeder Extraneural vessel
vessel
Figure 8-4
The blood supply of a multifascicular segment of peripheral nerve.
Note the inset of a blood vessel passing through the perineurial
lamellae. (Adapted from Lundborg G: Nerve injury and repair,
Edinburgh, 1988, Churchill Livingstone.)
range from one fascicle to many fascicles of varying sizes;
usually the more fascicles, the greater the ratio of connec-
tive tissue to conducting tissue (Figure 8-5).1 It is likely
that nerves are more resistant to pressure where there are
more connective tissues and more fascicles (e.g., sciatic
nerve in the buttocks), while nerves that have fewer con-
nective tissues will need to glide more (e.g., ulnar nerve at
the elbow) to avoid potentially dangerous forces.
These structural variations are significant for the cli-
nician. First, they mean that the sensorimotor outcome
from injury depends, in part, on the site of injury and
Figure 8-5
The effect of pressure on polyfascicular and oligofascicular peripheral
nerve. Where a peripheral nerve is multifascicular, a greater pressure
will be required to affect nerve fibers than where there is a small
number of, or only one, fascicle. (From Butler DS: Mobilisation of the
nervous system, Melbourne, 1991, Churchill Livingstone.)
the fascicular arrangement at that site. Second, it means
that injury to or forces placed on a peripheral nerve in
areas with less connective tissue may result in neurogenic
symptoms, such as tingling or paralysis. There is usually
a higher connective tissue percentage where nerves cross
joints (the ulnar nerve is an exception). In areas where
there is more connective tissue, the conducting tissues
would be better protected and neurogenic symptoms
less likely. In this case, the innervated connective tissues
(discussed later) may contribute to symptoms.
Neuroanatomical variations exist between nerve
roots and nerve trunks. Nerve roots lack the epineu-
rium and perineurium of a peripheral nerve, making
them more vulnerable to compressive forces from
structures such as a prolapsed disc or to irritation by
chemicals such as the byproducts of intervertebral
joint injury and nucleus pulposus in the intervertebral
foramina. However, they can withstand considerable
tensile force, as the peripheral nerve connective tis-
sues dissipate forces to the dura mater and the epi-
dural connective tissues. The dural sleeve is a funnel,
wider proximally than distally, and it may “plug” when
pulled into the intervertebral foramen, thus preventing
further elongation of the nerve root.1 This funneling
would occur in an outstretched arm position such as
an upper limb neurodynamic test.
The anatomy of the axon bundles in nerve roots is
similar to that of axons in nerve trunks. However, there
are differences in the dorsal root ganglion (DRG). This is
discussed later.
Connective Tissue Innervation
The neural connective tissues are self-innervated by the
nervi nervorum.16–18 This innervation, combined with
a superb but variable blood supply, makes the con-
nective tissues of nerve potentially reactive. Branches
form off primary afferent fibers and innervate the epi-
neurium, perineurium, and endoneurium. There is
also an extrinsic sympathetic innervation from fibers
entering the nerve from the perivascular plexuses.16–19
Mast cells exist in the epineurium, though few exist
in the endoneurium.20 With a nerve injury, the num-
ber of mast cells in the endoneurium increases.21 Mast
cells release inflammatory mediators such as histamine
and are a probable source of neurogenically mediated
inflammation.22,23
For the clinician, this means that nerves can be
potent contributors to a pain experience, perhaps with-
out damage to the conducting fibers. The innervated
connective tissues are the probable source of symptoms
of the local, sometimes intense, pain when a nerve is
palpated.1 It also means that nerve injury does not have
to be associated with paresthesia. The only symptom
may be pain.
 CHAPTER 8 • Peripheral Nerve: Structure, Function, and Physiology
Vasa Nervorum and Diffusion Barriers
Peripheral nerves possess a superb blood supply, which
is necessary because peripheral nerve function is highly
dependent on adequate oxygenation. The vasa nervorum
consists of a complex system of extraneural feeder vessels
and an intrinsic longitudinal interconnected supply in all
the neural connective tissues (see Figure 8-4).1,2,13 The
intraneural system is extremely well developed and may
still preserve nerve function if some extraneural feeders are
damaged.2 Intraneural blood vessels are sympathetically
innervated.24,25 The nerve supply to a particular blood vessel
arises from the nerve trunk that the blood vessel supplies.25
This arrangement probably allows an adjustable blood
supply for differing functional demands on the nerve.
To maintain the normal neuronal environment, the
endoneurial capillary bed and the perineurium have
acquired specialized features. The endoneurial capil-
lary bed is similar to the capillaries of the CNS, where
there is a barrier to certain substances circulating in the
blood that has been called (after the blood-brain bar-
rier) the “blood-nerve barrier.”26,27 It is also clear that
the perineurium presents a barrier to some external
substances such as inflammatory agents and bacteria.1
The barrier function also works from inside to outside
as well as outside to inside, as no lymphatic channels
cross it. Therefore, edema in the subperineurial spaces
may take a long time to disperse or lead to persistent
endoneurial edema.13,28
Researchers have observed that peripheral nerves can
pass through sites of infection without impairment of
nerve function.1 Although the perineurial barrier is quite
resistant to ischemia29 and mechanical deformation,30 long-
standing compression and pinching will breach it. Once
pathology becomes intrafascicular, because of the barrier,
it may be difficult to move, and there may be irreversible
aspects of the clinical picture such as persistent pain and
muscle weakness.
The design of the vasa nervorum supports the mobile
nervous system to ensure optimal neuronal function.
Feeder vessels to a peripheral nerve have some leeway so
that the nerve can stretch and the feeder vessel is not overly
stretched. Anatomically, the blood supply to nerve roots
develop in a spiraling “pigtail” formation31 so that stretch
does not hinder the flow and the nerve roots can move freely
in the intervertebral foramina. In general, most blood ves-
sels enter a peripheral nerve around joints, where there
is more protection, and nerve movement in relation to
surrounding tissues is not as extreme as in areas farther
from the joints.
Dorsal Root Ganglion
The dorsal root ganglia (DRG) is an enlargement or swell-
ing of the dorsal root, found just inside the interverte-
bral foramen of the bony spine. The DRG is the location
179
where the cell bodies of the somatic sensory (afferent)
neurons are found. Each DRG houses thousands of cell
bodies of somatosensory (afferent) neurons. These cell
bodies are densely packed and wrapped in tough connec-
tive tissue (the dura mater). Each cell body is completely
covered in a layer of flat satellite cells; research has deter-
mined these satellite cells are a type of neural glial cells
that are believed to play a role in the myelination process
of the peripheral nervous system.32
The cell bodies of the DRG can be classified into
smaller cells and larger cells. The smaller cell populations
are mainly dedicated to nociceptive functions (percep-
tion of painful stimuli) and the larger cell populations are
mainly dedicated to non-nociceptive functions (e.g., per-
ception of nonpainful stimuli such as touch and tempera-
ture). The axons of these cell bodies are bifurcated, and
peripherally they connect to the sensory nerve endings in
the skin, joints, and organs. They centrally synapse in the
spinal cord at the dorsal horn (nociception and non-noci-
ception) and the fasciculus gracilis and fasiculus cuneatus
(two point discrimination, vibration, and conscious pro-
prioception) of the dorsal lateral columns. Some afferent
fibers from the DRG have been found in the disc of L5-S1
and the skin in the groin area. This finding suggests that
referred pain in the groin area may originate from a lum-
bar disc, which is likely linked by convergence of afferent
pathways at the DRG level of the nervous system.33
Central and Peripheral Connections
An understanding of normal and abnormal peripheral
nerve function requires some knowledge of the connec-
tions to the central nervous system (CNS) and to tar-
get tissues such as muscles, joints, and skin. Motor fibers
emerge via rootlets from cells in the anterior horn of the
spinal cord and then join with sensory fibers to form
the spinal nerve and later the peripheral nerves. Sensory
fibers pass from the peripheral nerve to the spinal cord
via the dorsal roots. In the cord, they terminate within
10 designated laminae. The large-diameter myelinated
afferents (Aδ and β) pass into the dorsal columns. The
smaller diameter fibers (C and A α′ ) enter into the cord,
travel up or down a segment or two in Lissauer’s tract,
and then pass into the laminated dorsal horn, particularly
into laminae I, II, and V-VII. Lamina I and V are the
origins of the major ascending pathways related to noci-
ception, and they receive all forms of nociceptive input.34
Far more afferents enter the cord than go up to the brain,
resulting in significant convergence on dorsal horn cells.
Preganglionic sympathetic fibers emerge from the
lateral gray matter of the spinal cord segments C8-L3
and then exit via the anterior horn and white rami com-
municantes to join the sympathetic trunk. These neu-
rons pass up, down, or through the sympathetic trunk
before forming a synapse, from which postganglionic
180 SECTION I • Scientific Foundations
fibers emerge to join the peripheral nerves and innervate
nearly all the tissues in the body. Peripheral sympathetic
neurons, except those to the viscera, are efferent only
and innervate glands, smooth muscle, and the connective
tissue of peripheral nerves.
At the distal end of peripheral nerve are the terminal
boutons. These may be free nerve endings or specialized
receptor endings responding to combinations of thermal,
mechanical, and chemical stimuli, or the motor end plate
in the case of striated muscle. Researchers debate as to
whether a nociceptor actually exists,34 although the term
is used here as it is in most of the literature.
Basic Neurophysiology
Action Potentials
A unique feature of neural tissues is that they can gen-
erate and propagate electrical messages. This function
relates to the cell membrane. A difference in concentra-
tion exists across the cell membrane of potassium (K+),
sodium (Na+), and chloride (Cl−) ions. These ions can
selectively permeate ion channels in the membrane so that
an unequal distribution of net charge occurs. The resting
membrane potential results from an internal negativity
resulting from the active transport of sodium from inside
to outside the cell and potassium from outside to inside
the cell. Membrane potential ranges between −70 mv and
−90 mv. The generation of an action potential that occurs
at the threshold level of −55 mV ultimately converts the
negative resting potential into a positive depolarization
of around +40 mv. Sodium channel accumulation in the
membrane of damaged nerves is likely to lead to easier
depolarization and increased excitability, discussed later
in the chapter.
Motor axons conduct action potentials peripherally
toward the synaptic or neuromuscular junctions. Sensory
neurons conduct toward the cell body. These conduc-
tion directions are referred to as orthodromic conduc-
tion. However, currents can travel in both directions
along an axon. Antidromic impulses, most studied in C
fibers, travel in an opposite direction (away from the cell
body) to the orthodromic ones and are the signal for the
release of vasoactive chemicals such as the neuropeptides
substance P and calcitonin gene related peptide stored in
vesicles at the terminal boutons of C fibers.
Axonal Transport
Neurons are remarkable cells because they are so elon-
gated. From dendrites in the dorsal horn to terminal
boutons in the foot, for example, a neuron may be 4
feet long. Nearly all neuronal protein synthesis occurs
in ribosomes in the cell body and proximal dendrites.
Considering that the cell body in the dorsal root ganglion
or in the anterior horn produces the axoplasm, the trans-
port of channels and transmitters to the foot, passing
over and through different structures and even receiving
a different blood supply, is an exceptional feat. In addi-
tion, mammalian axoplasm is quite viscous, about five
times the viscosity of water,35 and is thixotropic, meaning
that it requires constant agitation and if it stops flowing,
it will gel.36 The energetics of axoplasmic flow require a
system of neurofilaments, microtubules, actin filaments,
and binding proteins.37 Mitochondria located along the
axon provide a source of energy for the transport.
Within the axon cylinder, there is a bidirectional flow
of axoplasm (Figure 8-6). This is obvious, because com-
pression causes damming of axoplasm on both sides of
the constriction. In antegrade transport (cell body out-
ward), there are two rates of flow. Materials destined for
the synapse, such as neurotransmitters, travel at up to
410 mm per day.38 A slower flow carries material such
as neurotubule constituents and structural proteins, in
essence the cytoskeleton of the axon; this flow travels at
no more than 30 mm per day.39 There is also a retrograde
flow back from nerve terminals to the cell body, traveling
quite rapidly at about 300 mm per day.40 The axoplasm in
Dendrite
Nucleus
200 mm / day
RETRO ANTERO
Target
tissue
Synaptic
cleft
400 mm / day
60 mm / day
Mitochondria
Figure 8-6
Bidirectional axoplasmic flow. (From Butler DS: Mobilisation of the
nervous system, Melbourne, 1991, Churchill Livingstone.)
 CHAPTER 8 • Peripheral Nerve: Structure, Function, and Physiology
this flow carries unused material from the antegrade flow
and neuronotropic factors, proteins that can “inform”
the cell body about the state of the axon and the target
tissues. Nerve growth factor, the most studied of these
neuronotropic factors, can regulate the production of
neuropeptides such as substance P and somatostatin.41
Thus, the material carried by the axoplasm is necessary
for the health of both the neuron and the tissues that it
innervates.
The action potential and the axoplasmic flow both
require a source of energy; they access a common pool
of adenosine triphosphate (ATP).8,42 In an anoxic nerve,
both axoplasmic flow and the action potential will stop
within 15 minutes. The relationship between these elec-
trical and chemical phenomena is further emphasized by
the fact that the axoplasm carries essential materials for
electrical conduction, such as axolemma constituents.
Alteration in axoplasmic flow may contribute to the
double crush syndromes and neurogenic inflammation,
as discussed later.
Endoneurial Fluid Pressure
A fluid exists in the endoneurial spaces (the intrafascicular
or subperineurial spaces). The pressure in this endoneurial
fluid (endoneurial fluid pressure) is always slightly greater
than in surrounding tissues such as muscle.2 The endo-
neurial space lacks lymphatic channels, and the endoneu-
rial fluid moves slowly in bulk. The pressure gives nerves
a stiffness and the perineurium an elasticity. Intraneural
edema increases following nerve injury play a major role
in acute and chronic nerve lesions. Even a moderate
pressure increase can interfere with the endoneurial cap-
illary flow,43 causing hypoxia and electrolyte imbalance.
Both mechanical constriction and inflammatory products,
such as proinflammatory cytokines from the nucleus
pulposus,44 may increase endoneurial pressure and lessen
blood flow. An endoneurial edema cannot escape rapidly
owing to the perineurial diffusion barrier, so it may persist
and be subject to fibroblast invasion.13,28
Neurodynamics
Neurodynamics is the study of the mechanics and physi-
ology of the nervous system.45 A neurodynamic test aims
to test the mechanics and physiology of a part of the ner-
vous system. For example, a mechanical component of a
straight leg raise would be the ability of the sciatic nerve
tract to move and strain in relation to surrounding tis-
sues such as lower lumbar discs. The physiological com-
ponents may relate to blood flow, ion channel activity,
and inflammation, as well as representational changes in
the CNS of the sciatic nerve, leg, and its movements.4
Peripheral nerves are not only impulse and chemi-
cal conduits; they are also highly mobile tissues, like
181
muscles and joints. Along with the CNS, the periph-
eral nervous system is designed to function during the
stretching, sliding, and compression that occurs during
everyday living. The spinal canal is approximately 7 cm
longer in flexion than in extension,46,47 and because the
centrode of the motion segment is in the center of the
disc, the neuromeningeal structures, especially the pos-
terior elements, are loaded on flexion.46,48 Peripheral
nerves are located on opposite sides of joint axes. For
example, during elbow flexion, the ulnar nerve at the
elbow stretches while the radial and median nerves
relax. Most neurodynamic studies have focused on the
median and ulnar nerves.12,49–55 In normal daily move-
ment, nerves may slide 2 cm in relation to surrounding
tissues and contend with strain of 10%. The fate of all
of the peripheral nerves while they contend with limb
and trunk excursions should be of interest to clinicians.
Peripheral nerve adaptation to movement also depends
on the surrounding tissues. For example, in 90 degrees
of shoulder abduction, from wrist and elbow flexion
to wrist and elbow extension, the median nerve has to
adapt to a nerve bed nearly 20% longer.12 With the inclu-
sion of pathological processes in the nerve bed that can
interfere with movement, the normal mechanosensitive
nerve may become hyperalgesic.
Activities of Nerves during Normal Movement
● Slide more than 2 cm
● Are strained 10% or greater
The following sections highlight some of the key fea-
tures of neurodynamics that have clinical relevance for
the assessment and management of peripheral nerve
problems.
Mechanical Continuum and Brain Representation
of Nerve Injury
A fundamental principle of neurodynamics is that the
nervous system forms a tissue continuum throughout
the body. For example, movement of the wrist and fin-
gers physically affects the median and ulnar nerves in the
upper arm and shoulder.51,52,56 Neck flexion alters knee
mobility in the slump sitting position,57 and ankle dorsi-
flexion in a straight leg raise mechanically affects lumbo-
sacral nerve roots.58 The implication of this mechanical
continuum is that injury or disease in one part of the
body can have repercussions elsewhere. The double crush
phenomenon59 is related to this mechanical continuum
and is discussed later.
The clinical presentation of a peripheral nerve injury
also needs to be considered in terms of the representation
182 SECTION I • Scientific Foundations
of the nerve, the tissues it supplies, the movements it
orchestrates, and the meaning of any injury within the
central nervous system. Now known to be remarkably
plastic, the somatosensory system in the brain also has
marked reorganizational abilities after peripheral nerve
lesions.60,61 Clinically, it may not be the local tissue that
determines pain and movement behaviors but more that
person’s thoughts, feelings, and understanding of the
injury. These emotions and cognitions are held in neu-
ral networks associated with the injured body part in the
neuromatrix in the brain.
Neural/Non-neural Tissue Relationships
During movement, neural tissue takes its lead from the
movement of joints and muscles. The physical loading
on a nerve depends on the location of the nerve in rela-
tion to the joint axis. For example, wrist extension clearly
loads the median nerve at the wrist. This concept led to
the development of neurodynamic tests.4 The health of
surrounding tissues, referred to as the interfacing tissue
or “neural container,” is therefore a critical concept in
peripheral neuropathy. Neural tissue must slide through
tunnels in muscles and through fascial openings; it must
be compressed against various structures such as bone,
and because of the continuum it is influenced by remote
joint positions. Research has shown that the addition of
sensitizing maneuvers in neurodynamic testing had no
effect on the intensity or area of experimentally induced
muscle pain utilizing the slump test or straight leg raise.62
This information lends some support to the validity of
neurodynamic testing as a preferential physical diagnostic
test that may bias the neural tissues even in the presence
of a painful muscle injury.
Ulnar nerve neurodynamics at the cubital tunnel has
been well studied and provides a nice example. On elbow
flexion, the ulnar nerve is pressed firmly onto bone at the
elbow after 90 degrees of elbow flexion. It even decreases
in diameter by as much as 50%.63 This pressure increases
if the shoulder is abducted or the wrist extended.56,64 The
interface that comes into play as well as the tunnel is up
to 50% smaller in flexion than in extension.63,65
Peripheral nerve neurodynamics and therefore neuro-
physiology may be adversely affected, with abnormalities
in interfacing tissues such as callus development, forma-
tion of bands of scar tissue, pressures from hematoma,
or enlarging tumors and ganglia. For clinicians treating
nerve entrapment or irritation, examination and perhaps
treatment of the interfacing structures is necessary.
Vulnerability of the Peripheral Nervous System
Despite the strength and arrangement of connective tis-
sues, peripheral nerves are vulnerable to various human
behaviors and injury at certain sites, and thus patterns
of nerve injury emerge. For example, the ulnar nerve
in Guyon’s canal at the wrist is vulnerable in cyclists,66
the superficial peroneal nerve is vulnerable in those with
ankle sprains,67 and hyperextension of the hip injuring
the femoral nerve has been described in dancers.68
Sites of peripheral nerve and nerve root vulnerability
can be identified:
1. Tunnels. Where a nerve is in a tunnel, especially one
with hard sides such as the carpal tunnel, spatial com-
promise of the nerve will be a greater possibility than
elsewhere. Within a tunnel, the contained nervous
system always has the potential to rub on the tunnel
structure, creating friction. Trauma and alterations to
tunnel structures, such as the intervertebral foramina,
could mechanically or chemically compromise the
neural structures contained within.
2. Branches. Where a nerve branches, it is more difficult
for the nerve to move away from forces (e.g., radial
nerve at the elbow, union of medial and lateral plantar
nerves in the forefoot).
3. Hard interfaces. Where a nerve lies on bone or passes
through fascia, it may be more readily compressed
(e.g., radial nerve in the spiral groove of the humerus,
cutaneous branches of the posterior primary rami of
thoracic spinal nerves as they pass through fascia).
4. Proximity to the surface. Nerves such as the sensory
radial nerve in the forearm or branches of the super-
ficial peroneal nerve on the dorsum of the foot are
vulnerable to external compression.
5. Where nerves are fixed to interfacing structures. Some
areas of nerve are more firmly adherent to interfac-
ing tissues than others—for example, the common
peroneal nerve at the head of the fibula and the radial
nerve at the elbow. It means that the adherent seg-
ment of nerve cannot move and slide next to adjacent
tissues during movement.
Sites of Peripheral Nerve and Nerve Root
Vulnerability
● Tunnels
● Branches
● Hard interfaces
● Proximity to the surface
● Where nerves are fixed to interfacing surfaces
Some nerves have a number of these vulnerable fea-
tures. For example, at the ankle, where the tibial nerve
branches into the medial and lateral plantar nerves in the
posterior tarsal tunnel, it is superficial and lies on a hard
interface.
Certain disease processes affect peripheral nerves
and make them more vulnerable to injury. Generalized
 CHAPTER 8 • Peripheral Nerve: Structure, Function, and Physiology
diseases such as diabetes mellitus, hypothyroidism, alco-
holism, immune deficiency syndromes, and rheumatoid
arthritis adversely affect neuronal function. The periph-
eral nerves of diabetics are more susceptible to compres-
sion than are those of nondiabetics,69 perhaps because of
the greater ease of blocking axonal transport in diabetics.
Texts on nerve entrapment invariably list vulnerable areas
for particular nerves, and the reader is referred to more
detailed sources.1,4,66
Extent of Strain and Neural Excursion
Nerves that have been physically loaded by functional
movement of the trunk or limbs react by moving and
by absorbing some of the pressure. Some classic studies
emphasize this. McLellan and Swash placed needles in the
median nerve epineurium of the upper arms of 15 volun-
teers and measured the amount of nerve movement in
relation to surrounding tissues during various upper limb
movements.50 The results were impressive. Among them,
wrist movement moved a needle positioned in the upper
arm by 7 mm. In one volunteer, the researchers noted
movements of 2 to 3 cm, although unfortunately they
did not record the position of the arm. Similar amounts
of movement have been recorded in a cadaver study.70
On slim individuals, the median nerve may be observed
or palpated moving in relation to surrounding tissue as
the arm is actively or passively moved.
Lumbosacral nerve roots are drawn caudally in rela-
tion to pelvic and spinal structures during a straight
leg raise.71,72 Movements in relation to adjacent tissues
occur all the way to the foot.73 Selective tension can be
placed on a peripheral nerve, as demonstrated by in vivo
experiments74 and cadaver experiments.51 In addition,
the loading on the meninges and spinal cord influences
loading on the peripheral nervous system. In this regard,
Breig’s work on the biomechanics of the CNS46 is highly
recommended for clinicians.
Because of the connective tissue sheaths, nerves are
strong structures, able to resist compression and tensile
forces. The median nerve, for example, can sustain a maxi-
mal load of 70 to 220 N before breaking,1 although dam-
age will occur at forces much less than this. These figures
equate to a length increase of 20% to 30%. During nor-
mal movement, as the nerve stretches, the perineurium
tightens, intraneural pressure increases, and intrafascicu-
lar capillaries stop flowing. This occurs at approximately
8% elongation,75,76 with intraneural microcirculation ceas-
ing at approximately 15%. Because the nervous system is
dynamic, forces that temporarily disrupt circulation are
easily handled and can occur regularly with athletics and
daily activities.
An athlete, for example, may load the sciatic nerve
enough for temporary disruption of circulation during
sustained hamstring stretching. If loading persists, as it
183
could from sustained nonphysiological postures or main-
tained local pressures from a swollen piriformis muscle,
for example, neural tissue damage may ensue.
When tensile forces are placed on a nerve, the intra-
neural pressure increases. It is possible to quadruple the
pressure in the ulnar nerve at the elbow in an ulnar nerve
stress position,77 and the nerve may stretch up to 15% at
the elbow.56 Compression can also occur from alterations
in interfacing tissues, such as changes in the size of a tun-
nel through which a nerve passes and the introduction
of foreign material, such as blood, into the nerve bed.
A critical level for nerve function occurs with compres-
sion of 30 mm Hg.30 Such pressures probably occur often
during human movement, but, if sustained, the viability
of the nerve may be threatened13 owing to edema forma-
tion. Thirty millimeters of mercury is enough pressure to
slow the flow of axoplasm, with 80 mm Hg enough to
stop intraneural circulation.13 These alterations are usu-
ally reversible within a few hours. Injury will depend on
the magnitude of compression (or tension) and the dura-
tion of the loading. In an acute compartment syndrome,
irreversible injury to nerve could be expected after 8
hours.78
With external compressive forces, if actual physical
damage to neurons occurs, it will usually happen at the
edge of the constriction,2,79 where electron microscopy
has revealed more myelin distortion and blood ves-
sel damage than in the center of a compressive force.
Tourniquets and plaster casts may be examples of such
compressive forces. With either vascular or mechani-
cally induced injury, larger diameter fibers, because of
their higher metabolic demands, are usually the first
affected.79,80
Thus, in a peripheral nerve injury, any of the fiber
types or parts of the fiber may be preferentially involved,
with the potential for a vast array of sensorimotor deficits.
Clinicians should take care not to overlook the possibility
of neural tissue involvement when examining peripheral
limb injuries.
Sympathetic Nervous System Neurodynamics
The sympathetic nervous system is part of the peripheral
nervous system, and sympathetic neurons in peripheral
nerves are subject to the same deformation and injury
potential during movement as somatic neurons. Areas
where the sympathetic nervous system is separate from the
somatic system (i.e., in the trunk, rami, and ganglia) are
also subject to deforming forces during movement.46,81,82
Animal experiments have shown that sympathetic trunk
stimulation has the potential to greatly reduce peripheral
nerve blood flow and hence nerve function.83 Commonly
used tension tests, such as the Slump test, induce sympa-
thetic responses in humans.84,85 Clinicians are urged to
consider the possibility that the structure and function
184 SECTION I • Scientific Foundations

of sympathetic neurons, either in the trunk or in periph-
eral nerve, may be adversely affected, particularly when
injuries are longstanding or recurrent in nature.
Nerve Injury
Modern Pain Concepts
There are no pain afferents in peripheral nerves. Nociceptors
send quantitative, not qualitative, information. Pain is con-
structed in the brain. While a damaged peripheral nerve
may contribute to a pain experience, this is not always the
case as a person can have damaged nerves yet experience no
pain or other symptoms.86 Whether an injury hurts or not
depends on the injury, available stimuli, the context of the
injury, and, critically, the state of the central nervous sys-
tem.87 This chapter is about peripheral neurogenic contri-
butions to pain experiences—that is, those that arise from
nerve trunks, plexuses, and roots (i.e., anywhere peripheral
to the dorsal horn in the case of limb and trunk pain or the
medullary horn in the case of facial pain).
Factors That Affect Injury and Pain
● Type of injury
● Degree of injury
● Available stimuli
● Injury context
● State of CNS
A peripheral nerve can directly contribute to a pain
experience in two ways. First, the innervated connective
tissue sheath of a peripheral nerve may be mechanically
or chemically sensitized and contribute; second, with
midaxon pathological changes, ectopic impulse produc-
tion may occur. Sensory neurons are somewhat plastic.
With midaxon injury, alteration in nerve terminals, dor-
sal root ganglia, and even altered gene expression in the
neuron can occur.88,89 Indirectly, once a nerve is dam-
aged, it may then contribute to inflammation in the tar-
get tissue via the process of neurogenic inflammation; it
may also contribute to changes in the central nervous sys-
tem, essentially amplifying any peripheral input. It is this
almost inevitable involvement of the rest of the nervous
system that is probably the main reason there is no con-
stant pattern of pain or functional loss following nerve
injury. In this regard, the reader is referred elsewhere.90
Categories of Nerve Injury
Nerve injuries have been classified according to severity
by Seddon (neurapraxia, axonotmesis, neurotmesis)91 and
Sunderland (grades 1 to 5).1 Similarities and differences
of the classifications and their relationship to abnormal
impulse generating sites are summarized in Table 8-2.
For clinicians dealing with peripheral nerve injuries, a
peripheral neuropathy may exist in which the pathology
is not as severe as in the categories shown in Table 8-2,
or mild pathology may not be demonstrable on current
measurement techniques. Seddon and Sunderland’s cat-
egorizations are based on gross pathology and functional
loss, and they do not register pain, sensory phenomena,
or minor disturbances in motor function. These catego-
ries are more relevant to surgical states. A preneurapraxic

Table 8-2
Categories of Nerve Injury
Increasing severity Abnormal Preneurapraxias
of neural damage Impulse-
Neurapraxia Sunderland I
Generating Site
Local conduction block, axon Local conduction block, axon
(AIGS)
continuous, innervated tissue patent continuous, innervated tissue patent
Increased Axonotmesis Sunderland II
excitability Loss axonal continuity, some Loss axonal continuity, some
degeneration of distal axons (e.g., degeneration of distal axons (e.g.,
severe entrapment or traction injury) severe entrapment or traction injury)
Neurotmesis Sunderland III
Loss of continuity by severance or scar Loss of axonal and endoneurial
continuity, perineurium intact
Sunderland IV
Loss of perineurium with epineurium
intact
Sunderland V
Complete nerve severance

Modified from Butler D: Nerve: structure, function, and physiology. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 179, Philadelphia, 1996, WB Saunders.
 CHAPTER 8 • Peripheral Nerve: Structure, Function, and Physiology
state surely exists in both clinical and subclinical forms.
Sunderland1 refers to irritative lesions in which conduc-
tion is normal, calling them “perversions of function.”
Lundborg defines two preneurapraxic categories.2 The
first is an immediately reversible metabolic block; the sec-
ond is a block occurring with intraneural edema, reversible
in a few days or weeks. The abnormal impulse generat-
ing sites (AIGS), discussed later, are difficult to include
in the Seddon and Sunderland classifications. Connective
tissue irritation and scarring that may involve the nervi
nervorum also cannot be classified along these classic
lines. Clinicians are urged to expand their categorization
of nerve injury to include the notion of AIGS.
Pathobiological Processes
Unlike the terminal boutons and perhaps dorsal root gan-
glia cells in which the axolemma is designed to generate
impulses, the vast majority of the nerve fiber is designed
for impulse transmission rather than impulse generation.
For a nerve to be a persistent source of pain, an abnormal
impulse generating site (AIGS), referred to sometimes as
an “ectopia,” must be present.
Abnormal Impulse Generating Sites (AIGS)
The vast majority of nerve injuries occur in continuity—
that is, the nerve is not cut. Midaxon impulse generation
relates to an increase in the number and kind of ion chan-
nels in the membrane (upregulation), particularly in
areas where the myelin sheath is disturbed or absent.3,92,93
Ion channel number and kind are constantly remodeling,
so the afferent neurons retain what the brain determines is
an appropriate level of sensitivity to stimuli. When nerves
are injured, further opportunities for channel insertion
occur. Known pathological processes related to ectopic
activity include neuromas,94 demyelination,95 immature
axon sprouts caught in scar,3 cross-excitation (ephaptic
synapses),3 and chronic hypoxia (Figure 8-7).96,97
With an accumulation of channels, normally innocu-
ous activity involving lengthening or pinching nerves may
involve ectopic discharges. Even sustained positioning
may evoke discharge from ischaemosensitive channels. For
Dorsal root
ganglion
Receptor
upregulation Axon hillock
Bare axolemma
Crosstalk
Spinal cord
185
example, some “trigger points” have been hypothesized
as sites of AIGSs.3
Some channels are adrenosensitive. Damaged nerve
fibers may become sensitive to sympathetic stimula-
tion.3,98-101 Another process likely to be clinically rel-
evant is the increase of adrenosensitive channels in the
dorsal root ganglia (DRG) and the associated sprouting
of sympathetic fibers.102-104 These processes may explain
the observation that emotional stress can exacerbate
symptoms of nerve injury.4,105
Some cases of ectopia display spontaneous activity,
although spontaneous activity is mainly confined to sensory
axons.106 The dorsal root ganglia are normally mechano-
and chemosensitive segments of nerve, displaying rhythmic
ectopic discharge, easily enhanced by mechanical probing
and chemical stimulation.6,106,107
Altered Pressure Gradients in Nerve
Neurons are particularly sensitive to ischemia, and a com-
plex series of pressure gradients exists around the neu-
rons to ensure optimal blood supply. This is the classic
work of Sir Sydney Sunderland.1 The median nerve in the
carpal tunnel can be used as an example (Figure 8-8). For
optimal nutrition, the pressure must be greatest in the
epineurial arterioles and progressively less in capillaries,
fascicles (endoneurial space), epineurial venules, and the
tunnel around the nerve.108 These pressure differences
allow blood to flow into the tunnel, nourish the neurons,
and then flow out again so that fresh oxygenated blood
can flow in. If the tunnel pressure increases to that greater
than in the vein, venous drainage stops. This stoppage
can occur at pressures as low as 20 to 30 mm Hg.13,109
Sunderland detailed three stages that could ensue follow-
ing persistent pressure around a nerve: hypoxia, edema,
and fibrosis.108 Once venous stasis is present, nerve fiber
nutrition will be impaired, and the resultant neuroisch-
emia may cause pain and other symptoms such as par-
esthesia. If hypoxia continues, damage to the sensitive
capillary endothelium follows, creating an edematous
situation. The blood-nerve and perineurial barriers, so
effective at protecting the nerve initially, are now a disad-
vantage. Endoneurial fluid pressure rises, intrafascicular
End bulb
(neuroma)
Axon sprout
Figure 8-7
Possible abnormal impulse-
generating sites represented on one
neuron. The parallel lines represent
an ion channel. (From Butler DS:
Receptor
upregulation The sensitive nervous system, Adelaide,
2000, Noigroup.)
186 SECTION I • Scientific Foundations
Fascicular Arterial
pressure (PF) pressure
(PA)
Pressure
in the vein
(PV)
Capillary
pressure
(PF)
Tunnel
pressure (PT)
Figure 8-8
Diagrammatic representation of the pressure gradient in the carpal
tunnel (transverse section). One fascicle is represented for ease of
demonstration. For normal neural nourishment, the pressure gradient
must be PA > PC > PF > PV > PT. (From Sunderland S: Nerves and
nerve injury, Edinburgh, 1978. Churchill Livingstone.)
pressure rises, and, because there are no intrafascicular
lymphatics, edema cannot disperse other than longitu-
dinally along the trunk, and the nerve may swell. This
edematous stage provides a superb environment for the
proliferation of fibroblasts and the beginning of the
intraneural fibrosis stage. If pathological forces persist,
the result will be intraneural fibrosis within the fascicle
and in the epineurial tissues. Sunderland referred to the
segment’s becoming a fibrous cord and noted that a
further development may be friction fibrosis elsewhere
along the nerve trunk.108
Stages of Nerve Injury from Persistent Pressure
● Hypoxia
● Edema
● Fibrosis
Blood pressure, both local and general, is an important
determinant in the pathogenesis of nerve lesions. The
common night pain of nerve entrapment and the higher
incidence of entrapment during pregnancy may, in part,
reflect a lower blood pressure. The vascular originated
pathological process described starts within the nerve.
Similar processes could occur with injury that affects
nerve beds and tunnels, such as by blood or edema or
scar strangling extraneural feeder vessels. Nerve damage
may occur with rupture of extraneural blood vessels.110
Some damage may follow if the nerve is adherent to the
nerve bed and repetitive movement distorts the nerve.
Those who rely on nerve conduction tests should be
aware that a nerve conduction test may be negative in
the presence of neuropathy. The process described here
could occur in one fascicle, and nerve conduction tests
cannot be fascicle specific; therefore, the nerve conduc-
tion test may be testing a “good” fascicle.78 In addition,
nerve conduction tests cannot measure the involvement
of the connective tissues.
Mechanical Trauma to Peripheral Nerve
Mechanical trauma may take the form of compression
(“cervical stinger,” tight cast), stretch (“brachial plexus
burner”), or friction (e.g., long thoracic nerve palsy
under scapulae). Anesthetists have long known of the
importance of positioning limbs off neural tension dur-
ing surgery.111,112 Acute compressive or tensile forces may
damage nerve fibers and make any ischemic contribu-
tion to symptoms less relevant. However, with a chronic
compression, a vascular component is obvious, as nerve
fibers can adapt and the mechanical forces present may
not be enough to deform them.113 Research has shown
that micro repetitive strains on a peripheral nerve may be
more injurious than a slow sustained stretch.114 This may
have relevance for cumulative trauma states.
The connective tissues of nerve are easily injured.
Slight trauma, such as mild compression or friction,
may result in an epineurial edema.115,116 Epineurial tears
in the common peroneal nerve are common in ankle
injuries, according to Nitz.117 Owing to the perineurial
diffusion barrier, an epineurial injury is unlikely to affect
conduction of the contained long nerve fibers unless it
is severe enough to compress fascicles or is deeply placed
in the internal epineurium.118 It would seem that symp-
toms from neural connective tissue pathology would be
more likely to be evoked by tensile than by compressive
forces. For example, suppose that the connective tissues
of peroneal nerve branches at the ankle were irritated
or involved in a postankle sprain scar. Although palpa-
tion of the nerves may provoke some symptoms, nerve
stretch such as plantar flexion/inversion of the ankle
plus a straight leg raise is likely to be more symptom
evocative.
Compressive forces distort myelin. Tourniquet
experiments on primate nerves have shown that most
nerve fiber injuries occur at the edge of the tourniquet.
On analysis, the myelin sheaths of the compressed seg-
ments were found to be stretched on one side of the
node of Ranvier and invaginated on the other side.79,119
Such dysmyelination and resultant sodium channel
upregulation could easily be a source of neuronal dis-
charge. Vascular injury is also likely with such forces,
and Schwann cell necrosis has been noted in similar
experiments.120
Clinicians will be aware of the potential mechanosen-
sitivity of the dorsal root ganglion. Impingement and
swelling of the dorsal root ganglion noted on imaging
 CHAPTER 8 • Peripheral Nerve: Structure, Function, and Physiology
studies appears to be well correlated with the severity of
clinical leg pain scores in patients with herniated discs
and narrowed intervertebral foramen.121 In comparison
to the nerve trunk, the dorsal root ganglion is extremely
mechanosensitive107 and chronic compression of the
DRG after injury or disease may contribute to a variety
of pain states such as low back pain, sciatica, hyperalgesia,
and tactile allodynia.122
Inflammation in the Peripheral Nervous System
Anti-inflammatory medications can be useful when
nerves are injured, particularly when the injury is acute.
This suggests an inflammatory mechanism, and since
the 1990s, old concepts of predominant physical com-
pression of nerves are giving way to more inflammatory
and mixed etiologies. Much evidence has accumulated
since the 1990s to suggest that the immune system has
a significant role in nerve injury and pain via inflamma-
tion. In particular, the immune system has been shown
to be a potent contributor to peripheral neurogenic pain
states.6,123 Of particular interest are the proinflamma-
tory cytokines, tumor necrosis factor, interleukin 1, and
interleukin 6. These immune derived compounds assist
in destroying pathogens but can also directly damage
myelin124,125 and directly increase nerve excitability.123,126
There is evidence that the symptoms of pain post discec-
tomy,127 neuropathies,128 and spinal stenosis129 correlate
with levels of proinflammatory cytokines. The nucleus
pulposus also appears to be a critical source of these
molecules.130
The dorsal root ganglia may be a potential phar-
macological target. For example, lidocaine will reduce
mechanical hyperalgesia and tactile allodynia in central
pain syndromes because of mechanical compression of
the L5 dorsal root ganglia,131 while corticosteroids have
been shown to significantly suppress substance P and
inhibit cytokine release at the dorsal root ganglia to aid
recovery of mechanically compressed nerve roots.132
Sequelae of Nerve Injury
With appropriate stimuli and threshold of the central ner-
vous system, an injury or upregulation of the peripheral
nervous system may contribute to a painful experience.
However, the nervous system is an electrochemical con-
tinuum and an initial nerve injury may potentiate prob-
lems elsewhere. The repercussions include the possibility
of the original injury weakening or altering the nervous
system to allow the development of another injury along
the pathway (double crush), abnormal concentrations of
neurotransmitters and modulators secreted into target tis-
sues (neurogenic inflammation), and altered responses of
the receiving cells in the spinal cord and brain leading to
central sensitivity.
187
Double and Multiple Crush Syndromes
Many clinicians are aware that after injury, symptoms will
not always be localized to one spot. Often pain or other
symptoms occur elsewhere, some of which the patient
may regard as insignificant. When these symptoms are
neurogenic, they may be a part of a double crush mecha-
nism. Upton and McComas formulated the double crush
hypothesis.59 The basis of the hypothesis was their study
of 115 patients with either carpal tunnel syndrome or an
ulnar nerve at the elbow. They found that 81 patients
had electrophysiological and clinical evidence of neural
lesions at the neck. The proposal was that minor serial
impingements along a peripheral nerve could have an
additive effect and cause a distal neuropathy. Upton and
McComas suggested that a neuron could become “sick”
from compression or from a disease such as diabetes,59
and because of altered neuronal ultrastructure includ-
ing slowing of axonal transport, the rest of the neu-
ron is rendered more pathologically susceptible. These
notions now have significant experimental and clinical
support,13,69,133-137 though not universally.138
The double crush syndrome “concept” can be use-
ful clinically, in particular as it encourages clinicians to
examine the whole nerve trunk and the tissues around it.4
However, a wise viewpoint would be to accept that the
spread of symptoms may be caused by multiple pathobio-
logical changes. These include remote nerve friction inju-
ries,113 increased expression of proinflammatory cytokines
along damaged neurons,6,139 and interacting discharge at
multiple sites.140 In addition, if second- and third-order
cells in the CNS are sensitized, minimal or even normal
input from the periphery may be interpreted as noxious.
Double crush is an inadequate term because the term
crush does not adequately describe minor neuropathies.
Some have suggested the term double neuropathy.113 The
literature on double crush syndromes includes tarsal tun-
nel syndrome and entrapment elsewhere in the leg,141,142
brachial plexus lesions and carpal tunnel syndrome,143
cervical injuries and carpal tunnel syndrome,137,144 and
failed lumbar surgery and leg pain.145
Mackinnon proposed the clinically valuable concept
of dynamic compression (i.e., there may be no pain at
rest, but certain postures that usually involve stretch of
nerve may evoke symptoms).146 The ulnar nerve provides
a good example. For instance, the wrist pain that a golfer
experiences at the end of the backswing could be com-
ing from the ulnar nerve in or near Guyon’s canal. This
position loads the ulnar nerve in the entire upper limb.
Neurogenic Inflammation
A damaged and discharging peripheral nerve may inflame
the tissues that the nerve supplies. Via antidromic impulses
(proximal to distal discharge in a sensory neuron), the
188 SECTION I • Scientific Foundations
terminals of primary afferent nociceptors, particularly the
unmyelinated afferents (C fibers), release vasoactive and
inflammatory compounds into the innervated tissues.
This evokes a tonic response, which is enhanced when
a peripheral nerve is injured.147,148 The most studied of
the neurogenic inflammatory mediators is substance P.
This and other peptides are synthesized in the dorsal root
ganglion and transmitted to the nerve terminals via the
axoplasmic transport. The majority goes to the periph-
ery, but some is also sent along dendrites into the CNS.
Substance P is particularly vasoactive, thus warming, and
its presence stimulates the release of histamine from mast
cells22 as well as inflammatory mediators such as leukot-
rienes. Other proinflammatory peptides are carried in C
fibers, such as the tachykinins (neurokinins A and B) and
calcitonin gene–related peptide (CGRP), an extremely
potent vasodilator.149
Antidromic impulses can arise from injury along the
nerve, nerve terminals, or dorsal root ganglion.150–152
Antidromic impulses can also arise from the spinal cord
where they are known as dorsal root reflexes.153
Clinicians are urged to consider the possibility of
concomitant nerve or nerve root injury in injuries that
take longer to heal than expected. Reddening, main-
tained edema, and linked positive neurodynamic tests
may be clues. Clinicians are reminded also that this
process is a defense that contributes to tissue health.
It is only when perturbed that persistent problems may
emerge.
Central Nervous System Upregulation and Perturbed
Homeostatic Systems
In response to repeated nociception and in the presence
of injured or altered descending control systems, sensi-
tization and later pathobiological alterations in dorsal
horn and brain cells may result; thus, a representation of
injury such as carpal tunnel syndrome is imprinted within
the CNS.154–156 Descending control systems offer inhibi-
tion and facilitation of afferent input.157,158 These systems
are influenced by factors such as time and environment.
For example, it may not be the nerve injury that is critical
but more the patient’s concept of the injury. Therefore
the influences of thoughts, beliefs, and previous ther-
apy come into play. Pain and the brain are discussed in
Chapter 10.
When the central nervous system is sensitized, there is
likely to be perturbed homeostatic systems—such as the
immune, endocrine, sympathetic, and motor systems—
that in turn may influence peripheral nerve healing and
firing. These systems, which are designed for coping with
acute threat, are not designed for the long term. The link
between the sympathetic and the immune system and
pain was discussed earlier.
Healing Potential of Peripheral Nerve
Compared with the CNS, peripheral nerves possess
a far greater healing potential. When a nerve is cut or
severely crushed and scarred, nerve fibers distal to the
injury degenerate, a process referred to as wallerian
degeneration. The Schwann cell–myelin complex breaks
up and macrophage activity occurs in the endoneurial
tube, degrading the myelin to fat. Schwann cells prolif-
erate, “waiting” for new axonal growth. Although the
connective tissue sheaths remain intact, the result is a
shrunken skeletal nerve with columns of Schwann cells.
Regeneration attempts occur within hours in severance
injury or up to a week later if a nerve has been badly
crushed. Axon sprouts emerge from the proximal side
of the injury and attempt to make contact with Schwann
cells on the distal side. Once contact has been made,
fine growth cones, or filopodia, anchor to the basement
membrane and then enter into the endoneurial tubes.
Results are never perfect. If sprouting axons fail to make
Schwann cell contact, perhaps because they are blocked
by scar or debris, a neuroma will form. Sometimes sprouts
enter inappropriate endoneurial tubules of a different
fiber type. Regeneration can be rapid, with an average
rate of 1 to 2 mm per day. Even with total severance,
skilled surgery can produce good results, although func-
tional improvement may take many months.
With injury in continuity, similar degeneration-regen-
eration processes will be occurring, although in only one
part of the nerve, perhaps a fascicle or part of a fascicle.
There is neither literature nor data on the healing of
injury to the connective tissue sheaths, but given that
they are highly innervated and vascularized, it is assumed
that they heal well. From what is known of the structure
of nerve tissue, axoplasmic flow alterations and meta-
bolically related action potential problems must also heal
well. This may occur by simply removing mechanical and
emotional stresses on the nervous system.
Recovery of function is extremely variable and depends
on the kind and severity of injury and the postinjury man-
agement. As long as axonal continuity is preserved, com-
plete functional recovery can be expected. Neurapraxias
or Sunderland category 1 injuries (e.g., “stinger”) have a
good chance for complete recovery in weeks or months2
depending on the area and severity of damage.
Mobilization and Immobilization
Nerve injury from intraoperative positioning while the
patient is immobilized is a reminder of the vulnerability
of the system.112 There is little literature on the effects
of immobilization of nerve. The potential of ill effects
following prolonged immobilization appears undercon-
sidered, especially in postoperative cases. However, early
 CHAPTER 8 • Peripheral Nerve: Structure, Function, and Physiology
mobilization after peripheral nerve neurolysis has been
encouraged,78 and over the years, there have been calls to
carefully mobilize nerves and their surrounding structures
following injury or surgery.47,50,159 Given the continuity of
nerve, mobilization of neural tissue can be accomplished
without movement or stress on neighboring tissues. For
example, knee extension movements with the hip held
in flexion will move and slide the neural tissues in the
spine with minimal movement of the interfacing tissues.
It means that early mobilization of neural tissue follow-
ing spinal surgery or severe trauma is possible without
adverse effects on neighboring tissues.
It is worth considering that it is nearly impossible to
immobilize the nervous system. Even with a plaster cast
immobilizing the wrist and elbow, movement of the
shoulder and neck will still load neural tissues in the wrist.
Likewise, the patient who wears a collar, post-“stinger,”
will be able to move cervical neural tissues via shoulder and
arm movements. Although a tension-free environment is
best for nerve regeneration following suture,49 modest lev-
els of tension are tolerated,160 and the beneficial effects of
gentle “microforces” to polarize the fibrin clot and guide
regenerating axon sprouts should be considered.2
Clearly, peripheral nerve can be mobilized and during
passive and active movements has always been mobilized,
usually inadvertently. This becomes clear with knowledge
of the structure of nerve that a nerve has built-in design
features that allow it to be mobilized, and if the design
features cannot accommodate the loading placed on it,
189
symptoms, or at worst injury, may ensue. Hamstring
stretches, for example, mobilize many tissues, the sci-
atic tract being one of them. Shoulder stretches mobi-
lize the brachial plexus, among other tissues. Techniques
proposed to mobilize the nervous system are discussed
elsewhere.4
Movement and pharmacology are not the only
therapies for damaged and painful nerves. If the nerve
becomes sensitive to various inflammatory (e.g., cyto-
kines) and stress-based compounds (e.g., adrenaline),
then therapeutic education87 that targets the threats,
fears, and challenges facing the patient should also be
considered as an additional therapeutic modality critical
to recovery.
Conclusion
Peripheral nerves are far more than conduits between tis-
sues and the central nervous system. Nerves are remark-
ably mobile and reactive to a variety of stimuli such as
mechanical forces, adrenaline, and immune compounds.
The role of damaged or upregulated peripheral nerves in
pain states may be underestimated.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 160 references for this chapter.

190 SECTION I • Scientific Foundations
A RTICULAR N EUROPHYSIOLOGY
AND S ENSORIMOTOR C ONTROL
Glenn N. Williams and Chandramouli Krishnan
Introduction
One of the defining characteristics of musculoskeletal
rehabilitation is the focus on movement and the res-
toration of functional movement patterns after injury
or disease. Movement requires a complex interaction
between the nervous system and the muscles, bones,
and joints of the musculoskeletal system. Accordingly,
a detailed understanding of the nervous system and its
interactions with the musculoskeletal system in produc-
ing safe and functional movement is of critical importance
to the rehabilitation specialist. This chapter focuses on
current theory related to articular neurophysiology,
sensorimotor control, and the interactions between the
nervous and musculoskeletal systems in maintaining joint
stability during movement.
Articular Neurophysiology
Somatosensory System
The somatosensory system is a unique sensory system
because it mediates signals related to multiple sensory
modalities (e.g., proprioception, thermal, and pain) that
are propagated by receptors distributed throughout the
body. Conversely, other sensory systems usually mediate
a single modality resulting from focused input. There are
three primary categories of specialized receptors in the
somatosensory system: (1) mechanoreceptors, which pro-
vide feedback related to the mechanical state of muscles,
joint tissues, and the skin; (2) thermoreceptors, which
provide feedback related to temperature; and (3) nocicep-
tors, which are pain receptors. Although each modality has
its own specialized receptors, all somatosensory feedback
190
9
C H A P T E R
is transmitted by neurons originating in dorsal root gan-
glions. Neurons associated with different somatosensory
modalities vary in morphology (Figure 9-1) and stimu-
lus sensitivity. The CNS continually receives input from
many receptors and processes it simultaneously. Although
this chapter emphasizes the function of mechanorecep-
tors that are sensitive to movement-related parameters,
it should be recognized that pain and abnormal tem-
perature may affect sensorimotor function and alter sta-
bility.1,2 For example, patients with inflamed joints often
have muscle inhibition that impairs their ability to gen-
erate force.3–6 Some of this inhibition is undoubtedly
because of pain, increased temperature, and the chemi-
cal environment within the inflamed joint. Such factors
may impact joint function even if the patient does not
consciously recognize them. It is critical that clinicians
recognize and treat such impairments as early as possible
because the resulting sensorimotor control deficits may
put patients at risk for further injury. Furthermore, it is
challenging to improve sensorimotor control without first
addressing impairments that adversely affect sensorimotor
function.
Mechanoreceptors
Mechanoreceptors are usually classified into three groups:
(1) joint receptors, (2) muscle receptors, and (3) cuta-
neous receptors. It is a common misconception that the
CNS deals with the signals arising from these receptors
separately. This misconception is understandable because
the function of these receptors is usually discussed
separately. In addition, researchers often isolate or focus
on the function of a single type of receptor in their stud-
ies. In reality, the current evidence suggests that the CNS
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control 191

Myelinated Unmyelinated

Diameter (micrometers)
20 15 10 5 1 2.0 0.5

Conduction velocity (m/sec.)

120 80 60 30 6 2.0 0.5
General classification

A C
α
β
γ
δ
Sensory nerve classification
I II III IV
IA
A B
IB
Sensory functions
Muscle spindle Muscle spindle
(primary ending) (secondary ending)

Muscle tendon
(Golgi tendon organ)
Hair receptors
Vibration
(pacinian corpuscle)
High discrimination touch Crude touch
(Meissner's expanded tips) and pressure
Deep pressure
Tickle
and touch

Pricking pain Aching pain

Cold
Warmth

Motor function
C D
Skeletal muscle Muscle spindle Sympathetic
(type Aα) (type Aγ ) (type C)
Figure 9-2
20 15 10 5 1 2.0 0.5 Photomicrographs of different types of joint receptors found in the
Nerve fiber diameter (micrometers) cat cruciate ligaments. A, Bare nerve endings in the posterior cruciate
ligament originating from a single axon (a). B, A Ruffini ending (r)
Figure 9-1 with fine capsules (c), arising from a single axon (a) in the anterior
Sensory and motor nerve fiber classification and functional cruciate ligament located close to the insertion on the epiphysis (e).
characteristics. (From Guyton AC, Hall JE: Textbook of medical C, A Golgi tendon organ–like ending with a thick axon (a) located
physiology, ed 11, p 577, Philadelphia, 2006, WB Saunders.) within the substance of the anterior cruciate ligament. D, A pacinian
corpuscle located adjacent to a nerve bundle (n) in the posterior
cruciate ligament. (From Sjölander P, Johansson H, Sojka P et al:
Sensory nerve endings in the cat cruciate ligaments: a morphological
investigation, Neurosci Lett 102:34, 1989.)

processes ensembles of sensory information from many
receptors simultaneously.7–9 Ensemble processing allows
thousands of impulses to be processed each second, which
enables the system to rapidly obtain an accurate picture
of the conditions at the periphery. As a result, effective
responses to potentially harmful disturbances are made
efficiently, and the system remains in relative homeostasis.
These responses are generated based on the net feedback
from a body region rather than to each individual signal
coming in from the region. Ensemble processing leads
to more appropriate responses because there is a level of
redundancy within the system that allows it to compensate
for errors in feedback.
Joint Receptors. There are four primary types of joint
receptors (Figure 9-2): Ruffini endings, pacinian cor-
puscles, Golgi tendon organ–like endings, and bare nerve
endings.10,11 These receptors are described (Table 9-1) by
the joint state in which they are active (static, dynamic,
or both), the stimulus intensity for activation (high versus
low threshold), and whether or not they remain active with
persistent stimuli (slowly versus rapidly adapting). Each
type of joint receptor relays unique sensory feedback to
the central nervous system (CNS). Although joint recep-
tors appear to exist in most articular connective tissues,
research indicates that the capsule is richly innervated,
whereas ligaments appear to be best described as sparsely
192 SECTION I • Scientific Foundations

Table 9-1
Functional Characteristics of the Four Types of Joint Receptors
Receptor Active Joint Activation Response to
Type Location Stimulus State Threshold Persistent Stimuli

Ruffini Capsule, Stretch/strain Static or Low Slowly adapting

endings ligaments, joint dynamic threshold
menisci position?
Pacinian Capsule, Compression, Dynamic Low Rapidly adapting
corpuscles ligaments, acceleration/ only threshold
menisci, and deceleration
fat pads
Golgi tendon Capsule, Strain, especially Dynamic High Slowly adapting
organ-like ligaments, at end range only threshold
receptors and menisci of motion
Bare nerve Widely Pain of Inactive High Slowly adapting
endings distributed in mechanical unless threshold
capsule, or chemical noxious
ligaments, and origin stimuli are
fat pads; fewer present, then
in menisci static or dynamic

innervated.12–14 Joint receptors in ligaments are most
densely located near the insertion sites and are most active
when a joint is rotated near its limits, which suggests that
the primary purpose of these receptors is to signal that
the joint is nearing its end range of motion.2,14–18 Signals
from these receptors may initiate protective reflexes from
appropriate muscles surrounding the joints that act to
resist motion and protect the joint.2 Although there is
evidence that some joint receptors are active in the mid-
ranges of motion, most evidence suggests that a minor-
ity of receptors function this way.2,18–20 Hence, although
joint receptors play some role in sensing joint position,
this does not appear to be the primary function of these
receptors.2,14,21,22
Joint Receptors
● Ruffini endings
● Pacinian corpuscles
● Golgi tendon–like or Golgi-ligament organs
● Free nerve endings
Ruffini Endings. Ruffini endings are primarily
located on the “flexion” side (the side that is stretched
with extension of the joint) of the joint capsule. For
example, in the knee they are found in the posterior
capsule.23,24 Ruffini endings are also found in ligaments,
primarily near the origin and insertion.18,25 The parent
axon (5 to 9 µm in diameter) of the Ruffini ending enters
the joint capsule and divides into multiple branches to
form a spraylike ending (see Figure 9-2B).26 The nerve
branches make contact with large numbers of collagen
fibers,27 which encapsulate them, creating the appear-
ance of cylinders (these may be complete or incomplete).
There are usually two to six of these thinly encapsulated
cylinders in each Ruffini ending. Nerve endings pass into
the joint capsule or ligament at the ends of the cylinder,
which allows them to be sensitive to mechanical changes
in the connective tissues of a joint.
Ruffini endings are stretch sensors. A maintained
stretch of the capsule produces a prolonged, slowly
adapting response in the form of a train of action poten-
tials.24 The neuron is primarily activated by stretching
along the axis of the cylinders and is not very sensi-
tive to compression.28 Thus, the orientation of collagen
fibers and of the cylinders determines the direction of
tissue stretch for which a given afferent will be most
sensitive. Under most circumstances, Ruffini endings
respond primarily when a joint is rotated near the limits
of motion because of increased strain on the connec-
tive tissues of the joint.14,16,17 Multiplanar joint motion
can cause Ruffini afferents to discharge in positions at
which they would otherwise be silent and increase the
sensitivity of these receptors. For example, the response
to rotation into extension is enhanced if the extending
knee joint is also externally rotated.17 Although Ruffini
afferents are usually not active when the knee joint is
rotated through the “intermediate” range of joint rota-
tion,15,17 some Ruffini endings become active in this
range with aggressive quadriceps muscle activation.29
This effect is only observed in a minority of afferents
with rather large loads;29 however, it confirms that
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control 193

Ruffini endings become active when the inherent laxity muscle spindles (Figure 9-3). Golgi tendon organs are
within the connective tissues of the joint is taken up, embedded within the collagen of the musculotendinous
straining the tissues. junction 90% of the time and in the tendon itself the rest
Pacinian Corpuscles. The largest percentage of of the time.42 Each Golgi tendon organ is attached to a
pacinian corpuscles are located in subcapsular fibro- small number of extrafusal muscle fibers (10 to 20) from
adipose tissue; however, they are also found in most a small number of motor units (≤15); the exact num-
other soft tissues of joints including the capsule, liga- ber of fibers varies according to the muscle-tendon unit
ments, and menisci.18,23,27,30 Pacinian corpuscles are the receptor is contained within.43–47 A mixture of motor
encapsulated, conical in shape, and somewhat smaller unit types can be included in the innervation.48 Golgi
(20 to 40 µm in width, 150 to 250 µm in length)
than pacinian corpuscles located in cutaneous tissues
(see Figure 9-2D). Signals recorded from the antero-
medial part of the knee capsule where these receptors Muscle
are found have shown them to be sensitive to compres-
sion but not stretch.30 Pacinian corpuscles respond to Muscle spindle (size exaggerated
joint compression and increased hydrostatic pressure in relative to whole muscle)
the joint.30 They are relatively silent when the joint is at
rest or rotated at a constant speed (i.e., they are rapidly
adapting), but they are sensitive to sudden acceleration Intramuscular nerve
and deceleration.26
Golgi Tendon Organ–Like Receptors. Golgi tendon
organ–like receptors (also called Golgi ligament organs) γd γs
γs
are “spraylike” receptors (see Figure 9-2C) like Ruffini Ia
endings and for that reason are sometimes grouped II β
with them.18,31–33 They are larger than the Ruffini end-
ings, have a thicker parent axon (13 to 17 µm), and are
found in the joint capsule, ligaments, and menisci.18,32,34
Golgi tendon organ–like receptors have high thresholds Nuclear
bag 1
to stimuli and are slowly adapting.26,33 They are not active fiber
unless the joint is moving, and like Ruffini endings, they
appear to function primarily as limit detectors because of Nuclear
their high thresholds. bag 2
fiber Ib
Bare Nerve Endings. Bare (free) nerve endings (see afferent
Figure 9-2A) are the most widely distributed of all of the Nuclear
joint receptors.21,23,33 These receptors are often referred chain fibers
to as fine afferents because they are innervated by small
group III and IV nerve fibers, rather than the larger
group II fibers that innervate other joint receptors.12,14,35
Bare nerve endings are distinct in several ways, including
the number of receptor sites, the diameter of the axons, Tendon
the structure of the cytoskeleton, and the number and
length of the branched endings.12 Under general move-
ment conditions, these fibers are quiet.35 Research
demonstrates that bare nerve endings are mechanically Golgi tendon organ
stimulated nociceptors that are often chemosensitive.36–39
They have high thresholds and become active when the
soft tissues of the joint experience potentially damaging
Figure 9-3
loads.19,40 The sensitivity of bare nerve endings usually Structure and innervation of muscle spindles and Golgi tendon
increases when joints are inflamed or swollen.36,37,39 organs. This sensory innervation of the spindle is through primary
For example, fine afferents are highly sensitive with (Ia) spindle afferents that innervate both nuclear bag and nuclear
experimental arthritis.41 Blocking feedback from these chain intrafusal muscle fibers and secondary (II) afferents that
endings is one of the mechanisms by which analgesics innervate nuclear chain fibers. Motor innervation of the spindle is
supplied by static and dynamic γ motor neurons (γs and γδ) and by
operate.36 motor neurons. (From Squire LR, Bloom FE, McConnell SK et al:
Muscle Receptors. Two types of muscle receptors Fundamental neuroscience, ed 2, p 785, Boston, 2003, Academic
are commonly described: Golgi tendon organs and Press.)
194 SECTION I • Scientific Foundations

tendon organs are in series with a few muscle fibers and

in parallel to other fibers inserting in the vicinity.49 A
single group I afferent enters the capsule of each Golgi
tendon organ and branches into a series of unmyelin-
ated fibers that are interwoven with the fibers of col-
Polar region
lagen in the tendon.42,50 When muscle contraction or
passive loading takes up the slack within the network of
collagen fibers, the nerve endings are stimulated; how-
ever, these receptors are more sensitive to contraction
to passive loading.51 Golgi tendons are sensitive to small
changes in force (sensitivity varies across receptors; it is as Intermediate region
little as <0.1 gram for some Golgi tendon units), which
allows the nervous system to provide specific responses
to force feedback.47,51 Although these receptors are sen-
sitive to force, it is actually strain on the receptors that Nuclear
activates them.52 Each tendon organ provides a picture (equatorial)
of the static and dynamic loading in the muscle fibers it region
is connected to.42 The CNS, however, appears to rely on
ensemble feedback from all of the Golgi tendon organs
in a muscle to obtain a picture of whole muscle force.53,54
Functionally, the force-feedback from these muscle recep-
tors is used not only to obtain a picture of muscle force
but also to reflexively prevent muscle damage, promote
phase transitions in gait, modulate joint stiffness, and
promote interjoint coordination.55–57

Intrafusal fibers
Muscle Receptors
● Muscle spindle
● Golgi tendon organs
● Free nerve endings

Extrafusal fibers

The second type of muscle receptor is referred to as the

muscle spindle. Muscle spindles are encapsulated recep-
tors (0.5 to 10 mm in length) that lie in parallel with
muscle fibers (Figure 9-4).58,59 The human body contains
25,000 to 30,000 muscle spindles (4000 per arm, 7000
per leg), and individual muscles can contain up to 500
spindles.58 The density is highest in muscles in which fine
control is important, such as the intrinsic muscles of the
hand and deep muscles of the neck.58,59 Muscle spindles
are sensitive to changes in length (stretch) and veloc-
ity.45,59 Three types of intrafusal muscle fibers are found
within muscle spindles: nuclear chain fibers and two types
of nuclear bag fibers (static and dynamic).45,58–60 These
intrafusal muscle fibers are innervated by both sensory
and motor (gamma) axons.59,60 The central capsular por-
tion of the spindle contains one to two primary group
I afferents and one to five secondary group II afferents
that are spiraled around the intrafusal fibers.59 Primary
afferents are highly sensitive to changes in length, and
Figure 9-4
Muscle spindles (intrafusal fibers) are connected in parallel with
skeletal muscle fibers (extrafusal fibers). (From Nadeau SE, Ferguson
TS, Valenstein E et al: Medical neuroscience, p 238, Philadelphia,
2004, WB Saunders. Modification of drawing by JJ Warner.)
feedback from these afferents varies based on the location
of the spindles within a muscle as all regions of a muscle
do not lengthen equally.42 The sensory “partitioning”
within muscles provides the CNS with specific informa-
tion regarding changes in muscle length.61 Rapid adjust-
ments in muscle length are achieved through muscle
stretch reflexes, which are a product of monosynaptic
connections between these sensory axons and the alpha
motor neurons that innervate the muscle in which the
spindles are found (Figure 9-5).45,62
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control
Sensory nerve
Motor nerve
Muscle spindle
Stretch reflex
Figure 9-5
The monosynaptic muscle stretch reflex. (From Guyton AC, Hall JE:
Textbook of medical physiology, ed 11, p 677, Philadelphia, 2006,
WB Saunders.)
The gamma motor neurons innervating muscle spin-
dles are known as the fusimotor system.60 Coactivation
between the alpha motor system and the fusimotor
system enables muscle spindles to remain sensitive to
changes in length and velocity throughout a joint’s range
of motion (Figure 9-6).45,60 Evidence also suggests that
the fusimotor system activation is directly influenced by
feedback from receptors located in the skin, ligaments/
195
capsule, and muscles (Figure 9–7).8,63,64 Integration of
muscle spindle function with that of mechanoreceptors
in other tissues may improve the accuracy and effective-
ness of motor responses by creating a more redundant
system and increasing the potency of responses.
Cutaneous Receptors. Nonhairy (glabrous) human
skin contains four types of cutaneous receptors (Figure
9-8): a type of Meissner’s corpuscle (rapidly adapting),
Pacinian corpuscles (rapidly adapting), Merkel’s discs
(slowly adapting), and Ruffini endings (slowly adapt-
ing).42 Hairy human skin contains hair-follicle receptors
(rapidly adapting) and pacinian corpuscles (rapidly adapt-
ing; primarily in the vicinity of joints), as well as Merkel cell
receptors (slowly adapting) and Ruffini endings (slowly
adapting) that are usually present near the hairs.42,65
Historically, sensory feedback from cutaneous receptors
has been discussed relatively little in association with joint
stability. It is now believed that cutaneous receptors play
an important role in the sensation of movement, either
by providing direct feedback or by facilitating feedback
from other receptors (e.g., muscle receptors).66–68 There is
evidence that cutaneous receptor feedback provides infor-
mation regarding movement of the knee joint.67 This may
help to explain the reported improvements in proprio-
ceptive acuity associated with wearing braces or neoprene
sleeves.69,70 Additional studies are needed to establish the
degree to which feedback from cutaneous receptors con-
tributes to dynamic joint stability.
Figure 9-6
The activity of γ motor axons can
counteract the effects of unloading
on the discharges of a muscle
spindle afferent. A, The activity
of a muscle spindle afferent is
shown during steady stretch. B,
The afferent stops firing when the
extrafusal muscle fibers contract,
owing to unloading of the muscle
spindle. C, Activation of a γ motor
neuron causes shortening of the
muscle spindle, counteracting
the effects of unloading. (From
Berne RM, Levy MN: Physiology,
ed 5, p 190, St. Louis, 2004,
Mosby. Redrawn from Kuffler SW,
Nicholls JG: From neuron to brain,
Sunderland, Mass, 1976, Sinauer
Associates.)
196 SECTION I • Scientific Foundations

Figure 9-7
Schematic organization plan of the mechanisms
and pathways by which the mechanical
and sensory properties of the ligaments
may contribute to joint stability, muscle
coordination, and proprioception. (From
Sjölander P, Johansson H, Djupsjöbacka M:
Spinal and supraspinal effects of activity in
ligament afferents, J Electromyogr Kinesiol
12:168, 2002.)

Cutaneous Receptors
● Meissner’s corpuscles
● Pacinian corpuscles
● Merkel’s discs
● Ruffini endings
● Free nerve endings

Sensorimotor Control
Sensorimotor control is a complex, highly integrated
process involving the hierarchical structure of the nervous
Dermis system and the muscles, joints, and various other tissues
of the musculoskeletal system. Large numbers of sensory
impulses carrying information about the conditions in
Papillary Sweat joints, muscles, and skin are received each second and pro-
ridge duct Epidermis
cessed by a network of neurons, interneurons, and CNS
centers that use an equally complex system of pathways
Epidermis

Meissner's
corpuscle and neurons to activate muscles and produce appropriate
Free nerve
responses and coordinated movement. The previous sec-
ending tion discussed the mechanisms by which somatosensory
Merkel's disk information is sensed and transmitted to the CNS. This
section discusses how that information is processed and
used functionally to control posture and movement.
Dermis

Subpapillary
plexus
Dermal plexus
Sensory Processing in the Central Nervous System
Pacinian The CNS is organized in a hierarchical fashion with the
corpuscle cortical centers of the brain being the location of the most
Subcutaneous complex processing and the spinal cord being the location of
plexus
the most basic processing (Table 9-2). Responses from the
Figure 9-8
Transverse section of skin illustrating the location of various cutaneous
higher centers of the CNS take longer than those mediated
receptors. (From Nadeau SE, Ferguson TS, Valenstein E et al: Medical lower in the system because of the distance that the signals
neuroscience, p 313, Philadelphia, 2004, WB Saunders.) must travel and the increased complexity of processing that
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control 197

Table 9-2
Sensorimotor Responses
Slowed with
Level of Degree of Increased Sensory
Response Type Mediation Typical Latency Flexibility Processing Demand

Spinal reflexes Segmental level of 30 to 50 ms Low No

the spinal cord
Long-loop reflexes Brain stem and 50 to 80 ms Low No
cerebellum
Triggered reactions Cortical centers 80 to 120 ms Moderate Yes
Reaction time Cortical centers >120 ms High Yes

takes place. Response processing time is also a function of RECIPROCAL INHIBITION

the complexity of information received from the periphery
(Hick’s law).71–73 Somatosensory feedback is mediated at
three levels of the CNS: (1) the spinal cord, (2) the brain
stem and cerebellum, and (3) the cerebral cortex. Rapid
motor responses to somatosensory feedback mediated in the
spinal cord are referred to as spinal reflexes. While some Excited
Inhibited Inhibited
spinal reflexes are simple monosynaptic circuits (e.g., muscle
stretch reflexes), others are more complex and involve syn-
apses with one or more interneurons (Figure 9-9). These
spinal reflexes can be excitatory or inhibitory and are part of
a distributed network that facilitates rapid postural adjust- Excited Polysynaptic
ments and regulation of limb mechanics in movement.56,57 circuit

Locations for the Mediation of Somatosensory Painful

Feedback stimulus
from hand
● Spinal cord
● Brain stem and cerebellum
● Cerebral cortex

FLEXOR CROSSED EXTENSOR

Responses to sensory feedback that is mediated in
the brain stem and cerebellum are referred to as long-
loop reflexes. Somatosensory signals ascend to the brain
stem and cerebellum through the dorsal column-medial
lemniscal system and the anterolateral system (Figure 9-
10).74 Motor responses descend from the brain stem and
cerebellum via the medial (vestibulospinal, reticulospinal,
and tectospinal tracts) and lateral (primarily rubrospinal)
pathways, which activate proximal and distal musculature,
respectively (Figure 9-11).74 Processing in the brain stem
and cerebellum leads to greater flexibility in the responses,
which are able to adapt based on experience, visual cues,
or instructions.75–77 Researchers have described evidence
of a long-loop reflex arc between the knee capsule or
ligaments and hamstring muscles in people with anterior
cruciate ligament ACL insufficiency.78 While some have
questioned a direct ACL-hamstring reflex loop,79,80 it
REFLEX REFLEX
Figure 9-9
Examples of reflexes with one or more synapses that have
interneurons. (From Guyton AC, Hall JE: Textbook of medical
physiology, ed 11, p 680, Philadelphia, 2006, WB Saunders.)
is likely that long-loop responses similar to this play an
important role in maintaining dynamic joint stability.81
Triggered reactions are preprogrammed, coordi-
nated responses that occur in response to feedback in the
periphery.71,82 These reactions appear to include processing
in the higher centers of the brain; however, preprogram-
ming as a result of motor learning enables some of the typ-
ical processing steps in the higher centers to be bypassed,
which results in faster responses than would be expected
with typical voluntary reaction time responses.71,82 Because
198 SECTION I • Scientific Foundations

A Postcentral B Second
gyrus (first
somatosensory
somatosensory
cortex
cortex)
Intralaminar and
Ventral posterolateral posterior groups
nucleus of thalamus of thalamic nuclei

Periaqueductal
gray matter

Spinal
Medial lemniscus
lemniscus

Pontine
Gracile
reticular
nucleus
formation
Cuneate
nucleus Decussation of the
medial lemnisci
Internal
arcuate Medullary
fibers reticular
formation

Cuneate
fasciculus Spinothalamic
tract
Cervical level

Dorsal part of
lateral funiculus Gracile Ventral white
fasciculus commissure
Thoracic level

Lumbosacral level

Figure 9-10
Anatomy of ascending somatosensory paths. A, Organization of the dorsal column-medial lemniscal system from entry of large-diameter afferents
into the spinal cord to the termination of thalamocortical axons in the first somatosensory area of the cerebral cortex. An obligatory synapse
occurs in the gracile and cuneate nuclei, from which second-order axons cross the midline and ascend to the ventral posterolateral nucleus of the
thalamus (VPL) by way of the medial lemniscus. B, Organization of the spinothalamic tract and the remainder of the anterolateral system. Primary
axons terminate in the spinal cord itself. Second-order axons cross the midline and ascend through the spinal cord and brain stem to terminate in
VPL and other nuclei of the thalamus. Collaterals of these axons terminate in the reticular formation of the pons and medulla. (From Squire LR,
Bloom FE, McConnell SK et al: Fundamental neuroscience, ed 2, p 682, Boston, 2003, Academic Press.)

these responses are processed at higher levels, they are
more complex and integrated. However, increased sensory
stimuli or unanticipated conditions may lead to slower or
errant responses because the increased processing rate
associated with the “preprogrammed” format of these
responses comes at the cost of response adaptation. The
task of stepping off a curb or step provides an example
of this concept. People step down off of steps and curbs
virtually every day of their lives. Because steps or curbs
are fairly consistent in terms of their height and our body
mass does not change rapidly, our CNS can preprogram
our muscle activity to slow our downward progression and
make a smooth transition between surfaces without requir-
ing close attention to the task. Our sensorimotor system is
able to respond to minor alterations in the support surface
(e.g., slightly uneven surfaces) and curb height differences.
But when the support surface or curb height is grossly
different than typical or when other sensory information
is competing for our sensory processing (e.g., a vehicle
comes to a screeching halt in the vicinity; someone yells,
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control 199

Skilled
Cerebral cortex - motor areas
movements

Initiation Thalamus Relay

Selection of station
motor programs
CS
Basal ganglia Posture
Brain stem Eye movements
Cerebellum
Motor RS VS RbS
coordination
and correction
1 2
Spinal reflexes
Spinal cord Locomotion

Muscle movement
and contraction
Sensory
receptors

Basic functions of descending tracts

Corticospinal-and rubrospinal
1. Transmission of commands for skilled movements.
2. Corrections of motor patterns generated by the spinal cord. Figure 9-11
Descending tracts of the motor system with
Reticulospinal
outlined interactions between processing
1. Activation of spinal motor programs for stepping and other
centers. CS = corticospinal tract; RbS =
stereotypic movements.
2. Control of upright body posture. rubrospinal tract; VS = vestibulospinal
tract; RS = reticulospinal tract. (From
Vestibulospinal Squire LR, Bloom FE, McConnell SK et
Generation of tonic activity in antigravity muscles al: Fundamental neuroscience, ed 2, p 763,
Boston, 2003, Academic Press.)

causing us to turn our head; or we are thinking deeply

about a stressful situation), the triggered reaction time
may increase or break down and lead to response errors
that may result in a stumble, fall, or injury.
The most complex and flexible responses are voluntary
responses, which are mediated in the cerebral cortex. These
responses are often referred to as reaction time responses.
Somatosensory feedback used in voluntary responses ascends
via the dorsal column of the spinal cord, synapses in the brain
stem, and continues to the primary somatosensory cortex
via the medial lemniscal system.83 The sensory and motor
cortices are somatotopically organized as is depicted with the
sensory and motor homunculi (Figure 9-12). Motor control
processing takes place in three specialized areas of the motor
cortex: the primary motor cortex, the premotor cortex, and
the supplementary motor area.84 Each of these cortical cen-
ters projects directly to the spinal cord via the corticospinal
tract and indirectly through pathways in the brain stem.74
Although voluntary responses take the longest to occur,
these are the most flexible, adaptable, and robust responses
as they are usually under conscious control.
Locations of Motor Control Processing
● Primary motor cortex
● Premotor cortex
● Supplementary motor area
Proprioception and Kinesthesia
Sir Charles Sherrington coined the term proprioception
a century ago from the Latin words proprius (one’s own)
and (re)ceptus (the act of receiving),85 which combined
infer the modality of sensing one’s own body position or
movement. In the contemporary medical literature, the
term proprioception is used for a wide range of param-
eters related to sensorimotor function, rather than being
reserved for a sensory modality. Because of this broad
use, it is best to define the term whenever it is used. The
authors are advocates of using proprioception exclusively
when referring to the following sensations: (1) detection
200 SECTION I • Scientific Foundations

Trunk
Hip
Neck

Leg
Head lder
Shou
Arm
Elbo rm
Fore
Wr
ot

Ha
Fo

w
ist
a
Lit g

nd
o e s

Ri
M

tle
T
In idd

n
Th x
de le
Genitals
u
Ey mb
e
No
se
Fac
e
Upp
er lip

Lips

Lower lip
Teeth, gums, and jaw
Tongue
l
nx ina
ary dom
Ph a b
ra-
Int

A
Gyrus precentralis (M)

Trunk

Foot Hand

Face

Figure 9-12 Tongue

Somatotopic organization of the sensory and
motor cortices. A, The sensory homunculus.
(Reprinted with permission from Penfield W,
Rasmussen T: The cerebral cortex of man: a
clinical study of localization of function, New Sulcus
York, 1950, MacMillan Company.) B, The lateralis
motor homunculus. (Adapted from Penfield
W, Rasmussen T: The cerebral cortex of man: a
clinical study of localization of function, New York,
1950, MacMillan Company.) B
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control
of the position and movement of joints, (2) sensation of
force and contraction, and (3) sensation of the orienta-
tion of body segments as well as the body as a whole.66
Kinesthesia is a submodality of proprioception that is
usually used to refer to the sense of movement of the
body or one of its segments.50 When referring to somato-
sensory feedback in combination with associated muscle
responses such as is typical for most functional tasks
and in rehabilitation, we advocate the use of the term
sensorimotor control or neuromuscular control rather than
proprioception because this is more accurate and consistent
with current neuroscience.
Exclusive Uses for the Term Proprioception 66
● Detection and movement of joints
● Sensation of force and contraction
● Sensation of body segment orientation
● Sensation of whole body orientation
The primary source of the proprioceptive modalities
has been a controversial issue and remains the subject of
debate.42,58,86 Most experts hold that muscle receptors are
the predominant source of proprioception.42,58,86 Joint
receptors, which have been the focus of a large number
of studies in the orthopedic-sports medicine literature
related to ligament injuries, are not considered to play
a primary role in proprioception because of the relative
paucity of receptors in ligaments and their general inac-
tivity in the midrange of motion.2,14,15 There is no doubt,
however, that joint receptors contribute proprioceptive
feedback to some degree, even if this is not their primary
function.42,86 The fact that joint receptors become more
sensitive when a joint is inflamed is clinically important as
it suggests that these receptors alter sensorimotor function
in those circumstances.19,36,37 There is a growing body of
evidence that cutaneous receptors also provide proprio-
ceptive feedback.66–68 The exact source of proprioception
is probably not important clinically. The most accurate
view is to think of proprioception as the result of the com-
bined feedback of muscle, joint, and cutaneous receptors.
Each of these tissues must be considered carefully in the
rehabilitation process as impairments in any of them can
have a meaningful impact on sensorimotor function. Joint
inflammation, adhesions at an incision site (scarring), and
muscle atrophy would have primary effects on different
receptor types, but each can adversely affect propriocep-
tion and requires special attention. The authors believe
that attempting to minimize muscle atrophy is especially
important. It is their theory that intrafusal fibers within
muscle spindles atrophy along with the extrafusal fibers of
the quadriceps muscle after knee joint injury and that this
may play an important role in the decreased proprioceptive
201
acuity and profound quadriceps dysfunction often observed
in knee injury patients.
Locations of Proprioceptive Receptors
● Muscle
● Tendon
● Capsules
● Ligaments
● Skin
Can proprioception be trained? The answer to this
question remains unclear. It is unlikely that clinicians
can significantly alter the physiological function of the
mechanoreceptors themselves;87 however, improvements
in the efficiency of signal processing, increased empha-
sis on converging feedback from other receptors, and
the development of triggered reactions may arise from
training and lead to improved proprioceptive acuity.
Regulation of Muscle and Joint Stiffness
The ability of a joint to remain stable depends in part on
its resistance to motion when subjected to external loads.
This resistance to motion is a product of sensorimotor
control and the material properties of the tissues in and
around a joint. Stiffness is typically determined by divid-
ing change in force (tension) by change in length. The
concept of stiffness is often described by the function of a
spring. Stiff springs require a great deal of force to change
their length, while low-stiffness springs are very compli-
ant. The material and mechanical properties of muscles
allow them to be the “springs” between a person’s skel-
etal system and the environment. Hence, muscles are
often modeled (Figure 9-13) as springs or a combination
of springs and dashpots (i.e., dampers or pistons).88,89
The following section discusses theoretical mechanisms
Q Mechanical properties:
FCE = f1(LCE, VCE, Q)
CE
SEE
FSEE = f2(LSEE)
FPEE = f3(LPEE)
State equation:
PEE dLCE
f3(LCE) + f1(LCE, ,Q) = f2(LM - LCE)
dt
LM
Figure 9-13
The traditional three-component Hill muscle model, which consists of
a contractile element (CE), series elastic element (SEE), and parallel
elastic element (PEE). Q indicates the level of activation (“active
state”) of the muscle. The state equation is a first-order differential
equation with length LCE of the contractile element as a state variable.
(From van den Bogert AJ, Gerritsen KGM, Cole GK: Human muscle
modelling from a user’s perspective, J Electromyogr Kinesiol 8:120, 1998.)
202 SECTION I • Scientific Foundations
by which the sensorimotor system may modulate muscle
and joint stiffness during functional tasks.
Muscle stiffness is the result of three components: (1)
passive factors associated with the material properties of
the musculotendinous tissues, (2) active intrinsic prop-
erties associated with the cross-bridge attachments and
length-tension properties of the muscle, and (3) reflexes
associated with length and force-feedback from muscle
spindles, tendon organs, and the influence of other somato-
sensory feedback on the fusimotor system.8,90–92 The net
stiffness of the muscles surrounding a joint allows it to
resist sudden translations or rotations.56,57 Perturbations
alter feedback from somatosensory receptors (especially
muscle receptors).92 Motor responses to this feedback
change muscle activity patterns (e.g., co-contraction),
which in turn result in changes in joint stiffness that are
appropriate to the environmental conditions.56,57,92
Components of Muscle Stiffness
● Passive factors
● Active intrinsic properties
● Reflexes
Intrinsic muscle stiffness associated with the material
properties of the muscle and tendon and the crossbridge
attachments within the muscles are thought to be the
first line of defense against perturbations because these
properties are always present, although the resulting stiff-
ness will vary somewhat based on joint angle.90,93 Reflex
stiffness appears to play its greatest role during postural
or slow movements because during faster movements,
the intensity of stretch reflexes is suppressed.94,95 The fusi-
motor system plays an important role in the regulation
of muscle stiffness by modulating muscle spindle sensitiv-
ity.8,64,93 Evidence from animal models suggests that joint
afferents in the ligaments and capsule have a direct impact
on fusimotor activity.96–98 Although it remains unclear
if similar direct pathways exist in humans, the results of
these studies suggest that joint receptor feedback may be
involved in modulating the muscle and joint stiffness. It is
widely held that reactive muscle responses are unlikely to
prevent joint injuries unless the rate of loading is relatively
slow or there is sufficient stiffness present from existing
muscle activation.10,99 Nevertheless, this continuous pro-
cess of muscle stiffness regulation, though debated among
neurophysiologists and still under investigation, appears to
be a critical factor in dynamic joint stability. Interestingly,
researchers have demonstrated that females have lower
active musculoskeletal stiffness than males when their
knees are subjected to anterior shear or rotatory loads.99–
102
This finding may have important implications related to
the female predisposition to knee ligament injuries.103–105
Control of Posture and Movement
Postural Control
The nervous system uses three sources of sensory informa-
tion in maintaining postural stability (the ability to main-
tain the body’s center of mass within its stability limits):
(1) somatosensory feedback, (2) vestibular feedback, and
(3) visual feedback.106,107 Although these sensory systems
are unique, research suggests that these systems interact
in producing postural stability.106,108 When feedback from
any one of these modalities is impaired, postural stability
suffers. In addition to this sensory feedback, the mechan-
ical properties of the musculoskeletal tissues of the body
and the properties of the support surface can also alter
postural stability.106
Sources of Sensory Feedback
● Somatosensory (proprioception)
● Vestibular (balance)
● Visual
Responses to postural perturbation vary accord-
ing to the direction and intensity of the perturbation
(Figure 9-14).77,109–111 Muscles on the posterior aspect of
the body (e.g., hamstrings, gastrocnemius, erector spinae)
are usually recruited when perturbations induce forward
sway, whereas muscles on the front side of the body
(e.g., quadriceps, tibialis anterior, rectus abdominis) are
recruited when posterior sway is induced.77,109,112 Different
control strategies are used with different perturbation
intensities. With small perturbations, an ankle strategy is
employed in which muscles around the ankle are used to
provide postural stability.107,110 With larger perturbations,
the muscles of the thigh, hip, and trunk are recruited (hip
strategy) and eventually a step must be taken to maintain
postural control (stepping strategy).107,110 Responses to
postural disturbances are usually predictable and auto-
matic, although postural control strategies are flexible
to the environmental conditions.107 Evidence suggests
that a person’s expectations of impending perturbations
and training can have a significant impact on the magni-
tude and variability of the responses.111,113 Consequently,
education and balance training exercises are important
components of fall prevention programs.
Control Strategies and Perturbation Intensities
● Ankle strategy
● Hip strategy
● Stepping strategy
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control
Hamstrings
Quadriceps
Gastrocnemius
Tibialis Ant.
0 100 200 ms
Hamstrings
Quadriceps
Gastrocnemius
Tibialis Ant.
0 100 200 ms
Figure 9-14
Sequencing of muscle activation in response to displacement of
a supporting platform. When the supporting surface is displaced
backward (at 0 ms), flexor muscles are excited first in the distal lower
limb segments (gastrocnemius, about 80 ms latency) and then in
the proximal segment (hamstrings, about 100 ms latency). Forward
displacement of the platform activates lower limb extensors, again
in a distal (tibialis anterior) to proximal (quadriceps) sequence.
Black arrows mark the first detected electromyographic response to
displacement. Based on studies by Horak and Nashner. (From Squire
LR, Bloom FE, McConnell SK et al: Fundamental neuroscience, ed 2,
p 799, Boston, 2003, Academic Press.)
Sensorimotor Control of Movement
Motor programs are codes within the nervous system
that when initiated, produce coordinated movement
sequences.114 These programs are usually under central
control, but sensory input is used extensively in selecting
the appropriate motor program, in monitoring whether
or not movement is consistent with expectations, and in
reflexively modulating the movement so that it is specific
to environmental variables.114,115 Animal studies have dem-
onstrated that once initiated, the rhythmic pattern of gait
can continue in the absence of feedback from the limbs or
descending control from the brain.116–118 This is achieved
by neural circuits in the spinal cord that are referred to as
central pattern generators (Figure 9-15).116–118
This spinal-level automation is important because
smooth, agile movement would be difficult if each of the
degrees of freedom involved in movement were processed
in the higher centers.114,115 These neural circuits can be
turned on and off by various stimuli, but they are generally
initiated or terminated by signals originating in the brain
stem.116,117 While the basic pattern of gait (regardless of
speed) is programmed, descending input from the brain
and somatosensory feedback play an important role in
maintaining flexible but stable movement patterns when
203
unexpected circumstances are encountered.114,116–118 The
complexity of the neural control strategies typical during
movement makes it difficult to extrapolate the results of
studies performed under static, controlled, or simplified
conditions to highly dynamic conditions such as sports
participation, because it is unclear how the results of such
studies would be integrated with the motor programs and
complex processing that are actively taking place. On the
other hand, the complexity of this neural processing and
the biomechanics of functional activities make interpret-
ing the findings of dynamic studies challenging and often
necessitate highly controlled, simplified study designs.
Hence, it is the confluence of evidence from a variety of
types of studies that clarifies the most likely sensorimotor
processes in functional movement.
Special Topics in Sensorimotor
Control
Sensorimotor Control Testing
Clinicians must have valid and reliable methods for
assessing sensorimotor control and its subcomponents if
they are to understand the impact of injury, disease, and
treatment. It is the authors’ opinion that the difficulties
associated with valid assessment of sensorimotor control
are a primary reason for the relative lack of understand-
ing of the role that sensorimotor control plays in injury
or disease and how clinicians can best modify it. This
section provides a brief overview of some of the various
methods being used in the literature and discusses the
benefits and challenges of each. The testing methods dis-
cussed are broken into five categories: (1) proprioceptive
acuity tests, (2) postural stability tests, (3) assessment of
muscle activity patterns, (4) motion analysis studies, and
(5) functional tests.
Proprioceptive Acuity Tests
Tests for proprioceptive acuity are directed at assessing
the sensory component of sensorimotor control. This
includes the assessment of proprioception and kines-
thesia. The primary methods for assessing propriocep-
tive acuity include threshold to detection of passive
movement, threshold to detection of the direction of
passive movement, and joint position sense studies.
When assessing threshold to detection of passive move-
ment and the direction of passive movement, clinical
scientists rotate the joint being tested at a very slow
rate (between 0.5 and 2.0 degrees per second).119–123
Subjects are blindfolded and white noise is played
through noise-reducing headphones to minimize other
sensory information that may assist the subject in per-
ceiving joint motion (noise from the testing device,
visual information). The extremity being tested is also
usually placed in an inflatable cuff to minimize the
204 SECTION I • Scientific Foundations

Selection Initiation Pattern generation

Forebrain Brainstem Spinal cord

Basal DLR
ganglia RS
Pharmacological
MLR activation
Locomotion Central spinal network
Sensory
Feeding Eye movements activation
Movement feedback
A

Walk Trot Gallop

Left
limb Right R-RS
turn L-RS
Right
limb

Left R-RS
Increasing activation turn L-RS
B of locomotor center C
Figure 9-15
Overview of the control of vertebrate locomotion. A, General control strategy. The locomotor CPGs in the spinal cord are turned on from the
brain stem via reticulospinal pathways. Disinhibition of the basal ganglia’s input to the mesencephalic (mesopontine, MLR) and diencephalic
(DLR) locomotor centers results in increased activity in reticulospinal neurons (RS), which, in cooperation with sensory feedback, activate the
central spinal network, which in turn produces the locomotor pattern. The basal ganglia exert a tonic inhibitory influence on different motor
centers. Once a pattern of motor behavior is selected, this inhibition is released, allowing, in this case, the locomotor centers to be activated.
B, With increased activation of the locomotor centers, the speed of locomotion increases. In quadrupeds, this also leads to a shift in interlimb
coordination, from walk to trot and, finally, to gallop. Experimentally, locomotion can also be elicited pharmacologically by administration of
excitatory amino acid agonists combined with sensory input. C, An asymmetric activation of RS neurons gives rise to an asymmetric output on the
left (L) and right (R) sides. This results in a turning movement to one side or the other. (Reproduced, in part, from Grillner S, Wallén P: On the
cellular bases of vertebrate locomotion, Prog Brain Res 123:297–309, 1999, with permission from Elsevier Science. From Grillner S, Wallén P:
Innate versus learned movements: a false dichotomy? Prog Brain Res 143:5, 2004.)

cutaneous feedback associated with attachment to the joint returns to the target position by pushing a button or
testing device. Laboratory studies generally utilize cus- performing a task like opening his or her fingers.123,125,126
tom-built testing equipment with low-speed servomo-
tors, but testing can be performed in a less sophisticated
manner using isokinetic dynamometers often present in
the clinical setting (Figure 9-16). When subjects sense
joint movement, they are instructed to either press a
button or perform a task such as opening or extending
the finger to signal their sensation (a potentiometer or
similar device is usually attached to the digit to provide
an electronic marker of their response).122–124
Joint position sense tests can be done passively or
actively. Active joint repositioning cannot be considered
a test of proprioceptive acuity alone because active repo-
sitioning involves the motor system and altered motor
function may cause overshoot or undershoot errors.
Hence, although active joint position sense studies may
signal altered sensorimotor control, we cannot differenti-
ate whether a person has sensory, motor, or a combination
of sensory and motor deficits. In passive joint position
sense studies, the subject’s joint is passively rotated to or Figure 9-16
through a certain target position and then returned to the Setup for proprioceptive acuity testing on an isokinetic dynamometer
start position. The subject is then asked to signal when the in the clinical setting.
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control 205

Proprioceptive acuity tests involve a reaction time pro-

cess that is mediated in the higher centers of the brain,
whereas in daily function proprioceptive feedback is often
mediated at the segmental level of the spinal cord or in
the brain stem and cerebellum. Consequently, these meth-
ods may overestimate the processing delays in movement.
Proprioceptive acuity tests are generally performed at low
speeds with all but the test joint stabilized. This design is
critical to the valid assessment of sensory deficits; how-
ever, sports participation and most daily activities require
the coordination of several joint segments that are moving
more rapidly. This discrepancy makes it difficult to interpret
the clinical meaningfulness of proprioceptive acuity stud-
ies, because it is unclear if the observed results from low-
speed testing are representative of sensory performance in
high-speed tasks. Moreover, the findings of propriocep-
tive acuity tests are often quite small (0.5 to 5 degrees)
with high variability.123,127,128 Considering that joints rotate
in the thousands of degrees per second in many sports
tasks,129,130 one must question whether such small differ-
ences are clinically relevant. Despite these difficulties, pro-
prioceptive acuity tests have an important role in defining
the sensory impairments after injury or in disease, as well
as further defining the sensorimotor neurophysiology.

Postural Stability Tests

Postural stability tests are often referred to as balance tests,
stabilometry, or posturography. The examiner may allow
all three systems providing postural input (vision, vestibu-
lar, and somatosensory) to be used during postural stabil-
ity testing, or one or more of the systems can be altered or
eliminated. For example, the subject can be blindfolded
to remove visual input and the surface that the patient is
standing on can be modified to alter somatosensory input.
More advanced techniques such as applying vibration to
the standing subject’s musculature can also be used to alter
input from muscle spindles.131,132 Postural stability tests can
be performed in static positioning with the patient stand-
ing with bipedal or unilateral support (Figure 9-17) or by
translating the support surface forward, backward, laterally,
or in a rotatory fashion.120,133 Testing systems may include
a force plate that is sensitive to changes in pressure, pres-
sure-sensitive mats, pressure-sensitive shoe inserts, or a
moveable platform that provides feedback related to the
change in the position of the platform. Clinical scientists
use these tests to quantify postural sway and the control
of the center of pressure. Information regarding postural
synergies can be gathered when this testing is used in
conjunction with electromyographic recordings.77,109,110
Several reasonably priced postural stability testing systems
are commercially available for clinical settings, whereas
more sophisticated systems are usually used in laboratory
research. Most postural stability studies are essentially
static, although the patient may sway and the platform may
translate or move. The relationship between the results of
Figure 9-17
Single-leg balance on Biodex balance systems. The level of difficulty
is progressed by decreasing the stability of the platform or removing
visual cues by having the patient close his or her eyes. (From Andrews
JR, Harrelson GL, Wilk KE: Physical rehabilitation of the injured
athlete, ed 3, p 204, Philadelphia, 2004, WB Saunders.)
static posture tests and the control of the center of mass
during movement has yet to be clearly defined.
Assessment of Muscle Activity Patterns
Sensorimotor control studies evaluating muscle activity
patterns can be broken into three primary categories:
studies evaluating responses to destabilizing loads, stud-
ies evaluating basic voluntary muscle control strategies,
and studies evaluating muscle activity patterns in move-
ment. A central component in each of these categories is
the use of electromyography, although other techniques
such as mechanomyography and magnetic resonance
imaging are becoming more prevalent.134,135
Several studies have evaluated muscle responses to
potentially destabilizing loads applied to the knee, ankle,
or shoulder.136–140 At the knee, scientists have evaluated
the effects of anterior shear loads, varus-valgus loads,
206 SECTION I • Scientific Foundations
and rotatory loads (Figure 9-18).81,136–138,141 Scientists
can evaluate short latency (spinal reflexes), medium
latency (long-loop reflexes), and long latency (voluntary)
responses with this method of testing. At the ankle, scien-
tists have evaluated similar reflexive responses to sudden
inversion in people with functional ankle instability and
those with no history of injury.139,142 Finally, researchers
have evaluated the responses to external rotation per-
turbations at the shoulder.140,143 Studies such as these
are important for explaining how joints respond when
subjected to loads during functional activity, although
it is again important to recognize that the degree to
which the observed results resemble those that would be
observed in athletic participation or everyday activity is
currently unknown.
Voluntary muscle control refers to the ability to select
and precisely control the activation of muscles that are
specific to a task being performed. It is believed to be an
important component in safely and successfully perform-
ing a task. The inability to regulate force with precision
and the use of counterproductive activation strategies may
increase the risk of injury or prolong recovery. Scientists
have used target matching protocols that require fine con-
trol of force to test voluntary muscle control strategies at
various joints.144–147 The subject’s objective in voluntary
muscle control testing is to move a cursor projected to a
screen in front of him or her over a target that appears in
Figure 9-18
The knee perturbation device uses an air-driven piston that can
apply both anterior and posterior translation forces to the tibia on a
fixed femur. Use of this device is integrated with electromyographic
measurement of the quadriceps, the hamstrings, and the
gastrocnemius. Two potentiometers and a compression load cell
precisely signal the onset and the amount of tibial translation as well
as muscle reflex characteristics. (From DeLee JC, Drez D, Miller MD:
DeLee & Drez’s orthopaedic sports medicine: principles and practice,
ed 2, vol 1, p 402, Philadelphia, 2003, WB Saunders.)
random order at many different locations. Cursor move-
ment is controlled via force-feedback from a load cell to
which the subject’s extremity is rigidly fixed (Figure 9-19).
The activity patterns of a series of muscles surrounding
the joint being tested are recorded while subjects match
the targets. This provides the investigator with a profile
of the muscles that the subject used to successfully match
each target. Muscle activity patterns can then be evalu-
ated by plotting them in polar coordinates and calculat-
ing indices that describe the specificity associated with the
muscle activity.147 Because voluntary muscle control test-
ing is usually performed in an isometric setup with the
subject seated, there is once again a challenge in extrapo-
lating the results to movement. As with the other study
designs discussed, careful control of the testing (e.g.,
subject positioning and fixation) is critical to test validity.
Consequently, limitations in the extrapolation of findings
Figure 9-19
Patient setup for voluntary muscle control testing. The patient’s
distal shank is fixed to a six-axis load cell with a fiberglass cylinder
cast and clamp. Electromyographic preamplifiers are placed on the
muscles of the thigh and covered with a self-adhering wrap. An
electroarthrometer and electrogoniometer are placed on the thigh to
assess the affect of tibial translation and change in joint angle. During
the experiment, the patient positions a cursor that moves by force-
feedback from the load cell over targets that appear in several locations
on the screen in front of him or her. Muscle activity patterns during
target matching are assessed to describe voluntary muscle control.
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control
are willingly accepted in order to obtain valid and mean-
ingful information related to muscle control strategies.
Muscle activity patterns have been assessed while
people have performed most sports tasks.129,148–150
Although this method provides meaningful information
and appears to be the most applicable to functional tasks,
it is also the most complex to interpret. The dynamic
nature of the studies increases the likelihood of noise
and therefore error in measurement. Furthermore, it is
difficult to uncouple what aspects of the muscle activity
patterns result from primary movement strategies versus
responses to mechanical events associated with injury or
motion at other joint segments. For these reasons, many
researchers use more than one sensorimotor assessment
method because this allows them to obtain general data
from tests that closely resemble functional activity and
more specific physiological data from highly controlled
sensorimotor testing designs.
Motion Analysis Studies
Motion analysis involves the use of cameras, electromag-
netic tracking systems, instrumented linkage systems, or
radiostereometric analysis (RSA) to assess joint kinemat-
ics and kinetics in movement.151–154 This method of study
is important in identifying alterations in movement pat-
terns and the loading of joints. Furthermore, it allows
clinicians to evaluate multiple joint segments simultane-
ously. We have learned about differences in the landing
strategies of males and females, the impact of ACL injury
on joint kinematics and kinetics, pitching mechanics,
and many other clinically relevant issues using motion
207
analysis.129,152,155 In addition to directly studying human
movement, scientists are able to use motion analysis data
to develop predictive biomechanical models that can
be used to evaluate injury risk factors or the impact of
treatments.156–158
There is some inherent error in most motion analy-
sis methods because sensors or markers are fixed to the
skin (Figure 9-20), which often moves differently than
the bones lying beneath.159,160 Despite this fact, the error
involved rarely leads to noteworthy problems because
differences in the kinematics and kinetics of injured and
uninjured people are usually quite large. Unfortunately,
the variability in observed patterns is sometimes substan-
tial, which can complicate analysis unless the sample size
is large. Studying groups with relatively minor differences
in movement patterns remains a challenge. The use of
RSA has provided additional insight because this method
has high precision and it eliminates the error associated
with skin motion because the motion of tantalum beads
inserted on the bones is tracked with video radiography
rather than external markers.151,161
Motion analysis provides meaningful information
regarding joint motion; but understanding the mecha-
nisms behind the observed biomechanics is challeng-
ing without the concomitant use of other technologies.
Making inferences related to sensorimotor control from
motion analysis data alone is difficult because it is pos-
sible for the same alterations in joint mechanics to result
from different sensorimotor strategies. Consequently,
the simultaneous use of electromyography is important if
sensorimotor control is the primary focus of the study.
Figure 9-20
An example of reflective surface markers typically used in
motion analysis studies. High-precision infrared cameras
are used to track the movement of the markers, which are
positioned to establish an anatomical coordinate system. (From
Ford KR, Myer GD, Smith R et al: A comparison of dynamic
coronal plane excursion between matched male and female
athletes when performing single leg landings, Clin Biomech
21(1):35, 2006.)
208 SECTION I • Scientific Foundations
Functional Testing
In typical clinical practice, rehabilitation specialists are
interested in making quick but sound assessments related
to a patient’s functional status. The use of most of the
methods discussed here is difficult and not cost beneficial
in the typical clinical environment. Instead, most clinicians
use some form of functional testing to obtain general
information related to sensorimotor control. These tests
may include tasks such as single-leg stance (closing the eyes
and decreasing the stability of the support surface make
this test more complicated) (Figure 9-21), square hopping
in which precision is assessed, or the ability to respond
quickly and appropriately while standing on a rollerboard
(Figure 9-22) or rocker board that is perturbed.162–164 The
most important consideration in tests like these is not
whether or not subjects can complete the test for a spe-
cific duration, but the quality of movement or response
that they exhibit. Clinicians should seek responses that are
specific to perturbations rather than generalized co-con-
traction, which is not functional. In dynamic drills, move-
ment should be quick and precise. Postural stability tests
should be marked by limited sway that is well controlled
under conditions of limited feedback. Before full return to
sport or return to functional activity, it is ideal to observe
Figure 9-21
Single-leg balance on a foam cushion with the eyes closed. (From
DeLee JC, Drez D, Miller MD: DeLee & Drez’s orthopaedic sports
medicine: principles and practice, ed 2, vol 1, p 411, Philadelphia,
2003, WB Saunders.)
the patient performing his or her sport-specific skills at full
game speed or activity-specific skills at functional speeds
to ensure the patient exhibits the necessary sensorimotor
control to safely participate again.
Differences in Sensorimotor Control by Sex
It is clear that the incidence of some injuries (e.g., non-
contact ACL injuries) are more common in females than
males with similar exposure to risk.103–105 The increased
incidence of noncontact ACL injuries in females is a mul-
tifactorial issue that results from anatomical, hormonal,
biomechanical, and neuromuscular factors.104,105,165,166
Experts believe that differences in sensorimotor control
are especially important because sensorimotor control
is modifiable, which provides hope for successful ACL
injury prevention programs.104,165 Several studies have
evaluated differences in sensorimotor control by sex. In
some of these studies, researchers have evaluated indi-
rect measures of sensorimotor control such as kinematics
and kinetics when walking, running, cutting, or landing
from a jump,155,167–170 whereas in other studies, scientists
have assessed direct measures such as proprioceptive acu-
ity, muscle activity firing patterns, and postural stabil-
ity.148,171–175 The majority of scientists studying this issue
have reported differences in sensorimotor function by
sex that may help explain the female bias in noncontact
ACL injuries.
Females have generally demonstrated decreased pro-
prioceptive acuity when compared with age- and activ-
ity-matched male subjects who performed the same
tasks.173,176 This decreased proprioceptive acuity appears
to be most significant when the knee joint extends, which
is meaningful because most ACL injuries occur between
15 and 30 degrees of knee flexion.173 Conversely, find-
ings related to postural stability have been inconsistent,
as females often demonstrate improved stability when
compared with age- and activity-matched males.173,177
Researchers have found that some females use altered
muscle activity patterns or exhibit altered kinematics
when perturbed in stance or gait.169,174,175,178 In particu-
lar, it has been demonstrated that females often contract
their quadriceps before their hamstrings muscle when a
destabilizing load is applied to their knee joint.169,171,175,179
Such a strategy is potentially injurious as it would increase
the anterior shear loads experienced by the ACL. Females
who experience noncontact ACL injuries generally
do so when either landing from a jump or decelerat-
ing quickly and changing direction (cutting).103,104,165
Scientists have routinely found that females land from
a jump with their knee in greater valgus than is evident
in their male counterparts, which also increases strain in
the ACL (Figure 9-23).155,168,169,180 In addition to land-
ing with the knee in greater valgus, most researchers
have also found that females land with their knees less
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control
Figure 9-23
A female athlete landing with the knees in valgus. (From Andrews JR,
Harrelson GL, Wilk KE: Physical rehabilitation of the injured athlete,
ed 3, p 324, Philadelphia, 2004, WB Saunders.)
209
Figure 9-22
Perturbation in single-leg stance on
a rollerboard. (From Chmielewski
TL, Rudolph KS, Snyder-Mackler L:
Development of dynamic knee stability
after acute ACL injury, J Electromyogr
Kinesiol 12:271, 2002.)
flexed than males, which reduces the shock-absorbing
capacity of the large thigh muscles;155,165,169 however, this
finding has not been universal.181 Researchers have also
reported that females exhibit increased quadriceps activ-
ity and similar or decreased hamstring activity during
landing when compared with males, which lends support
to the idea that alterations in sensorimotor control con-
tribute to the high incidence of noncontact ACL inju-
ries in females.169,171 Similar alterations in muscle activity
patterns have also been observed when female are com-
pared to males performing cutting maneuvers.169 Thus,
the confluence of evidence currently available suggests
that sensorimotor control is a critical factor in the female
predisposition to certain lower extremity injuries.
Can these sensorimotor and biomechanical differ-
ences in females be modified? Early evidence suggests
that they can. Females who have participated in intense
training programs that include education on land-
ing mechanics, balance training, knee strength training
including plyometrics to improve power and control in
landing, “core” strengthening, agility drills, and practice
in landing with feedback on their mechanics have dem-
onstrated improved mechanics and control in landing.182
Moreover, the early results from clinical trials evaluating
ACL prevention programs including these principles has
been quite promising.155,183–186
Injury and Sensorimotor Control
There is a considerable body of evidence that demonstrates
that musculoskeletal injuries have a profound impact on
the sensorimotor system, affecting both somatosensory
feedback and motor function. This appears to be true
210 SECTION I • Scientific Foundations
regardless of the joint injured. Clinical scientists have
described alterations in proprioceptive acuity, postural
stability, muscle activity patterns, and joint kinematics
and kinetics associated with injury. Unfortunately, it is
often difficult to determine whether people who sus-
tain injuries had altered sensorimotor control before the
injury that predisposed them to injury or if the full extent
of the altered sensorimotor control in comparison to that
of matched people without injury is due to injury itself.
Side-to-side differences suggest a large part of the altera-
tions are most likely a result of injury; however, without
preinjury data, it is difficult to rule out the idea that sen-
sorimotor control was altered before injury as both limbs
are affected by injury and the changes in activity level
that usually accompany it.
Proprioceptive Acuity
Many researchers have assessed the effects of ligament
injuries on proprioceptive acuity.122,123,128,187–194 The
majority of these studies have assessed the impact of an
ACL injury on proprioceptive acuity,122,128,187,192 but stud-
ies have also been done after posterior cruciate ligament
(PCL) injuries,193 ankle sprains,190,191 and shoulder instabil-
ity events (Figure 9-24).189,194 The findings of these stud-
ies have been fairly consistent in demonstrating decreased
proprioceptive acuity when the results of the injured limb
have been compared with those from the uninjured limb
or those from people without injury.122,123,187,189–192,194 An
interesting finding is that the alterations in acuity often
depend on the direction of joint rotation.123 For example,
after ACL injury, people have greater difficulty detecting
movement into extension than they do in detecting move-
ment into flexion.123 In terms of raw values in degrees
of threshold to detection of passive movement or joint
position sense, the impact of injury is usually quite large
when the difference between groups is compared with
mean values of uninjured people (up to a 100% change);
Figure 9-24
An individual performing either joint position sense or
threshold to detection of passive motion on a proprioceptive
testing device. The subject lies supine with the upper
extremity supported at 90 degrees of abduction and elbow
flexion. The subject is fitted with a blindfold, a pneumatic
air splint, and headphones to eliminate visual, tactile, and
auditory cues. Using a handheld switch, the subject signals
when either joint positions are reproduced passively or
motion is detected. (From DeLee JC, Drez D, Miller MD:
DeLee & Drez’s orthopaedic sports medicine: principles and
practice, ed 2, vol 1, p 401, Philadelphia, 2003,
WB Saunders.)
however, when these values are considered with respect
to the typical excursion of a joint or its angular velocity
observed in sports participation, the importance of these
findings with respect to performance and risk of injury
remains unclear.
The exact source of the diminished proprioceptive
acuity after injury is unclear and debatable. Joint effusion,
pain, and a change in the resting position of the joint sec-
ondary to injury may play an important role. Moreover,
atrophy and changes in muscle physiology may impact
the intrafusal fibers of the muscle spindle as well as alter
cutaneous feedback from the skin of the thigh. In reality,
diminished proprioceptive acuity probably results from
the combined effects of the preceding factors. The exact
source is not important to the clinician because the mini-
mization of pain, effusion, and atrophy are routine goals
in rehabilitation. Clinicians should be aware, however,
that the more pain, effusion, and atrophy a patient expe-
riences, the more likely he or she is to have propriocep-
tive deficits, which may be difficult to address until these
primary impairments have been mitigated.
Postural Stability
Most of the work related to the impact of musculoskel-
etal injury on postural stability has evaluated the effects
of either ankle injuries in athletes or injuries in older peo-
ple who are at risk for falls.195–198 Because the effects that
aging and osteoarthritis have on sensorimotor control are
discussed later, this section focuses primarily on injuries
in young people. The postural stability of athletes with
functional ankle instability (repeated giving-way of the
ankle in the absence of measurable structural instability)
has been a primary focus of research related to postin-
jury postural stability in athletes. Nearly all of the studies
performed in the functional ankle instability population
have demonstrated increased postural sway and poorer
postural stability. The evidence suggests that decreased
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control 211

postural stability is not universal in this population, but
most studies report that at least 50% of the functional
ankle instability patients tested have demonstrated dimin-
ished postural stability.195–198 Researchers have reported
20% to 65% decrements in postural stability, suggesting
that the effects are large. The exact source of the dimin-
ished postural sway has yet to be determined. Although
the degree to which altered sensorimotor control con-
tributes to ankle injury and chronic ankle dysfunction is
unclear, most experts believe that it is a primary factor.
Muscle Activity Patterns
The results of studies evaluating muscle activity patterns
after injury have been variable and sometimes contra-
dictory, which is most likely due to methodological dif-
ferences and dissimilarities in the samples studied. The
majority of studies indicate that injury leads to altered
muscle activity patterns. This alteration may be the result
of dysfunction or compensatory strategies associated
with the injury.
Clinical scientists have demonstrated that people who
sustain ACL injuries have slower reaction times when
their involved knees are subjected to destabilizing anterior
shear loads.137,141 In addition to this slowing, there is evi-
dence of altered recruitment when results of the injured
extremity are compared with those of the uninjured
extremity.137 Early after injury, a quadriceps first response
has been observed, which appears counterproductive as it
increases anterior shear loads and further destabilizes the
knee. A quadriceps first strategy (specifically the vastus
lateralis muscle) has also been observed when research-
ers have suddenly translated the support surface in the
horizontal direction while patients stood on one leg.138
Interestingly, people who have signs that they will be able
to cope with their ACL injuries do not display this quadri-
ceps first strategy; they fire their lateral hamstrings before
their vastus lateralis muscles.138 Over time, people with
ACL deficiency appear to learn compensatory strategies
that may increase the stability of the limb.137
Decreased voluntary control of the quadriceps has also
been observed in people with ACL deficiency.147,199,200
This quadriceps dysfunction is especially apparent the vas-
tus lateralis muscle, which is known to atrophy to a greater
extent than the other quadriceps muscles after injury
(Figure 9-25).147,199,201 Altered voluntary control has been
observed during isometric target matching experiments
as well as during dynamic tasks such as repeated terminal
knee extension.147,199 The observed quadriceps dysfunc-
tion has been marked by failure to turn off the quadriceps
muscles when such activity is seemingly counterproduc-
tive and potentially destabilizing.147,199 To compensate for
this quadriceps dysfunction during movement, people

Figure 9-25
Polar plots of the muscle activity patterns of quadriceps and hamstrings recorded during voluntary muscle control testing. The plots demonstrate
that the ACL-deficient limbs of the patients tested had diminished specificity of muscle action in comparison to the respective muscles of their
uninjured limbs and those of an age- and activity-matched uninjured control group. (From Williams GN, Barrance PJ, Snyder-Mackler L et al:
Specificity of muscle action after anterior cruciate ligament injury, J Orthop Res 21:1135, 2003.)
212 SECTION I • Scientific Foundations
with ACL deficiency would need to increase their ham-
string activity (especially on the lateral side), which has
been a common finding in motion analysis studies.152,202,203
Failure to effectively compensate for this quadriceps dys-
function may lead to giving-way episodes, which are
a primary reason that people who have sustained ACL
injuries undergo surgical reconstruction.147 Interestingly,
people who are able to cope with ACL injury demon-
strate greater vastus lateralis muscle control and have less
quadriceps atrophy, which further supports the clinical
importance of this quadriceps dysfunction and the need
for rehabilitation specialists to address it.200
As mentioned previously, the muscle activity patterns
of people with ACL deficiency have also been evaluated
during functional tasks such as walking, running, and hop-
ping.152,202,204–207 Altered muscle activity patterns have once
again been observed consistently in these studies. The
altered activity patterns during gait and hopping are usu-
ally marked by increased hamstrings timing and greater
coactivity of the muscles surrounding the knee, which
stiffens the joint.152,202,204,206 Although the short-term use
of this strategy helps to provide dynamic knee stability, its
long-term use may promote early osteoarthritis because of
the recurrent compressive loading of the joint.152,205 People
who are able to cope successfully with their ACL injuries
and return to sports participation without surgery do not
display this stiffening strategy, which provides further
evidence that it is dysfunctional for long-term use.205
The results of studies that have evaluated muscle activity
patterns in people who have sustained ankle injuries have
been less consistent. Some researchers have described dimin-
ished peroneal muscle reaction times,195,208 whereas others
have not observed deficits in this population.139,209,210
Studies of muscle activity patterns in people with
shoulder instability have demonstrated decreased rotator
50
Healthy
Low functioning
40
* High functioning
Knee flexion (degrees)>
30
20
10
0 −0.5
0 20 40 60 80
A % stance
Figure 9-26
Knee joint kinematics and kinetics of ACL-deficient and healthy people during a step-and-cut maneuver. A, Plot demonstrating decreased knee
flexion in people with ACL deficiency. B, Plot demonstrating a decreased knee extensor moment in people with ACL deficiency. (From Houck
J, Yack HJ: Associations of knee angles, moments and function among subjects that are healthy and anterior cruciate ligament deficient (ACLD)
during straight ahead and crossover cutting activities, Gait Posture 18:134–135, 2003.)
cuff response times when external rotation loads are sud-
denly applied to the joint.140,211 Altered activation strategies
have also been observed when overhead athletes with atrau-
matic shoulder instability have performed activities such as
pitching, elevation, and rehabilitation exercises.212–215
Kinematics and Kinetics
The analysis of joint kinematics and kinetics during move-
ment provides important information related to joint
mechanics and indirect information related to sensorim-
otor control. Researchers have investigated the effect of
joint injuries on the mechanics of the knee, shoulder, and
ankle joints.129,154,205,216,217 As with the other categories of
studies, the greatest volume of work is related to ACL
injuries. Researchers have demonstrated consistently that
people with ACL deficiency walk with increased knee
flexion and lower internal knee extension moments when
the results of the injured limb are compared with those
of their uninjured limbs or matched subjects without a
history of injury (Figure 9-26).152,207,217,218 This reduced
internal knee extension moment does not appear to be
the result of “quadriceps avoidance” because simulta-
neous collection of muscle activity patterns has rarely
demonstrated diminished quadriceps activity; instead,
the reduced internal knee extension moments appears to
be the result of increased hamstring activity and a shift of
control from the knee to the hip.205,207
Few studies have evaluated kinematics and kinetics
after shoulder or ankle injury. Most of the work related to
the shoulder joint has evaluated the movement patterns
of people with subacromial impingement syndrome.154,219
Researchers have demonstrated altered scapular rotation
and increased anterior tilting of the scapula in elevation,
with concomitant alterations in trapezius and serratus
anterior muscle activity in this population.154 In a study
Sagittal plane moment (N/Kg)
2
1.5 * Healthy
Low functioning
Extensor
1 High functioning
0.5
0 *
100 0 20 40 60 80 100
B % stance
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control
that compared the gait biomechanics of people who had
sustained inversion ankle sprains with those with no his-
tory of injury, researchers demonstrated that people with
a history of inversion sprain had more lateral centers of
pressure at initial contact with increased medial loading
during stance, a more mobile first ray, a longer period
of pronation, delayed knee flexion, and greater total
foot contact time.216 The results of these motion analy-
sis studies suggest that sensorimotor control is critical to
functional joint stability and adversely affected by injury.
Surgery, Rehabilitation, and Sensorimotor Control
Fewer studies have evaluated sensorimotor control after sur-
gery than have evaluated sensorimotor control after injury.
Most of the studies present are related to sensorimotor
control following ligament reconstruction or total joint
replacement procedures. The variability in subject popu-
lations and methodology (e.g., when postsurgical test-
ing was performed) has led to highly variable results.
Consequently, it is difficult to draw firm conclusions
from these studies. It is also challenging to differentiate
the effects of surgery from those of rehabilitation because
most people undergo rehabilitation after surgery and
there are no randomized trials comparing the effects of
surgery alone to those with postsurgical rehabilitation.
The results of studies assessing proprioceptive acuity after
ACL reconstruction are equivocal, with some research-
ers reporting no significant change in acuity and others
reporting noticeable improvement.192,220,221 The improve-
ments appear to be primarily observed at the end ranges of
motion rather than in the midrange and are not notewor-
thy until about 6 months later when they are observed.221
Postural stability in people who have undergone ACL
reconstruction is better than that in people with ACL defi-
ciency but not as good as that of people with no history
of injury.222 The findings of studies evaluating hamstring
muscle latencies following anterior shear loading have also
been equivocal on whether the latencies increase or decrease
after ACL reconstruction.223,224 Voluntary muscle control
appears to improve after ACL reconstruction; however, it
is unclear if this is a result of surgical stabilization, rehabili-
tation, or a combination of the two.225 Although kinemat-
ics in gait appear to improve after ACL reconstruction,
significant gait abnormalities are still present for up to 12
months after surgery.207,226–228 In particular, the internal
knee extensor moments and measured work and power
decrease.226,228 This is most likely because of the prolonged
knee extensor weakness after surgery.
A few studies have evaluated proprioceptive acuity after
shoulder stabilization procedures.189,229,230 These studies
suggest that surgical stabilization of the shoulder improves
proprioceptive acuity;189,194,229,230 however, a nonoperative
approach involving immobilization and rehabilitation yields
similar results to surgical stabilization of the shoulder.230
213
One study evaluated peroneal muscle reaction times
after anatomical repair of the lateral ankle ligaments.231
The results of this study suggest that there are no side-to-
side differences in peroneal reaction times after anatomi-
cal repair of the lateral ankle ligaments.
A number of research reports relate to propriocep-
tive acuity after knee, hip, or shoulder joint replacement.
The findings of these studies have also been equivocal.
Some researchers have reported improved proprioceptive
acuity after joint replacement,232–235 some have reported
that arthroplasty has no effect on proprioception,236–239
and others have reported that the acuity of the treated
limb is worse than that of age-matched healthy people
or the contralateral extremity after joint replacement.240
Retaining the joint capsule and cruciate ligaments does
not have a large effect on proprioception.232,236,239
Surprisingly, few studies have investigated the effects of
rehabilitation on sensorimotor control. Functional out-
comes are assessed frequently and have been the focus
of several studies in the literature; however, it is usually
difficult to differentiate whether sensorimotor control
was improved or not in such studies because sensorimo-
tor control has not been assessed directly. Several studies
demonstrate that sensorimotor training using balance
boards or perturbation training improves function.241–243
Researchers have also evaluated the effects of sensorimotor
training on postural stability,244,245 proprioceptive acuity,245
muscle activity patterns,178,246,247 and movement patterns
(kinematics and kinetics).247 The results of these studies
confirm that sensorimotor training has positive effects on
postural stability, muscle activity patterns, and movement
patterns, but little change in proprioceptive acuity was
observed. The results of these studies suggest that sen-
sorimotor training is important and should be included
as a routine part of physical therapy programs directed at
improving joint or postural stability. At this time, the opti-
mal training strategies, dose-response relationships, and
specific effects of neuromuscular training remain largely
unknown.
Age and Sensorimotor Control
As a person ages, there are changes in his or her anat-
omy and physiology that may alter sensorimotor control.
Anatomically, there is a reduction in the number of mech-
anoreceptors in joint tissues and a decrease in muscle mass
(sarcopenia) that is associated with a reduction in the size
and number of muscle fibers.248–251 Physiologically, there is
a decrease in proprioceptive acuity,252–254 slower sensorim-
otor processing,252,255,256 increased reaction times to distur-
bances,256 decreased balance,257,258 and a high likelihood
of muscle weakness.249,259,260 The combination of these
factors impacts function and decreases stability in stance
and movement.257,258,260,261 Consequently, it is no surprise
that approximately one third of people 65 years of age
214 SECTION I • Scientific Foundations
and older fall at least once each year;262,263 50% of these
falls will result in admission to a long-term care facility.264
Most of the studies related to the effects of aging on
proprioceptive acuity have examined acuity at the knee
joint.254,260,265 However, decreases in acuity have also
been observed at other joints,252,253,266 suggesting that
decreased proprioceptive acuity is a generalized phenom-
enon throughout the body. Lifestyle affects this acuity, as
the more sedentary a person is, the more likely he or she
is to have deficits in proprioceptive acuity.267 In addition to
activity level, injuries and disease processes such as osteo-
arthritis and diabetes have a profound impact on proprio-
ception.258,268–270 Fortunately, there is evidence that training
can significantly improve proprioception, postural stability,
and gait in older people.271–274 The take-home message here
is that proprioceptive training should be a routine compo-
nent of rehabilitation programs, especially in older people.
Muscle undergoes significant changes as it ages.275
Muscle fiber number and size decrease (Figure 9-27),
and the amount of noncontractile tissue (fat and other
connective tissue) within the muscle increases.250,251
Although the number of type I (slow) and type II (fast)
fibers appears to decrease in a similar fashion,276 type
II fibers appear to undergo selective atrophy.276,277 In
addition to this sarcopenia, people also have fewer α-
motoneurons and, consequently, fewer motor units with
age.278–280 Activation of the existing motor units may
also change.281,282 Finally, metabolic changes such as
reduced calcium release and related alterations in excita-
tion-contraction coupling have also been reported.283,284
The functional expression of these physiological changes
in skeletal muscle is weakness, decreased power, and
increased muscle fatigue. As with proprioceptive acuity,
the impairments associated with aging related to strength,
power, and fatigue can be limited with appropriate train-
ing measures.285,286 To promote these positive training
Muscle area (mm2/48)
90
70
Figure 9-27
The relationship between age and (A)
50
muscle cross-sectional area and (B) total
number of muscle fibers. (From Lexell J,
Taylor CC, Sjöström M: What is the cause
of the ageing atrophy? Total number, size 30
and proportion of different fiber types
studied in whole vastus lateralis muscle
from 15- to 83-year-old men, J Neurol Sci 10 20 30
84:284–285, 1988.)
adaptations, it is critical that the training is applied in
a manner that is consistent with the physiological prin-
ciples related to intensity, frequency, duration, and tim-
ing of training. Because older people are more likely to
experience muscle damage with training than are young
people,285,287 it is important that clinicians carefully moni-
tor patients and their exercise progression. This does not
imply that older people cannot be trained in an intense
fashion. Older patients should perform high-intensity
training, but only after the patient has had the appro-
priate preparatory training and demonstrates readiness
for increased intensity. It is the authors’ general observa-
tion that many rehabilitation specialists fail to train their
patients with sufficient intensity, duration, or frequency
to induce optimal changes in muscle function.
In addition to addressing proprioception and mus-
cle function, it is important that clinicians consider
sensorimotor processing when treating older patients. The
rate of sensorimotor processing and the degree of flexibility
within the sensorimotor system decrease with age (Figure
9-28).255,256 The coupling of decreased reaction times and
the likelihood of less forceful responses increase the risk of
falls and injuries. Moreover, the complexity of the circum-
stances older people are presented with (number of obsta-
cles, dynamics of the conditions) has a much greater impact
than it did when they were younger.255,256 Consequently,
clinicians need to educate their patients on safe movement
principles such as planning difficult movements ahead, per-
forming them slowly, and thinking about potentially dan-
gerous situations so that when they are presented with an
unexpected circumstance they may act in a safe manner.
Osteoarthritis and Sensorimotor Control
Although it is generally presumed that joint degeneration
precedes and results in the pain, weakness, and disability
Total number of fibers (*103)
900
(p<0.001)
700 (p<0.001)
500
300
100
40 50 60 70 80 10 20 30 40 50 60 70 80
Age (years) Age (years)
 CHAPTER 9 • Articular Neurophysiology and Sensorimotor Control 215

1 3500
Visual matching Y = 989 + 11.5(X)

Digit symbol reaction time (msec)

Crossing out 3000
0
2500
Standard score

2000

1500

1000

500
10 20 30 40 50 60 70 80 90 20 40 60 80
Chronological age (years) Chronological age (years)
Figure 9-28
Effect of age on (A) perceptual speed and (B) reaction time tests. (From Salthouse TA: Aging and measures of processing speed, Biol Psych
54:37–38, 2000.)

associated with osteoarthritis, it is equally plausible that system, reflex activity, and descending control pro-
altered sensorimotor control plays a primary role in cesses.288 Several researchers have demonstrated reduced
the pathogenesis and progression of osteoarthritis.288 proprioceptive acuity in the presence of osteoarthritis
Regardless of which of these pathways is conceptually using cross-sectional studies.233,265,269,290,291 Although the
more accurate, it is clear that sensorimotor dysfunction is primary focus of these studies has been patients with knee
prevalent in people with osteoarthritis.269,289 osteoarthritis, it is reasonable to expect similar findings
People with osteoarthritis exhibit both sensory and at other joints. Muscle weakness and activation deficits
motor deficits, which in combination result in altered are common in osteoarthritis,288,292–294 which may alter
movement, disability, and reduced quality of life.269,288 the magnitude and timing of responses and potentially
Joint effusion, pain, and joint degeneration may alter muscle spindle function. The end result of this senso-
joint receptor function, which impacts proprioceptive rimotor dysfunction is a cyclic process of dysfunction and
acuity and the function of the α-motor system, γ-motor disability (Figure 9-29).

Exercises to increase strength, Decreased disability and

Limb injury
Previous innocuous,
unilateral injury with
bilateral adverse effects
improve proprioceptive acuity, optimization of function
balance and coordination, function Participation in habitual exercise and
Rehabilitation functional activities (i.e., walking)
Joint damage
Abnormal movement and
instability causing pain, effusion
and stress on articular structures,
microtrauma to cartilage and
subchondral bone sclerosis

Disability or decrease
Muscle sensorimotor dysfunction
in habitual activities
Weakness, reduced voluntary activation (inhibition),
Atrophy of articular cartilage,
increased fatigue, decreased proprioceptive acuity,
subchondral osteoporosis
decreased neuromuscular protective mechanisms,
functional joint instability, postural instability
Persistent but “subclinical” deficits Aging process
Weakness, articular
wear and tear, slow
reflexes

Higher motor and sensory control

and psychological factors
Decreased motivation, loss of confidence,
fear of pain or (re)injury

Figure 9-29
The complex interrelationship between sensorimotor dysfunction of muscle, joint damage, and disability. (From Hurley MV: The role of muscle
weakness in the pathogenesis of osteoarthritis, Rheum Dis Clin North Am 25(2):283–298, 1999.)
216 SECTION I • Scientific Foundations
A global assessment of strength and control includ-
ing not only the muscles of the lower limb but the hip
and trunk (“core”) is critical when treating patients
with osteoarthritis. Because osteoarthritis appears to
preferentially affect the quadriceps muscle group (as
stated previously, this relationship is likely bidirec-
tional), the strength and control of quadriceps should
be a primary focus of rehabilitation. The good news is
that the strength and control of quadriceps are certainly
treatable.295,296
Summary
Sensorimotor control is achieved through a complex inter-
action between the nervous and musculoskeletal systems.
Mechanoreceptors in muscles, skin, and the connective
tissues of joints provide somatosensory feedback that is
mediated throughout the hierarchical structure of the
CNS. The CNS receives and processes a large number
of signals simultaneously each second. Reflexes and
descending motor commands modify muscle activity so
that it is specific to the environmental conditions the
somatosensory system senses. Motor programs and trig-
gered reactions expedite complex responses and reduce
the number of degrees of freedom that the CNS must
deal with at any given time. Locomotion is the result of
a specific type of motor program that is mediated in the
spinal cord but initiated and refined by somatosensory
feedback and descending commands from higher cen-
ters. The complexity of the sensorimotor control system
described in this chapter should be remembered when
considering the effects of perturbations in functional
activity or the impact of an injury. The redundancy and
plasticity of the sensorimotor control allow it to adapt to
perturbations, injury, and training.
The sensorimotor function of males and females is
grossly similar; however, some sensorimotor differences
that may contribute to the female predisposition to lower
extremity musculoskeletal injuries have been reported.
Aging leads to declined proprioceptive acuity and senso-
rimotor function, but training can minimize the effects of
aging and optimize function. Injury and osteoarthritis can
have a profound impact on sensorimotor control through
a multifactorial process involving muscular dysfunction,
pain and inflammation, and altered somatosensory feed-
back from the receptors of the involved limb. The results of
studies evaluating the effects that surgery has on sensorim-
otor control are best described as equivocal. Rehabilitation
appears to be effective at mitigating some of the effects
that injury, osteoarthritis, and surgery have on senso-
rimotor function, but at this time the optimal training
methods, dose-response relationships, and exact effects of
training remain unclear. Although we have learned a great
deal related to sensorimotor function in the past half cen-
tury, our knowledge of sensorimotor physiology and the
role that the sensorimotor system plays in musculoskeletal
health is constantly evolving. Overall, the evidence suggests
that sensorimotor control is a critical component in joint
stability and health; hence, sensorimotor training should
be a routine component of rehabilitation programs.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 296 references for this chapter.

P AIN : P ERCEPTION AND M ECHANISMS
Marie K. Hoeger Bement and Kathleen A. Sluka
Introduction
This chapter reviews the neurobiology of pain. Pain is
a complex subject; thus, the chapter only highlights
the major points. For more in-depth information on
the neurobiology of pain and pain management, refer
to the following texts: Sensory Mechanisms of the Spinal
Cord, Third Edition;1 The Textbook of Pain, Fourth
Edition;2 and Bonica's Management of Pain, Third
Edition.3 Further, where appropriate, reviews and
textbooks will be cited to offer sources for additional
information.
Pain is the most common reason a person seeks
medical attention. Yet pain is undertreated and man-
agement is difficult, particularly with chronic pain. The
International Association for the Study of Pain (IASP)
defines pain as an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage, or described in terms as such (Table 10-1).4
Inherent in this definition is both the subjective and
multidimensional nature of pain. Melzack and Casey
proposed three dimensions of pain: sensory-discrimi-
native, motivational-affective, and cognitive-evalua-
tive.5 The sensory-discriminative component of pain
is concerned with the quality (i.e., burning, sharp, dull,
aching), location, duration, and intensity. The moti-
vational-affective component of pain is concerned
with its unpleasantness and our motivational tendency
toward escape or attack. Lastly, the cognitive-evalua-
tive is based on past experience and the outcome of
different response strategies. All three dimensions are
linked and interact to affect the motor and behavioral
consequences responsible for the complex pattern of
responses to pain (for a review, see Textbook of Pain,
Chapter 172). The multidimensional aspect of pain dic-
tates a biopsychosocial approach when determining the
factors affecting pain reports (Figure 10-1).
10
C H A P T E R
Pain Dimensions5
● Sensory-discriminative
● Motivational-affective
● Cognitive-evaluative
Pain can be acute or chronic. Acute pain is protective
and serves as a warning sign that the body is experiencing
actual or potential tissue damage. Clinically, acute pain
usually results from an injury that can be pinpointed to
time and place, such as spraining an ankle, getting a sun-
burn, or breaking a bone. The pain in this case occurs
immediately at the time of injury and goes away once
healing is completed. On the other hand, chronic pain
is nonprotective and serves no biological purpose. The
International Association for the Study of Pain has pro-
posed several definitions of chronic pain. Pain can be
considered chronic if it outlasts normal tissue healing
time, is greater than would be expected from the extent
of the injury, or occurs in the absence of identifiable
tissue damage.4 Frequently with chronic pain, the self-
report of pain, which is considered the gold standard, is
greater than objective findings. Thus, the concept of pain
as a symptom, as occurs with acute pain, changes to the
concept of pain as a disease, as occurs with chronic pain.
Types of Pain
● Acute
● Chronic
Clinicians commonly use a number of other definitions,
suggested by the International Association for the Study
217
218 SECTION I • Scientific Foundations

Table 10-1
Pain Definitions
Term Definition

Pain An unpleasant sensory and emotional experience associated with actual or potential tissue damage
or described in terms of such damage
Pain is always subjective
Allodynia Pain resulting from a stimulus that does not normally provoke pain
Hyperalgesia An increased response to a stimulus that is normally painful
Primary: occurs at the site of injury (tissue damage)
Secondary: occurs outside the site of injury
Hypoalgesia Diminished pain in response to a normally painful stimulus
Analgesia Absence of pain in response to stimulation that would normally be painful
Referred pain Pain outside the area of tissue damage
Nociceptor A receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious
if prolonged

PAIN

Biological Factors Psychological Factors Social Factors

- disease activity - pain behavior - social support
- overall physical - pain coping - marital adjustment/
condition - self-efficacy spousal responses
- medication intake - helplessness
- cognitive distortion
- personality

Figure 10-1
Biological, psychological, and social factors are involved when an individual reports pain. (Redrawn from Keefe FJ, Bonk V: Psychosocial
assessment of pain in patients having rheumatic diseases, Rheum Dis Clin North Am 25:81–103, 1999.)

of Pain, to describe pain behaviors. Hyperalgesia is an
increased response to a noxious stimulus. Primary hyper-
algesia occurs at the site of injury, whereas secondary
hyperalgesia occurs outside the site of injury (Figure 10-2).
Primary hyperalgesia is thought to reflect changes in the
peripheral nervous system, and secondary hyperalgesia is
thought to be mediated by changes in the central nervous
system. Deep tissues (i.e., muscle, joint, and viscera) are
commonly associated with secondary hyperalgesia, particu-
larly at sites distant to the injury. For example, secondary
hyperalgesia occurs in people with kidney pain who have
tenderness with palpation over the lower back, whereas pri-
mary hyperalgesia is the increased pain felt by people with
osteoarthritis to pressure applied to the arthritic joint.
Allodynia, on the other hand, is defined as pain in
response to a previously innocuous stimulus. Allodynia
occurs after sunburn or in people with neuropathic pain
who have difficulty wearing clothes or who find that
brushing the skin is painful. Importantly, hyperalgesia is
different from referred pain. People feel referred pain
outside the area of injury; unlike hyperalgesia, referred
pain is not induced by a painful stimulus at the site of
referral. The most common example of referred pain is
that of pain down the left arm during a heart attack4 or
pressure on a nerve root from a herniated disc.
Deep Tissue Pain
Muscle pain can arise from a variety of disorders includ-
ing myofascial pain, fibromyalgia, myositis, or strain.6,7 Joint
pain occurs acutely after injury to ligaments or the joint
capsule, or chronically after conditions like osteoarthritis or
rheumatoid arthritis.8 Thus, deep tissue pain can be acute or
chronic with inflammatory and noninflammatory events.
 CHAPTER 10 • Pain: Perception and Mechanisms
Mechanical
hyperalgesia
A
B
C Cutaneous versus Deep (Muscle) Pain
Flare
1 cm
14 Before burn
After burn
12
Mechanical pain threshold
10
8
6 anatomical differences are discussed later. Briefly, dorsal
4 tin B4 and somatostatin and more calcitonin gene-related
2
Site A Site B Site C
Figure 10-2
Following a burn injury, tissue displays primary and secondary
hyperalgesia. Primary hyperalgesia occurs within the flare (A, B),
indicating tissue injury with a reduction in mechanical pain threshold.
Secondary hyperalgesia occurs outside the area of tissue injury (C)
with a similar reduction in mechanical pain threshold. (Redrawn from
Kandel ER, Schwartz JH, Jessel TM: Principles of neural science, ed 4,
New York, 2000, McGraw-Hill/Appleton Lange.)
The quality of pain associated with injury to a muscle
or joint differs from that associated with injury to the
skin. Injury to deep structures results in diffuse, difficult-
to-localize, aching pain.9,10 In contrast, injury to skin typi-
cally produces well-localized, sharp, stabbing or burning
pain.11 Using microneurography, intraneuronal stimulation
of muscle-nerve fascicles produces only the sensation of
deep cramplike pain10 in contrast to stimulation of cutane-
ous C-fibers (group IV), which produces burning pain.11
Stimulation of muscle nociceptors at a low intensity to acti-
vate a few primary afferent fibers produces pain that is well
localized.11 However, if the stimulus intensity is increased,
activating more primary afferent fibers, then the pain is less
localized and spreads to regions outside the area of innerva-
tion.12 For muscle pain, the size of the area of referred pain
correlates with the intensity and duration of the primary
219
muscle pain.13–15 In contrast to muscle nociceptors, high-
intensity stimulation of cutaneous nociceptors remains con-
fined to the area of stimulation and does not expand outside
the area of innervation unless secondary hyperalgesia is pro-
duced.11,12 In human subjects, muscle pain is rated as more
● Cutaneous: sharp and easily localized with minimal referral
● Deep: dull, poorly localized, and frequently refers
unpleasant and longer lasting with more frequent referred
pain compared with cutaneous pain.16,17 Pain associated
with injury to cutaneous tissue would be expected to differ
in quality than pain associated with injury to deeper tissues
such as a muscle or a joint. In summary, cutaneous pain is
sharp, easy to localize, and rarely refers, whereas deep tissue
pain is dull, difficult to localize, and frequently refers.
There are different central anatomical pathways and
biochemical mediators associated with muscles and joints
that could result in a different pattern of response. The
root ganglia neurons innervating muscle have less isolec-
peptide and substance P (see neurotransmitter section)
than dorsal root ganglia neurons innervating cutaneous
tissue.18,19 Interestingly, injection of neuropeptides into
skin or muscle results in different responses. For example,
substance P produces spontaneous pain when injected into
skin and a decrease in the pressure-pain threshold, without
spontaneous pain, when injected into muscle.20 Calcitonin
gene-related peptide does not produce pain when injected
alone into either skin or muscle but does produce pain
when injected intramuscularly with neurokinin A.21
Animal Models of Nociception
Pain is a subjective measure involving affective responses,
which is not quantifiable in animals. Therefore, when
using animal models the more accurate terminology is
nociception, which refers to the excitation of a noci-
ceptor. A nociceptor responds to a noxious (thermal,
mechanical, or chemical) stimulus, thus activating small-
diameter primary afferent fibers.
Several animal models of nociception mimic clinical
events, which are utilized to probe the mechanisms behind
the development and maintenance of different pain condi-
tions.22 Animal models of nociception are used to control
the extent of injury, examine the time course of injury, and
minimize the motivational affective component and placebo
effects of treatment. Animal models also allow research-
ers to investigate potential mechanisms that contribute
to the development and maintenance of pain, particularly
220 SECTION I • Scientific Foundations
those involving the peripheral and central nervous systems.
Furthermore, investigators can examine efficacy and safety
of pharmaceutical and nonpharmaceutical treatments, as
well as the mechanisms of action of these treatments.
Animal models exist for studying acute and more
persistent pain including cutaneous, neuropathic, and
musculoskeletal pain. Acute nociceptive (pain) models,
measuring responses to heat, mechanical stimulation,
or electrical stimulation, have been utilized for decades
as screening tools to test the efficacy of pharmacologi-
cal agents.23 Models of tissue injury were developed later
to more directly measure pain that might be similar to
clinical syndromes. Carrageenan can be injected into the
paw (in addition to the joint or muscle) to produce an
acute inflammatory event resulting in hyperalgesia.24,25
Injection of complete Freund's adjuvant, either systemi-
cally or into a joint, is a model of chronic inflammation
similar to rheumatoid arthritis and is associated with
mechanical and heat hyperalgesia.22,26 Other irritants
include injection of formalin into the paw, turpentine
oil, or capsaicin into the skin, muscle, or joint.22 Each
of these animal models allows potential pharmacological
and nonpharmacological treatments to be tested before
experimenting on human subjects.
The current models of musculoskeletal pain are both
inflammatory and noninflammatory in nature and pro-
duce an acute or chronic hyperalgesia.7,8 Interestingly,
injection of the inflammatory irritant capsaicin into mus-
cle or joint tissue results in long-lasting (weeks) bilateral
secondary mechanical hyperalgesia as compared to injec-
tion of capsaicin into the skin where secondary hyper-
algesia is unilateral and of shorter duration (hours).27
Similarly, injection of carrageenan into muscles or joints
produces a long-lasting bilateral hyperalgesia that is dose
dependent.28,29 In these models of deep tissue inflamma-
tion, there is an initial phase of acute inflammation that
converts to chronic inflammation by 1 week and lasts
through 8 weeks.28 A third model of musculoskeletal
pain, induced by repeated intramuscular acid injections,
is noninflammatory but produces long-lasting mechanical
hyperalgesia. Importantly, in this model, there is no dam-
age within the muscle tissue and the hyperalgesia is main-
tained by changes in the central nervous system.30 Thus,
for the study of musculoskeletal pain there are models
that mimic acute and chronic inflammation of muscles or
joints and chronic noninflammatory muscle pain.
To study postoperative pain, Brennan and colleagues
developed an animal model in which a longitudinal incision
is made through the skin, fascia, and muscle of the plantar
aspect of the hind paw.31 This model reflects both the super-
ficial and deep tissue injuries seen with surgical treatments.
Researchers study visceral pain by using pain models
that include hollow organ distension, urinary blad-
der inflammation, and artificial ureteral calculosis as
a model for generic visceral pain, cystitis, and kidney
stones, respectively.32 Colorectal distension in awake,
unanesthetized, unrestrained rats produces a quantifiable
aversive behavior and cardiovascular and visceromotor
responses indicative of acute visceral nociception.33 The
use of animal models helps to elucidate the mechanisms
involved and potential treatment of visceral pain.
Several models of neuropathic pain have been devel-
oped and are utilized extensively. The three most com-
mon models are (1) loose ligations around the sciatic
nerve,34 (2) tight ligations around one half to one third
of the sciatic nerve,35 and (3) tight ligations around the
spinal nerves (L5 and L6).36 Each of these neuropathic
pain models produces a measurable long-lasting hyperal-
gesia and changes in the central nervous system.
To summarize, there are several animal models of
nociception, which are used to increase our understand-
ing of pain mechanisms as well as the efficacy of phar-
macological and nonpharmacological treatments. These
models meld clinical and basic science research, ulti-
mately allowing clinicians to interpret the latest research
advancements relating to musculoskeletal, neuropathic,
visceral, and postoperative pain.
Neurobiology of Pain
Peripheral Pathways
The afferent component of the peripheral nervous system
is composed of sensory receptors that convert mechani-
cal, thermal, and chemical energy into electrical signals
and carry this information to the central nervous system.1
These primary afferent fibers vary in size and conduction
velocity from thickly myelinated (Ia) to unmyelinated (C)
fibers (Table 10-2). Cutaneous sensory receptors convey
electrical signals from encapsulated touch receptors to
the CNS via Aβ fibers. On the other hand, nociceptors
are unencapsulated receptors, termed free nerve endings,
respond to intense stimuli, and include Aδ (thinly myelin-
ated axons) and C fibers (unmyelinated axons). The pri-
mary afferent fibers contained in muscle and joint nerves
are classified as groups II, III, and IV.37,38 In addition to
these primary afferents, muscle nerves also contain motor
axons and groups Ia, II, and Ib primary afferents, which
carry information to the spinal cord from muscle spindles
and Golgi tendon organs, respectively.7,39 Group II primary
afferents in joint nerves are large myelinated afferents that
transmit information about proprioception of the joint.
Group III primary afferent fibers are thinly myelinated
fibers, and group IV are unmyelinated fibers. Both group
III and group IV fibers transmit nociceptive information
from free nerve endings in the periphery to the spinal cord
dorsal horn. Some nociceptors are normally silent and are
only activated following tissue injury.40,41
Following joint or muscle inflammation “sensitization”
of primary afferent fibers occurs.40–43 Sensitization refers to
 CHAPTER 10 • Pain: Perception and Mechanisms 221

Table 10-2
Types of Afferents Located in the Skin, Muscle, or Joint
Skin Muscle Joint

Thickly myelinated Aβ Ia—muscle spindles II

touch receptors Ib—GTO Proprioception
CV = 25–70 m/s II—muscle spindles CV = 25–70 m/s
Proprioception
CV = 25–120 m/s
Thinly myelinated Aδ III III
Nociceptors Nociceptor Nociceptor
CV = 2.5–25 m/s CV = 2.5–25/m/s CV = 2.5–25 m/s
Unmyelinated C IV IV
Nociceptor Nociceptor Nociceptor
CV = <2.5 m/s CV = <2.5 m/s CV = <2.5 m/s

CV = conduction velocity.

an increase in spontaneous activity, a decrease in the thresh-
old of response to noxious stimuli, an increase in responsive-
ness to the same noxious stimuli, or a change in receptive
field size. Recording the activity of the peripheral nerves
before and after induction of acute inflammation, Schaible
and Schmidt40,41 showed increased spontaneous activity and
responsiveness to noxious and innocuous joint movement
in primary afferent fibers, groups II, III, and IV (Figure
10-3). Similar changes occur following inflammation of the
muscle with carrageenan or following ischemia of the mus-
cle.42,44,45 In inflammation of either a muscle or a joint, there
is an increase in the response of the primary afferents to
weak mechanical stimuli, such as innocuous local pressure.
Following peripheral inflammation, silent nociceptors begin
to respond to both innocuous and noxious stimuli, such
as pressure and joint movement. Taken together, there is a
general increase in activity of nociceptors, thereby increasing
the number of afferents firing following a peripheral insult
and increasing input to the central nervous system.
A number of substances are released from inflammatory
cells and can directly activate or sensitize primary afferent fibers
(Figure 10-4). These include serotonin, bradykinin, prosta-
glandins, and cytokines. Serotonin is released from platelets,
activates muscle nociceptors, and causes pain in humans.46,47

Group III unit

Imp/s

20

Flexion
15
30s

10

0
72 87 90 105 125 147 170 173 198 205
Injection of
Kaolin Minutes after Kaolin
Figure 10-3
Group III primary afferent fiber (i.e., nociceptor) recording before and after the induction of joint inflammation by an injection of kaolin
and carrageenan into the knee. Before inflammation, the nociceptor did not respond to knee joint flexion (bar). Approximately 2 hours after
inflammation, the nociceptor started to respond to knee joint flexion. (From Schaible H-G, Schmidt RF: Direct observation of the sensitization of
articular afferents during an experimental arthritis. In Dubner R, Gebhart GF, Bond MR, editors: Proceedings of the Fifth World Congress on Pain,
pp 44–50, Amsterdam, 1988, Elsevier.)
222 SECTION I • Scientific Foundations
Figure 10-4
Inflammation induces the release of chemicals at the site of injury,
which sensitizes nociceptors. These inflammatory mediators therefore
contribute to the transmission of pain. Neurogenic inflammation
occurs with the release of substance P and CGRP, which induces
vasodilation and plasma extravasation. NGF = nerve growth factor;
ATP = adenosine triphosphate; H+ = hydrogen; TrkA = receptor
for nerve growth factor; BK= bradykinin; 5-HT = serotonin; P2X3
= purinergic receptor for ATP; ASIC = acid sensing ion channel;
PGE2 = prostaglandin E2; VR = vanilloid receptor; DEG/ENaC =
DEGenerin/Epithelial Na Channel; DRG = dorsal root ganglion;
CGRP = calcitonin gene related protein. (From Julius D, Basbaum AI:
Molecular mechanisms of nociception, Nature 413:203–210, 2001.)
Bradykinin is released from plasma after tissue injury, is pres-
ent in inflammatory exudates, sensitizes nociceptors, and
produces pain and heat hyperalgesia in humans.48–51 Further,
after inflammation, the sensitivity of nociceptors to bradykinin
increases.52 Prostaglandins are metabolites of the arachadonic
acid cascade and are produced in response to tissue injury.
Importantly, prostaglandins E2 and I2 directly excite and sen-
sitize joint afferent fibers.53 The nonsteroidal anti-inflammato-
ries (NSAIDs) produce their effects by reducing prostaglandin
production through inhibition of the enzyme cyclooxygenase,
which is involved in the breakdown of arachidonic acid.
During inflammation, macrophages release cyto-
kines that include interleukins (IL1β, IL-6) and tumor
necrosis factor (TNFα). These inflammatory cytokines
are increased in the synovial fluid from patients with
arthritis, sensitize primary afferent nociceptors, and pro-
duce mechanical and thermal hyperalgesia.54–60 Blocking
TNFα receptors or available TNFα reduces hyperalge-
sia in animal models of inflammation and neuropathic
pain.61-63 While the actions of each of these inflammatory
mediators were described individually, many mediators
act together to enhance the inflammation or hyperalgesia,
producing a potentiated response.
Central Pathways
The processing of nociceptive information and pain in
the central nervous system is complex, involving multiple
anatomical pathways and brain sites. The responses to
nociceptive information are coordinated within the spi-
nal cord, ascending nociceptive pathways, descending
facilitatory pathways, and descending inhibitory path-
ways. All of these are interrelated and control the level
of pain at a given time. Thus, pain processing is plastic
and modifiable. Although it is not feasible to describe
in detail all of the pain systems involved in nociceptive
processing, the more major and well-studied pathways
will be highlighted.
The greatest impetus to research into the central con-
trol of pain occurred as a result of the publication of
Melzack and Wall's gate theory of pain (Figure 10-5).
According to the gate control theory of pain, stimula-
tion of large-diameter afferent fibers inhibits nociceptive
fiber evoked responses in the dorsal horn.64 Melzack
and Wall proposed a model for the physiology of pain
in terms of a dynamic nervous system that is constantly
adapting to changing stimuli, with the spinal cord central
to this theory.64 Primary afferents conveying low-thresh-
old information affect the flow of noxious information
through the dorsal horn by inhibiting or gating activity
in small afferent fibers that respond to damaging stimuli.
The gate control theory also suggested that this spi-
nal gate was under control by the higher brain centers
and affected by both cognitive and subconscious activ-
ity. Thus, this theory predicted that the activation of
Figure 10-5
The gate control theory of pain states that activation of large-diameter
afferent fibers, by pressure, proprioception, touch, or vibration,
inhibits the transmission of pain by small afferent fibers. Specifically,
activation of large afferent fibers excites an inhibitory interneuron
in the substantia gelatinosa (lamina II), which blocks the pain
transmission of small afferent fibers. This theory demonstrates the
importance of the spinal cord in pain transmission and has expanded
to include the contribution of supraspinal sites in the perception of
pain. (From Melzack R, Wall PD: Pain mechanisms: a new theory,
Science 150:971–978, 1965.)
 CHAPTER 10 • Pain: Perception and Mechanisms
low-threshold afferents would close the spinal gate and
prevent the transmission of nociceptive signals. Specific
neurotransmitters or their receptors were not suggested
at the time since the pharmacology of the nervous system
was only beginning to be understood. The original the-
ory did suggest that descending inhibitory pathways exist
and that spinal neurons are under descending influences.
The theory clearly emphasized the importance of spinal
cord neurons, and the pharmacology of these neurons
has since been studied extensively. For example, animal
experiments were aimed at manipulating spinal neurons
by directly placing catheters in the intrathecal space of
the spinal cord for administration of drugs, such as local
anesthetics or opioids.65 The use of epidural administra-
tion of drugs, to act on spinal neurons, in humans has
now become common for the relief of many types of
pain, both acute and chronic.
Spinal Cord
Although the spinal cord is the first site of termination of
nociceptors in the central nervous system, it acts as much
more than a relay station. It integrates incoming informa-
tion and subjects it to both local spinal and supraspinal
modulation. The spinal cord has a well-defined struc-
ture that has facilitated studies aimed at understanding
its function and organization. Rexed divided the spinal
cord into 10 laminae based largely on the morphology of
cells.66 This anatomical division of the dorsal horn corre-
lates well with function and has provided a stable frame-
work for subsequent studies. Laminae I to VI constitute
the dorsal horn where the majority of sensory afferents
terminate. In general, the fine sensory fibers convey-
ing noxious information from the skin terminate in the
most superficial layers, laminae I, II, and V. In contrast
to those from cutaneous tissue, which have dense projec-
tions to lamina II, muscles and joints send nociceptive
information predominately to lamina I and the deeper
dorsal horn.7,8,67,68 Evidence suggests that primary affer-
ent fibers from muscle project primarily to lamina I and
II.69 The terminals of larger fibers conveying tactile infor-
mation are dispersed between laminae III and IV. Many
of these fibers terminate on spinal interneurons that relay
information to cells deeper in the spinal cord. Primary
afferent fibers from several peripheral structures (cutane-
ous, joint, muscle, and viscera) converge on one neuron.
This convergence is thought to be the basis for referred
pain and secondary hyperalgesia (Figure 10-6). Thus,
pain felt in one muscle is referred to another muscle
or skin that sends projections to the same dorsal horn
neuron.
Referred pain is felt remote from the area of injury,
with referral occurring predominantly distal to the area
of injury rather than proximal.70 Pain can be referred
from muscle, joint, and viscera.13,14,17,71 Pain rarely refers
from skin.17 In experimental pain models, referred pain
223
Thalamus Skin
Muscle
Joint
Viscera
Spinal cord
Figure 10-6
Convergence theory for referred pain. Primary afferent fibers
innervating different tissues (i.e., muscle, joint, viscera, or skin)
send convergent input onto a single neuron in the spinal cord. The
convergence of primary afferent fibers onto central neurons is thought
to be the basis for referred pain.
is correlated with the intensity, duration, and area of the
noxious stimulus.13–15,72
Referred pain involves both peripheral and central pain
mechanisms. Peripheral mechanisms are demonstrated by
the decrease in referred pain following the application of
anesthetic cream at the referred pain site.73 Not all studies
show the continuance of referred pain once the referred
area is anesthetized, which may be due to differences in
the intensity of the noxious stimulus.74 Central mecha-
nisms (i.e., central sensitization) are observed following
an intramuscular injection of bradykinin into the tibialis
anterior muscle of the rat (Figure 10-7).75 Specifically,
new receptive fields develop following the intramuscular
injection, which may explain the development of referred
pain following a noxious stimulus.
Neurons in the dorsal horn of the spinal cord are clas-
sified as high threshold, wide dynamic range, and low
threshold. High-threshold neurons respond only to
noxious stimulation. Low-threshold neurons respond
only to innocuous stimuli. Wide dynamic range neurons
respond to both noxious and innocuous stimuli. Thus,
transmission of nociceptive information through the dor-
sal horn activates high-threshold and wide dynamic range
neurons. Following tissue injury, sensitization of both
high-threshold and wide dynamic range neurons occurs.
This is manifested as an increase in receptive field size,
increased responsiveness to innocuous or noxious stimuli,
or decreased threshold to innocuous or noxious stimuli
(see Figure 10-7).75–78 These changes in spinal neurons
are commonly referred to as central sensitization.
Ascending Pathways
From the spinal cord, sensory information is conveyed
to the brain via projection neurons that receive inputs
from afferents directly or indirectly through interneurons.
Noxious information is considered to be largely relayed
by cells that have been defined either as high-threshold
224 SECTION I • Scientific Foundations

Before After

5 min 15 min
Noxious Moderate
Noxious deep
deep
deep pressure
pressure
pressure

Noxious Noxious
Bradykinin deep deep
86 ug, TA pressure pressure

Figure 10-7
The receptive field of a dorsal horn neuron was mapped before and after an intramuscular injection of bradykinin into the tibialis anterior. Before
injection of bradykinin, the receptive field was found in an area outside the site of injection. Following the intramuscular injection, the receptive
field expands to include the injection site. The stimulation threshold in the original receptive field decreases from noxious deep pressure to
innocuous deep pressure 15 minutes postinjection. (From Hoheisel U, Mense S, Simons DG et al: Appearance of new receptive fields in rat dorsal
horn neurons following noxious stimulation of skeletal muscle: a model for referral of muscle pain? Neurosci Lett 153:9–12, 1993.)

neurons or wide dynamic range neurons.1 Spinal neurons
that project to the brain show a distinctive pattern of orga-
nization. There are several ascending pathways that trans-
mit nociceptive information from somatic and visceral
tissue.1,79 The spinothalamic tract is the main pathway for
transmission of nociceptive information to higher centers
(relayed through the thalamus) involved in cortical pro-
cessing and ultimately the perception of pain (Figure 10-8).
The postsynaptic dorsal column pathway transmits noci-
ceptive visceral stimuli to higher centers. The spinomesen-
cephalic and spinoreticular pathways integrate nociceptive
information with areas involved in descending inhibition,
facilitation, and autonomic responses associated with pain.
Spinothalamic Tract. Many consider the spinotha-
lamic tract to be most important for the perception of
could relieve pain by preventing the signal from reach-
ing the brain. In fact, anterolateral cordotomy, which
would lesion the spinothalamic tract, does cause anal-
gesia. However, in some patients, the pain returns after
a few months, limiting the usefulness of this procedure.
In most cases, this procedure is utilized for patients with
cancer pain as a last resort.82
Spinothalamic tract (STT) cells originate primarily in
laminae I and V, with the majority crossing the midline
Somatosensory cortex
Ventral posterior
lateral nucleus Thalamus
(VPL)

pain. The spinothalamic tract transmits information to

neurons in the ventroposterior lateral (VPL) nucleus
and medial thalamic nuclei, which include the central
lateral, central medial, parafascicular, medial dorsal, and
posterior complex of the thalamus. From here, the VPL
projects to the somatosensory cortex (SI and SII), and
this pathway is thought to be involved in the sensory-
discriminative component of pain (i.e., location, dura-
tion, quality, and intensity). Neurons in the VPL receive
convergent input from the dorsal column pathway that
transmits information regarding touch sensation and
the spinothalamic tract conveying information regard-
ing pain and temperature sensation.80,81 The ascending
projections from the medial thalamic nuclei and the
posterior complex are more diffuse and include areas
such as the anterior cingulate and insular cortices. Thus,
this pathway is thought to be the basis for the moti-
vational-affective component of pain (i.e., unpleasant-
ness). Because spinothalamic tract cells are considered
to signal pain, it was thought that lesioning this pathway
Nociceptor
Dorsal root
Spinothalamic tract ganglia
(STT)
Injury
Figure 10-8
Schematic drawing of the transmission of nociceptive information
from the site of injury, through the spinal cord to supraspinal sites.
Nociceptive information travels in thinly myelinated (Aδ or group III)
afferents to the dorsal horn and synapses on spinothalamic tract cells
located in laminae I or V. These spinothalamic tract neurons then send
input to the thalamus, both the ventral posterior lateral (VPL) nucleus
(shown) and more medial nuclei (see the text). The VPL nucleus of
the thalamus then sends projections to the somatosensory cortex (SI)
for the perception of pain. This classical pathway (i.e., nociceptors-
STT-VPL-SI) is thought to mediate the sensory discriminative
component of pain.
 CHAPTER 10 • Pain: Perception and Mechanisms
to ascend in the contralateral anterolateral funiculus.
The STT cells from laminae I project via the lateral
and dorsolateral funiculi to the medial thalamic nuclei.
These cells respond almost exclusively to noxious ther-
mal and mechanical stimuli and may play an important
role in thermal nociception.83 It has also been suggested
that this pathway may be responsible for activating the
body's own control systems to limit pain.84–86 However,
some have questioned this model.87 Several investigators
support a role for wide dynamic range STT cells, par-
ticularly those in laminae V, which respond to both noci-
ceptive and mechanoreceptive stimuli.87 Sensitization of
wide dynamic range neurons to innocuous mechanical
stimuli may underlie allodynia, a painful response to an
innocuous stimulus.
Spinomesencephalic and Spinoreticular Tracts.
Cells of the spinomesencephalic tract originate in lami-
nae I, IV, and V and send projections to the midbrain,
particularly the periaqueductal gray, the nucleus cunei-
formis, and the pretectal nucleus.1,79 These are classified
as high-threshold and wide dynamic range neurons and
have complex receptive fields. The projection to the peri-
aqueductal gray likely activates descending modulatory
systems. The cells of origin of the spinoreticular path-
ways are located in the deep dorsal horn, laminae VII
and VIII, and project to brain stem areas known to be
involved in descending facilitation and inhibition of noci-
ception. These nuclei include the nucleus gigantocellu-
laris, nucleus paragigantocellularis lateralis, ventrolateral
medulla, and the parabrachial region. These neurons
are nociceptive specific and are proposed to activate the
endogenous analgesia system and signal homeostatic
changes to brain stem autonomic centers.
Thalamus and Cortex
A number of studies show the importance of the thala-
mus and cortex in processing nociceptive transmission.
These include work by Lenz and colleagues record-
ing and stimulating neurons in the human thalamus,88
recordings from thalamic and cortical neurons in ani-
mal models of pain,89 and imaging studies. Stimulation
of the principal sensory nucleus of the thalamus in
humans can produce pain sensations, and thalamic
neurons in humans respond to noxious thermal or
mechanical stimuli.88 Thus, the thalamus appears to
integrate information regarding peripheral noxious
stimuli. Recordings from neurons in animals show that
nociceptive information is processed in the VPL of the
thalamus as well as the somatosensory cortex, the insu-
lar cortex, and the anterior cingulate cortex. Neurons
in some of these thalamic and cortical areas sensitize
following tissue injury induced by inflammatory or
neuropathic injury.90,91
Central processing of pain has been assessed with
imaging techniques, such as PET scans that look at
225
cerebral blood flow changes following specific stim-
uli. Blood flow is thought to increase to an area with
increased neuronal activity. Imaging studies of cere-
bral blood flow in humans reveal that cutaneous tac-
tile/touch stimuli and painful stimuli activate separate
regions of the cerebral cortex.92–94 From these data,
the cortical regions most reliably activated by painful
stimuli are SI and SII, the anterior cingulate cortex,
and the anterior insular cortex. Innocuous tactile stim-
ulation also activates primary and secondary somato-
sensory cortex and additionally the posterior cingulate
cortex.92 The primary and secondary somatosensory
cortices are believed to be involved in the discrimi-
nation and localization of a painful stimulus (i.e., the
sensory-discriminative component). The motivational-
affective component of pain is thought to involve the
anterior cingulate and anterior insular cortices. Studies
by Bushnell and colleagues elegantly assess the role of
somatosensory cortex and cingulate/insular cortices
utilizing hypnosis to make suggestions that modulate
the sensory-discriminative component of pain or the
motivational-affective component of pain.95,96 These
studies demonstrate that the somatosensory cortex
mediates the sensory-discriminative component of pain
while the anterior cingulate and insular cortices mediate
the motivational-affective component of pain.
Descending Modulation of Pain
Descending modulation of nociceptive information
occurs through several nuclei, including the periaque-
ductal gray, the rostral ventral medial medulla (RVM),
and the lateral pontine tegmentum (Figure 10-9). These
sites were initially discovered and found to inhibit noci-
ception through projections either directly or indirectly
to the spinal cord.97 Later studies showed a role for these
structures in the descending facilitation of nociception.98
Anatomically, the periaqueductal gray sends projections
to the RVM and the lateral pontine tegmentum, but not
directly to the spinal cord. The RVM and lateral pontine
tegmentum then project to the spinal cord and modulate
dorsal horn neuron activity and ultimately nociceptive
information.
Descending Facilitation of Pain
Supraspinal centers can enhance nociception, resulting
in referred pain, secondary hyperalgesia, and “mirror-
image” or contralateral pain.98 Spinal cord transection,
which removes supraspinal connections, prevents A- and
C-fiber mediated windup of flexor motoneurons follow-
ing knee joint injection of carrageenan.99 Inactivation of
the rostral ventral medulla (RVM) by lidocaine reverses
and lesions of RVM with ibotenic acid completely
block secondary heat hyperalgesia produced by knee
joint injection of carrageenan.100 Interestingly, these
226 SECTION I • Scientific Foundations
Figure 10-9
Brain stem sites involved in the perception of pain. The RVM
contains both serotonergic and nonserotonergic neurons, whereas
noradrenergic neurons are found in the DLPT. Both the DLPT and
RVM send projections directly to the spinal cord. The PAG indirectly
sends projections to the spinal cord via the DLPT and RVM. 5HT
= serotonin; DLPT = dorsolateral pontomesencephalic tegmentum;
ne = noradrenergic; PAG = periaqueductal gray; RVM = rostral
ventral medulla. (From Melzack R, Wall PD: Textbook of pain, ed 4,
Edinburgh, 1999, Churchill Livingstone.)
manipulations in the RVM do not affect the primary
hyperalgesia produced by carrageenan injected into the
plantar paw.100 More rostrally, the anterior cingulate cor-
tex (ACC) appears to play a role in descending facilita-
tion, because electrical stimulation of the ACC enhances
the tail flick response to noxious stimuli.101 The facilita-
tion by the ACC is mediated through the RVM, as lido-
caine blockade prevented the facilitation produced by
ACC stimulation.101 Following digit amputation of the
rat hind paw, ACC responses are potentiated to periph-
eral electrical stimulation.102 Genetic manipulation, such
as forebrain NR2B overexpression and adenylate cyclase
knock out mice, further demonstrates the role of ACC
in tissue injury responses.103,104 Thus, supraspinal centers
play a major role in the production and maintenance of
hyperalgesia.
Descending Inhibition of Pain
PAG-RVM Pathway. The central inhibitory con-
trol of pain was initially discovered by Reynolds who
found that electrical stimulation of the periaqueductal
gray (PAG) in the midbrain produces analgesia in rats.105
This led to an explosion of work on so-called endog-
enous analgesia systems.97 The work focused primar-
ily on two sites, which were the midbrain PAG and a
site in the ventral medulla the nucleus raphe magnus
(NRM). Subsequent studies show that other nuclei in
the rostral ventral medial medulla (RVM) are similarly
involved in descending modulation of nociceptive infor-
mation. These include the RVM, the PAG, the anterior
pretectal nucleus, the locus caeruleus/A7 cell groups,
the hypothalamus, the somatosensory cortex, the thala-
mus, the red nucleus, the medial habenula, the parabra-
chial region, the hypothalamus, the prefrontal cortex, the
amygdala, the reticulospinal tract, and the rubrospinal
tract.79,97,106–112 Most of these sites relay either directly or
indirectly through the RVM, with the RVM serving as
one pathway to the spinal cord.
Electrical stimulation of either the PAG or the RVM
causes analgesia in rats, cats, and humans.113–115 Electrical
stimulation of the PAG and the RVM inhibits spinal neu-
rons that respond to noxious stimuli.116 The PAG does
not project directly to the spinal cord but projects to the
RVM.117 The RVM, in turn, projects to the spinal cord
via fibers running in the dorsolateral funiculus (DLF).
Hopes that activation of these endogenous analgesia sys-
tems leading to stimulation-produced analgesia would
be a useful clinical therapy were not realized. Deep brain
stimulation of the PAG often produces unpleasant side
effects and thus has not been used routinely.
The RVM includes a number of nuclei including the
nucleus raphe magnus, the nucleus reticularis giganto-
cellularis pars alpha, and the nucleus reticularis paragi-
gantocellularis lateralis.97,118 Efferent projections from
the RVM to the spinal cord are involved in inhibition
of nociception, and some of the projections contain
serotonin.119,120 Electrical or chemical stimulation of the
RVM inhibits reflex and behavioral responses to noxious
stimuli and also inhibits neurons in the spinal dorsal horn
that receive nociceptive input.121–125
Three types of neurons are located in the RVM that
play a role in descending nociceptive modulation: (1)
ON cells that increase their firing rate just before or
at the time of tail flick to noxious heat, (2) OFF cells
that decrease their firing rate just before or at the time
of tail flick to noxious heat, and (3) neutral cells that
do not respond consistently to noxious heat of the tail
(Figure 10-10).97,118 OFF cells are thought to be involved
in descending inhibition, while ON cells are thought
to be involved in descending facilitation of nociceptive
information. Morphine excites OFF cells and reduces
nocifensive behaviors when applied directly to neurons
in the RVM, the PAG, or systemically. Deltorphin, a δ-
opioid agonist, also inhibits ON cell firing.126 Morphine,
a µ-opioid agonist, or deltorphin II, a δ2-opioid recep-
tor agonist, suppresses ON cell firing and ON cells, thus
attenuating nociceptive responsiveness.126
 CHAPTER 10 • Pain: Perception and Mechanisms 227

Figure 10-10
The RVM is involved in both the facilitation and inhibition of descending pain modulation. ON and OFF neurons from the RVM send
projections to the spinal cord. Following application of noxious heat, ON cells fire just before or at the time of the tail flick response (pain reflex),
whereas OFF cells fire just before or at the time of the tail flick response. (From Melzack R, Wall PD: Textbook of pain, ed 4, Edinburgh, 1999,
Churchill Livingstone.)

Pontine Nuclei. Norepinephrine (i.e., noradrenaline)
terminals in the spinal cord arise primarily from descending
pontinergic nuclei, primarily the locus caeruleus and nucleus
subcaeruleus. Chemical or electrical stimulation of these
nuclei causes antinociception, reduces hyperalgesia, and
decreases activity of spinal neurons.127–131 Norephinephrine
may produce inhibition or facilitation of nociceptive stimuli
dependent on the activation of specific adrenergic receptors
in the spinal cord (see the neurotransmitter section).
Anterior Pretectal Nucleus. Stimulation of the ante-
rior pretectal nucleus results in long-lasting antinocicep-
tion without the additional aversive effects seen with
stimulation of PAG.132,133 The nucleus gracilis, which
carries large afferent fiber input, and the somatosensory
228 SECTION I • Scientific Foundations
cortex project to the anterior pretectal nucleus.110,134 The
anterior pretectal nucleus projects to the ventrolateral
medulla, the RVM, and noradrenergic cell groups.110
Lesions or local anesthetic blockade of the RVM partially
reduce anterior pretectal nucleus antinociception.135,136
Opiates, norepinephrine, and serotonin are implicated
in the analgesia produced by stimulation of the anterior
pretectal nucleus.133,137 Interestingly, Rees and Roberts
demonstrated that electrical stimulation of the dorsal
columns, at an intensity that only activates large afferent
fibers, (1) produces analgesia that outlasts the stimula-
tion, (2) excites cells in the anterior pretectal nucleus, (3)
results in analgesia that is abolished by transection of the
spinal cord rostral to the stimulation, and (4) results in
antinociceptive effects that are inhibited by GABA micro-
injected into the anterior pretectal nucleus.138 Thus, elec-
trical stimulation analgesia, like transcutaneous electrical
nerve stimulation (TENS), may involve a supraspinal
loop that includes the anterior pretectal nucleus.
The most reliable method of activating the PAG,
RVM, or pontine cell groups is by noxious stimulation
with input from spinal cord through the spinomesence-
phalic and spinoreticular pathways. The hypothalamus,
cortex, and limbic system can also activate these inhibi-
tory systems. Thus, noxious stimulation evoked activation
of descending inhibitory systems may explain the use of
certain treatments considered to be “counterirritants.”
Corticospinal Tract. In addition to the somatosensory
cortex receiving nociceptive input for the discrimination
of pain, this cortex also sends fibers that inhibit nocicep-
tive transmission through the corticospinal tract directly
to the spinal cord or indirectly through the thalamus or
PAG. Stimulation of somatosensory cortex inhibits spinal
neurons directly.139 In addition, stimulation of somatosen-
sory cortex causes primary afferent depolarization, which
would result in presynaptic inhibition.140 Lesioning of the
corticospinal tract blocks the primary afferent depolariza-
tion produced by stimulation of the somatosensory cortex,
demonstrating that presynaptic inhibition of the central
terminals of primary afferent fibers can be mediated by
activation of the corticospinal tract.140 Thus, stimulation
of the corticospinal tract (as with exercise) may reduce
nociceptive input through the descending inhibition of
spinal neurons or primary afferent fibers.
Neurotransmitters
A number of neurotransmitters, receptors, and ion channels
located within the peripheral and central nervous system are
capable of producing pain and inflammation. Peripherally,
neurotransmitters in primary afferent fibers have been
identified predominately in neurons located in the dorsal
root ganglia (DRG) that send axons to the periphery. In
some cases, neurotransmitters and receptors have been
located within the peripheral terminals. Mediators of the
inflammatory process can also activate primary afferent
nociceptors to initiate the nociceptive or painful response
to injury. Centrally, neurotransmitters have been identified
that mediate ascending pathways, descending inhibitory
pathways, and descending facilitatory pathways. This field
has expanded tremendously since the 1990s, with contin-
ued advances occurring exponentially. Therefore, only the
surface of the pharmacology of peripheral and central ner-
vous system involvement will be touched on here by high-
lighting a few well-established mechanisms.1,141
Neuropeptides
Although blood-borne factors are considered to be the
major initiator of inflammation, a substantial amount of
literature beginning at the turn of the century is devoted
to the involvement of the peripheral and sympathetic
nervous systems in this process.142,143 Neurogenic inflam-
mation is a term used to describe the role of the nervous
system in the development and maintenance of peripheral
inflammation. Neuropeptides such as substance P and calci-
tonin gene-related peptide (CGRP) are contained in small-
diameter afferents (group III and IV) and when released
from primary afferent fibers in the periphery produce an
inflammatory response.144–146 These substances intensify the
inflammatory events in the periphery, producing plasma
extravasation and vasodilation.144,145,147–150 In fact, substance
P and CGRP are also found in inflammatory exudate and
primary afferent fibers innervating inflamed joints in both
humans and animals.144,151–155 Elimination of primary affer-
ent fibers by peripheral neurectomy or capsaicin (which kills
group IV afferents) reduces the inflammatory response.156–158
Interestingly, the neurogenic component of inflammation
involves the central nervous system, specifically dorsal root
reflexes generated in the spinal cord.143
Neuropeptides
● Substance P
● Calcitonin gene-related peptide
Substance P and CGRP are also located in the cen-
tral terminals of primary afferent fibers and are densely
located in laminae I and II.159 Substance P exerts its effects
through activation of the neurokinin 1 (NK1) receptor,
located in the superficial dorsal horn. Activation of the
substance P receptor produces nocifensive behaviors,160
increases activity and responsiveness of dorsal horn neu-
rons,161 and enhances the NMDA glutamate receptor.162
In contrast, a blockade of neurokinin receptors reduces
hyperalgesia associated with tissue injury and reduces
sensitization of dorsal horn neurons.163–167 Further loss
of neurokinin 1 containing neurons in the spinal cord
similarly reduces hyperalgesia following tissue injury and
 CHAPTER 10 • Pain: Perception and Mechanisms
sensitization of dorsal horn neurons.168,169 CGRP antago-
nists reduce sensitization of dorsal horn neurons.170 In
addition, CGRP slows the degradation of substance P in
the spinal cord,41 resulting in a potentiation of the effects
of substance P.87 Both SP and CGRP are G-protein cou-
pled receptors producing effects through activation of
intracellular messengers such as protein kinase C and A.
There is a clear role for both protein kinase A and protein
kinase C in nociception.159
Opioids
After peripheral inflammation, in animals and human
subjects, there is an upregulation of opioid receptors on
the peripheral terminals of primary afferent fibers.171–173
Additionally, macrophages, monocytes, and lymphocytes
all contain opioid peptides,174 and there is an increase in
the amount of endogenous opioid peptides in these cells
in inflamed tissues.172 Thus, there appears to be a periph-
eral endogenous mechanism to reduce pain in inflamed
tissues. The effects of opioid agonists, such as morphine,
could produce their actions through the activation of
peripheral opioid receptors.
Opioid Peptides
● β-endorphins
● Methionine (met) enkephalin
● Leucine (leu) enkephalin
● Endomorphin 1 and 2
● Dynorphin A and B
Opioid analgesia has been extensively studied in
endogenous pain control mechanisms. The endogenous
opioids include β-endorphins, methionine (met)- and
leucine (leu)- enkephalin, endomorphin 1 and 2, and
dynorphin A and B.97 Each has a distinct anatomical
distribution and activates specific receptors. β-endor-
phins are found in hypothalamic neurons and the ante-
rior and intermediate lobes of the pituitary.97 Neurons
located in the hypothalamus send β-endorphin projec-
tions to the PAG and can “turn on” the endogenous
analgesia system.175 Release of β-endorphin from the
pituitary occurs with exercise and stress, and measurable
levels in the bloodstream increase.176,177 β-endorphins do
not readily cross the blood-brain barrier, and thus their
role in stress-induced or exercise-induced analgesia is not
known. However, removal of the pituitary decreases the
effectiveness of stress-induced analgesia.178 Since there is
an upregulation of opioid receptors on the peripheral ter-
minals of primary afferent fibers, and since β-endorphin
does not readily cross the blood-brain barrier, follow-
ing inflammation the increased plasma concentrations of
β-endorphin likely produce effects peripherally.
229
Enkephalins, endomorphins, and dynorphins are located
in neurons in the brain and dorsal horn in areas known
to be involved in analgesia such as the PAG, RVM, and
dorsal horn of the spinal cord.97 Activation of opioid recep-
tors with selective agonists, systemically or locally in the
PAG, RVM, or spinal cord, produces analgesia and reduces
hyperalgesia in a number of pain models including inflam-
matory, acid-induced muscle pain, and neuropathic.179,180
Most of the clinically available opioids produce their
effects through activation of µ-opioid receptors. Differences
in effectiveness are based on the potency of the drug.
Clinically available opioids include codeine, tramadol,
dipanone, percodan, oxycodon, levorphanol, methadone,
hydromorphone, buprenorphine, fentanyl, and morphine
(see Chapter 12).181 Long-term use of opioids clinically is
limited by the development of tolerance.
Glutamate
Glutamate, an important excitatory neurotransmitter in
the nervous system, is found in primary afferent fibers, and
glutamate receptors are found on primary afferent termi-
nals of nociceptors.182,183 Injection of glutamate peripher-
ally produces hyperalgesia and sensitizes primary afferent
fibers.184–186 Glutamate is upregulated in joint afferents
after inflammation, and glutamate increases in inflamed
tissues from humans and animals.187–189 Furthermore,
there is an increase in the proportion of nociceptors
expressing glutamate receptors after inflammation.190
Glutamate mediates excitatory synaptic transmission
between primary afferent nociceptors and dorsal horn neu-
rons.191,192 The role of spinal ionotropic glutamate recep-
tors in hyperalgesia resulting from tissue injury has been
well established.193 In particular, N-methyl-D-aspartate
(NMDA) glutamate receptors, calcium channels with a
voltage dependent Mg++ block, are implicated in synaptic
plasticity in a variety of systems including pain transmis-
sion.194 Spinal application of NMDA glutamate receptor
antagonists decreases hyperalgesia associated with hind paw
inflammation, joint inflammation, acid-induced muscle
pain, formalin injection, and neuropathic pain models.25,195–199
Blockade of spinal NMDA glutamate receptors prevents
“windup” of both dorsal horn neurons and α-motor
neurons resulting from C-fiber strength, conditioning
stimuli.200–202 Furthermore, NMDA receptor antagonists
prevent sensitization of dorsal horn neurons, including spi-
nothalamic tract cells, that occurs after joint inflammation,
formalin, capsaicin, or ultraviolet irradiation.203–205
The non-NMDA ionotropic glutamate receptors,
AMPA and kainate (AMPA/KA), form a complex with
cation channels that allow passage of sodium ions, but
some are also permeable to calcium depending on sub-
unit composition.206 These AMPA/KA receptors are
thought to mediate fast excitatory synaptic transmission
between primary afferent fibers and dorsal horn neurons
in response to noxious stimulation. There is mixed data
230 SECTION I • Scientific Foundations
on the role of AMPA/KA receptor antagonists in the
development and maintenance of hyperalgesia. AMPA/
KA receptor antagonists have no effect on hyperalgesia
following carrageenan paw inflammation once devel-
oped.25,207 In contrast, for knee joint inflammation or
acid-induced hyperalgesia, secondary hyperalgesia is
reduced by the spinal administration of AMPA/KA
receptor antagonists after the development of hyperal-
gesia.198,199,208 Further, AMPA/KA receptor antagonists
inhibit hyperalgesia associated with peripheral neuropa-
thy, burn injury, or carrageenan paw inflammation if given
either before or just after injury.197,207 Lastly, Brennan and
colleagues209,210 showed that hyperalgesia associated with
incision is preferentially reduced by AMPA/KA receptor
antagonists but not NMDA glutamate receptor antago-
nists when administered after the development of hyper-
algesia. Thus, several models and conditions are sensitive
to AMPA/KA receptor antagonists.
Although there are a number of selective NMDA
receptor antagonists, these agents cannot be used clini-
cally because of adverse side effects. However, there are
several clinically available drugs with NMDA antagonist
activity, including ketamine, dextromethorphan, and
memantine. These drugs are not selective antagonists but
block the NMDA receptor noncompetitively.211 Clinically,
Bell showed in three case studies that low doses of the
NMDA antagonist ketamine prevent the development of
analgesic tolerance to opioids.212
GABA
Gamma-amino-butyric acid (GABA) is an inhibitory
neurotransmitter located in neuronal cell bodies of the
dorsal horn exerting its actions through activation of
the ionotropic receptor, GABAA, and the metabotropic
receptor, GABAB. There is an upregulation of GABA fol-
lowing peripheral inflammation and a decrease in GABA
following peripheral neuropathy.213 One potential mech-
anism that may contribute to hyperalgesia is a reduction
in inhibition. Indeed, spinothalamic tract cells show a
reduced responsiveness to GABA agonists after induction
of inflammation with capsaicin.214 Further, activation of
GABAergic receptors in the spinal cord causes antinoci-
ception and reduces hyperalgesia.215,216 Clinically, several
muscle relaxants (such as baclofen and benzodiazepines)
exert their effects through activation of GABA receptors
(see Chapter 12).
Glial Cells and Pain
Glial cells in the central nervous system, particularly the
spinal cord, play a critical role in processing of nocicep-
tive information.113,117 Glia express receptors for many
neurotransmitters, including glutamate receptors, and
are involved in the clearance of neurotransmitters from
the synaptic cleft. Activation of astrocytes and microglia
occurs in a number of pain models including neuropathic
and inflammatory.106,109,180 Interestingly, glia release a
variety of neuroactive substances known to sensitize neu-
rons such as glutamate, nitric oxide, and proinflamma-
tory cytokines. Proinflammatory cytokines administered
spinally produce nocifensive behaviors and sensitize dor-
sal horn neurons, and spinal blockade of proinflammatory
cytokines reverses hyperalgesia.181,217,218
Serotonin
Serotonin is a neurotransmitter that is found in the RVM
in neurons that send projections to the spinal cord and
in PAG neurons that project to the RVM.219,220 Blockade
of serotonin receptors spinally prevents analgesia. In addi-
tion, application of serotonin to the spinal cord decreases
the activity of dorsal horn neuron, producing analgesia.221
Thus, it appear, that the PAG pathway producing analgesia
uses serotonin as its neurotransmitter in the spinal cord.
In the spinal cord, three families of receptors are pres-
ent: 5-HT1 (5-HT1A and 5-HT1B), 5-HT2, and 5HT3
receptors.222,223 The role of individual serotonin receptors
in nociceptive transmission is controversial and serotonin
receptors have been implicated in both facilitation and
inhibition of nociception. 5-HT3 receptors are located on
primary afferent fibers and dorsal horn neurons and are
involved in descending inhibition from stimulation of the
RVM but not descending facilitation.222,224–226 5-HT1A
receptors, on the other hand, are not found on primary
afferent fibers and mediate descending facilitation as well
as inhibition.225,227–230 5-HT2 receptors include a number
of subtypes that appear to be involved in inhibition but
not facilitation of nociceptive responses.230
Norepinephrine
Norepinephrine (i.e., noradrenaline) terminals in the spi-
nal cord arise primarily from descending pontinergic nuclei
including the locus caeruleus, nucleus subcaeruleus, and
parabrachial nucleus.231,232 Spinally, norepinephrine pro-
duces inhibition of nociceptive stimuli through activation
of α2 adrenergic receptors.233–236 In contrast, in the spinal
dorsal horn α1 adrenergic receptors mediate descend-
ing facilitation of nociception.218 Thus, norepineph-
rine is involved in descending facilitatory and inhibitory
nociceptive signaling depending on receptor activation.
The use of tricyclic antidepressants or selective
serotonin reuptake inhibitors (SSRIs) is commonly
utilized for chronic pain conditions. These inhibitors
can be nonselective (amitryptyline, imipramine) and
exert their effects by decreasing reuptake of noradrena-
line and serotonin, or selective (fluorxetine, paroxetine,
ritanserin, clomipramine) exerting effects by decreasing
reuptake of serotonin. As a result, more neurotransmit-
ters would be available and the inhibition of nociceptive
information would increase. SSRIs, clomipramine and
fluoxetine, enhance antinociception and pain reduction
in animals and humans.237–239 Further, 5HT1 agonists
 CHAPTER 10 • Pain: Perception and Mechanisms
such as sumatriptan, zolmitriptan, naratriptan, and
rzatriptan are effective for treating migraines.217,240
Adenosine
Adenosine is a neurotransmitter located in the dorsal
horn of the spinal cord that exerts inhibitory actions
through the A1 receptor.177 Spinal administration of ade-
nosine, A1 receptor agonists, or drugs aimed at reducing
the degradation of adenosine are analgesic and reduce
hyperalgesia in inflammatory and neuropathic pain con-
ditions.168,169,176,241,242 Studies have targeted adenosine
modulation in humans as a method of reducing pain.243
Ion Channels
Several ion channels, found on peripheral terminals, may
also be important in the response to noxious stimuli.
Low pH is found in inflamed tissues and produces pain
in humans and animals.244 Acid-sensing ion channels
are located in DRG neurons, are activated by low pH,
and are importantly involved in muscle pain.245,246 The
vanilloid receptor, TrpV1, is activated by the exogenous
ligand capsaicin, located in DRG, responds to low pH,
and mediates hyperalgesia to heat stimuli.247,248
Sodium channels are involved in fast synaptic transmis-
sion and action potential propagation. The dorsal root
ganglion (DRG) neurons express six different sodium
channels, including sensory-neuron-specific sodium chan-
nels not present within other parts of the nervous system.
The involvement of sodium channels in the peripheral
nervous system is complex but clearly important for
both inflammatory and neuropathic pain.249,250 A change
in sodium channel composition occurs after peripheral
neuropathy, resulting in physiological changes that con-
tribute to hyperexcitability in DRG neurons. A variety of
inflammatory mediators sensitize DRG neurons and thus
may mediate the sensitization of primary afferent fibers
that occurs after inflammation. Local anesthetics, such as
lidocaine, mediate their effects by blocking sodium chan-
nels, and future pharmaceutical agents may be aimed at
specific channels (see Chapter 12).
Combinational Therapy
Many neurotransmitters produce additive and suprad-
ditive (synergistic) effects when given simultaneously.
Combinational pharmaceutical therapy can therefore
enhance pain relief by reducing side effects. Medical man-
agement of pain is complex and multidisciplinary. Initial
treatments are aimed at nonpharmacological therapies
including exercise, heat and cold modalities, and TENS
(discussed later). One common pharmacological treatment
for pain is nonsteroidal anti-inflammatories (NSAIDs)
including both cyclooxygenase-1 (COX-1) and cyclooxy-
genase-2 (COX-2) inhibitors.251 NSAIDs produce their
effects by interfering with prostaglandin synthesis via inhi-
bition of cyclooxygenase (see Chapter 12). These effects
231
clearly occur in the periphery, interfering with inflamma-
tion. However, NSAIDs also have effects in the central
nervous system, particularly the spinal cord, to produce
analgesia through prostaglandin receptors.252,253 Clinical
and basic science studies show that NSAIDs, when com-
bined with µ-opioid agonists, synergistically reduce hyper-
algesia and pain in humans and animals. Either systemic
or intrathecal administration of the NSAIDs, ketorolac,
acetylsalicylic acid, piroxicam, and NS-398 (COX-2)
show synergism with morphine (systemic, intrathecal),
producing increased analgesia.252–256
The µ-opioid agonist, morphine, synergizes with
SSRIs, clomipramine and fluoxetine, to enhance antino-
ciception and pain reduction in animals and humans.237–239
Potentiation of antinociception, as measured by the
hot plate test, occurs with co-administration of either
µ-, or δ- opioid agonists and the SSRI, fluvoxamine.257
Additionally, opioid agonists (µ− and δ−) synergize with
α-adrenergic agonists, like clonidine, in pharmacological
studies in animals.258,259
Tolerance is pharmacologically defined as reduced
analgesic effect of a drug following repeated adminis-
tration. Clinically, development of opioid tolerance is
an important and limiting factor to long-term opioid
treatment. Tolerance is prevented by combining chole-
cystokinin (CCK) receptor antagonists, or NMDA recep-
tor antagonists, with opioids (discussed later). CCK, a
neuropeptide widely distributed in the mammalian cen-
tral nervous system,260 is implicated in the reversal of
the analgesic effects of opioids,261 and CCK antagonists
prevent opioid-induced analgesic tolerance.262 The spinal
administration of CCK-8 antiserum reverses the analge-
sic tolerance produced by morphine, implying that an
increased endogenous release of CCK-8 may be the likely
cause for the development of opioid tolerance.263–265
The systemic or spinal administration of NMDA recep-
tor antagonists prevents the development of morphine
tolerance in animals.266–269 Once developed, NMDA
receptor antagonists reverse this tolerance.270,271 Although
there are a number of selective NMDA receptor antago-
nists, these agents cannot be used clinically because of
adverse side effects. However, there are several clinically
available drugs with NMDA antagonist activity includ-
ing ketamine, dextromethorphan, and memantine.211
Clinically, Bell showed in three case studies that low doses
of the NMDA antagonist ketamine prevents the develop-
ment of analgesic tolerance to opioids.212 Thus, blockade of
NMDA receptors either spinally or systemically prevents
the development of opioid tolerance.
Nonpharmacological Treatment of Pain
Clinicians use several nonpharmacological therapeutic
interventions to manage pain (for a review, see Wright
and Sluka272). These therapeutic modalities are briefly
232 SECTION I • Scientific Foundations
reviewed here. The evidence to support the use of these
modalities will be given; however, several of these fre-
quently used interventions do not have solid supporting
evidence mainly because of a lack of properly con-
ducted research studies. Thus, hypothetical mechanisms
of action may be discussed, which will be indicated as
appropriate.
Electrical Stimulation
Transcutaneous Electrical Nerve Stimulation (TENS)
The American Physical Therapy Association defines
transcutaneous electrical nerve stimulation (TENS) as
the application of electrical stimulation to the skin for
pain control (Figure 10-11) (for a review, see Sluka
and Walsh273). TENS is frequently used to treat a num-
ber of pain conditions including osteoarthritis, back
pain, and fibromyalgia to name a few. The medical
field did not fully accept electrical stimulation for pain
relief until Wall and Sweet274 published the first paper
on TENS in direct response to the gate control theory
of pain.64
Clinically, TENS is applied at varying frequen-
cies, intensities, and pulse durations of stimulation.
Frequency of stimulation is broadly classified as high-
frequency (>50Hz), low-frequency (<10Hz), or burst
(bursts of high-frequency stimulation applied at a much
lower frequency) TENS. Intensity is determined by the
response of the patient as either sensory-level TENS or
motor-level TENS. Some clinicians may utilize stimu-
lation below a sensory intensity termed microcurrent
electrical stimulation. To date, there are no data to
support microcurrent electrical stimulation. In general,
high-frequency TENS is applied at sensory intensities
and is referred to as conventional TENS. In contrast,
low-frequency TENS is typically applied at high inten-
sities to produce a motor contraction. This mode of
Thalamus
Figure 10-11
Schematic drawing representing the most common
descending inhibitory pathways. The periaqueductal
gray (PAG) sends input to the rostral ventromedial Rostral
medulla (RVM), which then projects to the spinal ventromedial
cord dorsal horn. This pathway has been shown medulla
to utilize serotonin, mediates opioid analgesia, (RVM)
and is also involved in descending facilitation of
pain. TENS produces its effects by activating large-
diameter afferent fibers at the site of injury and by
activating opioid receptors in the spinal cord and
RVM. For more details on the pharmacology of
TENS, see the text.
stimulation is referred to as strong, low-rate, or acu-
puncture-like TENS.
The effects of TENS were analyzed in several animal
models. The spontaneous activity and noxious input
to spinothalamic tract cells are inhibited by low- and
high-frequency TENS.275–277 Garrison and Foreman
recorded from dorsal horn neurons in cats and exam-
ined the effect of varying frequency, intensity, and
pulse duration on the inhibition of dorsal horn cell
activity by TENS.276 Specifically, increasing intensity,
frequency, or pulse duration increases the amount of
inhibition of dorsal horn neurons produced by TENS.
Additionally, the effects of TENS on dorsal horn
cells are short lasting, returning to normal after the
TENS is removed. These data suggest that high- and
low-frequency TENS is effective, increasing intensity
increases inhibition, and the effects of TENS are short
lasting.
In one study, researchers evaluated the effect of
electrode placement by placing electrodes within the
receptive field for a spinothalamic tract neuron, out-
side the receptive field of the neuron but on the same
limb, and at the mirror site.277 The greatest degree of
inhibition of spinothalamic tract cell activity occurred
with electrodes placed within the receptive field for the
neuron, and only minimal inhibition occurred when
placed on the same hind limb but outside the receptive
field.277 Behaviorally, in animals without tissue injury,
TENS applied to the knee joint has no effect on the
paw withdrawal latency.278 These data suggest that
electrode placement is important and that the greatest
effect will occur if applied at the site of injury where
one would be expected to affect the receptive fields of
sensitized neurons.
Several theories are utilized to support the use of
TENS. The gate control theory of pain is most com-
monly utilized to explain the inhibition of pain by
Periaqueductal gray
(PAG)
Midbrain
Injury
Brainstem
Dorsal root
ganglia
TENS
Spinal TENS
 CHAPTER 10 • Pain: Perception and Mechanisms
TENS. Several studies support segmental mediated inhi-
bition in TENS analgesia. There are now much more
detailed data on mechanisms of actions of TENS that
includes anatomical pathways, neurotransmitters and
their receptors, and the types of neurons involved in the
inhibition. High-frequency TENS inhibition is partially
prevented by spinalization, which removes descending
inhibitory influences.279 However, a significant amount
of inhibition remains following spinalization. Thus,
TENS appears to produce both segmental and descend-
ing inhibition.
The release of endogenous opioids has been used
to explain the actions of TENS, particularly low-fre-
quency stimulation. Recent data support this theory
for both low- and high-frequency TENS stimula-
tion.280,281 Concentrations of β-endorphins increase
in the bloodstream and cerebrospinal fluid of healthy
subjects following administration of either high- or
low-frequency TENS.282,283 Increased concentrations
of methionine enkephalin, a δ-opioid agonist, and
dynorphin A, a κ-opioid agonist, are observed in the
lumbar cerebrospinal fluid following treatment of
patients with either low- or high-frequency TENS,
respectively.284 This suggests that at the spinal level,
different opioids are released with different stimula-
tion frequencies and thus possibly different opioid
receptors activated to produce analgesia with high- or
low-frequency TENS. Taken together, these data indi-
cate that several opioids and their receptors may be
involved in the ability of TENS to relieve pain. Animal
and human models of pain further demonstrate that
µ-opioid receptors are involved in the antihyperalge-
sia produced by low frequencies, and δ-opioid recep-
tors are involved in the antihyperalgesia produced by
high-frequency TENS.279,280,281,285,286 The activation of
opioid receptors occurs in the central nervous system
and involves descending inhibitory pathways from the
RVM and spinal cord.280,281
In addition to opioid receptors, low-frequency
TENS activates M1 and M3 muscarinic receptors, and
5-HT2 and 5-HT3 serotonergic receptors in the spinal
cord.287,288 High-frequency TENS activates M1 and M3
muscarinic receptors, but not serotonergic receptors
in the spinal cord.287,288 Furthermore, neither low- nor
high-frequency TENS utilizes noradrenergic receptors in
the central nervous system to produce its analgesia.288,289
However, peripherally, α-2 noradrenergic receptors par-
tially mediate the analgesia produced by both low- and
high-frequency TENS.289
Chronic pain patients are likely treated with a com-
bination of pharmaceutical and nonpharmaceutical
agents. Understanding the mechanisms of these treat-
ments will better assist the clinician in the appropriate
choice of pain control treatment; a particular modal-
ity such as electrical stimulation can be utilized in a
233
more educated manner. For example, if a patient is
taking opioids, currently those available activate µ-
opioid receptors, high-frequency TENS may be more
appropriate. Repeated application of opioids produces
tolerance to the opioid such that a higher dose is nec-
essary to produce the same effect. This is based on
the fact that low-frequency, sensory intensity TENS,
but not high-frequency sensory intensity TENS, is
ineffective if given in animals tolerant of morphine.290
Furthermore, it follows that repeated treatment with
the same frequency of TENS would produce tolerance
to its analgesic effects. Indeed, daily treatment with
either low-frequency or high-frequency TENS in ani-
mals with knee joint inflammation produces tolerance
to TENS and a cross tolerance to either spinally admin-
istered µ- or δ-opioid agonists, respectively.291 Thus,
TENS is ineffective if morphine tolerance is present
and produces opioid tolerance with repeated use.
Alternatively, combining pharmaceutical treatments
with TENS could enhance pain relief. In support, com-
bining the a-2 adrenergic agonist clonidine or mor-
phine with either high- or low-frequency TENS results
in a potentiation of the effect of TENS.273,291 Thus, a
lower dose of drug produces the same degree of pain
relief.
Interferential Current
Interferential current is the application of two high-
frequency currents that generate interference current.
Interferential current therapy increases blood flow and
skin temperature.292 Data regarding the effectiveness
of interferential current therapy are mixed. Subjects
without any known pathological condition, treated
with 15 minutes of interferential current therapy dem-
onstrated no change in mechanical pain threshold.293
In contrast, additional studies on healthy subjects
demonstrated that interferential current decreased
ischemic pain intensity and increased the threshold
in cold-induced pain.294,295 Clinically, interferential
current therapy is beneficial for treating painful con-
ditions such as osteoarthritic pain (for a review, see
Belanger296). Other research studies found no benefits
in treating low-back pain, jaw pain, and soft-tissue
shoulder disorders, as well as the previously mentioned
osteoarthritic pain.296
Potential mechanisms of action in interferential
current-induced hypoalgesia include the same mecha-
nisms as TENS. These include segmental inhibition
and activation of descending inhibitory pathways. The
increase in blood flow demonstrated with interferen-
tial therapy may also promote tissue healing. Thus, the
specific mechanisms for interferential current-induced
hypoalgesia are unknown, with only speculative mecha-
nisms proposed.
234 SECTION I • Scientific Foundations
Thermal Modalities
Superficial Heat
Examples of superficial heat include hot packs, paraf-
fin, fluidotherapy, infrared lamp, and whirlpool with
thermal energy transfer occurring by conduction, con-
vection, or radiation depending on which modality
is used. A wide range of results is reported clinically.
Moist heat is effective in relieving pain of sensitive trig-
ger points.297 In contrast, the addition of whirlpool
therapy to the standard treatment (i.e., massage, joint
mobilization, and exercise) of Colles’ fractures did not
provide any benefits compared to the group that did
not receive whirlpool therapy.298 In an animal model of
arthritis, a warm bath treatment decreased spontaneous
pain behaviors.299
The physiological effects of thermotherapy include
the following: vasodilation, relaxation, and increases
in soft tissue extensibility and metabolic rate.300 The
hypoalgesic effects of thermotherapy remain speculative.
Conceivably, the removal of waste products and healing
of injured tissue may eliminate the pain-producing sig-
nals that activate nociceptors. Alternatively, increasing
tissue extensibility may remove mechanical activation of
nociceptors created by constricted tissues.
Another hypothesis for thermal hypoalgesic effects
involves changes in afferent fiber activity. Increasing the
temperature of muscle increases the activity of group Ia
muscle spindle and Ib Golgi tendon organ afferent fibers,
whereas group II muscle spindle afferent fiber activity
decreases.301 Activation of type Ib Golgi tendon organ affer-
ent fibers potentially decreases muscle spasm and pain.
Deep Heat
Ultrasound and shortwave diathermy are the two most
common forms of deep heat. Shortwave diathermy
emits electromagnetic energy, causing both superfi-
cial and deep tissue heating. In normal subjects, pres-
sure pain thresholds increased following 20 minutes
of shortwave diathermy.302 Similar results are demon-
strated in pain conditions. Shortwave diathermy is more
effective than moist heat in relieving pain of sensitive
trigger points.297 Cervical collars fitted with a short-
wave diathermy generator effectively treat patients
with persistent neck pain or acute whiplash syndrome,
with improvements in pain and range of motion.303,304
Shortwave diathermy is beneficial in treating osteo-
arthritis, ankle sprains, subdeltoid calcified bursi-
tis, chronic neck pain, low back pain, soft-tissue and
ligamentous lesions, trigger points, and temporoman-
dibular joint disorders (for a review, see Belanger296).
Conversely, research studies have found that shortwave
diathermy is not useful in treating osteoarthritis, ankle
sprains, and low back pain.296 More conclusive data are
needed to make specific recommendations regarding
the use of shortwave diathermy in treating pain condi-
tions.
Deep heating-induced hypoalgesia likely involves
the same mechanisms as superficial heating therapy.
These potential mechanisms include tissue healing,
increases in tissue extensibility, and changes in afferent
fiber activity. As demonstrated with superficial heat-
ing modalities, additional research is needed to fully
understand the pain-relieving mechanisms as well as the
most suitable application in treating pain conditions.
Ultrasound is a therapeutic device that uses sound
waves with frequencies greater than 20,000 cycles
per second, resulting in both thermal and nonther-
mal effects.300 The purported thermal effects include
increases in blood flow, metabolic activity, and colla-
gen tissue extensibility, whereas the nonthermal effects
include increases in cell permeability, mast cell degranu-
lation, protein synthesis, and intracellular calcium.300,305
Much of the biological evidence describing the effects
of ultrasound was performed in vitro, therefore caution
must be utilized when inferring ultrasound effects to
clinical conditions.305
Ultrasound is used to treat a variety of musculosk-
eletal conditions including bursitis, calcifying tendon-
itis, osteoarthritis, low back pain, delayed-onset muscle
soreness, and myofascial pain (for a review, see van
der Windt et al.306). Unfortunately the effectiveness of
ultrasound in treating these conditions is unclear. Many
of the studies consist of methodological flaws includ-
ing discrepancies in the diagnosis, ultrasound param-
eters (treatment area, duration of treatment, intensity),
dosimetry, poor controls, and unknown functional out-
put of the ultrasound machine.307 Consequently, these
clinical studies provide evidence that both supports
and refutes the use of ultrasound in musculoskeletal
pain conditions. For example, patients with subacro-
mial bursitis demonstrated no changes in pain reports
or range of motion in a double-blind study compar-
ing ultrasound with a sham treatment, whereas sys-
tematic reviews support the use for tendonitis.306,308
Patients diagnosed with low back pain demonstrated
improved range of motion and pain control following
ultrasound treatments compared with a sham treat-
ment.309 Ultrasound is frequently used to treat mus-
culoskeletal pain; however, more studies are required
using improved methodology to determine the efficacy
of treatment.
The amount of thermal effects induced by ultrasound
can be manipulated by increasing the intensity, duty
cycle (continuous versus intermittent), and treatment
duration. Thus, the mechanisms of hypoalgesia are likely
similar to the previously mentioned systems for super-
ficial and deep heat. In addition to the thermal mecha-
nisms, ultrasound has purported nonthermal effects.
These nonthermal effects include changes in cellular
 CHAPTER 10 • Pain: Perception and Mechanisms
activity and promotion of tissue healing such as tendon,
bone, and nerve repair (for a review, see Nussbaum310).
Specific parameters as well as translation from animal
studies continue to be debated. Ultrasound-induced
hypoalgesia likely has both thermal and nonthermal
effects.
Cryotherapy
Cold therapy results in vasoconstriction, which lim-
its hemorrhage, inflammation, and swelling; decreases
muscle spasm; and produces anesthesia.311,312 In normal
subjects, crushed ice applied to the shoulder increases
pressure pain threshold, which was more effective than
shortwave diathermy applied to the shoulder.302 The use
of ice in treating musculoskeletal pain is well established.
Ice is frequently used in treating a number of musculosk-
eletal conditions including sprains, strains, postoperative
conditions, spasm, and arthritis.
The analgesic effects of ice have been reported, and
ice has been used to treat pain for centuries. In 1945,
Parsons and Goetzl first proposed the counter-irritant
theory using a cold stimulus.313 Specifically, cold applica-
tion using ethyl chloride spray increased the pain thresh-
olds produced by electrical stimulation of the tooth
pulp.313 The counter-irritant theory entails a noxious
stimulus that activates endogenous inhibitory mecha-
nisms thus decreasing the pain perception of a second
noxious stimulus.
An alternative theory in the hypoalgesic effects of
cryotherapy is based on the cold-induced decrease
in nerve conduction velocity.314,315 Decreasing nerve
conduction velocity may decrease nociceptor activity
including input to supraspinal sites. Consequently, the
decrease in pain signals being transmitted would affect
pain reports.
Manual Therapy
Massage
Massage therapy is the manipulation and mobilization of
skin and muscle tissue. Purported physiological effects
include increases in circulation, range of motion, tis-
sue healing, and relaxation/mood. Despite the univer-
sal appeal of massage, few controlled trials have assessed
the effectiveness of massage in relieving pain. Ernst has
published two systematic reviews on massage therapy as
a treatment for delayed-onset muscle soreness and low
back pain.316,317 Both reviews reported major method-
ological flaws in the research studies. Despite the short-
comings, Ernst concluded that massage therapy may
alleviate symptoms of delayed-onset muscle soreness.316
For low back pain, one study found that massage is supe-
rior to no treatment, whereas two studies implied that
massage therapy is equally effective as spinal manipula-
tion or TENS.317 Finally, one study found that massage
235
therapy was less effective than spinal manipulation.317
Ernst evaluated systematic reviews on massage therapy,
concluding that massage as an effective therapeutic inter-
vention for pain control has not been proven by clinical
trials.318 Thus, the clinical research on massage therapy
reveals a variety of therapeutic recommendations.
One hypothesis regarding the pain-relieving effects
of massage involves the gate control theory. Massage
activates large afferent fibers, thereby blocking the
nociceptive signals in the spinal cord. Thus, mas-
sage potentially closes the gate to the transmission of
pain.
The increase in circulation and tissue extensibil-
ity following massage likely affects pain reports (for
a review, see Goats319). Increasing blood flow may
promote tissue healing thus decreasing pain-produc-
ing signals. Increasing tissue extensibility could poten-
tially decrease mechanical activation of nociceptors. In
addition to decreasing nociceptor activation, increas-
ing range of motion may increase activation of large
afferent fibers in the joint, setting in motion the gate
control theory.
An alternative hypothesis regarding the pain-reliev-
ing effects of massage involves alterations in muscle
tension. Massage decreases the H-reflex, which mea-
sures motoneuron activity, thus decreasing muscle
spasm.320–322 Muscle spasm causes local tissue ischemia,
which activates nociceptors. By decreasing motoneuron
activity, the spasm is relieved, thereby decreasing the
activation of nociceptors. Interestingly, not all studies
demonstrate a decrease in motoneuron activity.323 This
lack of decrease may be due to the type of massage and
activation of deep tissue receptors. Deep massage results
in a greater reduction in motoneuron activity compared
with light massage.320 Furthermore, blocking cutane-
ous receptors with a topical anesthetic did not prevent
the decrease in the H-reflex caused by massage,321 and
thus the effects are likely a result of the manipulation
of deep tissue.
Joint Play Mobilization and Manipulation
Joint play mobilization and manipulation are fre-
quently used to manage both acute and chronic pain
conditions. A systematic review of randomized clini-
cal trials indicated that ∼50% of the articles reviewed
showed favorable results for manipulation for both
acute and chronic low back pain.324 However, the
review was inconclusive regarding the effects of spi-
nal manipulation therapy and low back pain because
of the poor methodology of the articles reviewed. In
contrast, a meta-analysis concluded that spinal manip-
ulation therapy was consistently more effective than
comparison treatments in treating low back pain.325
Barr performed a systematic review on manipulation
of the cervical spine and concluded there may be
236 SECTION I • Scientific Foundations
short-term benefits for patients with neck pain and
headache.326 A systematic review positively concludes
the use of manipulation in treating both low back and
neck pain conditions.327 Ernst evaluated randomized
clinical trials and concluded that spinal manipulation
was not more effective than conventional exercise
treatment in treating neck pain.328 The effectiveness of
spinal manipulation therapy in relieving pain continues
to be debated.
Hypoalgesia produced by joint play mobilization
and spinal manipulation may be due to changes in the
sympathetic nervous system function. Wright and col-
leagues demonstrated, in a randomized, double-blind,
placebo-controlled study, a strong correlation between
hypoalgesia produced by spinal manipulation and exci-
tation of the sympathetic nervous system in individuals
diagnosed with lateral epicondylitis.329
Another potential mechanism of action involves activa-
tion of descending pathways. In support of this hypoth-
esis, spinal blockade of serotonin receptors, 5-HT1 and
5-HT2, prevents antihyperalgesia by joint manipulation
in acute ankle joint inflammation; furthermore, partial
reduction is demonstrated with spinal blockade of nor-
adrenaline receptors with yohimbine.330 Thus, the antihy-
peralgesia produced by joint manipulation likely involves
descending inhibitory mechanisms from the RVM and
pontine nuclei.
One final hypothesis involves changes in muscle ten-
sion. Spinal manipulation decreases motoneuron activa-
tion as measured by the H reflex.323,331 This decrease in
motoneuron activity may reflect a decrease in spasm,
thus eliminating ischemic conditions and activation of
nociceptors. However, the changes in the H reflex are
short lasting, 20 to 30 seconds, and thus an unlikely
mechanism.
Exercise
Clinically, exercise is used to treat a number of pain
conditions including neuropathic pain, low back pain,
osteoporosis, fibromyalgia, and chronic musculoskeletal
pain.3,332–336 A number of studies demonstrate the benefits
of exercise in treating musculoskeletal pain. For exam-
ple, older adults diagnosed with osteoarthritis who per-
formed strength or aerobic training reported a decrease
in pain (for a review, see Koltyn337). The conclusion in
a Cochrane Database of Systematic Reviews stated that
therapeutic exercise reduces pain and improves physical
function in individuals diagnosed with osteoarthritis of
the hip or knee.338
Exercise is frequently used to treat individuals with
low back pain. Systematic reviews on exercise and low
back pain provided evidence that exercise therapy is
effective in treating chronic, but not acute, low back
pain.336,339 Another review assessed the type of exer-
cise used in treating low back pain, with the authors
concluding that strength training is frequently incor-
porated in low back pain exercises, with beneficial
results.340
Further research needs to be conducted to find the
optimal dosage (i.e., intensity, duration, type) of exer-
cise required to obtain the benefits. A number of stud-
ies support the use of exercise as a pain management
tool; however, these studies utilized a broad range of
parameters that cannot be combined into one exer-
cise prescription. Perhaps a wide range of parameters is
acceptable when using exercise as a pain management
tool.
Investigators continue to study the mechanisms of
action for exercise-induced analgesia. The most widely
accepted belief involves activation of the endogenous
opioid system, with activation of endogenous opioids
associated with high exercise intensities (for a review, see
Koltyn341,342). In addition to the activation of endoge-
nous opioids, there appear to be nonopioid mechanisms
of action because of the research conducted using nalox-
one. These hypotheses include the following: activation
of large afferent fibers incorporating the gate control
theory return of function and removal of mechanical and
shearing forces thus eliminating nociceptor irritation,
and enhancement of psychological well-being, altering
the motivational-affective dimension of pain.
Education
Educating individuals on pain mechanisms and man-
agement techniques likely affects the cognitive-evalu-
ative and motivational-affective components of pain.
Individuals who are well informed regarding a surgical
procedure require less pain medication than individuals
who did not receive this information.343 Patient educa-
tion includes incorporating behavioral strategies as part
of pain management. For example, behavioral strategies,
such as relaxation or biofeedback, are frequently used as
coping mechanisms in pain management.344 Cognitive
behavioral approaches are effective in treating headaches,
arthritis, fibromyalgia, low back pain, and chronic pain
(for a review, see Melzack and Wall2). Children edu-
cated on distraction techniques during routine blood
draws perceived less pain and exhibited less behavioral
distress.345 Adults who used cognitive strategies, such as
coping mechanisms, during a noxious stimulus reported
lower pain perception and higher tolerance.346 Thus, edu-
cating individuals regarding potentially painful events,
 CHAPTER 10 • Pain: Perception and Mechanisms
treatment interventions, and behavioral strategies may
significantly affect pain behaviors.
Acknowledgments
We wish to thank the Arthritis Foundation, American
Physical Therapy Association (Mary McMillan Doctoral
Scholarship), and the National Institutes of Health grants
K02 AR 02201 and R01 NS 39735 for financial sup-
port. We also wish to thank all our colleagues (graduate
237
students, postdoctoral fellows, and collaborators) who
contributed to much of the work presented in this chap-
ter: Drs. Westlund, Willis, Ma, Radhakrishnan, Skyba,
and Ms. Gopalkrishnan, Kalra, and Mr. Chandran.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 346 references for this chapter.

238 SECTION I • Scientific Foundations
P HYSIOLOGICAL B ASIS OF P HYSICAL
A GENTS
Mark A. Merrick
Introduction
With the notable exception of active exercise, therapeutic
modalities are probably the most frequently used tools
in all of musculoskeletal rehabilitation. Because the term
therapeutic modalities is actually very broad and techni-
cally encompasses a wide variety of treatments including
exercise and even surgery, this chapter focuses on just
physical agents.
Physical agents, including therapeutic cold, heat,
sound, light, diathermy, electrical current, LASERs, mas-
sage, and compression, comprise a formidable set of tools
in the hands of knowledgeable and experienced clinicians.
Used with proper technique and under the correct cir-
cumstances, these tools have the potential to significantly
affect a patient’s outcome. Even so, many clinicians do
not maximize the benefits of their use of physical agents,
and some produce little benefit from them at all or even
decline to use them in their patient care practices.
Common Therapeutic Modalities
● Cold and cryotherapy
● Superficial heat
● Ultrasound
● Infrared
● Diathermy
● Electrical current
● LASER
● Massage
● Compression
238
11
C H A P T E R
Although they are certainly common and familiar
to rehabilitation professionals, physical agents are used
improperly a surprisingly large percentage of the time.
They often are used for the wrong reason, at the wrong
time, with the wrong parameters, or as a substitute for a
more effective treatment. These errors often lead to poor
efficacy, which, in turn, can make it difficult to justify
the use of these agents to clinicians, patients, or their
insurance providers.
Prerequisite Concepts for Correct Use
of Therapeutic Modalities
● Their physiological effects
● Their benefits
● Their specific purpose for use
● That they are a tool in a total rehabilitation process
● That each patient’s pathology is unique
● That each patient’s response to treatment is unique
The incorrect use of the physical agents often stems
from an incomplete or inaccurate understanding of their
physiological effects and therefore their benefits and
limitations. Therapeutic ultrasound is the best example
of this. Some controversy exists regarding the effective-
ness of therapeutic ultrasound, which is reflected in a
review by Robertson and Baker.1 In their review, they
examined 35 published studies on therapeutic ultra-
sound and were forced to discard 25 of them based on
weak research methodologies. They then analyzed the
10 remaining papers and concluded that no evidence
 CHAPTER 11 • Physiological Basis of Physical Agents
existed that therapeutic ultrasound is clinically effective
in improvement of range of motion or pain. Indeed, in
only two of the 10 papers they examined was ultrasound
better than placebo. At first glance, this study appears
to be a condemnation of the clinical use of ultrasound,
and, in fact, this is the only reasonable conclusion that
Robertson and Baker could have reached based on the
published papers they examined.
Closer examination, however, reveals that this study is
an example of drawing problematic conclusions because
of poor data. Eight of the 10 studies evaluated in this
review had such serious flaws in their use of ultrasound
that no one could reasonably have expected the treatments
to succeed in the first place.2 Because the clinicians and
researchers in those studies apparently did not have an
adequate understanding of the physiological effects
and limitations of this modality, their treatments lacked
the capacity to benefit their patients. Their flawed but
published research actually led to dubious conclusions in
a review that has now become a primary reason for many
clinicians to be hesitant to use this modality at all.
Clearly, understanding the physiological basis for
using physical agents is critical if clinicians are to use
these agents effectively. In this chapter, the basis for using
physical agents during each of the main phases of the
rehabilitative continuum is examined. In each of these
phases, problems and goals that can be managed through
the scientific use of physical agents are addressed specifi-
cally. This is not a chapter that details how to use physical
agents, but rather why and when to use them.
In a discussion of the physiological basis for the use
of physical agents, a few overriding principles must be
observed. First, physical agents are rehabilitative tools
and are not replacements for a comprehensive rehabilita-
tive program. Physical agents can be used to assist clini-
cians and their patients to accomplish specific goals, but
they generally cannot accomplish goals by themselves.
Second, physical agents should be used only when the
clinician has a specific purpose or goal identified for
their use. A tool is effective only when it is used to do
the job for which it is designed. Wrenches are good for
tightening bolts, but they are lousy for cutting boards.
The same can be said for moist heat packs, which are use-
ful for combating soreness but not for inhibiting acute
edema formation. Matching a physical agent’s physiolog-
ical effects to the treatment goals is critical. Third, every
patient’s pathology and response to treatment are unique.
Although the clinician should choose the physical agents
based on their physiological effects and on the specific
therapeutic goal the clinician wishes to achieve, they
should recognize that the unique nature of each patient
requires an individualized approach. “Cookbook” pro-
tocols for physical agents are to be avoided and generally
are not effective. For example, using ice bags to produce
similar levels of cooling in patients with differing adipose
239
thickness requires wildly different treatment durations
(Figure 11-1).3,4
To make the use of physical agents truly effective, the
clinician must be able to match the specific physiological
effects of the agent to the immediate rehabilitative goals.
Likewise, this approach also clarifies the point in the,
clotting rehabilitative process when each modality can
be discontinued. Said simply, the clinician should discon-
tinue the use of a modality when the goal is accomplished
or when it is apparent that the modality is either not
working or is producing an unwanted effect. Generally
speaking, physical agents offer the greatest potential for
benefit in the inflammatory stage and reparative/prolif-
eration stage of an injury, and they generally offer much
less value in the remodeling phase. In fact, discussion of
physical agents in the remodeling phase is not addressed
in this chapter because they are generally used merely to
stave off reinitiation of the inflammatory process.
Stages at Which Therapeutic Modalities
are Most Effective
● Clotting
● Inflammation
● Repair/proliferation
Physical Agents During the
Inflammatory Phase
Perhaps no greater opportunity exists to influence the
outcome of an injury through the use of physical agents
than during the acute inflammatory phase, because it
is the only time the clinician can influence the actual
injury and not just the sequelae of the injury.5 Although
inflammation is certainly a necessary stimulus for tissue
repair and regeneration, it is not without its own newly
created problems.6–8 The physiological problems born
here often take weeks to resolve and can greatly impede
the rehabilitative progress of patients. Failure to address
the specific problems associated with the inflammatory
phase generally means that they will linger long into the
reparative phase, where they interfere with the speed and
quality of the repair. Worse yet, if ignored, the sequelae
of acute inflammation can lead to chronic or recurrent
inflammation, which can significantly affect a patient’s
outcome.
To be most effective during the inflammatory phase, cli-
nicians need to begin physical agent interventions as soon
as possible after the injury.5,7,9–11 Ideally, clinicians would
be physically present and able to intervene immediately
when the injury occurs so that the treatments can work
to counter the unwanted sequelae of inflammation.5–7,12,13
240 SECTION I • Scientific Foundations
70
60
50
Time (min)
40
30
20
Figure 11-1
Time required to produce uniform
cooling (decline of 7°C) with ice bag
10
application in patients with different
adipose thicknesses. (From Otte J,
Merrick M, Ingersoll C, Cordova
M: Subcutaneous adipose tissue 0
thickness alters cooling time during 0-10 mm
cryotherapy, Arch Phys Med Rehabil
83(11):1501–1505, 2002.)
In many cases, however, this is not possible, and clinicians
are unable to intervene until the acute phase response is
well underway or even near completion. The use of phys-
ical agents to manage inflammation already present is still
useful because it helps to resolve the symptoms; however,
it is not as useful as if it could have been begun imme-
diately after the injury when the opportunity existed to
influence the injury itself.
Physiological Problems and Goals
As discussed in Chapter 1 of this text, acute injury
results in a number of physiological problems. Because
most musculoskeletal injuries are aseptic and closed and
therefore do not have an associated risk of infection, the
body’s physiological response to them, inflammation, is
a mixed blessing. Inflammation provides a clear benefit
by limiting damage and initiating repair. However, at the
same time, it does harm by actually causing additional
tissue damage that is unnecessary in the absence of an
invading “bacterial army.” The severity of the harm and
of the physiological problems during this phase can be
minimized by the use of physical agents. By understand-
ing the problems, clinicians can identify which physical
agents to use, when to use them, and why to use them.
11-20 mm 21-30 mm 31-40 mm
Anterior thigh skinfold
Secondary Injury
The first and perhaps most important of the physiologi-
cal problems is secondary injury.7,9,13 When an injury
occurs, it involves immediate ultrastructural tissue dam-
age,14 such as the fracturing of a bone, which is referred
to as primary injury.7,9,13,15,16 This damage involves the
macroscopic or microscopic disruption of a variety of
structures such as ligamentous, muscular, tendinous,
nervous, vascular, and bony tissues.9,13,14 Because pri-
mary injury is the initial trauma itself, it already has
occurred before any possible treatment or interven-
tion. Therefore clinicians can do absolutely nothing to
counteract primary injury once it has occurred.16 For
example, clinicians cannot “unbreak” the bone that was
just fractured. If primary injuries were the only type of
injury to occur, clinicians would have no role in acute
injury management other than providing symptomatic
relief and immobilization to prevent further mechani-
cal damage. Clinicians can and should do more than
this, and clear anecdotal and empirical evidence exists to
support the overall positive effects of acute treatments,
particularly cryotherapy.5,17–21
The physiological response to primary injury can
lead to additional injury to otherwise uninjured
tissues. This resulting damage has been termed second-
 CHAPTER 11 • Physiological Basis of Physical Agents 241

ary injury.7,9,13,15,16 Knight,9 who originally applied this for the quantity of damage from secondary injury, its timing
theory to musculoskeletal injury in the mid 1970s, is beginning to be understood.11 From preliminary work, it
suggested that secondary injury occurred from enzy- appears that secondary injury processes begin immediately;
matic and hypoxic mechanisms. A recent update to they become measurable within 30 minutes of injury and
this theory7 points out that it is probably more correct then continue to worsen for at least the first 5 hours post
to think of these in terms of being immunological and injury (Figure 11-2). This implies that the earlier the inter-
ischemic mechanisms instead of hypoxic and enzymatic vention can be initiated, the greater the opportunity for a
ones. Immunologically, the actions of the complement positive therapeutic effect.
system22 and, more profoundly, the actions of leukocytes
such as the neutrophil22–34 are important contributors to Sequelae of Inflammation
secondary injury. These cellular events of inflammation Although inhibition of secondary injury is probably the
are marked by the early activity of neutrophils, which most important goal for use of physical agents during the
gradually give way over a period of hours into the activ- inflammatory phase of an injury, it certainly is not the
ity of macrophages.6,8,35 Neutrophils account for roughly only one. A second important problem during the inflam-
60% to 70% of all circulating white blood cells, do not matory phase is the classical signs of the acute inflam-
reproduce, and have only a 12- to 20-hour lifespan.6,8,35,36 matory response: redness, heat, pain, edema, and loss of
Their primary function is to fight an expanding bacterial function. Because acute inflammation occurs with every
infection by phagocytizing the bacteria and through injury to perfused tissues, clinicians can expect to see all
a respiratory burst, in which they release a variety of five signs of inflammation to some extent.6 Although
damaging enzymes and free radicals, the immune sys- the redness and heat are not necessarily problems that
tem equivalent of hand grenades, to destroy additional require a specific treatment goal, edema, pain, and loss of
bacteria.6–8,35 They are also active in amplification of the function certainly are.
overall immune response by releasing an assortment of
chemical messengers, and they appear to be a key factor
in the initiation of repair.37,38 Because most musculoskel-
Role of Therapeutic Modalities in Inflammatory
etal injuries do not involve open wounds and infection,
the activity of neutrophils with these injuries is probably
Stage
greater than is physiologically necessary and can lead to ● Inhibit secondary injury
unwanted secondary damage to otherwise uninjured ● Decrease inflammatory response
tissues.6–8,22–35 During the acute phase inflammatory ● Limit edema formation
response, humans have a strong neutrophilic response ● Control pain
regardless of whether the trauma involves an invading ● Decrease functional loss
pathogen.6,8,35
Ischemically, cells otherwise uninjured become
damaged because of the combination of hypoxia,
inadequate fuel delivery, and inadequate waste
removal.6–8 Unfortunately, additional cell death by any
of these mechanisms leads to liberation of arachadonic
acid from the fatty-acid portion of the phospholipid
bilayer of newly destroyed cell membranes. In addition
to being metabolized into inflammation magnifying
leukotrienes, prostaglandins, and thromboxanes (the
targets of nonsteroidal anti-inflammatory drugs), ara-
chadonic acid also has been shown to interfere with
mitochondrial function, which results in a loss of aero-
bic energy production.39–41 This is yet another example
of secondary injury to otherwise undamaged cells.
It is not presently known what the overall contribution
of secondary injury is to the total amount of tissue damage
with musculoskeletal injuries. Generally accepted theories
claim, however, that the time required for tissue healing (the
reparative phase) is partially dependent on the total quan- Figure 11-2
Loss of mitochondrial aerobic energy production across the first
tity of damaged and destroyed tissue. A smaller amount of 5 hours after contusion injury. (From Merrick MA, McBrier NM:
damaged tissue should translate into a more rapid repair Timeline for loss of cytochrome: c-oxidase function following blunt
and quicker return to activity. Although no estimate exists injury in skeletal muscle (submitted for publication).
242 SECTION I • Scientific Foundations
When an injury produces a hematoma, some of its
fluid is from hemorrhage from damaged blood vessels
and the remainder is from inflammation-induced increase
in exudate. The increase in exudate after acute trauma has
been explained through alteration6,16,42–44 of the minute
transcapillary forces governing fluid movement through
the walls of capillaries that were first described by Starling
in 1896.45 In normal vascular fluid dynamics, fluid escapes
from the vascular system through capillary walls at the
arteriole end of the capillary bed and is incompletely
reabsorbed through the walls at the venuole end of the
bed.42 The fluid escape and reabsorption at each end of
the capillary bed is the result of relative imbalances of
the Starling forces at these points. Normally, three of
the Starling forces, capillary fluid (hydrostatic) pressure,
interstitial fluid (hydrostatic) pressure, and tissue colloid
osmotic pressure, cause fluid to migrate from the capil-
lary into the extravascular space, whereas only one force,
capillary colloid osmotic pressure, resists this extravascu-
lar migration of fluid.6,42,43 An overall imbalance is cre-
ated across the entire length of the bed, with net fluid
escape forces being slightly greater than fluid retention
forces.6,42,43 This overall imbalance results in slightly more
fluid escaping from the capillaries than is reabsorbed by
them. This small net fluid loss, totaling about 3 L per
day,46 subsequently is collected by the lymphatic system
under normal circumstances.6,42,46 With inflammation, one
of the escape forces (interstitial colloid osmotic pressure)
is thought to increase substantially because of the release
of free protein and other molecules from the damaged
tissue and activated immune cells (Table 11-1).6,8,16,44
The result would be an even greater net balance of forces
that favors fluid escape. This additional fluid loss from
the capillaries during inflammation exceeds the immedi-
ate removal capacity of the lymphatic system, and edema
accumulation is the result. Physical agents that help to
limit the alteration in Starling forces and/or the bleeding
Table 11-1
Starling’s Law 45: Forces Controlling Fluid Movement Across the Capillary Membrane6,16,42,45,118
Force Description
Capillary fluid Fluid pressure
hydrostatic (Pc) within the capillary
Capillary colloid Osmotic pressure
osmotic (πp) exerted by plasma proteins
Interstitial fluid Fluid pressure in the
hydrostatic (Pi) interstitial space
Interstitial colloid Osmotic pressure
osmotic (πi) exerted by interstitial fluid
Net force under normal
conditions
*The negative interstitial fluid hydrostatic pressure (a partial vacuum), which holds tissue layers together, reverses with injury to become a positive
pressure that separates tissue layers. This loss of vacuum creates an actual space from what had been a potential space, and this space serves as a
pocket where edema collects.
from damaged vessels that accompanies injury would be
logical candidates for acute edema management.
Although limiting edema formation often is thought
of as a primary reason to use physical agents during
the acute phase, clinicians also should not overlook the
importance of management of acute pain. The manage-
ment of post-injury pain can present a bit of a riddle for
the clinician because pain is prolonged and multi-fac-
eted.47–56 Pain in the first few minutes to hours after a
typical musculoskeletal injury results from chemical and
mechanical sources. In such cases, the earliest pain (epi-
critic or “first” pain) is generally mechanical in nature,
well localized, sharp, and carried on myelinated Aδ affer-
ent fibers.49,55 As inflammation progresses, a much larger
contribution to total pain from chemical sources, includ-
ing mainly prostaglandins and other inflammatory medi-
ators, is seen.49,52,56–61 This pain (protopathic or “second”
pain) is generally burning or aching, poorly localized,
and transmitted on unmyelinated C afferent fibers.49,55
Although “fast” pain predominates initially, over a period
of hours, “slow” pain becomes the primary variety of
pain. Because pain is caused and transmitted in different
ways at different times, a variety of physical agents can
be used for its management. The key to clinical efficacy
is matching the specific modality to the specific sources
and/or transmission pathway that control the patient’s
pain at the time of physical agent use.
Although clinicians often refer to the four cardinal signs
of inflammation (i.e., edema, pain, redness, and heat), a
fifth sign, loss of function, is also critical in acute care
management. Functional loss is sometimes overlooked as
a problem for acute management because it is primarily
an indirect phenomenon. That is, loss of function gener-
ally is thought to be the result of the other inflamma-
tory problems. For example, most clinicians have been
taught15,16,62–64 about the importance of the pain-spasm
cycle that accompanies injury. Pain and spasm serve as
Direction Normal Value Effect of Injury
Fluid loss −17.3 mm Hg −17.3 mm Hg
(no change)
Fluid retention +28 mm Hg +14 mm Hg
Fluid loss* −3 mm Hg +4 mm Hg
Fluid loss −8 mm Hg −28 mm Hg
Fluid loss −0.3 mm Hg −27.3 mm Hg
 CHAPTER 11 • Physiological Basis of Physical Agents
psychological deterrents to further use of the injured
body part. Spasm plays a further role as a biomechanical
deterrent by making function uncoordinated and diffi-
cult. Perhaps an even more important cause of the loss of
function is neuromuscular inhibition, in which the central
nervous system actively restrains the function of motor
nerves. Pain has long been thought to be an important
cause of neuromuscular inhibition.15,16,64–67 More recent
work has demonstrated clearly that joint effusion is also a
significant cause of neuromuscular inhibition, even in the
absence of pain.65,67–72 Time saved by limiting the loss of
function during the acute phase is important because it
will pay dividends in terms of the time saved during reha-
bilitation in both the reparative and maturation phases of
the injury. As was the case with the other inflammatory
phase goals, strategies for limiting the loss of function
center on limiting its causes. The main targets of pain,
edema, and voluntary disuse should help the clinician to
select the physical agents for acute use.
Management with Physical Agents
As already emphasized, the use of physical agents dur-
ing any phase of the injury rehabilitative process must
be governed by a specific set of clinical goals based on
the actual physiological problems present during that
phase. During the inflammatory stage of an injury,
the most important of these goals is to limit the total
quantity of tissue damage associated with the injury
and to limit the debilitating sequelae of inflammation.
Several physical agents appear useful for this purpose
(Table 11-2).
Table 11-2
Common Modalities for Managing Acute Injury
Modality Physiological Target
Cryotherapy Reduce pain
Retard secondary injury
Retard edema formation
Retard bleeding
Retard acute inflammation
Compression Retard edema formation
Improve cooling efficacy of
cryotherapy
Elevation Retard edema formation (unproven)*
Retard bleeding
High-voltage electrical Retard edema formation†
stimulation
* No published evidence states that elevation retards edema formation
with acute injury over and above that documented to occur with
cryotherapy and compression. Its use remains largely historical rather
than evidence based.
†
Requires a specific protocol described by Dolan et al.93
243
Secondary Injury
A theoretical argument would be easy to make that to
limit secondary injury would be useful clinically. On the
other hand, another easily made theoretical argument is
that to limit the inflammatory response possibly would
compromise the repair process and lead to a worse out-
come. The reality is that even the strongest approaches
to limiting secondary injury are not likely to prevent a
meaningful inflammatory response and that a clinically
adequate repair with their use can be seen.
Modalities to Decrease Secondary Injury
● Medication
● Cold and cryotherapy
Potentially useful strategies in combating secondary
injury include limiting the delivery of damaging immune
cells to the injury site; limiting the immune cells’ ability to
emigrate from the vasculature; limiting their phagocytic,
enzymatic, and chemotactic activities; and enhancing the
ability of uninjured tissues to withstand the immunologi-
cal attack and the metabolic siege that occurs with isch-
emia. Presently, two clinical approaches exist to limiting
secondary injury.
Immediate Use of Medication. The less common
and more controversial of the two is not a physical agent
at all but is instead the immediate use of drugs/medica-
tion to suppress the inflammatory response. Although
the use of anti-inflammatory medications is certainly
not uncommon post injury, the immediate use of fast-
acting NSAID medications, such as injectable ketorolac
tromethamine (Toradol)58,73–76 within minutes of injury,
is less common but may hold some promise therapeuti-
cally. This approach has the potential to minimize the
attraction and activation of the immune cells respond-
ing to injury and by extension. This may help to mini-
mize secondary injury and many of the sequelae of
inflammation. The controversy is whether this approach
may provide too much immune suppression and ulti-
mately interfere with the reparative phase.38,75,77 If it
does, unwanted consequences such as a delay in repair
or more likely a lower quality repair actually may be
seen. This is a new area of thought and requires sub-
stantially more research before a reasoned conclusion
can be drawn.
Cryotherapy. The more common and more widely
studied of the approaches to managing secondary injury
is through the use of cryotherapy. Cryotherapy, the ther-
apeutic use of cold, takes many different forms, all of
which are designed to produce physiologically meaning-
ful cooling of affected tissues. Although the application
techniques differ, the underlying physiology is largely the
244 SECTION I • Scientific Foundations
same. Few data suggest which form of cryotherapy is the
most effective.78–86 Although it has not yet been estab-
lished empirically, clinicians generally assume that cold
modalities that produce greater cooling without actually
freezing tissues are most effective at combating second-
ary injury and acute inflammation.5
To date, little research exists regarding secondary
injury in musculoskeletal tissues. Although the litera-
ture is sparse, some evidence suggests that secondary
injury may be reduced or perhaps even prevented by
cryotherapy (Figure 11-3).5 In the fight against second-
ary injury, the most important physiological effect of
cryotherapy may be a reduction in the metabolic rate
of the cooled tissue. A reduced metabolic rate translates
to reduced demand for ATP and therefore improved
ability to survive the ischemic condition that follows
acute injury.5,7,9,15,16,87 Because ischemia leads to an
inadequate supply of oxygen and fuel substrates, cells
quickly become dependent on anaerobic metabolism
during ischemia. The byproducts of anaerobic metabo-
lism, particularly lactate, accumulate because of the isch-
emia-induced lack of waste removal. These byproducts
actually inhibit the glycolytic pathway, which reduces
the already limited ATP production.42 This alone poses
a metabolic hazard, however, when this is coupled with
ischemia’s inadequate fuel availability6: ATP production
can quickly decline to the point where survivability is
questionable. A cold-induced reduction in ATP demand
then would have an obvious benefit.
In addition to its ATP-sparing effects, a hypother-
mia-induced decrease in the rate of chemical reactions
would help to minimize the activity of the damaging
enzymes and free radicals released by inflammatory
cells.5,7,9,15,16 These enzymes and radicals lead to dam-
Figure 11-3
Cryotherapy retards secondary injury after contusion injury.
(From Merrick M, Rankin J, Andres F, Hinman C: A preliminary
examination of cryotherapy and secondary injury in skeletal muscle,
Med Sci Sports Exerc 31:1516–1521, 1999.)
age to cells and their organelles6–8,35,39–41,59 and may
be an even more important contributor to secondary
injury than ischemia.7 The rate of chemical reactions
is reduced at lower temperatures42 and is described
through a physical chemistry concept referred to as
Q10.6,42 The Q10 of a chemical reaction is simply the
magnitude of the change in the reaction rate that occurs
with a 10°C change in temperature. Clinicians gener-
ally speak of Q10 in physiology to describe metabolic
rate, usually determined by examination of either O2
consumption or NH3 excretion.6,42 Although it often is
suggested that physiologically, Q10 = 2 (i.e., the reac-
tion rate doubles with each 10°C temperature increase),
Q10 is actually somewhat variable88–91 and depends on
the specific temperature range, metabolic pathway, and
organism being studied. Generally, Q10 falls between
1.2 and 2.5, which means that a decrease in temperature
of 10°C leads to a decrease in the reaction rate of 1.2
to 2.5 times (i.e., a 20% to 150% decrease). Although a
decline in metabolic rate is clearly an important aspect
of the acute use of cryotherapy, much is still unknown
in this area. For example, it is unknown what the actual
Q10 is for bioenergetic pathways or immune enzymatic
reactions during cryotherapy. Similarly, although the
evidence for the role of damaging enzymes and free
radicals in secondary injury is getting stronger, most of
this research has been performed in organs and nervous
tissues.7 Very little is known about the progression
of secondary injury in musculoskeletal tissues,7 and
post-injury ischemia theories have not yet been well
examined.
Edema and Effusion
Edema and effusion result from the combination of
bleeding from vascular damage and from the alteration
of Starling forces already described. Three widely used
nonpharmacological approaches exist to limiting them:
elevation, cryotherapy, and compression. Electrotherapy,
an approach that is not as widely used, may be just as
effective.44,92–100
Modalities to Control Edema and Effusion
● Elevation
● Cold and cryotherapy
● Compression
● Electrical stimulation
● Therapeutic exercise
Elevation. Clear evidence supports the use of cryo-
therapy and compression to combat edema formation.
Surprisingly, the evidence supporting elevation for any
purpose is very limited,101–104 and virtually no literature
 CHAPTER 11 • Physiological Basis of Physical Agents
isolates its effects for acute musculoskeletal injury. In
fact, the limited literature examining elevation addresses
its use for post-acute edema removal.101,102,104 Post-
acute elevation for edema reduction is described as
only minimally effective (a decrease of less than 20 mL
of fluid), and even then the reduction lasts only until
a gravity-dependent position is resumed.104 The effects
of elevation are improved by active exercise or other
treatments,101–103 but post-acute elevation alone does not
appear to be very valuable, and no data exist to describe
the efficacy of acute elevation.
Cryotherapy. Although some conflicting data exist
from animal models,10,105 cold generally is accepted as use-
ful for limiting bleeding and the inflammation-induced
increase in Starling extravasation forces.* The bleeding is
managed through a reduction in local perfusion. As was
true with metabolic rate, perfusion also is reduced as tis-
sue temperatures become colder.85,108–112 The decrease in
blood flow is the result of local hypothermia-induced vaso-
constriction.18,108,110–112 As blood vessels become colder,
the smooth muscle layer in their walls begins to contract,
which causes the vessel’s diameter to constrict. Compelling
evidence113 suggests that this vasoconstriction is the result
of the activity of norepinephrine on adrenergic receptors
within the smooth muscle. Although vasoconstriction is
well documented with cryotherapy, it does not occur in
capillaries. Capillary walls are single-cell thick endothelium
and do not contain contractile muscular tissue.
Although the hypothermic decline in perfu-
sion through vasoconstriction is a well-documented
physiological certainty,108,110–115 some confusion still
exists regarding a phenomenon known as cold-induced
vasodilation (CIVD).15,16,108 When a noncapillary blood
vessel is cooled, sympathetic nervous system activ-
ity causes its smooth muscle wall to contract, which
results in vasoconstriction that leads to decreased blood
flow.42,108,110–113 If allowed to remain hypothermic, the
vessel’s constricted state relaxes slightly after several
minutes because of a cyclical decline in norepinephrine
release.113 This results in a slight dilation of the vessel
relative to its constricted state, but this dilation does not
even return the vessel to its normal resting diameter113–
115
and blood flow is still considerably less than nor-
mal.108,110–113 This slight vasodilation is cyclical, that is,
the vessel will alternate between a severely constricted
and partially constricted state as long as it remains
hypothermic.113 This cyclical phenomenon, sometimes
known as the Hunting response,113,114,116 often is misun-
derstood to be a cold-induced hyperperfusion, in which
the vasodilation is an active phenomenon that produces
vessel diameter and blood flow greater than are found
at rest.15,16,108 This misconception is sometimes used as a
*References 5,10,13,16–19,85,94,105–107.
245
rationale for limiting cryotherapy treatments to less than
20 to 30 minutes in duration, ostensibly so that blood
flow does not increase and magnify the inflammatory
problems.
This notion is a misinterpretation of a 1930 study by
Lewis,117 who described cyclical fluctuations in finger
temperature during immersion in ice water. He observed
that finger temperature fluctuated during immersion and
actually become warmer than the baseline temperature.
The misinterpretation comes from the fact that Lewis did
not examine blood flow nor vessel diameter, and his sub-
jects began the study somewhat hypothermic as a result
of being underdressed in a very cold room. The subjects’
baseline finger temperatures were already depressed well
below normal, and the fluctuations Lewis described were
most likely the Hunting response. In reality, cryotherapy
does not cause greater-than-normal perfusion, and the
body of literature documenting this physiological certainty
is extensive. Instead, cold causes a decline in perfusion.
The hypothermia-induced decline in perfusion creates
a theoretical quandary for injury management.118 On
the good side, reduced perfusion would translate to less
hemorrhaging, less edema formation, and decreased accu-
mulation of inflammatory cells that may cause secondary
injury. These may all translate to improved outcomes
of the injury. On the bad side, decreased perfusion also
would mean less delivery of O2 and nutrients and less
removal of metabolic waste products. These potentially
would worsen secondary injury. Because blood flow with
cryotherapy is not stopped completely, clinicians can
speculate that the pros outweigh the cons. However, this
remains a theoretical argument, because a conspicuous
lack of data exists to build a strong case for either side.
Compression. The use of external compression
to limit the formation of edema and effusion is rooted
in two separate effects. The first and most obvious is
compression’s ability to alter transcapillary Starling
forces.12,119 External compression increases the tissue
hydrostatic pressure, which thereby reduces the magni-
tude of the pro-edema pressure gradient present during
acute inflammation.12,119 At rest, tissue hydrostatic pres-
sure is actually slightly negative (i.e., a vacuum).42 This
negative pressure contributes to the small loss of fluid
from the vascular system and also helps to hold tissue
layers together. This is one of the reasons that a patient’s
skin clings to the contours of the underlying structures.
During edema formation, this pressure reverses from
negative to positive and the result is that the potential
space that exists between tissue layers at rest becomes an
actual physical space and serves as a collecting place for
exudate. External compression dramatically increases this
pressure119 and causes it to resist the fluid loss from the
vascular system, which retards the formation of edema.
Unfortunately, external pressure does not offset
completely the increase in tissue osmotic pressure during
246 SECTION I • Scientific Foundations
inflammation, so some edema forms even with the use
of external compression. Likewise, edema is formed not
only by fluid leaking through intact capillary walls. A
considerable portion of the edema or effusion associated
with injury is from bleeding vessels damaged during the
injury.6 This is why trauma-induced edema (exudate
+ bleeding) is associated with ecchymosis and allergic
edema (exudate only) is not. Compression of greater
than 30 to 40 mmHg reduces blood flow120–122 and there-
fore can be used to limit this bleeding. Compression
also slows the rate of flow, which allows for more rapid
development of the fibrin scaffolding that eventually
forms a clot and stops the blood loss6,42 and serves as
the foundation for the granulomatous tissue that brings
about repair.6 This reduction in blood flow also may help
to explain compression’s second useful effect in acute
injury management.80 Compression has been shown to
increase the rate of cooling and to produce colder tis-
sue temperatures when used with cryotherapy (Figure
11-4).78,80 Reduced blood flow likely would translate to
decreased inflow of warm blood into the cooled area and
therefore partially explain the improved cooling during
cryotherapy.80
Electrical Stimulation. Although the ice, compres-
sion, elevation (ICE) approach to acute injury manage-
ment is steadfastly used, the acute electrotherapy model
is generally less familiar to most clinicians. Nonetheless,
some compelling data support this approach for combat-
ing acute edema formation,44,92–94,98,100 and it deserves
serious consideration. This approach uses a specific elec-
trotherapy protocol using cathodic high-voltage pulsed
current (CHVPC) at 120 pulses per second and a volt-
age that is 90% of the visible motor threshold.92–94,99 Data
Figure 11-4
Cryotherapy with compression produces
colder intramuscular temperatures than
cryotherapy alone. (From Merrick M,
Knight K, Ingersoll C, Potteiger J: The
effects of ice and compression wraps on
intramuscular temperatures at various
depths, J Athl Train 28(3):236–245,
1993.)
suggest that the protocol is most effective if applied con-
tinuously during the entire acute period in which edema
is forming.93 Other electrical waveforms and protocols
may not be as effective.99 Some data suggest that elec-
trotherapy, cold water immersion, and their combination
are similarly effective.93,94 Conceptually, the most likely
explanation for the efficacy of CHVPC in curbing edema
formation is that it alters capillary permeability or Starling
forces44,92–94,99 or possibly arteriole diameter.98
Acute Pain
Although a number of physical agents are effective for
pain management, the specific choice during the acute
phase is limited to those that will not further exacer-
bate the inflammation and injury. For this reason, no
physical agent is used more frequently for acute pain
management than cryotherapy.13,21,53,107,123 Three over-
lapping theories may explain the ability of cold to allevi-
ate pain during the acute phase. First, cold application
stimulates temperature receptors, causing stimulation of
Aβ afferent nerve fibers. These may inhibit pain trans-
mission on second order neurons through gating at the
substantia gelatinosa in the dorsal root ganglion of the
spinal cord as explained through the gate control the-
ory.124 A second possibility is that the conduction of the
pain impulse along the afferent nerves may be slowed
by cryotherapy. Cold has been shown to decrease nerve
conduction velocity by as much as 30%,125 and this may
interfere with pain signaling. A third possibility is that
cold may affect pain receptors themselves. Local cold
application may reduce the sensitivity of pain receptors
much in the same way that it reduces sensitivity of touch
and pressure receptors.16,42
 CHAPTER 11 • Physiological Basis of Physical Agents
Modalities to Control Acute and Chronic Pain
● Cold and cryotherapy
● Electrical stimulation
● Acupuncture
● Medication
● Massage
● Heat
Although cryotherapy is an outstanding agent for
pain control, its application actually can be painful. This
is particularly true of cryotherapy treatments that involve
immersion in ice water or for patients unaccustomed to
cryotherapy. The pain generated with cold application is
initially intense but often subsides after several minutes.
A repeated application over a period of days or weeks
generally leads to better tolerance by patients as they
grow accustomed to the treatment. The use of an insulat-
ing toe cap or confounding sensory information has been
shown to decrease cold application pain.126,127
Loss of Function
The loss of function with acute injury is a relatively new
target for physical agent use. This is probably because his-
torically the loss of function has not seemed as important,
or at least not as urgent a therapeutic goal, in comparison
with the other inflammatory sequelae or secondary injury.
Clinicians traditionally attributed the loss of function to
these other acute problems and more or less assumed that
function would return once they are alleviated. Clinicians
are now beginning to think about the loss of function as
its own entity as more is learned about the neuromuscular
inhibition that accompanies injury.16,67,68,70 Neuromuscular
inhibition clearly results from joint effusion,65,67,69,70 but
it also may result from other causes. The use of physical
agents to hinder the formation of joint effusion therefore
would be useful. As clinicians learn more about the causes
and initiation of inhibition, acute interventions targeting it
will evolve. Until that time, clinicians tend to address inhi-
bition primarily as a reparative phase issue. Nonetheless,
this is a potential target for attention during the acute
phase intervention because it has the potential to save the
patient time in the rehabilitative process.
Physical Agents During the
Reparative Phase
During the reparative phase, the physiological problems
and clinical goals facing the patient change and therefore
so should the use of physical agents. Because the acute and
reparative phases are part of a continuum, the transition
between them is somewhat blurred and no clear defin-
ing point exists between them. This indistinct transition
247
between the inflammatory and reparative phases creates
opportunities and pitfalls. The opportunities lie in the
early initiation of controlled activity and its potential to
help overcome the inhibition and loss of function while at
the same time helping to resolve inflammatory sequelae,
particularly edema. The pitfall is that if clinicians are too
aggressive, the desired therapeutic effect will not be pro-
duced, and the acute inflammation may be worsened and
prolonged. An indistinct transition also exists from the
reparative phase to the maturation phase. Care also must
be exercised here to avoid damage to newly repaired
structures that may not yet be ready for full functional
stresses, while at the same time progressively adequate
force must be provided to maximally strengthen these
tissues. The early portion of the reparative phase is rather
different from the final portion. Hence, the use of physi-
cal agents during the reparative phase is rather diverse
because the problems and goals are diverse.
Physiological Problems and Goals
Unlike the acute phase, in the reparative phase with
closed musculoskeletal trauma the point is reached at
which the balance of physiological events tilts in favor of
benefit instead of harm. Early in this phase, the immune
system is finalizing its “housekeeping” role by clearing
tissue debris from the injury site. Simultaneously, it is
stimulating the body’s anabolic machinery into action,
whereby damage will be repaired through a combination
of regeneration of damaged tissue and sclerotic repair
of tissues that do not regenerate. Therefore the early
goals during this phase largely center on resolution of
the “leftovers” of inflammation, such as residual edema
and pain, and also on facilitation of the start-up of repair
and regeneration phases. Later in this phase, repair and
regeneration are fully underway, and therapeutic goals
change to focus on maximizing the quality of the repair
while minimizing the time required for the repair. At
the same time, work to prevent additional losses in joint
motion or muscular strength and endurance that result
from disuse must occur.
Remnants of Inflammation
At the beginning of the reparative phase, patients still
have many problems related to inflammation. From a
use of physical agents’ standpoint, residual edema and
pain are chief among these and all three are interrelated.
That is, resolution of one contributes to resolution of
the other.
Post-Acute Edema. Although clinicians fight to
limit edema formation acutely, the reality is that some
edema will have formed, which has positive and nega-
tive effects. On the positive side, some degree of edema
is necessary because it forms a medium through which
macrophages and fibroblasts can more easily travel to
248 SECTION I • Scientific Foundations

where they are needed for resolution and repair.6 On
the negative side, excessive edema potentially can inter-
fere with restoration of function with injury resolution
and rehabilitation post-acutely. In fact, if excess edema
is allowed to remain for more than a few weeks, con-
nective tissues produce additional cells and fibers to fill
in the edematous space and the edema becomes per-
manent.6 Likewise, once present, edema is thought
to increase pain, cause neuromuscular inhibition, and
reduce functional level.16,67,68,70 Although edema does
lead to measurable neuromuscular changes,65,69,70 some
recent evidence shows that altered functional level does
not correlate as well with the quantity of edema as
previously thought.128
The resorption of post-acute edema and effusion is a
critical early treatment goal and the physiological target
is maximization of the function of the peripheral lym-
phatic system: a system whose anatomy and physiology
are described poorly in most rehabilitation literature.
Under normal, noninjured conditions, the vascular sys-
tem constantly loses a small amount of fluid (transudate)
because of incomplete reabsorption of fluid leaked in
the capillary beds as a result of the imbalance of Starling
forces.6,42,43 Without the lymphatic system, this fluid loss
eventually would accumulate and form massive peripheral
edema as is seen with some patients whose lymph nodes
have been removed surgically. Fortunately, this fluid does
not normally accumulate because it is instead reabsorbed
by the lymphatic system.6,42,46,129–131 When edema does
accumulate after trauma and inflammation, its removal
also is accomplished through the functioning of the lym-
phatic system,46,129,131 although the exact mechanisms for
absorption of interstitial fluid by the lymphatic system
have yet to be resolved.131
Anatomically, the lymphatic system is an “open” sys-
tem, in which fluid can enter from the interstitial spaces.
That is not to say that lymph vessels are open ended (like
a soda straw) but instead they have closed-ended terminal
branches (cul-de-sacs) with gap junctions between cells
that function as perforations. Interstitial fluid, includ-
ing edema, is reabsorbed by entry into these terminal
branches, clinically described as lymph capillaries,17,46 or
as initial lymphatics in the microcirculation literature.129–
131
These initial lymphatic vessels have walls consisting of
single-layer thick endothelium, which overlap, forming
endothelial microvalves (primary valves) at the junctions
between individual cells.130–131 These valves prevent back-
flow of fluid out of the lymphatic into the interstitial space
(Figure 11-5). The initial lymphatics do not have valves
preventing backflow along their lumens (i.e., secondary
valves).130,131 The initial lymphatics join together (anasto-
mose) to form networks (plexi) from which larger afferent
lymphatic vessels arise and eventually end at lymph nodes.
Along the afferent lymphatic vessels, sometimes called
secondary lymphatics, the walls become multilayered and
gain secondary valves and a smooth muscle layer.132 The
efferent lymph vessels leaving the lymph nodes eventually
join to form even larger lymphatic vessels that eventually

Primary lymphatics
(lymph capillaries - 1 cell thick)

Efferent lymphatic
Smooth muscle in wall
appears here Lymph
node
Primary lymphatics
(lymph capillaries -
1 cell thick) Afferent lymphatic

Secondary lymphatic

Epithelium
Secondary
Figure 11-5 valves
Lymphatic microanatomy. Fluid enters
through the primary lymphatics and is Fluid
Lum
prevented from escaping by overlapping en
epithelial cells (primary valves). Secondary Primary
valves arise in the secondary lymphatics, valves
which prevents backflow. The afferent
lymphatics add smooth muscle to their walls,
which generates a small amount of pressure,
which promotes lymphatic return.
 CHAPTER 11 • Physiological Basis of Physical Agents
empty into one of the two lymphatic ducts, where the
fluid rejoins the vascular system.
Fluid enters the initial lymphatics through the gap
junctions between the endothelial cells and is prevented
from escaping by the primary valves.130,131,133 Because
the initial lymphatics lack a muscular layer in their walls,
they can neither constrict nor dilate nor do they actively
generate pressure to move the fluid toward the afferent
lymphatic vessels. Instead, the pressure to move the fluid
comes entirely from external sources, mainly contraction
of the skeletal muscles (the “muscle pump”) surround-
ing the lymph vessels. Once the fluid reaches the affer-
ent lymph vessels, it can no longer backflow because of
the secondary valves. Likewise, the smooth muscle layer
allows the lymph vessel to generate pressure and actively
contribute to the flow of fluid. Even at this point, the
contribution of constriction pressure to lymph flow is
probably minor compared with the contribution from
external pressure.
Residual Pain. In the reparative phase, pain evolves
from its acute, sharp, epicritic form to a more diffuse, dull,
protopathic form. Protopathic pain during the reparative
phase is largely the result of stimulation of chemical pain
receptors by inflammatory chemical mediators such as
bradykinins and prostaglandins,6,49,50,54,55 although pain
also emanates from other sources, including neurological
trauma. Protopathic pain is also different than acute
epicritic pain in that it is predominantly carried on unmy-
elinated C afferent nerve fibers.49,50,54,55 Because pain is
predominantly an inflammatory chemical pain at this
point in the rehabilitative process, goals should largely
center on resolving the inflammation; a goal that far
easier to conceptualize than to actually achieve.
Promoting Repair/Regeneration
One of the hallmarks of contemporary musculoskeletal
rehabilitation is a quest to maximize the quality of tissue
repair after trauma with a simultaneous attempt to mini-
mize the time required for this repair. The stark reality,
however, is that clinicians have little evidence to tell them
if they can actually do so. Before the discovery of growth
factors, it was widely accepted that wounds heal at their
maximal rate all by themselves.6 Clinicians now have
convincing evidence that adding growth factors to their
cellular environment can speed up the process.6,134,135
Unfortunately the cost of this approach is too prohibitive
for routine clinical use, and clinicians are left attempting
to stimulate the local release of growth factors134,136–139
rather than supplementing these externally.
The healing of tissues is actually a balance between two
separate but simultaneous processes. The first is regener-
ation, the replacement of damaged cells with cells of the
same type, whereas the second is repair, the replacement of
damaged cells with sclerotic (scar) tissue (see Chapter 1).
Sclerotic tissue has considerably weaker tensile strength
249
than the tissue it replaces,6,140 and it tends to indiscrimi-
nately adhere tissue layers to each other in a detrimental
way. For these reasons and because regenerated tissue
retains its functional properties, clinicians would prefer
regeneration over sclerotic repair.
Unfortunately, outside of epithelial tissues, humans
are not terribly gifted at regeneration. Regenerative
capacity in humans appears to be age related141 (children
have more capacity than adults), probably because of the
relatively greater number of stem cells (satellite cells)
present in children. To regenerate a nonepithelial tissue
such as skeletal muscle, satellite cells located adjacent to
the injured muscle cell must be activated, must prolifer-
ate, and then must differentiate into muscle tissue.136,142
This process appears to be primarily complete within a
few days of the injury,6,142 yet clinicians certainly do not
see full restoration of function with muscle injuries in
this timeframe. The reason for this discrepancy is that
humans are able to regenerate only a very small portion
of the damaged tissue, and the rest is repaired by sclerotic
tissue: a process which takes much longer.
Sclerotic repair of tissue follows one of two paths
depending on whether the wound is incisional (closely
approximated edges) or excisional (a gap between
edges).6 With incisional wounds, the closely approxi-
mated edges are temporarily “glued” together with a
weak mesh of fibrin produced during blood clotting.
This mesh acts as a scaffold upon which fibroblasts crawl
into the wound and permanently glue it together. In
excisional wound healing, the edges are too far apart
to be held together with a fibrin mesh, and instead the
wound must be “filled-in” with granulation tissue. This
process then involves maturation of the scar tissue, where
it contracts and reabsorbs nearly all of its cells and leaves
a fibrotic mass, a process that can take more than a year
from injury to completion.
Goals for wound healing are simple to understand
and yet difficult to achieve. Clinicians simply want to
facilitate regeneration while minimizing sclerotic repair
to the absolutely smallest amount possible. To date,
this has involved primarily attempts to keep incisional
wounds closed (sutures and steri-strips), promote
early mobility, and minimize factors that interfere with
wound healing such as infection, presence of foreign
bodies, poor nutrition, and chronic disease (e.g., dia-
betes). These are reasonable for promoting healing, but
they do little to influence the balance between repair
and regeneration.
Minimizing Sequelae of Disuse
Disuse can be a double-edged sword after injury. As a
general rule, clinicians need to minimize the potentially
detrimental stress to an injury to prevent further damage
and to allow the edges of a wound to approximate to
maximize healing.143 On the other hand, disuse causes an
250 SECTION I • Scientific Foundations
entirely new set of problems. Chief among these prob-
lems are the loss of range of motion (ROM) in addition
to a softening of articular surfaces.66 All of these can pro-
long the rehabilitative process144 and significantly inter-
fere with the return of normal function.
Although immobilization formerly was the favored
treatment for most musculoskeletal injuries, contempo-
rary injury management involves early mobilization.143,144
Unfortunately, even with early mobilization, some
patients still develop joint motion limitations. Although
some movement limitations that are the result of exces-
sive pain are best approached through pain treatments,
most lingering motion deficits are the result of disuse
related tissue shortening, sclerotic adhesions, or from
wound contraction. All tissues in the body are remod-
eled based upon repetitive stresses, and the relative lack
of stresses with immobilization can cause unwanted
positional shortening of tissues that are no longer being
stretched. This shortening can be remedied by stretch-
ing and increased functional demands. More insidious,
however, are the adhesion and wound contraction limita-
tions. Sclerotic repair involves the laying down of collagen
fibers produced by fibroblasts that are indiscriminately
located along the fibrin meshwork of a healing wound.
The randomness of the fibroblasts, location in the healing
wound6,140,141 virtually guarantees that the collagen they
produce will adhere to and thereby link multiple tissues,
even when those tissues are not normally adhered to each
other. If mobilized early in the healing process, these
misplaced collagen fibers can be broken free before they
proliferate and have a chance to cross-link. Once cross-
linked, however, it becomes a much more daunting task
for the clinician to free the restricted tissues. Likewise,
with the healing of excisional wounds, in which a gap
in the tissue must be filled in, wound contraction is cer-
tainly biological.
From a physiological perspective, wound contraction
through the contraction of myofibroblasts6 is beneficial
in that it makes the wound smaller (more incisional in
shape) and shortens the length of time necessary to fill
the void with sclerotic tissue. The unfortunate conse-
quence is that in some cases, and especially with severe
burns, the contraction of the wound is so profound as
to interfere with virtually any movement of the tissue.6
Wound contraction with large excisional wounds can
limit mobility profoundly. To this end, the therapeutic
goal is to minimize disuse other than what is absolutely
necessary to ensure approximation of tissues so that they
may reconnect as quickly as possible. In cases in which
the patient’s motion limitations have already developed
already, the goal becomes to alter the properties of the
adhesions and contractions so that patients can improve
their mobility. This is much more readily achieved early
on and becomes exponentially more difficult if clinicians
allow the motion limitations to persist for very long.
Another common problem with disuse is atrophy of
muscles, tendons, ligaments, and cartilage (see Chapters
2 to 7). Virtually all mammalian tissues undergo a near-
constant state of remodeling, and this remodeling is
specific to the stresses imposed on these tissues.6,42 In
the presence of repetitive stress with interspersed peri-
ods of rest, these tissue undergo anabolic changes that
make them stronger and more adept at withstanding
the stresses. If one applies the stress without adequate
opportunity for recovery, these tissues undergo catabolic
changes that ultimately make them incapable of with-
standing these stresses, and an overuse injury results.
In the event of disuse, clinicians also observe catabolic
changes that ultimately weaken these tissues. This is not
generally problematic during the disuse itself; however,
it presents a major rehabilitative challenge when patients
attempt to resume activity.
Management with Physical Agents
A variety of physical agents are commonly used in the
reparative phase (Table 11-3), some with well-demon-
strated efficacy, and some with no demonstrated efficacy.
This section does not delve into the specific use for each
modality, but instead common physiological approaches
during this phase will be discussed.
Remnants of Inflammation
Edema Removal. The use of physical agents to aug-
ment edema resolution must be rooted in normal lym-
phatic physiology. Edema resolution is a slow process and
no agent provides large-scale immediate relief; however,
several agents hold some degree of promise. Physical
agents whose actions are based on increasing local
external pressure, such as compression treatments,95,145
are likely to succeed because they provide an increased
force (interstial fluid pressure) that will encourage fluid
to enter the initial lymphatics and move it within these
lymphatic capillaries toward the secondary lymphatics.
Likewise, agents that encourage the spreading of the
edema over a larger surface area, such as massage,146–149
are theoretically useful because they expose the fluid to a
larger number of initial lymphatic capillaries, where it can
enter the lymphatic system.
Mixed data exist regarding the efficacy of edema-
reducing massage.146–149 This literature must be exam-
ined cautiously because most of it examines lymphedema
caused by damage to the lymphatic system and may not be
applicable to traumatic edema associated with musculosk-
eletal injury in situations in which the lymphatics are still
intact. Physical agents that alter the permeability of lym-
phatic vessels, such as electrical stimulation, also may be
useful for post-acute edema resolution95; however, most
literature examines their effect on acute edema formation
rather than resolution.44,92–94,98,100 Although it does not
 CHAPTER 11 • Physiological Basis of Physical Agents
Table 11-3
Common Modalities in the Reparative Phase
Modality
Cryotherapy
Ultrasound (thermal)
Shortwave diathermy
Ultrasound (non-thermal)
Electrical stimulation
Low power LASER
Hyperbaric oxygen
Massage
Intermittent compression
*Iontophoresis requires an uninterrupted monophasic waveform available only from a specially designed
stimulator.
involve a physical agent, perhaps the most important part
of an edema removal strategy is controlled active exercise.
It is exercise that produces the pulsatile pressure waves
that ultimately cause the movement of fluid within the
lymphatic system. Without active exercise, edema merely
moves around in peripheral tissues rather than moving
along the pathway to removal.
On the other hand, one common treatment, contrast
bath therapy, has little theoretical support. Contrast bath,
or the alternation of heat and cold agents, is based on
causing alternating vessel dilation and constriction in an
attempt to create a pumping effect that moves fluid. This
generally is explained to be targeted at venous pump-
ing, which ignores normal edema physiology because
post-acute edema is not absorbed by the vascular system.
The physiologically savvy could make an argument that
contrast would create alternating constriction and dila-
tion of the secondary and larger lymphatics, and that this
would create useful lymphatic pumping. However, this
also does not hold up to scrutiny because contrast bath
has been shown repeatedly to not produce temperature
fluctuations in subcutaneous tissues.150–152 However, these
fluctuations are the theoretical basis for the purported
251
Physiological Target
Reduce neuromuscular inhibition
Reduce pain
Minimize reinitiation of inflammation
Increase perfusion
Increase metabolism
Facilitate healing (unproven)
Reduce pain
Increase collagen extensibility
Promote tissue regeneration (unproven)
Promote edema resolution (unproven)
Reduce pain
Neuromuscular reeducation
Retard atrophy
Reduce muscle spasm
Remove post-acute edema
Transport drugs across the skin (iontophoresis)*
Promote healing (sclerotic)
Reduce pain
Promote healing (literature inconclusive)
Promote edema resolution
Reduce pain
Retard adhesion formation
Increase perfusion (largely disproved)
Promote edema resolution
pumping effect with contrast bath. Although it is a
physiological fallacy to use contrast bath for edema reso-
lution, contrast bath may hold some therapeutic value for
managing post-acute pain.
Residual Pain. A number of physical agents have
proven efficacious in the management of protopathic
pain. In fact, physical agents are probably more effec-
tive with protopathic pain than with epicritic pain. Recall
that three strategies exist for alleviation of epicritic pain;
namely to interfere with the function of pain recep-
tors,16,42 to interfere with nerve conduction,125 and to
inhibit pain transmission through stimulation of ascend-
ing neurological pathways.124 These same strategies hold
true when using physical agents to manage protopathic
pain, and to them clinicians can add central biasing and
descending pain control strategies.47,55,127,153–155 Of these
strategies, interfering with pain receptors and interfering
with nerve conduction are probably the least common
mechanisms for the physical agents used in the repara-
tive phase; cryotherapy is the only likely candidate for
each. Because cryotherapy can cause additional discom-
fort,126,127 it often is phased out of use once the signs and
symptoms of acute inflammation diminish.
252 SECTION I • Scientific Foundations
A number of physical agents appear to capitalize on
ascending pain control strategies including cryotherapy,
thermotherapy, massage, and electric stimulation in its
many forms. All of these produce sensory information
that has the potential to interfere with pain transmission
at the substantia gelatinosa within the dorsal horn of
the spinal cord through the gate control mechanism as
classically described in Melzack and Wall in 1965.156 The
literature has begun to reflect more complex explanations
of pain formation and control, such as the neuromatrix
theory,55 in which pain is conceptualized as multifaceted
and is modulated by somatic and nonsomatic inputs.
Promotion of Repair/Regeneration
Although myriad physical agents exist whose developers
and marketers tout as promoting tissue healing, actu-
ally very few exist for which sufficient evidence supports
their claims. Unfortunately, many of the claims that have
been made regarding healing have not directly examined
microscopic tissue healing at all.134,137,139,157,158 Instead,
many have used indirect variables such tissue mass. Mass
can be increased by healing, but it also can be increased
by edema, hematoma, or an influx of inflammatory cells,
and none of these actually would represent healing. For
this reason, older studies used as evidence in favor of the
use of physical agents to increase tissue healing may not
demonstrate tissue healing at all.
Modalities to Increase Metabolic Rate and Perfusion
● Thermal ultrasound
● Shortwave diathermy
● Moist hot packs
● Warm whirlpool
● Paraffin bath
● Therapeutic exercise
Many physical agents are thought to improve heal-
ing indirectly through their ability to cause an increased
metabolic rate or increased perfusion. Although this is
certainly true of the hyperthermic modalities, including
thermal ultrasound, shortwave diathermy, moist heat
packs, warm whirlpool, and paraffin bath, modalities
such as these, which increase tissue temperatures, have
been shown very clearly to increase metabolism via the
Q10 effect and increase perfusion through vasodilation.
Although the idea that any physical agent that would
promote increased metabolism and increased perfusion
should promote healing seems logical, little evidence
exists to suggest that improved healing actually occurs
from any of these forms of therapeutic heat. In fact, no
evidence suggests that either sclerotic repair or tissue
regeneration is at all limited by perfusion or metabo-
lism with most musculoskeletal injuries, and therefore
improving these variables would not necessarily promote
more rapid healing. Although a period of hypoxia fol-
lows trauma in which the oxygen tension in the wound
space is close to zero,6,159 it typically is resolved by the
formation of granulation tissue, which is extraordinarily
rich in temporary capillary networks.6 In fact, this soon-
to-be-resolved hypoxia is actually one of the most impor-
tant driving forces in the formation of these granulation
capillary networks. They do not form if oxygen tension is
raised artificially.159
Repair and regeneration are limited by factors other
than perfusion and metabolism. Likely candidates for
limiting regeneration include the exceedingly low num-
ber of satellite cells in adult humans.141 Some physical
agents, specifically non-thermal ultrasound, have been
shown to cause satellite cell activation and prolifera-
tion.160 Although this holds a great deal of promise for
improved wound healing, satellite cells are still limited
by another candidate for limiting regeneration; namely,
the differentiation of these satellite cells into actual
regenerated tissues.136,160 Until this link can be made,
ultrasound remains little more than an interesting can-
didate for improved regeneration. In fact, a great deal
of controversy still exists over whether non-thermal
ultrasound produces satellite cell proliferation160 because
others are having difficulty with the reproduction of
these results.136
In contrast to the relatively rapid process of regen-
eration, sclerotic repair begins quickly but matures
rather slowly.6 Increasing the rate of scar formation
presents us with a clinical conundrum. Rapid scar
formation typically leads to adhesions and limita-
tion in motion, and clinicians must work diligently to
prevent this in normally healing patients. Increasing
the rate of scar formation holds a potential hazard in
exacerbation of the adhesion problem; however, it
holds some promise for faster repair of tissues. Some
modalities such as therapeutic LASER158,161,162 and
microcurrent138,163–165 have been shown to increase
fibroblastic activity and thereby increase the rate of
collagen synthesis, particularly in the skin. The depth
of penetration of these physical agents is remarkably
small, and they are not likely to be of therapeutic use
in the improvement of healing in tissues more than a
few millimeters deep.
Modalities to Increase Superficial Scar Formation
● LASER
● Microcurrent
 CHAPTER 11 • Physiological Basis of Physical Agents
Minimizing Sequelae of Disuse
The primary sequela of disuse that can be improved with
physical agents is motion limitation secondary to adhe-
sions. Limitations from large scale wound contraction
are prevented effectively only by the use of skin grafting.6
With adhesions, the best approach is to disrupt unwanted
connections between tissue layers as they form, and this
is accomplished most easily with early joint mobility and
soft-tissue mobilization. In the event that a motion limi-
tation does form and collagen fibers have been permit-
ted to crosslink, the most common approach to breaking
them free is to increase the elasticity of these fibers before
mobilization. This is accomplished most easily by the
increase of the temperature of these fibers into what has
been referred to as the “therapeutic range” before manual
therapy intervention or other forms of exercise.
Numerous published articles have detailed the study
of this “therapeutic range.” Most of the early work was
completed by Lehman and colleagues.166–169 In several
papers, they and others170 attempted to identify the
temperature range for elasticity changes in collagenous
tissues. They collectively observed that the therapeutic
range was somewhere between 39°C or 40°C and 45°C.
Temperatures below 39°C or 40°C did not produce
meaningful elasticity changes, and temperatures above
45°C were observed to cause damage. A critically impor-
tant and often overlooked aspect of this early therapeu-
tic range defining work170 was that it was not studied in
vivo and was not studied in humans. Instead, therapeutic
temperature range was determined using excised sections
of rat tail tendon immersed in a heated buffer solution
at various temperatures. Although clinicians commonly
apply the findings from this work to therapeutic ultra-
sound and diathermy, neither ultrasound nor diathermy
was used in identification of the range nor was this work
performed on in vivo pathological tissues. Collectively,
we are making a relatively significant leap of faith that
most clinicians do not realize they are making.
Interestingly, Lehman later describes this range in
relative terms, that is, he described it in terms of the tem-
perature change from baseline rather than the absolute
temperatures, and he referred to it as “vigorous heat-
ing.”168 This relative description has become popular
recently, largely because of the prolific work of Draper and
colleagues,171–183 whose papers often cite that Lehman’s
“vigorous heating” temperature increase of 3°C to 4°C
is required for elasticity changes.
The use of relative temperature change as a clinical
guideline may be problematic, however. Tissues in the
extremities treated commonly with ultrasound have
baseline temperatures in the neighborhood of 35.5°C,
and some baseline temperatures have been recorded that
are below 35°C.184 For these tissues, a 4°C temperature
change barely reaches the lower bound of the therapeutic
253
range or may not reach it at all.118 In a recent paper,185
neurologically normal subjects reported a noticeable
heating sensation with thermal ultrasound. This sensation
became uncomfortable to the point of discontinuation of
the treatments when temperatures exceeded 41°C. This
anecdotal observation eventually may form the basis of
a clinical guideline for thermal ultrasound treatments
in which the beginning of patient discomfort may serve
as an indicator that the temperature has reached the
therapeutic range.118,184
Another aspect of disuse that can be addressed through
physical agents is the loss of function and atrophy of the ill-
used tissues. Certainly the best and often easiest approach
to management of atrophy is to prevent it in the first place.
Whenever possible, active exercise is the most efficient
approach to prevention of atrophy. However, active exer-
cise is not always possible and even when it is, the clinician
must expect to see some degree of atrophy because the
exercise intensity and duration are typically not at the level
performed before the injury. When exercise is not pos-
sible, electrotherapy offers a possible means to minimize
atrophy.186,187 Electrotherapy protocols that produce active
muscle contraction, particularly tetanic contractions, pro-
duce adequate stress to maintain some degree of muscle
mass and muscle contractility that would have been oth-
erwise lost.186,187 Likewise, the muscular force generated
also can help to maintain some degree of bone density in
addition to connective tissue strength.
Electrotherapy is not capable of total prevention of
muscular atrophy for three reasons. First, electrotherapy
typically is used to retard atrophy during prolonged and
purposeful immobilization. In such situations, strong
muscle contractions generally are avoided so that dis-
placement of the immobilized structures does take
place. Therefore clinicians tend to use mild isometric
contractions that retard atrophy but do not prevent it.
Second, motor unit recruitment with electrical stimu-
lation is not the same as that which occurs with a vol-
untary contraction. In volitional contractions, smaller
diameter motor neurons that supply small muscle fibers
of small motor units are recruited, which first results in
finer motor control. As the need for increased force or
to overcome fatigue occurs, larger neurons with larger
and stronger motor units are recruited. During elec-
trotherapy, this order is reversed and the larger diameter
motor neurons are recruited first and smaller diameter fibers
recruited less and only when sufficiently high voltage is used.
This leads to a reversed order of atrophy, in which smaller
motor neuron motor units, responsible for fine motor tasks,
atrophy more than the larger motor neuron motor units
responsible for gross motor tasks. The third reason that
clinicians cannot completely prevent atrophy is because
patients, especially athletes, have high levels of athletic
skill and training. Even disregarding the consequences of
254 SECTION I • Scientific Foundations
displacement of the immobilized tissue with strong, elec-
trically induced contractions, the available electrical cur-
rents are unlikely to produce strong enough contractions
to prevent most muscle loss in injured patients. Because
athletes undergo extensive training and conditioning
programs, they have dramatically larger muscle masses
and force-producing capacities than the general public.
Because electrical stimulation tends to recruit the same
motor units repeatedly, atrophy in the lesser recruited
motor units still is seen.
A final concept involves neuromuscular inhibition.
After musculoskeletal injury, a period of neuromuscular
inhibition is seen, which results in motor weakness,
impaired coordination of motor activities, and impaired
joint proprioception. These impairments are observed
even before the patient has had sufficient time for muscle
atrophy to occur. These functional losses are not the result
of loss through muscle atrophy. Instead, they result from
neurological inhibition of muscular activity. Previously the
predominant theory regarding this inhibition was that it
was mediated by pain.16 Now a growing body of evidence
that examines this inhibition suggests another source:
arthrogenic muscle inhibition.68,71,188,189 This research
examines the availability of the motor neuron pool and
how it changes with injury. Under normal circumstances,
patients voluntarily can recruit only a portion of their
total motor neuron pool, because total recruitment of
the pool would produce muscle and joint forces that
would literally pull muscles off of their bony attachments
and cause fractures and other injuries. During an injury
and the subsequent post-injury rehabilitative period, the
percent of the motor neuron pool that can be recruited is
less than normal and can be quantified by measurement
of the Hoffman reflex (H-reflex).68,71,188,189
In several recent studies, creation of an artificial joint
effusion through injection of sterile saline into the syno-
vial space has been demonstrated to diminish the available
motor neuron pool and thereby produce inhibition in the
absence of actual injury.68,71,188,189 Findings demonstrate
that neuromuscular inhibition is related to pain and to
joint effusion. Interestingly, the use of cryotherapy has
been shown to counteract this effusion-induced reduc-
tion in motor neuron pool availability and lead to motor
neuron pool facilitation.68,71,189 That is, cold application
actually increased the amount of the motor neuron pool
available for recruitment. This potentially makes cryother-
apy a useful adjunct to post-acute rehabilitation, because
it may allow the earlier initiation of exercise than would
have been otherwise possible. Another possible approach
to overcoming inhibition involves neuromuscular reedu-
cation, in which electrical muscle stimulation can be used
to cause contraction in a muscle that is inhibited. This
potentially can allow the patient to “learn” to recruit
motor units not otherwise available.
Physical agents frequently are used in interventions
for musculoskeletal rehabilitation. Physical agents com-
prise a formidable set of tools in the hands of knowl-
edgeable and experienced clinicians. Used with proper
technique and under the correct circumstances, these
therapeutic tools have the potential to significantly
influence a patient’s outcome.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 189 references for this chapter.

P HARMACOLOGY AND I TS I MPAC T ON
THE R EHABILITATION P ROCESS
Ellen M. Schellhase, Judy T. Chen, Joseph Jordan, Deanna S. Kania, Brian R. Overholser,
Brian M. Shepler, Kevin M. Sowinski, and Craig D. Williams
Introduction
Pharmacology and the study of drugs and drug therapy
is a continuously growing and changing practice. Drug
therapy had a broad impact on health care and the reha-
bilitation process. Because of the advances in health care,
consideration of the impact of drug therapy is becoming
increasingly important in all areas of patient care, including
the rehabilitation process. Therapeutic effects and adverse
effects of drug therapy may influence rehabilitation. This
chapter provides insight into pharmacology and its effects
on rehabilitation to provide the best patient care. The gen-
eral overview of the principles of pharmacology is followed
by disease-specific drug therapy discussions.
General Principles 1–4
Definitions
Pharmacology involves the study of drugs. Pharma-
cotherapeutics extends this discipline to refer to the
specific use of drugs to prevent, treat, or diagnose dis-
eases. The goal of therapeutics is to achieve a desired
effect while minimizing adverse effects. The major focus
of the remainder of this section includes the concepts of
pharmacokinetics and pharmacodynamics. Figure 12-1
illustrates the interrelationship between pharmacokinet-
ics and pharmacodynamics. Pharmacokinetics refers to
the study of the time course of a drug and its metabo-
lites in the body after administration: in other words, the
study of the actions of the body on the drug. Conversely,
pharmacodynamics refers to the actions of the drug on
the body, or how the body responds to the drug.
12
C H A P T E R
Drug Nomenclature
In most cases, a single drug compound has three distinct
names: chemical, generic, and brand. Prescription drugs
have trade or brand names to distinguish them as being
produced and marketed by a particular manufacturer. In
the United States, drugs usually are registered as trade-
marks, which confer certain legal rights with respect to
their use. A chemical substance marketed by several man-
ufacturers may have several trade names. Additionally, a
drug may be marketed under different trade names in
different countries. Prescription drugs in the United
States also are given generic names, which are approved
by the Food and Drug Administration (FDA). Drugs can
be produced and marketed under their generic name by
companies other than the original manufacturer upon the
expiration of the legal rights associated with drug discov-
ery. Table 12-1 shows examples of two chemical, generic,
and brand names for drugs discussed in this chapter.
Routes of Drug Administration
Drugs are administered in numerous ways, but the most
common mode is extravascular administration. However,
because most drugs work systemically, drugs must move
from the extravascular spaces to the intravascular space to
move into the systemic circulation. This mode includes the
oral or enteral route, which is the most common route of
drug administration. Drugs administered by this route can
be absorbed at any location through the gastrointestinal
tract, including sublingual (i.e., under the tongue) or buc-
cal, rectal, and most commonly oral drug administration.
255
256 SECTION I • Scientific Foundations

Dosage regimen Drug

in tissues
Absorption Site of
Distribution action

Systemic drug
concentration
Drug
Elimination effect

Drug metabolism
or excretion
Efficacy Toxicity

Pharmacokinetics Pharmacodynamics
Figure 12-1
Interrelationship of pharmacokinetics and pharmacodynamics.

Table 12-1
Pharmacokinetics
Drug Naming
Brand or
● Absorption
Chemical Generic Name Trade Name
● Distribution
● Metabolism
N-(4-hydroxyphenyl) Acetaminophen Tylenol, etc. ● Excretion
acetamide
N,N,6-trimethyl- Zolpidem Ambien
2-p-toyl-imidazo
Absorption
(1,2, -a)pyridine-
3-acetamide
Processes of Drug Absorption and Transport. The
L-(+)-tartrate systemic absorption of a drug from the gastrointestinal
tract, lung, or other location is determined by many
factors. These factors include the physiochemical proper-
ties of the drug (e.g., pKa, solubility); surface area of the
absorption site; anatomy, physiology, and pathophysiol-
ogy of the absorption site; blood flow to the absorption
Numerous other extravascular routes of administration
site; dosage form (e.g., tablet, capsule, syrup, inhalant)
include subcutaneous, topical, and many others.
used; and in the case of gastrointestinal absorption, the
The second most common method of drug adminis-
motility of the gastrointestinal tract. Membranes play a
tration is via the parenteral route. This type of admin-
key role as barriers to compound transport.
istration commonly is used in a hospital setting. The
Passive processes represent mechanisms by which
most common route of parenteral drug administration
drugs are absorbed that are not energy requiring. Passive
is the intravenous route. Drugs administered by this
diffusion is a major mechanism of drug absorption and is
route are given directly into the systemic circulation.
the process by which drugs simply move from a higher
The location of administration can be into either a vein
concentration to a lower concentration, sometimes
or an artery, although most drugs are administered
referred to as “down the concentration gradient.” For
into veins because of their easier accessibility. Drugs
passive diffusion to occur, the membrane that the drug is
are given by the intravenous route for numerous rea-
being transported across must be permeable to the drug.
sons, but namely to allow for rapid drug administra-
Important factors that affect permeability are lipid solu-
tion or to bypass the gastrointestinal tract, or simply
bility, degree of ionization, and molecular size. For exam-
because the drug cannot be given orally. Drug dosage
ple, most drugs exist as either weak bases or weak acids.
forms and routes of administration are summarized in
At a physiological (i.e., plasma/blood) pH of 7.4, most
Table 12-2.
weak acids and bases are in the nonionized or neutral
form, which allows the substances to diffuse more readily
than in their ionized form.
Pharmacokinetics
Facilitative diffusion, like passive diffusion, is not an
The four major components of pharmacokinetics are energy-requiring process and involves the movement of
absorption, distribution, metabolism, and excretion. drugs from higher concentrations to lower concentrations.
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process 257

Table 12-2
Drug Dosage Forms and Routes of Administration
Route Dosage Forms

Enteral
Sublingual and buccal Drugs placed under the tongue or in the cheek; Tablets, sprays
avoids first pass effect
Oral Drugs administered by mouth and absorbed in the Solutions, suspensions, tablets,
gastrointestinal tract; subject to first pass effect capsules
Rectal Drugs administered in the rectum as a suppository Suppositories, solutions,
or enema; useful in patients who cannot take suspensions
medications by mouth
Parenteral
Intravenous (IV) bolus, Drugs administered directly into a vein (i.e., Solutions
Infusion systemic circulation), either rapidly as a bolus or
slowly as an infusion. Drugs bypass the
gastrointestinal tract and are not subject to
first pass effect
Intramuscular (IM) Drugs administered into the muscle Solutions
Subcutaneous (SC) Drugs administered below the dermis Solutions
Intradermal (ID) Drugs administered into the dermis Solutions
Intraarticular Drugs administered directly into the synovial Solutions
fluid of a joint
Intrathecal Drugs administered directly into the Solutions
subarachnoid or subdural spaces. Route bypasses
the blood-brain barrier
Epidural Drugs administered into the epidural space, Solutions
the space outside the dura in the spinal column
Other Routes
Topical Drugs in formulations are applied to the skin; Creams, gels, ointments,
cornea; mucous membranes of the nose, eye, suspensions, solutions
mouth, oropharynx, rectum, urethra, and vagina
Ophthalmic Drug administration into the eye Solutions, suspensions
Intranasal Drugs administered in an aerosolized fashion Solutions, suspensions
into the nasal cavity
Transdermal Lipid-soluble drugs administered on the skin; Patches, creams, ointments
usually administration is via a disc or patch that
allows for controlled administration
Otic Drug administration into the auditory canal of Solutions, suspensions
the ear, either external or internal
Inhalation Drugs administered in an aerosolized fashion Solutions, suspensions
into the lungs

However, it is a carrier-mediated process in which a carrier
is required to “assist” in the transport of the molecule across
the cell membrane. Although this process is not energy
dependent, it is dependent on drug and carrier concen-
trations and exhibits capacity-limited properties similar to
active transport systems. Transport of insulin is an example
of this method.
Active transport processes differ from passive pro-
cesses in that drugs move against the concentration gra-
dient, that is, drugs move from lower concentrations
to higher concentrations. These processes are energy
requiring and carrier mediated and are responsible for
regulating the absorption of a large number of drugs
and nutrients from the gastrointestinal tract. In addition,
this type of transport also plays a prominent role in the
excretion of drugs via renal tubular secretion and bili-
ary secretion. Another method of absorption, vesicular
transport, is the process by which a particle or dissolved
material is engulfed by the cell. During pinocytosis, the
cell membrane surrounds and engulfs a particle outside
the cell and transports it into the cell. This method of
transport is important for larger proteins, such as orally
administered polio vaccine, which is absorbed in this
manner. Finally, two other modes of drug absorption are
convective transport, typically important for small mol-
ecules, and ion pair formation.
258 SECTION I • Scientific Foundations
Bioavailability. Bioavailability refers to the extent
of drug delivery into the systemic circulation. It is the
amount of a dose given extravascularly (e.g., orally,
rectally, and subcutaneously) that actually reaches the
systemic circulation. On the other hand, the absorption
rate instead of the extent of absorption influences the rate
at which a drug is absorbed. Pharmacokinetic parameters
that assess the rate of absorption are maximum (or peak)
concentrations (Cmax) and the time to reach the maxi-
mum concentration (Tmax).
Distribution
Drug distribution describes the process by which drugs
leave the systemic circulation and are transported to the
extravascular spaces of the body. Volume of distribution is
an apparent term that relates the amount of drug in the
body to the concentration of drug in the plasma or blood.
The rate and extent of drug distribution throughout
the body are determined by several factors: blood flow
and tissue permeability, plasma protein binding, and tis-
sue binding. Tissues with higher blood flows, such as the
heart and kidneys, usually are more accessible to drugs.
In addition, for a drug to gain access to a tissue or organ,
the drug needs the ability to pass through the membranes
“surrounding” those tissues.
The major determinants for the extent of distribution
of a drug are the relative strength and extent of binding
to tissue components (proteins) versus plasma proteins.
For example, if a drug is highly bound to tissues and to a
small extent to plasma proteins, the drug will have a large
volume of distribution. An example of this is the drug
digoxin. These drugs are distributed widely throughout
the body. The converse to this is a drug with a relatively
small volume of distribution, which is highly bound to
plasma proteins but not highly tissue bound. Warfarin
(Coumadin) is an example of such a drug.
Elimination
Drug elimination refers to the irreversible removal of
drug from the body by all routes of elimination. This
concept typically is broken into two major physiological
components: metabolism or biotransformation and excre-
tion. Biotransformation is the process by which drugs are
changed or transformed into a metabolite. Typically, the
resulting metabolites are more polar or ionizable substances
that can be excreted from the body more readily. The major
metabolizing organ in the body is the liver, although sev-
eral other sites (i.e., gut, kidney, and lung) have metaboliz-
ing capacity. Two major types of drug metabolism exist:
phase I and phase II metabolism. Phase I biotransforma-
tions refer to chemical modifications to the parent drug,
such as oxidation, reduction, and hydrolysis reactions. The
predominant mode of phase I metabolism is oxidation by
the cytochrome P450 enzyme system. Phase II metabolism
refers to a reaction in which an endogenous compound, a
conjugate (e.g., glucuronide), is added to the molecule.
Excretion refers to the removal of drug from the body
in an unchanged form. The most common means of drug
excretion is by the kidney. Other nonrenal means of excretion
of nonvolatile drugs are biliary secretion, through the sweat
and salivary glands and reticuloendothelial system. Highly
volatile drugs, such as anesthetics, are removed via the lungs.
The kidney plays a major role in the excretion of drugs
and metabolites from the body. Typically, substances
that are water soluble and have a low molecular weight
may be excreted by the kidney. Three major processes
are involved in renal excretion of drugs or their metab-
olites and may include any combination of glomerular
filtration, tubular secretion, and tubular reabsorption.
Another mode of excretion is biliary excretion.
Pharmacokinetic Parameters Describing Drug
Elimination and Excretion. The decision on how to
dose a particular drug regimen is based partly upon the
rate at which the drug is eliminated. Two pharmacokinetic
parameters that reflect, at least partly, drug elimination
or excretion are elimination rate constant and clearance.
Elimination rate constant is a hybrid parameter determined
by volume of distribution and clearance. Elimination rate
constant is inversely related to volume of distribution and
directly related to clearance. Elimination half-life is a recip-
rocal function of elimination rate constant and describes
the time it takes for plasma concentrations of a drug to
decrease by one half. Half-life is useful to determine how
long it will take to reach steady-state concentrations or the
duration of action of a drug. Half-life is important in the
construction of drug dosing regimens to avoid large fluc-
tuations in concentrations during the dosing interval.
Importance of Half-Life
● Helps determine time drug needs to reach steady-state
concentrations
● Helps determine duration of action of drug
Like volume of distribution, clearance is a primary
and independent pharmacokinetic parameter. Clearance
describes the efficiency of irreversible elimination (by bio-
transformation and/or excretion) from the body. From a
physiological sense, clearance is the volume of blood cleared
of a drug per unit time (e.g., mL/min, L/hr). Clearance
typically is represented as the total or systemic clearance or
the sum of all elimination and excretion pathways, renal
(kidney) and nonrenal (e.g., liver, lung). It is the parameter
that determines the maintenance dose required to achieve
an average plasma concentration of a drug.
Importance of Clearance Time
● Helps determine dosage required to maintain average
concentration of drug
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
Pharmacodynamics: The Pharmacological
Response to Drugs
As described in the previous section, the field of pharma-
cokinetics incorporates a theoretical description of drug
absorption, distribution, and elimination from the body.
In many cases the pharmacokinetics of a drug dictates the
amount of drug that reaches the site of action and there-
fore influences the pharmacological response. However, it
does not include the theoretical or mathematical framework
by which drugs elicit their effects upon the human body.
The field of pharmacodynamics characterizes the amount
of a drug in a living organism with its corresponding phar-
macological response, outlining the theory of drug action.
Simply stated, the pharmacodynamic profile of a given
drug describes the effect that the drug is exerting upon the
body, such as the perception of pain relief or sedation. The
mathematical manipulations involved in pharmacodynam-
ics are beyond the scope of this text. However, the broad
field of pharmacodynamics includes topics such as mecha-
nisms of drug action, drug sensitivity, and the development
of drug tolerance. These mechanisms are discussed in the
remainder of this section.
Mechanisms of Drug Action
The observed response to a drug can be that of either the
desired (positive) effect or a toxic (negative) outcome. In
general, drugs exert these effects through specific interac-
tions with receptors. A receptor is a component of a cell that,
upon physical contact with a drug, can attenuate or intensify
a biological response. This theory of drug action implies that
drugs do not create new biological phenomena but instead
alter present physiology. Receptors are therefore endogenous
to all living organisms and generally have a high degree of
specificity for naturally circulating endogenous compounds.
When an endogenous substance comes into contact with its
receptor, the receptor’s structure generally is altered, which
leads to a cascade of biochemical events that propagate into
an observed physiological response.
In most cases, drugs are developed and designed to
mimic endogenous compounds and therefore attenuate
or intensify a physiological effect by binding to a receptor.
For example, the drug class called the β-adrenergic recep-
tor blockers have been designed to mimic structurally cir-
culating endogenous chemicals known as catecholamines.
Catecholamines exert their effects by binding to and
modulating receptors on the cellular membranes of a vari-
ety of cells, most notably myocardial cells. When bound
to their receptors, catecholamines propagate a cascade
of cellular events that ultimately lead to observed physi-
ological consequences, such as an increased heart rate.
However, when a β-adrenergic receptor blocker binds to
its receptor, the drug-occupied receptor can no longer be
activated by endogenous catecholamines. The result is a
decreased heart rate resulting from the drug blocking the
effects of endogenous catecholamine activity.
259
Surface membrane proteins are the most important
receptors, in terms of actual numbers of drugs that interact
with them. Receptors, however, are not limited to surface
proteins located on cellular membranes. Certain drugs bind
and alter protein activity in the cytoplasm, mitochondria,
and nucleus, among other cellular locations. Drug receptors
are dispersed in cells throughout the body and can be located
in the circulating bloodstream, in organs, and in all tissue.
Drug-Receptor Interactions. Receptors have a high
specificity for the endogenous chemicals and exogenous
drugs that activate them. Receptor specificity refers to
a high affinity for binding a specific endogenous com-
pound or drug with similar molecular structures or chem-
ical properties. Because receptors have high specificities,
the chemical structures of drugs must contain specific
molecular components that allow them to come into
contact with and bind to the active site on a receptor.
A drug-receptor complex is formed when a drug comes
into physical contact with its specific receptor. This drug-
receptor formation can be stabilized by physical (e.g.,
electrostatic) or chemical interactions between a drug and
the reactive protein receptor. These drug-protein interac-
tions lead either directly or indirectly (through a cascade
of biochemical events) to an observed response to a drug
(e.g., heart rate reduction).
The basic theory behind this concept of drug-receptor
interactions is based on the law of mass action. As applied
to pharmacology, the theory assumes that the intensity
of a response to a drug is proportional to the number
of drug molecules and available active receptor sites that
come into physical contact with each other. Thus the
greater the number of drug-receptor complexes formed,
the greater the observable response.
The formation of a drug-receptor complex can have
several biological consequences that can be broken
down into two fundamental concepts: receptor activa-
tion (agonism) and receptor inhibition (antagonism).
Agonists are drugs or endogenous chemicals that activate
receptors and intensify a biological response. Antagonists
inhibit receptor activation, generally by promotion of a
conformational protein change or by direct blockade of
the active site, which inhibits receptor activation through
agonist binding. Antagonistic drugs therefore reduce or
attenuate a biological response. Partial agonists bind to
and activate receptors but do not have the potential to
confer a full biological response. The biological response
to a partial agonist is somewhere between the observed
response to a “full” agonist and an antagonist. Examples
of an agonistic and antagonistic effect have been described
for the catecholamines and β-adrenergic receptor blockers,
respectively. An example of a partial agonist that acts on
adrenergic receptors is pindolol (Visken). Pindolol acti-
vates the adrenergic receptors but not to the same extent
as endogenous catecholamines. This results in heart rate
changes that are between those of β-adrenergic receptor
blockers (antagonist) and catecholamines (agonist).
260 SECTION I • Scientific Foundations
Other Drug Mechanisms. Drug-receptor interac-
tions encompass the underlying mechanisms of most
drugs, even though the term receptor generally is limited
to that of macromolecular protein structures. However,
drugs can act by several other mechanisms, such as being
incorporated into essential nonprotein entities. For
example, certain chemotherapeutic agents exert their
effects by structurally mimicking nucleotides and inter-
fere with the synthesis of deoxyribonucleic acid (DNA).
A commonly used nucleotide analogue for the treatment
of cancer includes 5-fluorouracil, Adrucil. When incor-
porated into DNA, 5-fluorouracil can interfere with the
growth of rapidly dividing malignant cells, which are
destroyed eventually.
The mechanisms of drug action described thus far are
determined largely by the specific molecular structure of
a drug and its ability to interact with and have a high
affinity for an active site in a receptor or a specific DNA
sequence. However, certain drugs elicit their effects
largely because of their physical properties and not spe-
cific molecular structure. One example includes certain
antacids (e.g., calcium carbonate, Tums), which decrease
the acidity of gastric fluid secondary to their neutraliza-
tion properties in the gastrointestinal tract. The observed
response is therefore not mediated by a biological recep-
tor but instead depends on the ability of the drug to bind
and neutralize acidic ions in gastric secretion.
Drug Sensitivity
Two functionally diverse drugs that modulate the same
receptor may necessitate different amounts at the site of
action for the same biological response to be observed.
The receptor is more sensitive to the drug that exerts
the greatest effect with the same number of drug-recep-
tor complexes formed. The sensitivity of a receptor can,
in some cases, be described by the potency of a given
drug. Potency refers to the amount of a drug required
to exert an observable response. The effect could be that
of a desired outcome or a toxic event. Potency can be
classified by the dose required to exert a pharmacologi-
cal response. However, it is more appropriate to relate
response to drug concentrations at the active site (e.g.,
plasma) to truly classify the potency of a given drug. This
allows for better control over pharmacokinetic variability
such as drug absorption.
Importance of Potency
● Determines the amount of drug necessary to have an observable
effect
Therapeutic Index. Optimally, drugs are designed so
that they are more potent for the desired versus toxic
effects. That is, a lower concentration of drug is required
to exert the preferred response than is needed for a toxic
event to occur. The most desirable drugs are those for a
given condition in which a large range in drug concen-
tration can exist and still propagate a desired outcome
without toxicity. Drugs in which a small difference exists
between the effective and toxic concentrations can be
defined as having a narrow therapeutic index. Narrow
therapeutic index drugs need to be monitored closely
in clinical practice because of interindividual variability
that exists in pharmacokinetics and pharmacodynamics.
One example of a drug with a narrow therapeutic index
is the anticoagulant agent warfarin (Coumadin). Patients
receiving warfarin need to be monitored closely because
of the potential for serious bleeding complications that
can transpire with this therapy. Adverse events can occur
with warfarin doses that are very close to doses that are
needed to exert the desired effect. Furthermore, the
response to warfarin is highly variable among individuals,
which necessitates intensive drug monitoring programs.
Importance of Therapeutic Index
● Determines range of drug concentration needed to have a
therapeutic effect without having a toxic effect
● Varies between individuals
Tolerance. The sensitivity of a receptor, and thus the
therapeutic index of a drug, is not generally identical
between individuals and can change with time in any
given individual. Common intraindividual differences
in drug response can develop with aging, disease pro-
gression, drug interactions, or continued drug expo-
sure. An example of a well-characterized intraindividual
drug-response change is the phenomenon called drug
tolerance. Tolerance refers to a decreased observable
biological response over time with repeated or continual
exposure to a drug or chemical.
Factors That Affect Response to Drugs
● Age
● Disease progression
● Drug interactions
● Continued drug exposure
Tolerance can develop to antagonistic and agonistic
drugs and in most cases is due to a receptor upregulation
(increased receptor amount) or downregulation
(decreased receptor amount), respectively. These phe-
nomena are possible because receptor expression is not
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
static in any given cell and the amount expressed can
be regulated by an assortment of physiological systems.
Downregulation (receptor desensitization) may tran-
spire when an intracellular biological feedback mecha-
nism is turned on as the result of continued receptor
activation by an agonist. This can alter the machinery
of the cell that leads to a decrease in receptor produc-
tion and therefore a decrease in total receptor number.
A decrease in the number of receptors expressed in a cell
is called receptor downregulation. This results in a loss of
full receptor activation and ultimately a decreased observ-
able effect. However, continued antagonist exposure
can lead to the opposite effect and an increased cellular
production of receptors or an upregulation (receptor
sensitization). The antagonistic properties of the drug
are masked following a receptor upregulation because a
greater number of receptors are available for activation
by naturally circulating endogenous agonists. When the
antagonistic drug is stopped, a withdrawal phenomenon
can be observed because of the increased number of
available receptors (see Barbiturate Sedative-Hypnotics).
The remaining sections of this chapter address key
medications and drug classes that may affect musculosk-
eletal rehabilitation. To address all areas of drug therapy
in one chapter is impossible. Therefore the disease-related
therapies and ancillary medications discussed are those
commonly seen in patients undergoing musculoskeletal
rehabilitation.
Sedative-Hypnotic Agents
Sedative-hypnotic agents are medications used in the
treatment of insomnia. A variety of different classes of
sedative-hypnotic agents currently are available, and the
purpose of this section is to classify the different sedating
medications and review some basic information about
the agents including their mechanism of action, indica-
tions, adverse effects, and dosing. Other medications are
indicated for the treatment of different disorders such
Table 12-3
Nonbarbiturate Sedative-Hypnotics
Generic Name Brand Name Classification
Estazolam ProSom BZD*
Flurazepam Dalmane BZD
Quazepam Doral BZD
Temazepam Restoril BZD
Triazolam Halcion BZD
Zolpidem Ambien Imidazolpyridine
Zaleplon Sonata Pyrazolopyrimidine
Zopiclone Imovane Cyclopyrrolone
*Benzodiazepine.
261
as anxiety, depression, and psychosis, which also have
the potential to produce sedation; these are mentioned
briefly at the conclusion of this section. The sedative-
hypnotic agents are broken into two broad classes: the
barbiturates and the nonbarbiturates. The nonbarbitu-
rates, and specifically the benzodiazepines, have largely
replaced barbiturates as hypnotic agents because of the
more favorable side effect profile and the lower risk for
the development of physical and psychological depen-
dence associated with these agents.5
Nonbarbiturate Sedative-Hypnotics
Benzodiazepines
The largest subfamily of medications that make up the
nonbarbiturate sedative-hypnotics is the benzodiazepines.
In the United States there are five benzodiazipnes with an
FDA indication for the treatment of insomnia, even though
other benzodiazepines work as well.5 The nonbarbiturate
sedative-hypnotics are listed in Table 12-3. The first five
listed are benzodiazepines. Benzodiazepines induce sleep
by decreasing the number of arousals between the differ-
ent stages of sleep and allow for more continuous total
sleep time.6 Clinicians select the most appropriate benzo-
diazepine based on the pharmacokinetic profiles of each
individual agent. For example, those agents with shorter
half-lives are eliminated from the body more quickly and
their duration of pharmacological effect is decreased.
Because these agents tend to work quickly and wear off
sooner, they generally are preferred for a patient who
has difficulty falling asleep initially. Those with lon-
ger half-lives remain in the body and produce longer-
lasting effects and would be ideal for patients who expe-
rience problems either staying asleep or waking up early.
Unfortunately, these long half-life agents also have the
potential to produce some unwanted daytime sedation
and performance impairment.5,7 The half-lives of the dif-
ferent benzodiazepines also are listed in Table 12-3. The
adverse effects associated with the benzodiazepine class
Dosage (mg/day) Half-life (hours)
1–2 12–15
15–30 8
7.5–15 39
15–30 10–15
0.125–0.25 2
10 2.6
10 1
7.5 5
262 SECTION I • Scientific Foundations
of medications include excessive drowsiness, impaired
psychomotor coordination, decreased concentration,
and cognitive deficits.5 In addition, some patients may
experience some rebound insomnia after discontinuation
of these medications. Although all benzodiazepines have
the potential to produce this phenomenon, it is more
common with triazolam because of its pharmacokinetic
profile.6
Zolpidem
The imidazolpyridine, zolpidem, is unrelated chemically
to the benzodiazepines; however, it does act on the same
receptor as the benzodiazepines and shares some of the
same pharmacological properties. Zolpidem binds to the
receptor in a slightly different fashion; this is a possible
explanation for why the drug does not possess anxiolytic
or myorelaxant (muscle relaxing) properties in addition
to its hypnotic effect.5 When compared with the ben-
zodiazepines and zopiclone, zolpidem appears to impair
acute and delayed memory to a greater degree.8 The
half-life of zolpidem is approximately 2.5 hours and can
produce a pharmacological effect that lasts 6 to 8 hours.
Common adverse effects associated with zolpidem when
administered at the standard dose include drowsiness,
dizziness, and diarrhea.5 However, when compared with
the benzodiazepines, zolpidem is less likely to have an
effect on next-day psychomotor performance.5
Zaleplon
Similar to zolpidem, zaleplon also selectively binds to the
same receptor as the benzodiazepines to exert its phar-
macological effect.5 Because of its rapid onset and short
duration, zaleplon is indicated to help patients who have
difficulty falling asleep, and no significant impairment of
psychomotor performance, arousal, memory, or cogni-
tive function occurs the next morning. The most com-
mon adverse effects associated with zaleplon are dizziness
and headache but they are not usually severe.6 Even in
the elderly population (age 65 and over), a study of 422
patients treated with 5-mg and 10-mg doses of zaleplon
demonstrated no difference in adverse events when com-
pared with placebo.7 The half-life is approximately 1 hour
and the duration of action ranges from 0.9 to 1.5 hours.5
Table 12-4
Barbiturates
Generic Name Brand Name Sedative Dose (mg/day)
Mephobarbital Mebaral
Phenobarbital Barbita
Aprobarbital Alurate
Pentobarbital Nembutal
Secobarbital Seconal
Zopiclone
Another nonbenzodiazepine hypnotic similar to zolpidem
is zopiclone; however, this agent is slightly less selec-
tive than zolpidem in binding to its receptor, where it
exerts the pharmacological effect.7 Although zopiclone
has the potential to produce residual sedation, this effect
was seen only at doses greater than 7.5 mg.9 When com-
pared with the benzodiazepines, zopiclone produced less
impairment of psychomotor and physical performance.10
One study revealed that it also may have some effect on
memory storage during sleep: patients treated with the
drug at bedtime were able to recall fewer words upon
awakening compared with those treated with placebo.11
Barbiturate Sedative-Hypnotics
The barbiturate class of medications is not used routinely
for its sedative-hypnotic effects because of the superiority
of the benzodiazepines and the newer agents like zolpi-
dem, zaleplon, and zopiclone. Barbiturates are associated
with a rapid development of tolerance, often after only 2
weeks of therapy. They also carry a high risk of physical
and psychological dependence, withdrawal syndromes,
fatalities by overdose, and significant drug interactions.5
Some of the more common oral barbiturates are listed in
Table 12-4.
Other Sedating Medications
As previously mentioned, other benzodiazepines are not
classified as sedative-hypnotics yet still have the poten-
tial to cause some drowsiness. These are the benzodiaz-
epines approved for the treatment of anxiety and include
alprazolam, chlordiazepoxide, clonazepam, clorazepate,
diazepam, halazepam, lorazepam, and oxazepam. Adverse
effects for these agents would be similar to those previ-
ously stated for the sedative-hypnotic benzodiazepines.
Many medications used for the treatment of depression
also can cause sedation. The most noteworthy agents
include amitriptyline, clomipramine, doxepin, trimipra-
mine, mirtazapine, and trazodone. Certain antihistamines
also can cause sedation because of their ability to cross the
blood-brain barrier where they can block histamine, one
Hypnotic Dose (mg/day)
32–200 –
30–120 100–320
120 40–160
40–120 100
- 100
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process 263

of the many neurochemicals that can affect sleep in the
hypothamalus region of the brain. These include diphen-
hydramine, clemastine, carbinoxamine, tripelennamine,
promethazine, and azatadine.5
Implications for the Clinician
Patients taking sedative-hypnotic medications do so at
night before going to bed and should wake up feeling
refreshed and energized. However, because of the phar-
macokinetic profiles of some agents and the pharmaco-
dynamic differences among patients, some patients may
experience daytime sedation or drowsiness. Clinicians
should check to see if the patient is currently taking any
sedative-hypnotic agents, which could affect perfor-
mance. In addition, some antidepressant medications
and over-the-counter cough and cold remedies have the
potential to produce drowsiness.
Corticosteroids
Steroid drugs are derivatives of naturally secreted adrenal
corticosteroids and have many uses in clinical practice.12
Natural mineralocorticoids are involved in maintaining
fluid and electrolyte balance and are not the subject of
this section. Glucocorticoids, represented by endoge-
nous cortisol and drugs such as prednisone (Table 12-5),
are used primarily for their anti-inflammatory effects.
Because they affect cellular protein synthesis, however,
glucocorticoids affect a wide range of organ systems. This
has implications for therapeutic use and adverse events.
Because altering protein production in cells takes time,
often a delay occurs in the full onset of action of these
drugs and a persistence of their effects after they have
been stopped. This persistence may last days, particularly
in the case of the longer-acting agents (see Table 12-5).
Glucocorticoids fundamentally affect nearly every
major organ system but their primary role is to regu-
late blood glucose. This is accomplished largely through
increasing the production of glucose in the liver, which
reduces peripheral glucose utilization and increases
breakdown of peripheral fat and protein. These processes
ensure a supply of glucose to vital organs (e.g., brain,
heart) in times of fasting or extreme physiological stress.
Notably, glucocorticoids also suppress inflammation
resulting from a wide variety of inciting events (e.g.,
mechanical or chemical injury, infection, radiation).
Higher doses are generally more effective than lower
doses but an upper limit exists to their anti-inflammatory
effects.12 Generally, doses greater than 100 mg/day of
prednisone or its equivalent (see Table 12-5) have little
further anti-inflammatory effect.
Glucocorticoid drugs may be used systemically (orally
or intravenously) or topically (ocular, inhaled, nasal
instillation, dermatological). Because of the inflamma-
tory pathophysiology of a number of disease states, the
therapeutic use of corticosteroids is broad and includes
osteoarthritis and rheumatoid arthritis, asthma, auto-
immune diseases such as lupus and psoriasis, hepatitis,
myocarditis, and cancer chemotherapy. This broad use
means that the clinician may encounter a wide spectrum
of patients who may be using a glucocorticoid drug.
The rehabilitation impact of topical steroid use is
minimal because adverse effects are minimized by the
local delivery of these agents to their desired site of action.
However, patients on inhaled steroids (e.g., beclometha-
sone [Beclovent, QVAR], triamcinolone [Azmacort], or
fluticasone [Flovent]) are using them to treat the pulmo-
nary inflammation of asthma or bronchitis. When these
conditions are poorly controlled, patients can quickly
become short of breath with minimal exertion, which could
impose obvious limitations on a rehabilitation regimen.
Use of inhaled steroid agents should therefore be noted
by the clinician and consideration given to a patient’s pul-
monary status when designing a rehabilitation regimen.
Unlike the disease-limiting concern of inhaled steroids,
the rehabilitation concern with patients on systemic steroids
is their long-term toxicities. The adverse effects that occur
with long-term steroid use are extensions of their physi-
ological actions. These include worsening of glycemic

Table 12-5
Equivalent Potencies and Doses of Representative Glucocorticoids
Drug (Generic Name) Anti-inflammatory Potency Duration of Action Equivalent Dose

Cortisol (hydrocortisone) 1 S 20 mg
Prednisone 4 I 5 mg
Prednisolone 4 I 5 mg
Triamcinolone 5 I 4 mg
methylprednisolone 5 I 4mg
Betamethasone 25 L ∼1 mg
dexamethasone 25 L ∼1 mg

S, short (<12 hours); I, intermediate (12–36 hours); L, long (36–48 hours).

264 SECTION I • Scientific Foundations
control in diabetic patients, increases in blood pressure,
which may be slight or notable, suppression of the immune
system and diminished work capacity because of loss of
both skeletal muscle and bone mass.
The long-term loss of bone and muscle mass is of con-
cern to rehabilitation medicine. A general lack of activ-
ity by the patient worsens the catabolic effects of these
drugs.12 Strength training and weight-bearing activi-
ties help to lessen these drug-induced losses. Clinicians
should be particularly cautious though when beginning
work with patients who may have sustained injuries partly
as a consequence of long-term steroid use. The differ-
ence between helpful and harmful strength training will
be smaller in these patients because of their reduced mus-
culoskeletal mass and increased susceptibility to further
injury with vigorous exercise.
Adverse Effects of Long-Term Steroid Use
● Worsening glycemic control in diabetics
● Increased blood pressure
● Immune system suppression
● Decreased work capacity
● Osteoporosis
● Decreased muscle mass
● Increased susceptibility to injury
● Skin breakdown
● Subcutaneous connective tissue breakdown
Use of topical thermotherapy, whether heat or cold,
also should be used with care because thinning of the
skin and breakdown of subcutaneous connective tissue
also may be present in these patients. Last, clinicians
can help ensure good long-term outcomes by making
sure that blood pressure is monitored in all patients on
glucocorticoids and that glycemic control is watched in
patients with diabetes.
Pain Management
Overview
Pain continues to be one of the most common and devas-
tating symptoms of many diseases and conditions. More
than 50 million people are partially or totally disabled
because of pain, and the annual cost of pain to society is
estimated at $79 billion.13 It has a significant effect on a
person’s quality of life and is a societal burden because of
health care costs, disability payments, and lost productiv-
ity.14 Pain is often undertreated, especially in elderly or sur-
gical patients or in those with cancer and HIV or AIDS.15
The management of pain is often difficult because it is
affected by various physical, psychological, and social fac-
tors. Barriers to effective pain management include those
associated with the patient (reluctance to report pain,
fear of addiction, and noncompliance with medications)
and the provider (lack of knowledge, underestimating
analgesic requirements of the patient, prejudice against
the use of analgesics, and fear of controlled substance
regulations).13,15,16 For a more comprehensive review of
pain, the reader is referred to Chapter 10.
Because pain is a complex phenomenon that involves
peripheral and central sensations, effective pain manage-
ment should target different mechanisms of action.17 For
this reason, many patients end up on a combination of
nonopioid and opioid analgesics, in addition to adjunc-
tive pain therapies. A review of adjunctive medications
is beyond the scope of this chapter, but the opioid and
nonopioid analgesics are discussed.
Opioid Analgesics
Opioid analgesics are natural, semisynthetic, or synthetic
agents used for the relief of moderate to severe pain.18
They commonly are used to treat cancer pain, various
chronic pain conditions, and pain after surgeries, traumas,
or myocardial infarctions. They are more effective in pain
of constant duration versus sharp intermittent pain.
The amount of opioid required to relieve the pain depends
upon the patient’s prior exposure, severity of pain, hepatic
and renal function, and route of administration.18
Mechanism of Action
The pharmacological activity of opioids depends on their
affinity for various opioid receptors located in the brain,
spinal cord, and peripheral nervous system.13 Opioids are
classified as either opioid agonists, partial agonists, or
agonist-antagonists, based on their activity at the opioid
receptors. An agonist stimulates opiate receptors, a partial
agonist stimulates some receptors but does not have any
antagonist qualities, and an agonist-antagonist stimulates
some receptors while it antagonizes others.19,20
The efficacy and side effect profile of different opioid
analgesics depend upon their activity at various opiate
receptors. The primary receptors responsible for an
analgesic response are the µ, κ, and δ receptors, each
of which has different subtypes.13,20,21 The µ receptor
is the most important in mediation of the analgesic
effects of opioids, but stimulation of this receptor also
can lead to habituating and withdrawal effects, respi-
ratory depression, constipation, miosis, sedation, and
euphoria.13,16,18,21 The κ receptor causes less respiratory
depression versus the µ receptor but is more likely to
cause hallucinogenic and dysphoric effects.13,16,18 The
δ receptor also can cause euphoria, hallucinations, and
dysphoria,18 whereas the σ receptor can cause dysphoria,
hallucinations, and confusion.16,20 The analgesic effect
from opiate receptor activation occurs as a result of a
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
decrease in the release of inflammatory neurotransmit-
ters from afferent neurons, a decrease in the activity of
neurons along their pathways, and an inhibition of neu-
ronal activity via gamma amino butyric acid (GABA).
Overall, patients often report that pain still exists while
taking opioid analgesics but the intensity and unpleas-
antness of the pain are decreased.13,19
Adverse Effects
Patients may experience a variety of adverse effects with
opioid analgesics. One of the most common adverse
effects is sedation, which affects 20% to 60% of patients.22
Sedation usually manifests itself as drowsiness, lethargy,
and an inability to concentrate, but tolerance to the seda-
tive effects usually develops with continued use. A con-
cerning adverse effect is respiratory depression, especially
in those patients who are seriously ill, have preexisting
pulmonary problems, or have overdosed the medication.
To avoid an increase in the risk of opiate central ner-
vous system (CNS) depression, opioid analgesics should
not be used in combination with alcohol or other CNS
depressants.
Gastrointestinal complications also may occur.
Constipation results from the antiperistaltic activity of the
opiates, and often one of the most debilitating adverse
effects leads to patient noncompliance. Unfortunately,
tolerance to the constipation does not develop. Nausea
and vomiting are other GI effects from the direct stimu-
lation of opioids on the chemoreceptor trigger zone and
the decrease in gastric motility.
Adverse Effect of Opioid Analgesics
● Sedation (drowsiness, lethargy)
● Respiratory depression
● Gastrointestinal complications
● Hypogonadism
● Myoclonus
● Pruritus (itching)
● Cognitive dysfunction
● Urinary retention
Other adverse effects may include hypogonadism
(decreased functional activity of the gonads that can result
in deficiencies with growth and sexual development),
myoclonus (muscle spasms or twitching), pruritus (itch-
ing), cognitive dysfunction, and urinary retention.19,22
In addition to these adverse effects, opioid analge-
sics also can lead to tolerance and physical dependence.
Tolerance is the need for more drug to achieve the
same effect, and it can happen if a drug is used for a pro-
longed period of time. Physical dependence is the onset of
withdrawal symptoms after the drug is removed abruptly.
265
Patients experiencing withdrawal may experience body
aches, diarrhea, insomnia, irritability, shivering, gastroin-
testinal upset, sweating, rhinorrhea, and tachycardia. For
opioids, signs and symptoms usually occur within 6 to 10
hours after the last dose of the medication, peak on day
2 or 3, and continue for up to 5 days after completion.
Fortunately, the risk of tolerance and dependence is very
low when opioids are used correctly for chronic pain.21
Individual Agents
Table 12-6 lists available opioid analgesic agents, starting
dosages, equivalent doses to assist with changing agents,
and the onset, peak, and duration of activity.13,18,20
Strong Opioid Agonists. These agents are most
commonly used for acute or chronic severe pain.
These drugs have strong pharmacodynamic effects on
µ and κ receptors. Examples of agents in this group
include morphine, hydromorphone (Dilaudid), fen-
tanyl (Duragesic), meperidine (Demerol), methadone
(Dolophine), and levorphanol (Levo-Dromoran).
Despite the development of newer agents, morphine
remains the prototypical opioid analgesic. It is often the
drug of first choice because of its efficacy and afford-
ability and can be given via multiple routes of adminis-
tration. Hydromorphone has comparable efficacy with
morphine, with less potential to cause nausea, vomiting,
constipation, or sedation.23 Levorphanol has a longer
duration of action when compared with morphine, but
with some increased sedation.23 Meperidine is less potent
than morphine and does have the ability to accumulate
in patients with decreased renal function.13,20 This can
increase the risk of seizures with this particular agent.
Methadone, most well known for its use in narcotic
detoxification, is now being used more for analgesia.
It has a long duration of action, which allows for less
frequent dosing. Methadone is equivalent to morphine;
however, it does accumulate upon repeated use of the
product, requiring dosage adjustment.
Mild Opioid Agonists. These agents are used for
mild to moderate pain. They have less affinity for the
opioid receptors versus other agents previously discussed.
Examples in this category include codeine and its deriva-
tives hydrocodone (Vicodin, Lorcet, Lortab) and oxy-
codone (Percocet, Oxycontin), propoxyphene (Darvon,
Darvocet), and tramadol (Ultram). Tramadol demon-
strates weak opioid receptor activity, and it also inhibits
norepinephrine and serotonin reuptake. The advantages
of tramadol are less abuse potential and respiratory
depression, but it can cause such adverse effects as diz-
ziness, sedation, constipation, and an increased risk of
seizures.20,23
Mixed Agonist/Antagonists. These agents have
varying effects at different opioid receptors. Their advan-
tages are less risk of respiratory depression and addiction.
They may cause more psychotomimetic effects, including
266 SECTION I • Scientific Foundations

Table 12-6
Opioid Analgesics
Onset of Peak of Duration
Equianalgesic Analgesia Analgesia Analgesia
Drug Product Usual Starting Dosage Dose (mg) (minutes) (hours) of (hours)

AGONISTS
Morphine PO: 10–30 mg IR q3–4h 30–60 mg PO 15–30 0.5–1 4–5 (IR)
PO: 15–30 mg SR q12h 10 mg IM 3–4 12 (SR)
IM: 5–10 mg q3–4h 30 mg PR (SR form)
IV: 1–2.5 mg q5 min
PR: 10–20 mg q3–4h
Hydromorphone PO: 2–4 mg q3–4h 7.5 mg PO 15–30 0.5–1 4–5
(Dilaudid) IM: 0.5–1 mg q3–4h 1.5 mg IM
IV: 0.1–0.5 mg q5 min
PR: 2–4 mg q3–4h
Oxymorphone PR: 5 mg q3–4h 5–10 mg PR 5–15 0.5–1 3–6
(Numorphan) IM: 1–1.5 mg q3–4h 1–1.5 mg IM
Levorphanol PO: 2–4 mg q6–8h 4 mg PO 30–90 0.5–1 6–8
(LevoDromoran) IM/IV: 2 mg q6–8h 2 mg IM
Hydrocodone 5–10 mg q3–4h 20 mg PO 15–30 1 4–5
(Vicodin, Lorcet,
Lortab, etc.)
Codeine PO: 15–60 mg q3–4h 65 mg PO 15–30 0.5–1 4–5
IM/IV: 15–60 mg q3–4h
Oxycodone PO: 5–10 mg IR q3–4h 20–30 mg PO 15–30 (IR) 0.5–1 (IR) 4–5 (IR)
(Oxycontin, PO: 10–20 mg SR q12h 3–4 (SR) 12 (SR)
Percocet,
Percodan, Tylox)
Merperidine PO: 50–150 mg q3–4h 200–300 mg PO 10–45 0.5–1 3–4
(Demerol) IM: 75–100 mg q3–4h 75–100 mg IM
IV: 5–10 mg q5 min
Fentanyl IM: 0.05–0.1 mg q1–2h 0.15 mg IM 7–8 1–2
(Duragesic, Transdermal: 25 mcg/h 25 mcg/h patch
Sublimaze)
Methadone PO: 10–20 mg q6–8h 2.5–20 mg PO 30–60 0.5–1 4–5
(Dolophine) 2.5–10 mg IM
Propoxyphene PO: 65–100 mg q3–4h 65 mg PO 30–60 2–2.5 4–6
(Darvon, Darvocet)
Tramadol (Ultram) PO: 50–100 mg q4–6h 50–100 mg PO <60 2–3 6
AGONIST-
ANTAGONISTS
Pentazocine (Talwin) PO: 50–100 mg q3–4h 50–200 mg PO 15–20 0.25–1 3–4
IM: 30 mg q3–4h 30–60 mg IM
Butorphanol (Stadol) IM: 1–4 mg q3–4h 2–3 mg IM <10 0.5–1 3–4
IV: 0.5–2 mg q3–4h 1 mg Intranasal
Intranasal: 1 mg q3–4h
Nalbuphine (Nubain) IV/IM: 10 mg q3–6h 10–20 mg IV/IM <15 1 4–6
Buprenorphine IM/IV: 0.3 mg q6h 0.3 mg IM 15 1 4–6
(Buprenex, Transtec) Transdermal: 35 mcg/h
SL: 0.15–0.8 mg q4–6h
Dezocine (Dalgan) IV: 2.5–10 mg q2–4h 10 mg IV/IM 15–30 0.17–1.5 3–5
IM: 10 mg q3–6h

q, every; PO, by mouth; IM, intramuscular; IV, intravenous; PR, per rectum; IR, immediate release; SR, sustained release.
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process 267

hallucinations and vivid dreams, and they may cause a
ceiling effect of analgesia, which could increase pain lev-
els over time.13 Examples of mixed agents include butor-
phanol (Stadol), nalbuphine (Nubain), and pentazocine
(Talwin).
Antagonists. Naloxone (Narcan) and naltrexone
(Revia) are narcotic antagonists that block all opioid
receptors and are used to treat opioid overdose or addic-
tion.20 Naltrexone is a longer-acting agent with a slower
onset. Both can precipitate withdrawal if overly used.
Nonopioid Analgesics
Nonopioid analgesics, which include salicylates, acetamino-
phen, and nonsteroidal anti-inflammatory drugs (NSAIDs)
are some of the most commonly prescribed medications
available.24 They have analgesic, antipyretic, and anti-inflam-
matory properties. At lower dosages, nonopioid analgesics
provide more pain relief, whereas at higher doses, they
achieve a stronger anti-inflammatory response.24,25 Unlike
opioid analgesics, these agents do not produce physi-
cal dependence of tolerance, nor are they associated with
addiction. Nonopioids often are used for mild or moderate
pain conditions and in combination with opioids for more
severe pain. Table 12-7 lists individual agents, common
doses, analgesia onset and duration, and unique character-
istics, where applicable.13
Mechanism of Action
Aspirin inhibits the synthesis and release of prostaglan-
dins, a major cause of inflammation and pain. Aspirin
also inhibits the formation of platelet aggregation by

Table 12-7
Nonopioid Analgesics
Maximum Onset of Duration of
Daily Analgesia Analgesia
Drug Product Usual Dosage Dose (hours) (hours) Comments

Acetaminophen 325–1000 mg 4.0 gm 0.5–1 3–6 Higher dosages required for

(Tylenol) q4–6h anti-inflammatory effect
Salicylates
Aspirin 325–650 mg 4.8 gm 0.5 3–6 Antipyretic and anticoagulant
q4–6h effects as well
Choline 1000–1500 mg 4.8 gm – 4 Better tolerated than aspirin with
magnesium q12h minimal GI effects and no effect
salicylate on platelet aggregation
(Trilisate)
Salsalate 500–1000 mg 4.8 gm – – Better tolerated than aspirin with
(Disalcid) q8–12h minimal GI effects and no effect on
platelet aggregation
Diflunisal 250–500 mg 1.5gm 1 8–12 ↑ risk for renal impairment, but no
(Dolobid) q8–12h effect on platelet aggregation
Sodium 325–650 mg 4.8gm – 4 Better tolerated than aspirin with
salicylate q6–8h minimal GI effects and no effect on
(Uracel) platelet aggregation
Acetic Acids
Diclofenac 50 mg q8–12h 150 mg 0.5 6–8 More potent than naproxen;
(Voltaren) intermediate risk for GI bleeds
Etodolac 200–400 mg 1.2 g 0.5–1 6–8 Less risk for GI upset and ulcers;
(Lodine) q6–12h uricosuric effect
Indomethacin 25–50 mg 200 mg – – 20% to 25% of patients experience ↑
(Indocin) q8–12h headaches, dizziness, and
GI upset; ↑ risk for renal
function impairment
Ketorolac 10 mg q4–6h 40 mg 0.5–1 4–6 ↑ risk of bleeding, esp. with long-term
(Toradol) (oral) use (avoid using for >5 days;
15–30 mg q6h avoid use pre-operatively and
(parenteral) intraoperatively if bleeding
control necessary

(Continued)
268 SECTION I • Scientific Foundations

Table 12-7—Cont’d
Nonopioid Analgesics
Maximum Onset of Duration of
Daily Analgesia Analgesia
Drug Product Usual Dosage Dose (hours) (hours) Comments

Nabumetone 500–1000 mg 2 gm – – Less GI ulceration and bleeding

(Relafen) once or twice
daily
Sulindac 150–200 mg 400 mg – – Less likely to cause renal toxicity, but
(Clinoril) twice daily > GI side effects
Tolmetin 200–600 mg 1.8gm – – Increased risk of anaphylactic reactions;
(Tolectin) three times short half-life
daily
Propionic Acids
Fenoprofen 300–600 mg 3.2 gm 0.25–0.5 4–6 As effective as naproxen; ↑ chance for
(Nalfon) q6–8h rashes and some CNS effects;
best on empty stomach
Flurbiprofen 50–100 mg 300 mg – – Similar to ketoprofen
(Ansaid) q8–12h
Ibuprofen 200–800 mg 3.2 gm 0.5 4–6 Fewer GI side effects, but weaker
(Motrin) q6–8h anti-inflammatory activity
Ketoprofen 25–50 mg 300 mg 1 4–8 Intermediate risk for GI bleeds;
(Orudis) q6–8h efficacy = ibuprofen; may cause fluid
retention and ↑ serum creatinine
Naproxen 250–500 mg 1 gm 1 up to 12 Greater anti-inflammatory effect over
(Naprosyn) q12h ibuprofen, but increased side effects
Naproxen 275–550 mg 1.375 gm 0.5–1 up to 12 Greater anti-inflammatory effect over
sodium q12h ibuprofen, but increased side effects
(Anaprox)
Oxaprozin 600–1200 mg 1.8 gm – – Long half-life that accumulates with
(Daypro) chronic dosing (may reach
40–60 hours)
Fenamates
Meclofenamate 50 mg q4–6h 400 mg – 4–6 Less effect on platelet aggregation
(Meclomen)
Mefenamic acid 250 mg q6h 1 gm – 6 Less effective agent; ↑ risk of diarrhea
(Ponstel) and hemolytic anemia
Pyrazoles
Phenylbutazone 100–200 mg 400 mg – – Long-term use limited by ↑ side effects
(Butazolidin) q6–8h
Oxicams
Piroxicam 20 mg daily 20 mg – – ↑ GI side effects
(Feldene)
Meloxicam 7.5–15 mg daily 15 mg – –
(Mobic)
COX-2
Inhibitors
Celecoxib 100–200 mg 400 mg 1 12–24 Cross-sensitivity with sulfa or aspirin
(Celebrex) q12h allergies
Valdecoxib 10 mg daily 10 mg 1 up to 24
(Bextra)

q, every; GI, gastrointestinal

 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
inhibiting prostacyclin, and this is responsible for the car-
dioprotective effect with an increased risk of bleeding.20
The nonacetylated salicylates have the same analgesic
effects as aspirin, without affecting platelet aggregation.
Like aspirin, NSAIDs inhibit cyclooxygenase, the
enzyme that converts arachidonic acid to prostaglandins.
Besides causing inflammation and pain, prostaglandins
are important in the protection of gastric mucosa, in the
support of renal function, and in hemostasis through
platelet activation. Cyclooxygenase exists in two forms,
COX-1 and COX-2. COX-1 produces prostaglandins that
mediate gastroprotection, renal perfusion, and platelet
aggregation, whereas COX-2 produces prostaglandins that
lead to an anti-inflammatory response.25 Certain NSAIDs
are more selective for COX-2 and have some improved
gastrointestinal tolerance over other agents.17,25 Some
NSAIDs, specifically indomethacin (Indocin) and flur-
biprofen (Ansaid), also can inhibit leukocyte migrations,
which contributes to the anti-inflammatory effect.20,25
Selection of Agents
No one NSAID has been shown to provide superior anal-
gesia over another.13,16,24–27 Patient response varies con-
siderably between agents. If one NSAID fails, another
one can be tried and may be efficacious. The choice of
which agent to use often depends upon cost, safety, and
efficacy.13,16,24–27
Adverse Effects
NSAIDs can cause serious gastrointestinal (GI) and renal
complications, inhibit platelet aggregation, and produce
central nervous system (CNS) effects.24 The complication
rate tends to increase if higher dosages are used for longer
periods of time.16 The most common GI side effect is dys-
pepsia, but NSAIDs also can produce ulcers. Perforations,
obstructions, and major GI bleeds have occurred in
approximately 4% of patients who have taken NSAIDs
for more than 1 year.28 Approximately 5% of patients
may develop renal toxicity secondary to an NSAID as a
result of decreased renal prostaglandins, and decreased
renal blood flow, which can lead to fluid retention and
acute renal failure. Common CNS effects include cogni-
tive dysfunction, dizziness, and drowsiness, especially in
the elderly.16,24 COX-2 agents cause fewer problems with
the intestinal mucosa, but other effects are comparable,
including the effect on renal prostaglandins and fluid
retention.16 Recent studies have demonstrated an increase
in cardiovascular complications with the use of COX-2
agents, especially when used in patients with a history of
or who are at risk for cardiovascular and/or cerebrovascu-
lar events.29,30 At the present time, as with any medication,
practitioners should weigh the risks versus the benefits for
use, and when COX-2 agents are used, the lowest effective
dose should be prescribed for a very short period of time.
269
Adverse Effects of Nonsteroidal
Anti-inflammatory Drugs
● Gastrointestinal upset (dyspepsia, ulcers)
● Renal toxicity and failure
● Inhibit platelet aggregation
● Cognitive dysfunction
● Dizziness
● Drowsiness
Implications for the Clinician
Clinicians work with patients who are taking various
medications for pain control. If the analgesic regimen is
effective, the patient has an increased ability to complete
a thorough treatment session, but this depends upon the
timing of the therapy session and the onset and dura-
tion of activity of the patient’s pain medications. The
disadvantages of the analgesics are the possible side
effects, especially sedation, respiratory depression, con-
stipation, and dyspepsia/nausea. Clinicians can help
identify problems that patients are experiencing early
on and provide education to patients and caregivers. In
addition, they can alert other health care providers to
enhance optimal therapy regimens in an appropriate and
efficient manner.
Medications for Rheumatoid Arthritis
Overview
Rheumatoid arthritis is a chronic, systemic, immuno-
logical disorder that affects primarily synovial fluid and
articular joint tissue.31 The exact etiology of this disease
is unknown. Rheumatoid arthritis affects approximately
1% of the population.31 Characteristics of the disease
include symmetrical joint swelling, stiffness, and pain.
Extraarticular manifestations, which include rheuma-
toid nodules, vasculitis, ocular inflammation, neurologic
dysfunction, and cardiopulmonary disease, also may be
present. Drug therapy is the focus of the disease treat-
ment and is aimed at treatment of symptoms, mainte-
nance of joint function, and prevention of further joint
destruction and deformity. In addition, rest, rehabilita-
tion, and in some severe cases, surgery is recommended.
Advances in the treatment of rheumatoid arthritis
include new medications and evidence that earlier and
more aggressive treatment is beneficial.32 The manage-
ment of rheumatoid arthritis emphasizes the use of early
aggressive therapy, including anti-inflammatory agents,
corticosteroids, and disease-modifying antirheumatic
drugs (DMARDs).31
270 SECTION I • Scientific Foundations

Nonsteroidal Anti-inflammatory Drugs
Initial therapy for rheumatoid arthritis includes NSAIDs,
salicylates, or cyclooxygenase (COX-2) inhibitors. These
medications reduce inflammation, pain, and swelling but
do not reverse or prevent joint damage and destruction.31
Thus they should not be the only agents used for treat-
ment.31 For discussion of NSAIDs, including mechanism
of action and adverse effects, see the previous discussion.
For information about specific agents, see Table12-7.
Corticosteroids
Corticosteroids are effective in controlling the disease but
can be associated with serious adverse effects, especially with
long-term use. Their role in rheumatoid arthritis treatment
is primarily during periods of flare-up and for symptom relief
as bridging therapy when initiating DMARDs or changing
regimens.33 As disease progresses, many patients end up on
low-dose, chronic corticosteroids.31 Another role for corti-
costeroid use is direct intraarticular injection. This is effective
when a flare occurs in a single joint as it decreases the need
for systemic corticosteroids. These should be administered
no more frequently than every 3 months because of the risk
of increased joint damage.31 Aseptic technique is important
for administration to prevent infection. Intraarticular injec-
tions may provide symptom relief and improve a patient’s
ability to participate in rehabilitation programs.31 For addi-
tional discussion of corticosteroids including mechanism
of action and adverse effects, see previous discussion. For
information about specific agents, see Table 12-5.31
Disease-Modifying Antirheumatic Drugs
DMARDs are the mainstay of rheumatoid arthritis
therapy because of their ability to prevent further joint
damage and destruction.31 These agents act slowly and
take weeks to months before the benefits are seen. They
can be used alone but often are used in combination with
each other.32 Combination therapy may be synergistic
without increasing adverse effects.34 This is particularly
important because use of these medications is often lim-
ited by toxicity. With the use of DMARDs, the approach
is often to use them early and aggressively because of the
effect on joint inflammation and destruction.34 Synthetic
and biological DMARDs exist. The most frequently used
synthetic (traditional) DMARDs are methotrexate, sul-
fasalazine, and hydroxychloroquine.31 Dosing for the
various agents can be found in Table 12-8.13,31
Synthetic Disease-Modifying Antirheumatic Drugs
Methotrexate. Methotrexate is the DMARD of
choice and the “gold standard” in treatment of rheuma-
toid arthritis. This is due to its efficacy, demonstrated in
numerous clinical trials, and affordability.31 Methotrexate
is a folic acid antagonist, which suppresses leukocytes and
decreases inflammation.35
The most common adverse effects are gastrointestinal
upset, mucositis, and myelosuppression.35 These can be
reduced by the addition of daily folic acid supplementa-
tion.31 Additional adverse effects include liver dysfunc-
tion, pulmonary changes, and alopecia.35 Methotrexate is
teratogenic and is contraindicated during pregnancy.35
Hydroxychloroquine. Hydroxychloroquine is less
effective than some other DMARDs.31 Therefore it
often is used early in therapy for more mild disease or in
combination with other DMARDs.31 Although the med-
ication does have anti-inflammatory activity, the exact
mechanism of action is unknown.35
One advantage of hydroxychloroquine is the lack of
hematological effects seen with most other DMARDs.

Table 12-8
Rheumatoid Arthritis Medications
Generic Name Brand Name Route(s) of Administration Dosage

Methotrexate Rheumatrex Oral 7.5–20 mg once weekly

Injectable 7.5–20 mg once weekly
Auranofin (gold) Ridaura Oral 3 mg twice daily
Gold sodium thiomalate Aurolate Injectable 25–50 mg every 2–4 weeks
Azathioprine Imuran Oral 50–150 mg daily
Sulfasalazine Azulfidine Oral 1000 mg twice or three times daily
Hydroxychloroquine Plaquenil Oral 200 mg twice daily
Leflunomide Arava Oral 100 mg/day for 3 days then 20mg/day
Etanercept Enbrel Subcutaneous 50 mg once weekly or 25 mg
twice weekly
Infliximab Remicade Intravenous 3–10 mg weekly at weeks 0,4,6;
then every 4–8 weeks
Adalimumab Humira Subcutaneous 40 mg every other week
Anakinra Kineret Subcutaneous 100 mg daily
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
The potential for ocular toxicity exists, which can lead
to visual impairment, but overall, the medication is
well tolerated and requires less monitoring than other
DMARDs.36
Sulfasalazine. Sulfasalazine frequently is used early
in therapy and for milder disease.31 It often is used in
combination with methotrexate and/or hydroxychlo-
roquine.32,33,37 Sulfasalazine is a pro-drug cleaved to
5-aminosalicylic acid (5-ASA) in the colon. The exact
mechanism of action is unknown.13
The use of this agent is limited by the adverse effects
including gastrointestinal upset (e.g., nausea, vomit-
ing, diarrhea, and anorexia), rash, photosensitivity, and
myelosuppression.31,36 This medication should not be
used in patients with an allergy to sulfa medications.31,36
Gold. Gold compounds are not used as routinely
because of the adverse effects.31,35 Gold, alone or in com-
bination with other DMARDS, is used in patients who
do not respond to other treatment regimens. Gold is
available in oral and injectable dosage forms. The oral
form is preferred because it is less toxic but unfortunately
less efficacious.35 The mechanism of action is unclear.
Gold compounds do affect lymphocyte, monocyte, and
neutrophil activity.35
The most common adverse effects are dermatitis (rash
and itching), gastrointestinal upset (diarrhea and indiges-
tion), and mucositis/stomatitis.13 The major concerns
are the adverse hematological and renal effects seen with
gold use.13 The most serious concerns are nephrotic syn-
drome and aplastic anemia.36
Azathioprine. This medication usually is reserved
for more refractory cases of rheumatoid arthritis.38 The
exact mechanism of action is unknown. The medication
does suppress T-cell function and therefore inhibits the
immune process.35
The most common adverse effects include gastro-
intestinal upset (nausea and vomiting) and rash.36
Myelosuppression and its complications are potential
effects of azathioprine use.31 The potential also exists for
a hypersensitivity reaction.38 These adverse effects often
limit the use of azathioprine.
Adverse Effects of Synthetic Disease-Modifying
Antirheumatic Drugs
● Gastrointestinal upset
● Myelosuppression
● Liver dysfunction
● Visual impairment
● Photosensitivity
● Dermatitis
● Alopecia
● Kidney dysfunction
271
Leflunomide. Leflunomide is the newest synthetic
DMARD.33 The medication works by inhibition of
pyrimidine synthesis. This results in an inhibition of lym-
phocyte proliferation and a reduction in inflammation.13
The most common adverse effects are gastrointestinal
upset and alopecia.13 The medication should not be used
in patients with preexisting liver disease because it can
cause liver toxicity.31 Leflunomide is teratogenic (leads
to deformities in developing embryos) and therefore
contraception is recommended for all male and female
patients. Because of its long half-life the drug remains
in the system for many months. Cholestyramine can be
used to clear the medication more rapidly if pregnancy is
being considered.13
Biological Disease-Modifying Antirheumatic Drugs
The newest DMARDs are biological agents and as a
group have advantages over traditional agents such as
more predictable outcomes and a quicker onset of activ-
ity.34,39 The biological DMARDs specifically target and
block interleukin-1 (IL-1) or tumor necrosis factor
(TNF). TNF and IL-1 are cytokines that play a role in
the inflammatory process of rheumatoid arthritis.39
Etanercept. Entanercept is indicated for use alone
or in combination with methotrexate.40 Etanercept is a
soluble tumor necrosis factor (TNF) receptor antagonist.
The medication works by binding to circulating TNF,
which makes it inactive and prevents it from binding to
cell surface receptors, which prevents the inflammatory
response.39
The most common adverse effect is a skin reaction at
the site of injection. TNF has a role in helping to fight
infection. Therefore TNF antagonists may interfere with
the ability to fight infection. Etanercept should not be
used in patients with preexisting infection or in those
at high risk for infection.31 It should be discontinued in
patients who develop serious infection while using etan-
ercept.40,41 Other adverse effects include the risk of rare
but serious central nervous system demyelinating disor-
ders and malignancies.40
Infliximab. Infliximab is indicated for use only when
used in combination with methotrexate. This medica-
tion is an intravenous medication, which means that
it cannot be self-administered like the other biological
DMARDs. Infliximab is an anti-TNF antibody, which
contains human and mouse portions, that interacts with
TNF receptors on inflammatory cells. It binds to soluble
and membrane-bound TNF.39 An infusion-related reac-
tion may result in fever, chills, pruritus, and rash.31
This medication may increase the risk of infection,
including sepsis, tuberculosis, and fatal infections. The
medication carries a warning recommending that patients
be evaluated for latent tuberculosis before initiation of
infliximab therapy.42 Like etanercept, concerns exist
regarding demyelinating conditions and malignancies.42
272 SECTION I • Scientific Foundations
Adverse Effects of Biological Disease-Modifying
Antirheumatic Drugs
● Injection site reactions
● Increased chance of infection
● CNS demyelinating disorders
● Malignancy
Adalimumab. Adalimumab is the most recent TNF
antagonist to be marketed. It is indicated for use alone
or in combination with other DMARDs in patients who
have had a poor response to one or more DMARD regi-
mens.43 Adalimumab is a monoclonal antibody that binds
to TNF and thus affects the inflammatory process.44
The adverse effects of adalimumab are similar to
those of the other available TNF antagonists. Injection
site reactions were the most common adverse effect. An
increased risk exists for infection while taking adalim-
umab. The medication should be discontinued if seri-
ous infection develops. The medication carries a warning
suggesting patients be evaluated for latent tuberculosis
infection with a tuberculin skin test before initiation of
therapy. In addition, concern exists regarding rare demy-
elinating disorders and malignancies.43
Anakinra. Anakinra is the only available agent that
targets interleukin-1 (IL-1). It is indicated for patients
who have failed one or more DMARDs. It can be used
alone or in combination with DMARDs other than TNF
antagonists. Studies of the use of anakinra with etaner-
cept demonstrated an increase in the incidence of serious
infection and no increase in clinical benefit.45
Anakinra inhibits the activity of IL-1, a proinflamma-
tory cytokine.44 The most frequent adverse effect is a mild
skin reaction at the site of injection.44 A risk of neutro-
penia exists while taking anakinra, for which monitoring
is recommended.45 As with other biological DMARDs,
concern exists regarding the risk of serious infection and
malignancy.41,45
Other Disease-Modifying Antirheumatic Drugs
Other DMARDs are indicated in rheumatoid arthritis
treatment. These include d-penicillamine, cyclosporine,
and minocycline. These medications typically are reserved
for refractory patients because of significant toxicities
and decreased efficacy compared with other available
DMARDs and a discussion is beyond the scope of this
chapter.31,33
Implications for the Clinician
The impact of these medications in rheumatoid arthritis is
critical to the rehabilitation process. The medications may
allow for symptom relief, improvement in rehabilitation
progress, and prevention of further joint destruction.21
The efficacy of the medications may allow for more
extensive and intensive rehabilitation.21
The influence of the medications on rehabilitation
depends upon the medications used. The therapeutic
regimen, timing of therapy initiation, and adverse effects
of these agents should be considered in development of a
rehabilitation program. The onset of activity of the vari-
ous medications used is variable and should be consid-
ered in initiation of rehabilitation and when goals and
expectations for progress are set.
Finally, the clinician may identify patients in need of
medication adjustment whether because of efficacy con-
cerns, adverse effects, or inadequate control of pain/
inflammation.
Medications for Osteoporosis
Overview
Osteoporosis also is known as the “silent disease” because
bone loss often occurs without any symptoms. The disease
is characterized by low bone mass and structural deterio-
ration of bone tissue, which cause bones to become frag-
ile and more likely to fracture.46 Fracture can affect any
bones in the body; special concerns are fractures of the
hip, spine, and wrist.
To maintain bone integrity, bones continuously
undergo remodeling, a coupled process that involves
resorption (breakdown) and formation (buildup) of the
bone. Osteoclasts are cells responsible for bone resorp-
tion; osteoblasts are cells responsible for bone forma-
tion. Bone loss occurs with an imbalance between bone
removal and replacement, which causes less bone to be
replaced than removed.47 Although no known cure exists
for osteoporosis, several medications are available for
prevention and/or treatment of osteoporosis to reduce
the risk of fractures (Table 12-9).
Drug Therapies for Osteoporosis
Antiresorptive agents are medications that affect the
osteoclastic bone resorption, whereas anabolic agents
are aimed at osteoblastic bone formation. Selection of
drug therapy for osteoporosis encompasses the long-
term effects on bone, safety concerns, and the potentially
beneficial effects on other tissues. Because compliance
with drug therapies often is challenging in patients
with asymptomatic diseases, the once-weekly dosing of
bisphosphonates (alendronate or risedronate) is cur-
rently the preferred drug regimen for prevention and
treatment of osteoporosis. These have demonstrated effi-
cacy in reducing fractures of the spine and the hip. Other
therapies for osteoporosis are reserved for patients who
cannot tolerate bisphosphonates, and patients at high
risk of fractures may warrant treatment with an anabolic
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process 273

Table 12-9
Agents with FDA-Approved Labeling for Use in Prevention or Treatment of Osteoporosis
Generic Name
Antiresorptive Agents
Alendronate sodium
Alendronate sodium +
cholecalciferol
Risedronate sodium
Ibandronate sodium
Raloxifene hydrochloride
Calcitonin
Estrogen
Anabolic Agent
Teriparatide
Brand Name Prevention Treatment Adverse Effects
Fosamax 5 mg PO daily 10 mg PO daily
Nausea, vomiting, abdominal
35 mg PO weekly 70 mg PO weekly
pain, esophageal ulceration,
Fosamax – 70 mg + 2,800 int.
bone pain
plus D units PO weekly
Actonel 5 mg PO daily 5 mg PO daily
35 mg PO weekly 35 mg PO weekly
Boniva 2.5 mg PO daily* 2.5 mg PO daily
150 mg PO 150 mg PO monthly
monthly* 3 mg IV every 3 months
Evista 60 mg PO daily 60 mg PO daily Hot flashes, headache, GI
disturbances, joint or muscle
pain, leg cramps, weight gain,
edema, flulike symptoms
Miacalcin – 200 int. units (1 spray) Intranasal: nasal dryness,
intranasally daily soreness, irritation, nosebleed
100 int. units SC/IM SC/IM: flushing, nausea,
every other day rash, allergic reaction
Various Equivalent to – Nausea, vomiting, headache,
forms 0.3–0.625 mg abdominal pain, edema,
of oral conjugated breast tenderness
estrogen per day
Forteo – 20 mcg SC daily Joint pain, dizziness, nausea,
weaknessd, increased serum
calcium levels

– = not indicated; PO, by mouth; Int. units, international units; SC, subcutaneous; GI, gastrointestinal; IM, intramuscular.
*Safety and efficacy of ibandronate 150 mg/month in postmenopausal women without osteoporosis are currently being studied; data are not
yet available.

agent. Adequate calcium consumption (at least 1200 mg
of elemental calcium per day) and vitamin D (400 to 800
international units per day) is essential to maximize the
effect of all drug therapies for osteoporosis.47
Antiresorptive Agents
Bisphosphonates
Bisphosphonates are the most common class of medica-
tions used for prevention and treatment of osteoporosis.
The three FDA-approved bisphosphonates are alendro-
nate (Fosamax), risedronate (Actonel), and ibandro-
nate (Boniva). Bisphosphonate is the structural analog
of pyrophosphate (the normal component of the bone).
It exerts its effects by self-incorporation into the bone
and later becomes a permanent part of the bone struc-
ture. The bisphosphonates inhibit bone resorption by
decreasing the osteoclast activity and inducing apoptosis
(cell death). The results are decreased bone remodel-
ing, indirectly increased bone mass, and reduced risk of
fractures.48
Adverse effects commonly associated with the bisphos-
phonates are limited to GI problems such as nausea,
vomiting, and abdominal pain. The most serious adverse
effect is esophageal ulceration.48 In addition, osteone-
crosis of the jaw has been reported in patients taking
bisphosphonates.48a Symptoms included nonhealing
extraction socket or an exposed jawbone. Dental exams
and preventive dentistry should be performed before
placing patients with risk factors for osteonecrosis such
as cancer, concomitant chemotherapy, radiotherapy or
corticosteroids, anemia, infection, or preexisting dental
disease. Alendronate has demonstrated sustained thera-
peutic effects and long-term safety over 10 years in post-
menopausal women.49
Bisphosphonates are poorly absorbed (0.7% or less)
when administered orally. In the presence of food,
ingested 1 hour before or up to 2 hours after, the bio-
availability is further reduced to a negligible amount.48
To facilitate the delivery of the medication to the stom-
ach and reduce the potential for esophageal irritation,
patients taking bisphosphonates must be counseled to
274 SECTION I • Scientific Foundations
follow strict administration guidelines. The medication
must be taken upon rising from sleep, on an empty stom-
ach, with full glass of plain water, and patients need to
remain upright for at least 30 minutes after administra-
tion. Furthermore, they need to wait at least 30 minutes
before eating, drinking, or taking other medications.
Patients taking ibandronate should remain upright for
at least 60 minutes and wait at least 60 minutes before
eating.
Estrogen
Menopause is accompanied by accelerated bone loss, and
the central role of estrogen deficiency in postmenopausal
osteoporosis is well established. Postmenopausal women
taking estrogen receive either estrogen alone (estrogen
replacement therapy [ERT]) or in combination with
progesterone (hormone replacement therapy [HRT]).
The progesterone component of the HRT is necessary
for women with an intact uterus to prevent endometrial
cancer. ERT and HRT are the most effective therapies to
reduce the vasomotor symptoms associated with meno-
pause. Various formulations such as oral and transdermal
products are available.
Estrogen decreases bone remodeling and indirectly
increases bone mass by inhibition of bone resorption and
subsequent reduction of the risk of fractures.48
Common adverse effects associated with estrogen
include headache, abdominal pain, nausea, vomiting,
edema, and breast tenderness.48 The Women’s Health
Initiative (WHI) study suggested that the risks of using
HRT in postmenopausal women exceeded its benefits
because of the small increased risks of heart attacks,
stroke, breast cancer, pulmonary emboli (PE), and deep
vein thrombosis (DVT) detected over 5 years of treat-
ment.50 The Women’s Health Initiative Memory Study,
a subset study of the WHI, reported an increased risk
of development of probable dementia without significant
effects on the global cognitive function in postmeno-
pausal women at age 65 or older during 4 to 5.2 years of
treatment with HRT or ERT compared with placebo.51,52
Thus ERT or HRT is recommended only for use at the
lowest effective dose for the shortest duration of time if
hormonal replacement therapy is needed.
Selective Estrogen Receptor Modulator
The selective estrogen receptor modulator (SERM) is a
nonhormonal medication that acts as an estrogen agonist
in bone to suppress bone remodeling without unfavor-
able stimulation of the estrogen receptors located on the
breast tissue or the uterus.48 Raloxifene (Evista) is the
only SERM indicated for prevention and treatment of
postmenopausal osteoporosis. Raloxifene decreases bone
resorption, which increases bone mass and reduces the
risk of fractures.
The most common adverse effect associated with ral-
oxifene therapy is hot flashes.48 In perimenopausal or
postmenopausal women already experiencing vasomo-
tor symptoms, this medication may cause worsening of
their symptoms. Less commonly observed adverse effects
reported with use of raloxifene include joint or muscle
pain, leg cramps, headache, GI disturbances, weight
gain, peripheral edema, and flu-like symptoms. Similar to
estrogens, this medication is associated with an increased
risk of thromboembolism (i.e., pulmonary embolism,
deep venous thrombosis) and fatal stroke,53 but it reduces
the risk of invasive breast cancer.53,54
Calcitonin
Calcitonin is a calcium-lowering hormone secreted by
the thyroid gland in response to elevated serum calcium
concentrations. Calcitonin salmon exerts its effects by
direct inhibition of the osteoclast activity, promotion of
renal excretion of calcium and other minerals thereby,
and increase in bone mass and reduction of the risk of
fractures.48 This medication currently is approved for the
treatment of postmenopausal osteoporosis in women
who are more than 5 years post menopause. Calcitonin
is available only as an injection or a nasal spray because
gastric acids easily destroy the oral formulations.
Although calcitonin does not affect other organs or
systems in the body, the injectable calcitonin may cause
unpleasant adverse effects including flushing of the face
and hands, local reactions, nausea, skin rash, and rare
systemic allergic-type reactions that have limited its use.
Adverse effects are rare with the nasal spray and consist
primarily of complaints of nasal dryness, soreness, irrita-
tion, and nosebleeds.48
Calcitonin may have some analgesic effects for patients
experiencing pain as result of acute compression frac-
tures. The exact mechanism for this analgesic effect still is
not completely understood. If a patient is not responding
to traditional pain management interventions, calcitonin
may be considered. However, it is not the first-line osteo-
porosis therapy in high-risk patients.
Anabolic Agent
Parathyroid Hormone (Teriparatide)
Teriparatide is a recombinant formulation of endog-
enous parathyroid hormone (PTH). It is the first medi-
cation approved for the treatment of osteoporosis and
aims to stimulate new bone formation through osteo-
blastic activity, increase calcium absorption in the intes-
tines, increase renal reabsorption of calcium to effectively
increase bone mass, and reduce risk of factures.48 This
medication is intended for use in postmenopausal women
and in men with primary or hypogonadal osteoporosis
at high risk of having a fracture. Teriparatide is available
only by subcutaneous injection.
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
Common adverse reactions associated with teripara-
tide are joint pain, dizziness, nausea, weakness, and a
transient increase in serum calcium levels. Although no
cases of osteosarcoma (a malignant bone tumor) have
been observed in human or monkey studies, an increased
incidence of osteosarcoma risk was noted in rat studies.55
Therefore this medication should be avoided in patients
with an increased risk of osteosarcoma, including patients
with Paget’s disease of bone or unexplained elevation
of alkaline phosphatase, open epiphyses, prior radiation
therapy, history of bone metastases, or other metabolic
bone diseases. Patients who receive teriparatide need to
receive extensive patient education on the proper use and
storage of the syringes.
Dual Antiresorptive and Anabolic Agent
Strontium Ranelate
Strontium ranelate (Protos), a unique bone-seeking
agent, is the first osteoporosis medication that offers
the dual mechanisms of action of combining the anti-
resorptive effect with the anabolic effect. It acts as an
uncoupling agent but the exact mechanism of action still
is not known. Its efficacy is similar to other antiresorp-
tive agents. Strontium is approved for treatment of post-
menopausal osteoporosis to reduce the risk of vertebral
fractures in various countries. The most commonly asso-
ciated adverse effect is diarrhea.56 However, this product
currently is not available in the United States.
Implication for the Clinician
Osteoporosis is prevalent in clinical practice. Although
most patients may not experience pain with osteoporosis,
many patients are enrolled in therapy programs because
of complications from osteoporosis. Certain patients
who experience bone pain may necessitate alteration of
therapy activities. Patients who experience fractures often
are challenged with significant physical impairments and
disabilities. Thus comprehensive rehabilitation inter-
ventions are essential to help patients restore maximum
physical function, reduce disability, and lower risk of sub-
sequent falls.47 Clinicians can help provide goal-oriented
exercise regimens, modalities for pain relief, and various
assistive devices for patients with osteoporosis.47 Patients
with spinal fractures should avoid spinal flexion and rota-
tion exercises. Various strategies to reduce fall risks (e.g.,
undergarments with hip protectors) should be considered
when working with patients at high risk for hip fractures.
National guidelines recommend routine physical activities
to improve agility, strength, balance, and to reduce risk
of falls.47 Several studies have suggested that regular weight-
bearing exercise and muscle-strengthening exercise can cause
modest increases in bone mass and complement drug thera-
pies for osteoporosis.57–61 Extended outpatient rehabilitation
275
that incorporated progressive resistance training for 6
months has shown more benefit than low-intensity home
exercises to the community-dwelling elderly patients with
hip fracture, which results in improved physical function
and quality of life and reduced disability.62
Gaining awareness of adverse effects associated with
osteoporosis medications also can help the clinician
inform the patient of the possible causes of their con-
cerns. Furthermore, clinicians can help minimize adverse
effects of drug therapy by scheduling physical activi-
ties around drug administration. Activities that require
patients to lie down should be avoided 60 minutes after
taking ibandronate (Boniva) or 30 minutes after taking
alendronate (Fosamax) or risedronate (Actonel). For
patients who experience hot flashes taking raloxifene
(Evista), making the environment cool is important to
ensure patient comfort.
Skeletal Muscle Relaxants
Overview
This section focuses on the centrally acting oral skeletal
muscle relaxants most often indicated for the treatment
of spasticity from multiple sclerosis, for the relief of mus-
cular rigidity, and/or as adjuncts to rest and physical
therapy for the management of painful musculoskeletal
conditions such as back pain. Medical treatment gener-
ally is recommended when the musculoskeletal condition
begins to interfere with posture, motor capacity, or activi-
ties of daily living.63 According to data from the National
Health and Nutrition Examination Survey (NHANES
III), which studied skeletal muscle relaxant use in the
United States from 1988 to 1994, an estimated 2 mil-
lion Americans reported muscle relaxant use. No dif-
ferences were reported between men and women, and
the median user age was 42 years. Back pain and muscle
disorders were the most common conditions responsible
for muscle relaxant use and were reported in 85% of the
population.64 The centrally acting oral skeletal muscle
relaxants are listed in Table 12-10 with dosing guidelines
and adverse effects.3,5 A brief overview of each muscle
relaxant is given below.
Baclofen
Baclofen is indicated for the relief of signs and symp-
toms of spasticity from multiple sclerosis, including
the relief of flexor spasms, clonus, and muscular rigid-
ity, and also may offer some benefit to patients with
spinal cord injuries and disease. In patients with mul-
tiple sclerosis, baclofen has been shown specifically to
reduce spasticity, decrease the frequency and severity of
sudden muscle spasms, and increase the range of joint
movement.65 A recent small study of male veterans
276 SECTION I • Scientific Foundations

Table 12-10
Skeletal Muscle Relaxants
Drug Product Starting Dosage Maximum Dosage Adverse Effects

Baclofen 5 mg/day 80 mg/day in Muscle weakness, sedation, fatigue, dizziness, nausea

(Lioresal) divided doses
Carisoprodol 350 mg three to – Tachycardia, facial flushing, dizziness, drowsiness,
(Soma) four times daily vertigo, ataxia, nausea
Chlorphenesin 800 mg three times – Drowsiness, dizziness, confusion, insomnia, increased
(Maolate) daily initially, then nervousness, headache, nausea
400 mg four times
daily
Chlorzoxazone 250–500 mg three 750 mg three to Drowsiness, dizziness, lightheadedness, malaise,
(Paraflex) to four times daily four times daily some GI upset
Cyclobenzaprine 10 mg three times 60 mg/day in Drowsiness, tachycardia, syncope, dry mouth
(Flexeril) daily divided doses
Dantrolene 25 mg/day 400 mg/day in Hepatotoxicity, weakness, sedation, diarrhea
(Dantrium) divided doses
Diazepam 2 mg twice daily or 40–60 mg/day in Sedation, cognitive impairment, depression
(Valium) 5 mg at bedtime divided doses
Metaxalone 800 mg three to – Drowsiness, dizziness, headache, nausea
(Skelaxin) four times daily
Methocarbamol 1.5 g four times 8 g/day Lightheadedness, dizziness, drowsiness, nausea,
(Robaxin) daily urticaria
Orphenadrine 100 mg each – Dry mouth, tachycardia, weakness, headache,
(Norflex) morning and dizziness, nausea
evening
Tizanidine 2–4 mg/day 36 mg/day in Drowsiness, dry mouth, dizziness, reversible
(Zanaflex) divided doses dose-related elevated liver transaminases

treated with baclofen suggests that the drug also may
have some benefit in treatment of posttraumatic stress
disorder.66 Baclofen is started at a low dose (i.e., 5 mg
three times per day) and then titrated up but should
never exceed 80 mg per day. This drug is structurally
similar to gamma-aminobutyric acid (GABA), which is
an inhibitory neurotransmitter. It stimulates the GABAB
receptor subtype and can inhibit reflexes at the spinal
level. Baclofen has the potential to produce some CNS
depression, including sedation, somnolence, ataxia, and
some respiratory and cardiovascular depression.67,68
Sedation is the most common adverse effect reported
with cyclobenzaprine use and has an incidence of 39%
in early controlled trials and 16% in post marketing sur-
veillance programs. One large study reported that dos-
ages as low as 5 mg three times per day could effectively
control signs and symptoms of muscle pain and stiffness
while producing significantly less sedation.70 Because of
the drug’s pharmacokinetic profile, elderly patients often
experience plasma concentrations up to twice those of
normal healthy controls, which can place these patients
at additional risk for sedation and somnolence.71

Cyclobenzaprine
Cyclobenzaprine is used to treat painful muscle spasms
originating from some acute musculoskeletal injury and
also carries an “off-label” use for sleep disturbances in
fibromyalgia syndrome.67,69 Cyclobenzaprine generally
is indicated for short-term use, and treatment beyond 2
to 3 weeks is not recommended. The drug generally is
well tolerated and does not produce serious adverse reac-
tions. The drug is dosed at 10 mg three times per day
and can be increased to 60 mg per day; however, sedation
may be a problem even with the 10-mg starting dose.
Dantrolene
The oral form of dantrolene is indicated for the control of
spasticity resulting from spinal cord injury, stroke, cere-
bral palsy, and multiple sclerosis. “Unlabeled” uses for
dantrolene include exercise-induced muscle pain, neurolep-
tic malignant syndrome, and heat stroke.67,72 Dantrolene’s
mechanism of action is different than those previously
mentioned. It acts directly on muscle contractile elements,
specifically, decreasing the release of calcium from the sar-
coplasmic reticulum and thereby reducing the muscle’s
ability to contract. Dantrolene is dosed at 25 mg daily and
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
then may be increased to twice daily to four times daily.
The maximum recommended dosage is 400 mg per day.
Because the drug works directly on peripheral muscles,
its most common adverse effect is weakness and therefore
it may not be the most appropriate agent for ambulatory
patients. Dantrolene is metabolized through the liver and
also has the potential to produce hepatotoxicity, which can
be irreversible. For this reason, clinicians should perform
liver function tests before therapy and every 3 months
thereafter for any patient receiving dantrolene.65
Diazepam
Diazepam is a benzodiazepine and is indicated for the
treatment of anxiety disorders, panic disorders, status
epilepticus, and alcohol withdrawal symptoms. It also
can be used as a skeletal muscle relaxant. The typical
dose of diazepam is 2 to 10 mg given two to four times
per day.65,67 Diazepam’s muscle relaxant properties are
thought to occur at the spinal level through GABA-
mediated presynaptic inhibition and at the supraspinal
sites. Diazepam differs from baclofen in that it targets
the GABAA receptor subtype.65,67 As with most benzodi-
azepines, the most common adverse effects are sedation
and cognitive impairment.
Tizanidine
Tizanidine is an α2-adrenergic agonist and exerts its effect
by inhibiting the release of excitatory amino acids in spi-
nal interneurons.65 In an open label dose titration study
of 47 patients with spasticity, treatment with tizanidine
resulted in significant improvement while preservation of
muscle strength.73 Tizanidine is dosed at 2 to 4 mg three
times per day (although generally only started at 4 mg
once per day and then increased) with a maximum rec-
ommended dosage of 36 mg per day.65,67
The most common adverse effects reported with this
drug include somnolence, fatigue, and dizziness.73,74
Tizanidine also has the potential to cause hepatotoxicty.
Aminotransferase levels should be measured within the
first 6 months (i.e., at baseline, 1, 3, and 6 months) of
treatment and periodically thereafter to monitor for any
signs of liver damage.67
Other Muscle Relaxants
Carisoprodol, chlorphenesin, chlorzoxazone, metaxalone,
methocarbamol, and orphenadrine are other skeletal
muscle relaxants used along with rest and therapy to help
relieve sore, painful muscles. None of the above agents
directly relax tense skeletal muscle and their mechanisms
of action have not been completely determined.67 Dosing
information and adverse effects associated with each
agent may be found in Table 12-10.
277
Implications for the Clinician
Because nearly all of the oral skeletal muscle relaxants
have the potential to produce drowsiness, sedation, or
muscle weakness, these agents can have an effect on a
patient’s ability to perform motor-related tasks or par-
ticipate in therapy programs. Some agents, such as
cyclobenzaprine, are more likely to produce a noticeable
effect in geriatric patients because of the pharmacoki-
netic characteristics of the drug, whereas other agents
such as dantrolene can produce muscle weakness in
nearly all patients. The clinician may wish to ask patients
if they are taking any skeletal muscle relaxants or review
the patient’s medication list before initiation of any reha-
bilitation program because these medications may affect
the patient’s performance.
Local Anesthetics
Overview
General anesthesia or local (regional) anesthesia is used
for pain relief in acute and chronic conditions for surgical
and medical conditions. Local anesthetics are adminis-
tered selectively for the surgical the site or the site that is
in pain and have allowed patients a faster recovery time
from procedures and effective pain relief.75,76 A reduction
in perioperative opioid analgesic requirements has been
demonstrated with the use of local or regional anesthe-
sia, resulting in a lower incidence of postoperative nausea
and vomiting.75,77,78 Controlling postoperative pain and
postoperative nausea and vomiting possibly can lead to
shorter stays in recovery rooms and decreased likelihood
of hospital readmissions.76,78–80
Local anesthetics decrease sensation in a body part
without the loss of consciousness or resultant impair-
ment of vital functions that can come from the use of
general anesthetics.81,82 Several different methods exist
for administration of local anesthetics including topical,
infiltrative, spinal (subarachnoid), epidural, or by periph-
eral nerve (regional) or field block.75,83 These agents can
provide pain relief in many different types of joint sur-
geries. When selected, the choice of local anesthetic is
based on operative site, type of local anesthesia desired,
patient size and general health, and duration of anesthe-
sia needed.84–91 A closer look at the mechanism of action
and adverse effects of these agents is warranted for all
clinicians who practice in areas where these agents may
be used.
Basics of Local Anesthetics
Local anesthetics are used to block nerve transmission so
the desired procedure or activity can be performed with-
out pain. Mechanistically, all local anesthetics have the
same mechanism of action, resulting in part from their
278 SECTION I • Scientific Foundations
similar structures. Lipophilic and hydrophilic compo-
nents make up the common structure with either an ester
or amide linkage joining these groups. Local anesthetics
with an ester linkage are degraded rapidly in the plasma by
esterases, whereas amide linkages require transformation
in the liver, resulting in a longer duration of action.92
Lipophilicity is correlated with the potency and toxic-
ity of these agents. The lipophilic component probably
is necessary for the drug to partition into the cell mem-
brane, where it binds to a sodium channel and prevents
the generation and conduction of nerve impulses.92 The
net effect is a decrease in the propagation of the action
potential and resultant failure of nerve conduction. In
general, highly lipophilic agents can be given in lower con-
centrations but also are potentially more toxic if systemic
accumulation of the agent occurs. Some local anesthetics
do not penetrate intact skin and are used only topically.93
The diameter of the nerve, in part, dictates the degree
of neuronal block that results from a given concentration
of the drug. In general, larger diameter (type C) fibers
require larger concentrations of a drug to achieve the same
degree of block as a smaller diameter (type A) fiber.93 The
action of local anesthetics causes loss of sensation of pain
first, then temperature, touch, deep pressure, and motor
function.
Many local anesthetics are combined with a vasocon-
strictor (i.e., epinephrine) to decrease the rate of metab-
olism and thereby increase the duration of blockade at
the sodium channel. Cocaine, one of the original local
anesthetics, has vasoconstrictor properties that potenti-
ate the effects of norepinephrine. However, this apparent
advantage also means that it is toxic in systemic amounts.
Other local anesthetics have some slight vasoconstrictory
properties but much less than cocaine. Adverse effects
that can be seen with using a vasoconstrictory agent such
as epinephrine are delayed wound healing, tissue edema,
and necrosis because of increased oxygen consumption.
Epinephrine is not recommended for concomitant use in
areas with limited collateral circulation.94
Adverse Effects
Adverse events are important concerns for anyone who
works with local anesthetics. The adverse reactions can
be broken down into either systemic or local reactions.
Several local anesthetics have been discovered over the
years that either do not find wide use because of their
toxicity or are used only as a topical agent (e.g., benzo-
caine, pramoxine, dibucaine) because of potential toxic-
ity if entered into the systemic circulation. The majority
of the serious effects result from distribution into the
systemic circulation, where cardiovascular and cerebro-
vascular effects can be fatal. They can have a toxic effect
on the myocardium, which results in decreased excit-
ability, conduction rate, and contractions. The central
nervous system effects of these agents can range from
drowsiness to tremors and ultimately respiratory depres-
sion depending on the systemic concentration. Factors
that increase the risk of systemic introduction include the
dose of the drug, the rate injected, the site (vascularity)
injected, and the age (the elderly have decreased volume
for drug to accumulate).95,96
Adverse Effects of Local Anesthetics
● Toxic effect on myocardium
● Respiratory depression
● Hypersensitivity
Local reactions usually are represented as a hypersensi-
tivity reaction. This can be expressed in allergic dermatitis
or asthmatic attacks. This is seen primarily in the ester type,
although preservatives such as methylparaben have been
known to cause this. Allergies reported to local anesthet-
ics are likely not a result of the original drug structure but
from a para-amino benzoic acid-like metabolite (PABA).
Allergies to the amide type anesthetics are much rarer,
and they are options in individuals with a true allergy to
the PABA metabolite in ester anesthetics.97
Examples of specific agents and their relative potency,
duration, and toxicity are given in Table 12-11.
Implications for the Clinician
The rehabilitation practitioner needs to be aware of anal-
gesic agents given for pain and adjunctive therapy that
may have been given intraoperatively or postoperatively.
The use of local anesthetics may lower the required
dosage of analgesic agents that a patient requires. The
site and degree of block the anesthetic agent is exhibit-
ing will likely have an impact on the therapy session of
the patient. A reduction in pain may allow the patient
to perform at an increased level and ultimately recover
faster from their procedure or illness. Timing the therapy
sessions close to the time of administration of the anes-
thetics can ensure that the patient experiences a pain-free
session. Alternatively, depending on the degree of block-
ade experienced by the patient, certain movements may
not be feasible or appropriate for the patient.
Ancillary Agents
This section deals with ancillary drug classes that do not
necessarily fit into any of the previous disease states but
are of importance to the rehabilitation clinician. The
underlying disease state is often as important to take into
account as the medications themselves. Clinicians should
try to look at prescribed medications as a guide to what
underlying diseases they will have to deal with in the
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process 279

Table 12-11
Pharmacodynamic and Pharmacokinetic Properties of Local Anesthetics
Local Speed of Duration
Anesthetics Onset Potency of Action Toxicity Uses

Esters
Cocaine Slow High Long Very high Topical use only
Procaine Slow Low Short Low Infiltration, peripheral nerve block, spinal
(Novocaine)
Chloroprocaine Rapid Intermediate Short Low Infiltration, peripheral nerve block, epidural
(Nesacaine)
Tetracaine Slow Intermediate Intermediate Intermediate Topical, spinal
(Pontocaine)
Amides
Lidocaine Fast Intermediate Intermediate Low Infiltration, peripheral nerve block, epidural,
(Xylocaine) spinal, transdermal, topical, sympathetic
block, intravenous regional block
Mepivacaine Slow Intermediate Intermediate Low Infiltration, peripheral nerve block, epidural,
(Carbocaine, intravenous regional block
Polocaine)
Bupivacaine Slow High Long High Infiltration, peripheral nerve block, epidural,
(Marcaine, spinal, sympathetic block
Sensorcaine)
Levobupivacaine Slow High Long Intermediate Infiltration, peripheral nerve block, epidural
(Chirocaine)
Ropivacaine Slow Intermediate Long Intermediate Intravenous regional block, epidural,
(Naropin) peripheral nerve block, infiltration
Etidocaine Fast Intermediate Long Intermediate Infiltration, peripheral nerve block, epidural
(Duranest)
Prilocaine Fast Intermediate Intermediate Low Infiltration, peripheral nerve block (dental
(Citanest) procedures)

patient, in addition to thinking about the effects of the
medications.
Medications for Parkinson’s Disease
Parkinson’s disease is marked by a selective loss of neu-
rons involved with the coordination of motor skills.98
The resulting loss of the inhibitory neurotransmitter
dopamine and resulting relative overabundance of the
excitatory neurotransmitter acetylcholine results in pro-
gressive dysfunction of motor coordination. Although
it does not directly affect cognition, the motor dysfunc-
tion eventually becomes so severe (i.e., impaired swal-
lowing, loss of facial expression) that Parkinson’s often is
mistaken for a cognitive disease. However, patients with
Parkinson’s do not have impaired hearing and compre-
hension skills.98 Therefore repeating instructions multiple
times, speaking slowly, or raising your voice is not neces-
sary. Treating advanced Parkinson’s patients as though
they have a cognitive disorder frustrates the patient and
the clinician.
Although a complete discussion of Parkinson’s medica-
tions is beyond the scope of this chapter, an important
note is that current therapies are designed to either replace
dopamine or prevent its further breakdown.99 The result
of either approach is an increase in dopaminergic drive.
This commonly results in adverse effects in the cardiovas-
cular and central nervous systems.99
Cardiovascular adverse events may include palpi-
tations, arrhythmias, and orthostatic hypotension.
Orthostatic hypotension increases the risk of fall in
patients with Parkinson’s when they move suddenly from
a more prone to a more upright position and is most
common with a class of medications called the dopamine
agonists.100 These are represented by pergolide (Permax),
bromocriptine (Parlodel), pramipexole (Mirapex), and
ropinirole (Requip). Central nervous system side effects
are also common because of the increased dopaminer-
gic stimulation. Confusion, dizziness, somnolence, and
even hallucinations all may occur more with dopamine
agonists.
The most commonly used and most effective medica-
tion for Parkinson’s disease is levodopa.99 Levodopa is a
prodrug for dopamine, meaning that, once it is taken, it
is converted physiologically to dopamine. This occurs in
peripheral tissues and the central nervous system. Because
280 SECTION I • Scientific Foundations
excess peripheral dopamine is associated with cardiovas-
cular and gastrointestinal side effects, levodopa always is
dosed with carbidopa. Carbidopa inhibits dopa-decar-
boxylase, which is the enzyme that converts levodopa to
dopamine. Because carbidopa cannot cross the blood-
brain-barrier (BBB), it does not inhibit CNS conversion
of levodopa to dopamine. This actually allows for lower
doses of levodopa to be used because more is able to pen-
etrate the CNS before being converted to dopamine in the
periphery (dopamine also cannot cross the BBB). In the
United States, fixed combinations of levodopa and carbi-
dopa are available as the drug Sinemet, which is available
as extended-release (Sinemet CR) and non–extended-
release formulations. The combinations are available in
fixed ratios of 1:4 and 1:10 of carbidopa to levodopa. It
is important that at total daily doses of less than 500 mg
of levodopa, the 1:4 ratio Sinemet is used (typically the
25 mg/100 mg dose). This allows for enough carbidopa
to be taken to adequately inhibit dopa-decarboxylase.
An important consideration in the rehabilitation of
Parkinson’s patients is to individualize their sessions to
take into account symptomatic fluctuations in motor
skills that commonly occur in their disease manage-
ment. Regardless of the combination of drugs used,
patients typically have better and worse times of the day
for symptomatic control. As these times become more
extreme, which is common after several years of levodopa
or Sinemet therapy, they are referred descriptively to as
“on” times and “off” times.99 An “on” time refers to a
period when the medication is at near optimal effects
and the patient is near optimal motor function. “Off”
times, when motor control is poor, could pose obvious
problems for a rehabilitation session that requires active
patient involvement. Therefore discuss with the patient
or their caregiver when the best time of day may be for
their session. Of particular note, the symptom improve-
ment with the controlled-release formulation, Sinemet
CR is delayed compared with the non–controlled-release
formulation because of a slowed absorption. Many
patients therefore also take a dose of immediate-release
Sinemet to help with early morning symptom control.
If they do not, however, an early morning rehabilitation
session may be particularly problematic for patients on
Sinemet CR.
Medications for Cardiac Disease
Several classes of medications used for cardiac disease also
deserve special mention. Beta-blockers and nitrates com-
monly are used in patients with chronic stable angina.
Angina results from a mismatch between oxygen supply
and oxygen demand in myocardial tissue when coronary
arteries are narrowed because of atherosclerosis.101
Nitrate drugs, represented by nitroglycerin (taken sub-
lingually or topically), isosorbide dinitrate (Isordil,
Sorbitrate, Dilatrate-SR), and isosorbide mononitrate
(ISMO, Imdur), work by dilating coronary vessels to
help improve oxygen supply.101 Beta-blockers work by
reducing heart rate and contractility, which results in
reduced oxygen demand.102 Commonly used beta-block-
ers include metoprolol (Lopressor, Toprol XL), ateno-
lol (Tenormin), carvedilol (Coreg), bisoprolol (Zebeta),
and propranolol (Inderal). Because physical rehabilita-
tion increases oxygen demand, it potentially can trigger
angina. Angina that occurs while the patient is at rest is
known as unstable angina and is a medical emergency.103
Patients who are known to require sublingual or topical
nitroglycerin for occasional relief of anginal pain should
have these medications readily accessible during any reha-
bilitation session. The clinician also should be cognizant
of the physical thresholds for angina in these patients.
Repeated exercise increases these thresholds and is of great
value to the cardiovascular rehabilitation of the patient.101
Although nitrates often increase the exercise capacity
of rehabilitation patients by prevention of their angina,
beta-blockers may reduce it. Because beta-blockers
reduce the patients’ ability to increase their heart rate
and contractility, they reduce their ability to respond to
physical demand.104 This may have obvious effects on any
rehabilitation session or regimen that increases a patient’s
cardiovascular demand. This is also true when patients
are taking beta-blockers for hypertension.
When these drugs are used for chronic heart failure
(CHF), however, the relationship is different. In CHF,
patients already have compromised cardiac function,
resulting in a reduced capacity for cardiac output.105 This
characteristic is notably improved by chronic beta-blocker
therapy in these patients, although this may be worsened
acutely for a period of weeks to a couple of months when
these agents are initiated.106 Therefore, although patients
with CHF have a reduced capacity for physical exertion,
it is due to preexisting cardiac disease and not to the use
of the beta-blocker drug. The limitations on the physical
aspects of rehabilitation, however, are the same.
Medications for Pulmonary Disease
Inhaled bronchodilator drugs, which are used to treat
obstructive pulmonary diseases, also deserve special con-
sideration from the rehabilitation clinician. Aside from
recognizing that patients on these medications have
some reduction in pulmonary capacity, exercise also can
be a trigger for bronchoconstriction in patients with
underlying obstructive lung diseases.107
The most common bronchodilating drugs are ipratro-
pium (Atrovent) and beta-agonists. Both work by direct
relaxation of the bronchial smooth muscle, and both can
acutely blunt exercise-induced bronchoconstriction if
used before exercise. They also may partly relieve exercise-
induced bronchoconstriction when it occurs. Although
 CHAPTER 12 • Pharmacology and Its Impact on the Rehabilitation Process
they commonly are used to provide chronic broncho-
dilation for patients with COPD, they generally should
be used only on an “as needed” basis for patients with
asthma. If it is noticed that a patient with asthma routinely
requires bronchodilator agents during rehabilitation or is
using them daily in their regular routine, it could signal
poor underlying control of the disease and an attempt
should be made to inform the medical prescriber. Often
more optimal use of inhaled steroids (see above) improves
asthma control and lessens the need for bronchodilator
therapy. Commonly used beta-agonist drugs include alb-
uterol (Ventolin, Proventil), metaproterenol (Alupent),
salmeterol (Serevent), and terbutaline (Brethine). These
agents are commonly delivered by a pocket-sized inhaler
as either an aerosolized mist or a dry powder. Although
exercise can improve lung function in the long term,107
the possibility of immediate reactions of bronchoconstric-
tion means that patients should have their medication
close at hand during rehabilitation sessions.
281
Summary
Drug therapy has broad implications for the contem-
porary management of musculoskeletal conditions
including the rehabilitation process. The clinician must
be cognizant of the desired therapeutic effects and
the adverse effects that may accompany drug therapy.
An understanding of the general principles of pharma-
cology and common medications used in the manage-
ment of acute and chronic musculoskeletal conditions
will prepare the clinician to render the best possible
patient care.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 107 references for this chapter.

282 SECTION I • Scientific Foundations
E FFECTS
FFECT OFOFAAGING
GING-G
-GROWTH
ROWTHCCHANGES
HANGES
AND L IFE S PAN C ONCERNS (0–40)
Lori Thein Brody and Jill M. Thein-Nissenbaum
Introduction
Numerous changes occur to the human body throughout
the life span. Changes in muscle strength, balance, motor
control, power, and flexibility are normal throughout
development. Any clinician helping to rehabilitate an
injured patient must be prepared to examine and provide
effective interventions for patients and clients throughout
the life span. As such, it is imperative that clinicians have a
good understanding of normal physical development.
This chapter provides an overview of normal physical
development and changes from birth to age 40 years.
Although every individual grows and develops motor
skills at different rates, this chapter explores general
development and progression. Additionally, special con-
siderations specific to various age groups are discussed.
Infant-Toddler (0 to 3 Years)
The infant and toddler undergo numerous changes from
birth to the age of 3 years. Lifelong skills such as language
development as well as psychomotor skills such as dress-
ing, grooming, walking, and running are achieved during
this period. Although general milestones are provided,
the clinician must bear in mind that children achieve these
milestones at different rates. A child’s progression of skill
development often goes through stages of ebbs and flows;
all children—even identical twins—develop differently.
Clinicians or parents should only become concerned when
the infant or child is significantly delayed or shows delays
in more than one area of skill development. How these
delays are defined and measured will vary by measure or
scale used, but they should be consistent throughout the
patient’s health care system.
282
13
C H A P T E R
This section presents the systems and skills that
undergo the most significant changes from birth to the
age of 3 years. Torticollis, a musculoskeletal condition
specific to this age group, is also discussed.
Physical Growth/Physiological Development
Musculoskeletal System
Before discussing the positions of various bones and joints
in the newborn, the reader should have a general under-
standing of bone modeling in the newborn and infant.
The infant skeleton is composed primarily of cartilaginous
tissue, rendering it highly plastic.1 This cartilage is much
weaker than the bone it ultimately forms and is therefore
capable of much greater unit creep than bone. Most bones
are formed by the destruction and replacement of hyaline
cartilage, a process called endochondral ossification. In
long bone, this ossification occurs at primary and second-
ary ossification centers; the primary ossification center is
present after the second month of fetal life. However, the
secondary centers do not appear until after birth.
The spine of the newborn is kyphotic, forming a
C-curve, with the lumbar spine in flexion, rendering
the kyphosis evident from the neck to the sacrum.2 The
pelvis is tilted posteriorly, which is a reflection of the
kyphotic position of the spine.3 The acetabular roof of
the hip is shallow at birth and is inclined downward
7° from the sagittal plane. By 3 years of age, the roof
is angled downward 17° and is considered mature.1
These changes incurred by the acetabulum are due to
muscle tension and body weight applied in appropriate
magnitude and direction.2
The hips of the newborn are held in a position of flex-
ion and lateral rotation by a combination of contracture
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40)
of the capsular structures and tightness in the muscles of
flexion and lateral rotation.3 At birth, the hip flexion con-
tracture averages 30°, and the total amount of rotation
available is 120°, with lateral rotation exceeding medial
rotation for the first 18 to 24 months of life.3,4 In children
younger than 6 months of age, lateral rotation is three
times greater than medial rotation. However, by 3 years
of age, this variance normalizes.4 Hip abduction in the
newborn is measured at 90° hip flexion and is normally
approximately 76° at each hip. By 9 months, abduction
decreases to 59°; it remains at 59° until 24 months. After
that, 45° of abduction range at each hip is normal.5
Normal Musculoskeletal Growth from Ages
0 to 3 Years
● The spine is kyphotic at birth; elongation of anterior structures
reduces this curve.
● A hip flexion contracture is present in the newborn’s hips, and
increased lateral rotation is also present. This is primarily due to
positioning in the uterus.
● The femur of the newborn presents with coxa valga, antetorsion,
and varus bowing. Increased activity of the muscles that surround
the hip joint causes these features to reduce by age 2.
● The knee flexion contracture, which is present at birth, is due
to the maturation of the nervous system, which increases flexor
activity. Normal movement of the lower extremities elongates the
hamstrings and decreases this angle by 6 months.
● The tibia and fibula twist in response to muscular forces; this
moves the malleoli into proper position to stabilize the talus with
weightbearing.
● The newborn is born with excessive dorsiflexion; this rapidly
decreases during the first few weeks of life.
● The newborn’s foot is long and hypermobile at birth.
The femur of the newborn has three structurally
unique features, which are due to position demanded
by intrauterine confinement during the final 2 months
of gestation. The features include coxa valga, antetor-
sion (also called retroversion), and mild varus bowing.3,6
The angle of inclination between the shaft and the neck
of the femur increases as compared to adult values and
averages 150°.6 Between birth and 18 months, the angle
decreases to 145°. The greatest influence on the reduc-
tion of coxa valga is muscle action about the hip joint.7
Antetorsion, the medial twist of the distal femoral shaft
on the proximal shaft, is 40° at birth. Despite this medial
twist, the newborn femoral head and neck are anteverted
by soft tissue contracture.3,7,8 Reduction of femoral tor-
sion correlates with a reduction in hip flexion contrac-
ture, increased activity of the hip extensors, and loading
of the muscles that extend the hip, in conjunction with
longitudinal bone growth. This occurs predominantly
through the first 2 years of life.8
283
A knee flexion contracture of up to 30° is present
in the newborn, when measured with the hips fully
extended.9 The flexion contracture is due to maturation
of the nervous system, which increases flexor activity, and
also due to adaptive shortening because of the position
in utero. By the age of 6 months, most infants engage in
playing with and mouthing of the feet, which elongates
the hamstrings, thereby decreasing the knee flexion con-
tracture.3 In addition, genu varum is present in the new-
born, although its presence is usually masked by the knee
flexion contracture. However, the combination of coxa
valga, lateral hip rotation, mild lateral femoral bowing,
and medial tibial rotation results in a tibiofemoral angle
of up to 17°. By age 2 years, genu varum resolves and
genu valgum is present. This is due to the variable loads
of compression on the medial and lateral condyles of the
femur in standing and walking.3,10
The tibia and fibula of the newborn are straight-neither
bowed nor twisted.1,3,8 The tibia may appear rotated because
the knee flexion contracture allows the tibia to rotate medi-
ally on the femur, which can cause the appearance of medial
tibial torsion in the shaft of the bone. Because the tibia and
fibula are highly cartilaginous, they are highly responsive
to forces. As the newborn develops, the shafts of the tibia
and fibula gradually twist laterally in response to muscular
forces. This occurs in order to move the malleoli into posi-
tion to stabilize the talus during weight bearing. The distal
third of the lower leg often appears to bow laterally 15° to
20°, but the long bones are, in fact, straight. Interestingly,
the apparent lateral bowing is due to lateral displacement
of the posterior compartment muscles laterally, which is
caused by shortening of the medial knee joint musculature
and connective tissue. As the knee joint gains mobility, the
lateral displacement of the posterior compartment resolves.
By the age of 1 year, tibial varum decreases to 6°; by age 2
years, it is 2°.3,10 The proximal tibial plateau is retroverted
up to 27° at birth, rendering the anterior tibial plateau
more proximal than the posterior tibial plateau. The knee
flexion contracture masks this angle, which reduces to 5°
by the end of adolescence.1
The talocrural joint of the newborn can be passively
dorsiflexed up to 70°, with plantar flexion limited to 30°.
The resting position of the newborn ankle is 15° dorsi-
flexion. This excessive hypermobility is most likely due to
intrauterine positioning. This mobility decreases rapidly
in the first few weeks of life, resulting in a normal infant
range of 50° passive dorsiflexion.3,9
The length of the newborn foot averages three to four
inches in length, which, when compared to the length of
the leg, is long. The first ray is pitched medially, and is
abducted away from the second metatarsal by 10°. The
newborn also has 10° of rearfoot varus and the forefoot is
inverted an additional 15° of varus relative to the rearfoot.
This is due to the baby’s intrauterine position and is why
the newborn is able to get the plantar surfaces of both feet
284 SECTION I • Scientific Foundations
to touch.1 Rearfoot varus deviates into valgus by 1 year as
the foot pronates in stance. The soft tissue structures on
the medial side of the foot, which were shortened dur-
ing uterine confinement, are able to elongate under the
stresses placed upon them in standing. Forefoot varus
reduces to 5° in the first year and continues to decrease
until age 5 years. This reduction is due to growth of the
navicular and strengthening of the peroneus longus.1
Lastly, although the toes are hypermobile in infancy, they
are often in a flexed position because of the lack of oppor-
tunity to extend the toes. The first effort of the infant to
utilize toe hyperextension can be seen with belly crawling.
The infant utilizes the plantar surface of the toes for push-
off. At 7 to 8 months, with supported standing, the infant
will rise onto the toes, which also requires hyperextension
of the metatarsophalangeal joints.
Cardiorespiratory System
The cardiorespiratory system and circulation of the fetus
are markedly different from adult circulation. As such,
numerous changes occur in the cardiovascular system
immediately after birth. One of the biggest changes is the
closure of the ductus arteriosus, which is a vascular link
outside the heart between the pulmonary artery and the
aorta. This link allows blood to exit the pulmonary artery
and be delivered directly into the aorta for systemic circu-
lation. The ductus arteriosus closes within a few weeks of
life. After closure, only one route of blood flow remains,
the route similar to adult circulation.11 The infant con-
tinues to experience altered pressures and forces on the
developing chest wall throughout the first few months of
life. Many of these alterations, such as a transient heart
murmur, are considered benign if there is no accompany-
ing symptomatology. Because of the numerous changes
that occur during the first months of life, an infant’s car-
diac system is assessed routinely throughout growth. Any
abnormalities deserve documentation and follow-up.11
Normal Cardiorespiratory System Changes from
Ages 0 to 3 Years
● The ductus arteriosus closes within the first few weeks of life;
circulation is then similar to that of an adult.
● The pulmonary system begins to functional with the first postnatal
breath, which forces fluid from the airways into the lymphatic
system.
● Infants are born with a larynx higher than that of an adult, allow-
ing the infant to breathe better while feeding.
● The diaphragm of the infant is predisposed to easy fatigue
because of its fiber composition; the accessory muscles of the
cervical spine assist with ventilation in the infant.
● The vital signs of the infant include a higher heart rate and respi-
ratory rate and a lower blood pressure when compared to that of
an adult.
The respiratory system undergoes numerous changes
after birth as well. The pulmonary system is not func-
tional until the first postnatal breath.11 During the first
few breaths, the infant must generate large inspiratory
pressures to inflate the lungs and force the fluid within
the airways and alveolar units into the lymphatic sys-
tem. For the first few hours after birth, this diffusion
process occurs naturally. Transient newborn tachypnea,
or an occasional rapid increase in respiration rate, is not
uncommon even in the healthiest of infants.11
Important differences exist between the pulmonary
system of the adult and the pulmonary system of the
infant. Infants are born with a larynx that is structur-
ally higher than that of an adult, enabling the infant to
breathe better while feeding. However, this makes the
infant a nose breather, and this may present a problem if
the infant has nasal congestion or nasal obstruction. The
smooth muscle within the bronchioles is less developed,
providing a greater risk of bronchiolar collapse, until
approximately the age of 5 years.11
The compliance, configuration, and muscle action
of the chest wall of an infant differ from those of older
children. The muscles of the infant’s chest wall are the
primary stabilizers of the thorax to counteract the nega-
tive pleural pressure of the diaphragm during inspiration.
In the adult, this is done by the ribs, but in the infant,
the increased ribcage compliance results in decreased
thorax stability. The infant’s diaphragm is also aligned
differently than the adult’s and has decreased efficiency
of ventilation and increased distortion of the chest wall.
In addition, only 20% of the fibers of the diaphragm in
the newborn are fatigue resistant, as compared with 50%
in adults. This predisposes the infant to earlier diaphrag-
matic fatigue. Elongation of the cervical spine, seen early
in life, improves the length-tension relationship of some
of the accessory muscles of inspiration, which helps over-
come diaphragmatic fatigue. As the child is exposed to
more antigravity and upright positions, muscular and
gravitational forces help mold the shape of the thorax
into a more typical adult configuration.11
The infant’s vital signs are significantly different from
that of a child or adult. The infant’s heart rate is 100 to
140 bpm, blood pressure is 80/40 mmHg, and respira-
tory rate is 30 to 40.11
Nervous System
Although brain maturation is a major force driving devel-
opment of the newborn and infant, it is probably no
more important than any other system. Experience drives
brain development, and a hierarchy of important func-
tions exists.12 Lower levels of the nervous system, such
as the spinal cord, are capable of controlling many finely
coordinated movements, not only simple reflexes. In the
first 3 to 4 months of life, infants shift from subcorti-
cally organized movements to increasing involvements of
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40)
cortical circuits at age 4 to 5 months. By 6 months, an
infant is able to grasp, manipulate, and release an object
from his or her hand. This is due to a combination of
maturation of cortical systems, anthropometric changes,
and learning gained from experiences.12 By 8 months,
monosynaptic connections between the motor cortex and
the spinal cord allow for selective control of digital move-
ments.13 This occurs about the same time reciprocal coor-
dination of muscle activity occurs, which characterizes
more mature movement patterns.12 At 8 months, the
frontal areas of the brain also develop dramatically. This
area processes information related to goal-directed behav-
ior and anticipated consequences; it reaches a maximum
at 2 years of age.12,13
Normal Nervous System Changes from Ages
0 to 3 Years
● The infant shifts from subcortically organized movements to
movements involving cortical circuitry at age 4 to 5 months. This
allows a 6-month-old infant to manipulate an object in his or her
hand.
● At 8 months, monosynaptic connections between the motor cortex
and spinal cord allow the infant to move selective digits. This
occurs about the same time that reciprocal coordination of muscle
activity occurs.
Body Composition
Body composition refers to the relative proportions of
lean body mass and fat mass. The proportion of the body
that is fat mass is referred to as percent body fat. Fat is
the most variable component of body composition dur-
ing infancy and childhood. Part of this change is due to
chemical maturation as a result of increasing mineral mass
and hydration of adipose tissue.14,15 The disproportionate
contribution of fat content to overall increases in body
mass over the first 8 months of life causes infants to be
relatively weak during a time when they are developing
motor control and coordination skills. From birth to 6
months of age, the body fat of an infant rises from 12% to
25% of body mass. As age and mobility increase, fat con-
tent drops and muscle mass increases. By approximately 4
months of age, water content stabilizes at approximately
60% to 65%; it remains at this level until puberty.14,15
Normal Body Composition Changes from Ages
0 to 3 Years
● From birth to 6 months, body fat increases from 12% to 25%.
● Newborns weigh approximately 7 to 8 pounds at birth.
285
At birth, the newborn boy weighs, on average,
just shy of eight pounds. By 12 months, he weighs
approximately 22 pounds; by 2 years, average weight
is 28 pounds, and by age 3, he weighs 31 pounds
(Figure 13-1). The average weight gain for girls is
similar, although girls may weigh slightly less than
boys (Figure 13-2). The length of the average new-
born male is 19.75 inches; by 12 months he is 29.5
inches in height. At 2 years, boys average 34.5 inches
in height, and by age 3, they average 38 inches in
height (Figure 13-3). Females progress at a similar rate
(Figure 13-4). Fifty percent of adult height is reached
between the ages of 2 and 2.5 years.12,16
Performance Development
Motor/Skill Development
Motor and skill development in the newborn devel-
ops in a cephalocaudal, head-to-foot, direction. In
the prone position, achievement of the first antigrav-
ity component appears as neck extension, followed by
extension of the arms, trunk, and hips.2 As the infant
progresses from age 2 to 6 months, the point of stabil-
ity shifts caudally, which allows the infant to first lift
his or her head, followed by his or her upper back and
chest.12 The active contraction of the spine extensors
also reduces the kyphosis seen in the spine. The hip
flexion contracture continues to reduce through the
contraction of the hip extensors. By age 5 months, the
infant is able to use the upper extremities to push the
point of stability distally, onto the pelvis. Eventually,
the infant can shift weight onto one side of the pelvis
and unload the opposite side, providing the infant with
the preliminary stages of belly crawling. By 6 months,
the infant can use the upper and lower extremities, in
combination with weight shifting, to belly-crawl to
locomote in prone. By 7 months, the infant can achieve
the hands-and-knees position.2
Normal Motor/Skill Development from Ages
0 to 3 Years
● Motor skill development develops in a cephalocaudal direction.
● In prone, the infant is able to raise his or her head first, followed
by the arms, trunk, and hips. By 6 months, the infant can use the
upper and lower extremities to belly crawl.
● In supine, the infant progresses from a position of flexion of the
extremities to extension. By 6 months, the infant can lift his or her
head off of the surface and rotate the pelvis on the shoulders.
● The infant is able to stand with support as early as 4 months;
standing posture improves as the kyphosis in the spine decreases.
By 12 months, the infant can stand independently.
286 SECTION I • Scientific Foundations

Birth to 36 months: Boys NAME

Length-for-age and weight-for-age percentiles RECORD #

Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS)
cm in
41 41 L
40 95 40 E
100 90 100 N
39 39
75 G
38 38
95 50 95 T
37 37 H
25
36 36
90 10 90
35 5 35
34
85
33
32 95 38
80 17
31
L 30
90 36
E 75 16
N
29
34
G 28 75
70 15
T 27 32
H 26 50
65 14
25 30 W
24 25 E
60 13
23 28 I
10 G
22 55 12 H
5 26
21 T
20 50 11 24
19
18 45 10 22
17
16 40 9 20
15
8 18

16 16
7 AGE (MONTHS)
kg lb
12 15 18 21 24 27 30 33 36
14
6 Mother’s Stature Gestational
W Father’s Stature Age: Weeks Comment
E 12
Date Age Weight Length Head Circ.
I 5 Birth
G 10
H
4
T
8
3
6
2
lb kg
Birth 3 6 9
Published May 30, 2000 (modified 4/20/01).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts SAFER HEALTHIER PEOPLE TM

Figure 13-1
CDC growth charts. Length-for-age and weight-for-age percentiles: boys, birth to 36 months. (Developed by the National Center for Health
Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion, the Centers for Disease Control and
Prevention, and the US Department of Health and Human Services, May 30, 2000 [modified April 20, 2001], www.cdc.gov/growthcharts.)
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40) 287

Birth to 36 months: Girls NAME

Length-for-age and weight-for age percentiles RECORD #

Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS)
cm in
41 41 L
40 40 E
100 95 100
39 90 39 N
38 G
75 38
95 95 T
37 50 37 H
36 25 36
90 90
35 10 35
5
34
85
33
32 38
80 95 17
31
L 30 36
E 75 90 16
N
29
34
G 28
70 75
15
T 27 32
H 26 65 14
25 50 30 W
24 E
60 13
23 25 28 I
G
22 55 12 H
10 26
21 5 T
20 50 11 24
19
18 45 10 22
17
16 40 9 20
15
8 18

16 16
7 AGE (MONTHS)
kg lb
12 15 18 21 24 27 30 33 36
14
6 Mother’s Stature Gestational
W Father’s Stature Age: Weeks Comment
E 12
Date Age Weight Length Head Circ.
I 5 Birth
G 10
H
T
4
8
3
6
2
lb kg
Birth 3 6 9
Published May 30, 2000 (modified 4/20/01).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts SAFER HEALTHIER PEOPLE TM
Figure 13-2
CDC growth charts. Length-for-age and weight-for-age percentiles: girls, birth to 36 months. (Developed by the National Center for Health
Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion, the Centers for Disease Control and
Prevention, and the US Department of Health and Human Services, May 30, 2000 [modified April 20, 2001], www.cdc.gov/growthcharts.)
288 SECTION I • Scientific Foundations

2 to 20 years: Boys NAME

Stature-for-age and Weight-for-age percentiles RECORD #

12 13 14 15 16 17 18 19 20
Mother’s Stature Father’s Stature cm in
Date Age Weight Stature BMI*
AGE (YEARS) 76
95
190
74
90
185 S
75
72
180 T
50 70 A
175 T
25 68 U
*To Calculate BMI: Weight (kg) ! Stature (cm)! Stature (cm) " 10,000
or Weight (Ib) ! Stature (in) ! Stature (in) " 703
170 R
10 66
165 E
in cm 3 4 5 6 7 8 9 10 11 5
64
160 160
62 62
155 155
S 60 60
T 150 150
A 58
T 145
U 56
140 105 230
R
54
E 135 100 220
52
130 95 95 210
50
125 90 200
90
48 190
120 85
46 180
115 80
75
44 170
110 75
42 160
105 50 70
150 W
40
100 65 140 E
25
38 I
95 60 130 G
10
36 90 5 H
55 120
T
34 85 50 110
32 80 45 100
30
40 90
80 35 35 80
W 70 70
30 30
E 60 60
I 25 25
G 50 50
H 20 20
40 40
T
15 15
30 30
10 10
lb kg AGE (YEARS) kg lb
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
Published May 30, 2000 (modified 11/21/00).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts SAFER HEALTHIER PEOPLE TM

Figure 13-3
CDC growth charts. Stature-for-age and weight-for age percentiles: boys age 2 to 20 years. (Developed by the National Center for Health
Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion, the Centers for Disease Control and
Prevention, and the US Department of Health and Human Services, May 30, 2000 [modified April 20, 2001], www.cdc.gov/growthcharts.)
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40) 289

2 to 20 years: Girls NAME

Stature-for-age and Weight-for-age percentiles RECORD #

12 13 14 15 16 17 18 19 20
Mother’s Stature Father’s Stature cm in
Date Age Weight Stature BMI*
AGE (YEARS) 76
190
74
185 S
72
180 T
70 A
95
175 T
*To Calculate BMI: Weight (kg) ! Stature (cm)! Stature (cm) " 10,000 90
68 U
or Weight (Ib) ! Stature (in) ! Stature (in) " 703
170 R
75 66
165 E
in cm 3 4 5 6 7 8 9 10 11 50
64
160 25 160
62 62
155 10 155
60 5 60
150 150
58
145
56
140 105 230
54
S 135 100 220
T 52
A 130 95 210
50
T 125 90 200
U
48 190
R 120 85
E 95 180
46
115 80
44 170
110 90 75
42 160
105 70
150 W
40
100 75 65 140 E
38 I
95 60 130 G
50
36 90 H
55 120
25 T
34 85 50 110
10
32 80
5
45 100
30
40 90
80 35 35 80
W 70 70
30 30
E 60 60
I 25 25
G 50 50
H 20 20
40 40
T
15 15
30 30
10 10
lb kg AGE (YEARS) kg lb
2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
Published May 30, 2000 (modified 11/21/00).
SOURCE: Developed by the National Center for Health Statistics in collaboration with
National Center for Chronic Disease Prevention and Health Promotion (2000).
http://www.cdc.gov/growthcharts SAFER HEALTHIER PEOPLETM

Figure 13-4
CDC growth charts. Stature-for-age and weight-for age percentiles: girls age 2 to 20 years. (Developed by the National Center for Health
Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion, the Centers for Disease Control and
Prevention, and the US Department of Health and Human Services, May 30, 2000 [modified April 20, 2001], www.cdc.gov/growthcharts.)
290 SECTION I • Scientific Foundations
In the first 6 months of life in the supine position, the
infant undergoes many changes. At 1 month, the elbows,
hips, and trunk remain in flexion, with random kicking
occurring. The infant is in his or her “floppiest” stage at
2 months, as demonstrated by a total head lag with pull-
to-sit. Symmetry occurs during the 3rd and 4th months,
and bilateral kicking, which rolls the pelvis into anterior
and posterior tilt, occurs, which requires activation of the
abdominal musculature.12 By 4 months, the infant is often-
times able to roll into side lying, and eye-foot and hand-to-
foot contact appear. By 5 months, the baby can grasp a foot
and bring it to the mouth. By 6 months, the component
of antigravity flexion control and strength is complete, and
the infant can maintain all extremities extended into space
above the trunk, lift the head off the support surface inde-
pendently, and rotate the pelvis on the shoulders.2
Standing features in the newborn exist. When the
infant is placed in the standing position as a newborn, the
baby can accept part of his or her own weight but cannot
achieve upright trunk extension in standing because of
the kyphotic posture. For the first 4 months of life, the
infant can only take part of her or his weight in stand-
ing, but the infant will assume a more upright posture
as his or her trunk kyphosis decreases. By 6 months, a
mild lordosis in the spine appears, and the infant wid-
ens his or her base of support. Although foot control is
poor at this age in standing, by 7 to 8 months, ankle and
foot strength increases. At this age, infants stand on their
toes, as if to prepare for push-off for gait. By 12 months,
infants should stand indepently.2
Balance and Gait
In the first 6 months, the infant gradually achieves the
ability to maintain the position of sitting when placed in
this position.12 The infant typically sits in a “ring” posi-
tion, with the legs arranged in a ring position and the soles
of the feet directed toward each other. This arrangement
provides positional stability, which helps prevent a fall.2
As the infant learns antigravity trunk control in sitting,
vaulting transitions occur between sitting and the quad-
ruped position. This occurs at approximately 9 months.
Vaulting occurs when the trunk is shifted over the lower
extremities when the infant is sitting to a position of all
fours; the infant must shift his or her body weight and
catch their body weight with his or her upper extremi-
ties. As the infant continues to gain strength and balance
in the extremities and trunk musculature, she or he will
shift into creeping. Creeping is locomotion on the hands
and knees and consists of rocking forward, backward, and
diagonally in the quadruped position. It is the precursor
to bear-standing, which can occur as early as 6 months
but typically occurs later because of the required upper
extremity strength and control of the pelvis that is required
to maintain the position.12 Bear-standing consists of the
infant being on the feet and hands with knee extension
and hip flexion. Another logical progression from the
quadruped position is kneel-sitting, which occurs at 8 to 9
months. The transition from kneel-sitting to kneel-stand-
ing occurs when the infants have lumbar extension control
and adequate strength in the knee extensors to lift their
pelvis off of their feet.12 Infants continue with preambula-
tory skills during this stage, by creeping on their hands and
knees and pulling themselves to standing. These activities
can occur anywhere from 6 to12 months.2 Interestingly,
infants often first learn to pull to standing using the rails
of a crib and then cannot sit back down again without
help. This is due to the fact that extension skills in the legs
emerge in advance of the flexion that is needed as a coun-
terforce. Once the infant is able to overcome the extension
and buckle at the hips to sit down, cruising is natural pro-
gression.12 Cruising, or side-stepping with upper extrem-
ity support, along furniture can begin as early as 8 to 9
months and begins in the frontal plane. Eventually rotary
motion is added to cruising. Climbing is the culmination
of the dissociation between the lower extremities and anti-
gravity power in the quadriceps and hip extensors. All of
these activities prepare the infant for ambulation.12
Normal Balance and Gait Changes from Ages
0 to 3 Years
● The infant can sit upright at approximately 6 months when placed
in a “ring” position.
● Vaulting occurs at approximately 9 months.
● Kneel-sitting occurs at 8 to 9 months.
● Creeping and pull-to-stand activities occur anywhere from 6 to 12
months.
● Cruising occurs at approximately 8 to 9 months in the frontal plane.
● Ambulation occurs anywhere from 9 to 15 months of age.
● By 2.5 years, the toddler can walk with reciprocal arm swing and
a longer step length and can jump with both feet.
Ambulation can begin as early as 9 months or as
late as 15 months in the normally developing child.14
At 1 year of age, the infant typically has skeletal struc-
ture, joint alignment, and posture that are conducive to
ambulation. In addition, they possess dynamic balance
and postural control. The infant’s first few steps are typi-
cally slow and deliberate, all while maintaining a wide
base of support. The body and limbs are maintained in
an upright posture.14 Infants also frequently squat dur-
ing the first month of walking, which strengthens the
quadriceps eccentrically and lowers the infant’s center of
gravity. After the infant has walked independently for 3
months (at about 15 months of age), the base of support
will narrow, and the child squats less and stands more
erect.14 Because children have good trunk stabilizing
musculature, they lift and pull objects as they ambulate.
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40)
Ambulation continues to be refined through the follow-
ing year as the child becomes stronger and motor skills
continue to improve.
By 2.5 years, the transition from immature sagittal
plane walking to mature sagittal plane walking occurs.
Reciprocal arm swing is also evident. In addition, an
increase in walking velocity also occurs, primarily the
result of a longer step length.14 The 2-year-old child can
kick a ball and steer a push-toy. By 2.5 years, the child
can walk on tiptoes, jump with both feet, and stand on
one foot. By 2.5 years, the child is able to spend over 35%
of gait cycle in single limb support, which is an increase
from 32% seen at 1 year of age. (The normal adult value
is 40%.)2 The mechanics of gait continue to improve until
the age of 3 years.14
Musculoskeletal Problems More Commonly Seen
in 0-to-3 Age Group
● Congenital torticollis
● Developmental hip dysplasia
● Congenital club foot
● Brachial plexus injury
Common Musculoskeletal Problems
Torticollis
Torticollis is defined as any asymmetrical posturing of the
head and neck; the term is derived from the Latin terms
tortus, meaning twisted, and collum, meaning neck.17 The
most common type of torticollis is congenital muscular
torticollis (CMT), although other forms exist. Congenital
muscular torticollis is caused by unilateral fibrosis of the
sternocleidomastoid (SCM).17 Although the etiology of
the SCM fibrosis is unknown, many theories exist. The
reported incidence of CMT ranges from 0.084% to 1.9%,
and affects males and females equally.
A majority of patients with CMT present with evi-
dence of a nodule or benign tumor in the SCM within
the first 3 months of life; the tumor gradually disappears
at about 4 to 6 months.17, 18 Biopsies of the tumors reveal
the histological appearance of a fibroma.
The unilateral fibrosis of the SCM seen with CMT
causes the head to be tilted toward the side of the tumor
and the chin rotated toward the opposite side.17 The
opposite SCM is lengthened and weak and cervical sco-
liosis is convex toward the side opposite the tumor (con-
vex toward the side of the lengthened SCM).18 Infants
may also have associated problems, including hip dyspla-
sia, club foot, metatarsus adductus, and brachial plexus
injury.17 In addition, many infants with CMT present as
fussy, irritable babies with poor self-calming skills and a
low tolerance for positional changes and stimulation.18
291
The diagnosis of CMT is usually made in the first few
months of life. A thorough examination includes palpa-
tion of the SCM bilaterally; findings of a fibrotic nod-
ule will most likely be present on the involved side. The
tumor is hard, painless, and 1 to 3 cm in diameter.18 In
addition, shoulder elevation on the affected side or a lat-
eral shift of the head toward the affected side may be
present.18
Management of the infant with CMT includes stretch-
ing of the SCM upper trapezius and ipsilateral trunk
muscles. The clinician should bear in mind that a child
may lose range of motion (ROM) of the SCM during
a growth spurt because the SCM on the involved side
does not grow at the same rate as the muscle on the
uninvolved side.18,19 Other interventions utilized in the
early phases of rehabilitation include strengthening exer-
cises of the trunk, soft-tissue mobilization, and the use
of a collar, if necessary.18 The collar is typically added to
conservative treatment of infants with CMT if they are 4
months of age or older and show a consistent head tilt
of 5° or more. The infant must have adequate ROM and
head control and strength to lift his or her head away
from the side of the collar.20 Collars can be made out of
PVC tubing or foam. The reader is referred elsewhere for
specifics of collar design (Figure 13-5).20
Fewer than 16% of children treated conservatively
before 1 year of age require surgery; but when conserva-
tive management of CMT fails, surgical intervention is
warranted. The actual surgical technique involves dissec-
tion of the SCM at the level where the sternal and cla-
vicular heads converge; the central portion of the muscle
is removed. Physical therapy is resumed 1 to 2 weeks fol-
lowing the operation; postoperative bracing may also be
recommended.21
Researchers have examined the outcomes for infants
with CMT.22,23 Studies have shown that children who
were treated in the first year of life had better results
than those treated later, regardless of the intervention.
In addition, the duration of the condition as well as the
severity of the deformity before the operation had the
major effects on surgical results.22,23
Developmental Dysplasia of the Hip
The term developmental dysplasia of the hip (DDH) is
replacing the term congenital dysplasia of the hip. Dysplasia
describes the abnormal development or growth. Normal
muscle balance and a femoral head that is congruent and
seated within the acetabulum are necessary for normal
hip development. The concave acetabulum develops in
response to the spherical femoral head.24
The etiology of DDH is multifactorial; factors that
predispose an infant to DDH include mechanical,
physiological, and environmental factors. Mechanical fac-
tors include a small intrauterine space, breech presenta-
tion, and positioning of the fetal hip against the mother’s
292 SECTION I • Scientific Foundations

Figure 13-5
Child wearing a foam collar. (From Jacques C, Karmel-Ross K: The use of splinting in conservative and post-operative treatment on congenital
muscular torticollis, Phys Occup Ther Pediatr 17[2]:81–90, 1997.)

sacrum in utero. Physiological factors include maternal

hormone influence of estrogen and relaxin, which results
in ligamentous laxity of the female infant. This is thought
to account for the 6:1 ratio of female-to-male incidence
of DDH.24
Physical exam in an infant with DDH reveals hip
abduction limitation or an asymmetry in the amount of
abduction available at the affected hip. Typical abduc-
tion ROM for the neonate is 75° and 90° abduction in
each hip. If a side-to-side difference of as little as 5° to
10° exists, DDH should be considered. Other physical
exam findings include skinfold asymmetry, pistoning,
or an apparent leg length discrepancy.25 In addition,
Ortolani and Barlow signs are used to assess hip stabil-
ity. The Ortolani sign is the palpable sensation of the
femoral head gliding over the cartilaginous ridge as it
moves back into the acetabulum. This is performed with
the infant’s hip flexed to 90°; the thigh is then gently
abducted, which brings the femoral head from its dislo-
cated posterior position forward into the acetabulum. In
a positive test, there is typically an audible “clunk.” In
the Barlow maneuver, which is a more aggressive test,
the hip is flexed and the thigh adducted while pushing
posteriorly in the line of the shaft of the femur, causing
the femoral head to dislocate posteriorly. Both of these
tests must be performed one leg at a time.25
The most common intervention for DDH in a neonate
or an infant is the Pavlik harness, which maintains the hip
in a position of flexion and abduction that can promote
acetabular development while avoiding the positions of
subluxation (extension and adduction) (Figure 13-6).
Figure 13-6
This harness has a success rate of 85% to 95% if used The Pavlik harness can be used to reduce a dislocated hip. (From
correctly. Frequent monitoring of the hips is required to Campbell S, VanderLinden D, Palisano R, editors: Physical therapy for
avoid avascular necrosis or femoral nerve palsy.24,25 children, p 409, Philadelphia, 2000, WB Saunders.)
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40)
Congenital Clubfoot (Talipes Equinovarus)
Congenital clubfoot, the most common form of which
is talipes equinovarus, occurs in approximately 1 per
1000 live births and is a seen in a 2:1 male-to-female
ratio.24 Talipes equinovarus is characterized by forefoot
adduction, rearfoot varus, and ankle equines. The calca-
neus, foot, and calf are generally smaller on the involved
side than on the uninvolved side. Although the precise
etiology is unknown, it likely results from an abnormal
intrauterine restriction in someone who is genetically
predisposed. The genetic predisposition is supported by
the finding that, in many children, congenital clubfoot
is only one manifestation of more serious congenital find-
ings.24 However, epidemiological research suggests other
contributing factors. A population-based study found
strong associations between maternal smoking and idio-
pathic talipes equinovarus.26 Another study examined the
effects of family history (genetics) and smoking separately
and together. Results showed a strong and significant
effect for the combination of family history and smoking
history.27
Intervention for congenital clubfoot typically consists
of manipulation and serial casting started immediately
after birth, followed by surgical correction at some point
later in the first year of life. The Ponseti method of treat-
ment for talipes equinovarus has been advocated. This
treatment requires applying the initial cast with the fore-
foot supinated such that the plane of the metatarsal heads
is parallel to the long axis of the tibia. An important com-
ponent of this treatment is addressing the cavus deformity
immediately to prevent persistent rigidity and incomplete
correction.28 The Ponseti method utilizes serial manipula-
tion and casting with limited surgical correction.29 Long-
term follow-up of this treatment finds it to be successful
in most cases, with noncompliance and parental educa-
tion as strong factors influencing outcome.30–32
Brachial Plexus Injury (Erb’s and Klumpke’s Palsy)
Brachial plexus injury (BPI) can occur from a variety of
trauma to the shoulder and spine, but it often occurs
because of a difficult vaginal delivery. During a breech
delivery, traction on the newborn’s shoulder can injure
the cervical roots; forceful traction and rotation during
a vertex delivery can injure the C5 and C6 nerve roots.
Other factors that may contribute to BPI include pro-
longed maternal labor, high birth weight, a heavily
sedated mother, and a difficult cesarean section.33
Erb’s palsy, which involves C5 and C6, is the most
common type of BPI and accounts for 73% of BPIs. On
examination, the child’s shoulder is held in extension,
internal rotation, and adduction with the elbow extended
and the forearm pronated. Many scapular muscles are
also affected. This gives the classic “waiter’s tip” posi-
tion. In contrast, Klumpke’s palsy is rare and only affects
2% of all cases. It involves the lower roots, C7, C8, and
293
T1. The child will present with good shoulder and elbow
movements, but the forearm will rest in supination and
the wrist and hand muscles will be paralyzed.33
Physical examination for children with BPIs includes
examination of range of motion, motor function, sen-
sation, functional status, and occasionally electromy-
ography. The majority of infants (90% to 95%) with
birth-related BPI require only physical therapy and no
surgical intervention. Successful interventions include
range of motion, sensory awareness, positioning or
splinting, and occasionally electrical stimulation.33
Preschool (3 to 5 Years)
From ages 3 to 5 years, numerous developmental changes
occur. Preschoolers have developed many of their life
skills in the first 3 years of life, and many skills are fine-
tuned from the ages of 3 to 5 years. Children may also
undergo changes in their level of confidence related to
their motor skills; 3.5-year-old children may seem hesi-
tant regarding motor skills but regain their confidence
by the age of 4 years. The pendulum may actually swing
in the opposite direction, and the 4-year-old may appear
exuberant!12
This section discusses the changes that are relevant to
the musculoskeletal physical therapist. In addition, the
issues of in-toeing, out-toeing, and toe-walking, all of
which can be seen in the preschooler, are discussed.
Physical Growth/Physiological Development
Musculoskeletal System
The musculoskeletal system continues to develop.
Physical activity, including play, causes an increase in
strength in the preschooler. Strength is needed for skills
acquired during this time frame, including riding a tricy-
cle, skipping, hopping, and climbing. In the preschooler,
strength-assessing maneuvers include getting up from
the floor in a mature fashion, jumping, standing on one
foot, the ability to ascend and descend stairs, and stand-
ing on tiptoes.34
The strength of children age 3 to 4 years can be tested
reliably with a standard handheld dynamometer as long
as they understand the directions and are given verbal
praise to help them put forth their best effort. Four-year-
olds can generate 65 N of force with their deltoids and
74 N with their biceps. In their lower extremity, they can
generate approximately 102 N of force with their ham-
strings and 73 N of force with their ankle dorsiflexors.34
Although variations exist between boys and girls, this is
most likely because of skill development with the task
and not actual strength differences. Strength differences
caused by hormonal changes are not typically seen until
puberty. Until that time, the strength of boys and girls
remains similar.34
294 SECTION I • Scientific Foundations
Changes Seen in the 3-to-5 Age Group
● Increased confidence
● Improved motor skills
● Increased strength
● Handedness well established
● Improved cardiac output
● Improved ventilation
● Decreased body mass index
Cardiorespiratory System
The cardiorespiratory system continues to develop in
the preschooler. As in adults, the response of a child to
exercise includes physiological changes in the cardiovas-
cular and pulmonary systems, as well as metabolic effects.
In children, however, the responses depend on the rate
of growth of skeletal muscle, the skeleton itself, and, of
course, the myocardium.15
Many tests used to assess the aerobic capacity of the
individual are geared for children age 5 and older; little
information exists on children younger than the age of 5
years. Maximal oxygen consumption (VO2max) is approxi-
mately 1 L/min at age 5 years; it will increase to 3 to
4 L/min by puberty. Cardiac output, a result of heart rate
and stroke volume, is similar to that in adults, despite the
fact that stroke volume in a 5-year-old is approximately
25% of the stroke volume of an adult. This results in the
increased heart rate seen throughout childhood.15
Ventilation, the rate of exchange of air between the
lungs and ambient air, increases with age. It is normal-
ized by body weight and is the same for children and
adults when activity is maximal. However, at submaximal
levels, ventilation is higher in children and decreases with
age. This suggests that children have a lower ventilatory
reserve than adults.15,35 Vital capacity in a 5-year-old is
about 20% of that in an adult and increases with age. It
is highly correlated with the size of the child, particularly
with height.15
The vital signs in the preschooler also undergo changes
when compared to those of an infant. The young child’s
heart rate is typically 80 to 120 bpm, blood pressure is
100/60 mm Hg, and respiratory rate is 25 to 30.11
Body Composition
The preschooler will experience a change in body com-
position as compared to that of an infant/toddler. Body
mass index, or BMI, is determined by dividing body
weight (in kilograms) by height2 (in meters). BMI actu-
ally decreases between the ages of 3 and 5 years. The
average boy will experience a decrease in BMI from 16
at age 3 years to 15.5 at age 5 years. Girls at this age will
experience a similar drop. After the age of 5 years, BMI
slowly increases.36
Performance Development
Motor/Skill Development
The child between the ages of 3 and 5 years experiences
many rapid changes in motor and skill development.
Three-year-olds have advancing fine motor skills, which
allow them to paste, color, and draw.36 They can alter-
nate feet easily when ascending stairs and can control
their speed of movement. They are able to ride a tricycle
successfully. They may be able to hop, but only on the
preferred leg. Three-year-olds can feed and dress them-
selves, although buttoning may be difficult.12
By age 4 years, self-confidence seems endless. Four-
year-olds can walk downstairs with one foot per step,
catch with the hands only, and learn to ride a small bicy-
cle. They enjoy running, jumping, and climbing. They
can gallop. They may be able to dress themselves with
the exception of tying their shoes.12,36
Five-year-olds tend to be more conforming than 4-year-
olds. The 5-year-old child can skip, jump about 2 feet,
jump rope, and hop in a straight line. Handedness is well
established, and the child can throw overhead. Children
can feed themselves with utensils, with the exception of
cutting meat. Dressing and undressing are independent,
with the (occasional) exception of shoe tying.12,36
Musculoskeletal Problems More Commonly Seen
in 3-to-5 Age Group
● Lower leg alignment
● Idiopathic toe walking
Special Issues
In-Toeing, Out-Toeing, and Idiopathic Toe-Walking
One of the most common reasons for elective referral of a
child to an orthopedist is concerns about in-toeing or out-
toeing. A thorough history—including birth history, the
age when in-toeing or out-toeing began, and family his-
tory—should be noted; also, determining the child’s sit-
ting and sleeping positions is an important first step before
the physical examination.24 Clinical examination should
include documentation of the foot progression angle in
standing, hip rotation ROM, thigh-foot axis, and align-
ment of the foot.
The foot progression angle is defined as the angle
between the longitudinal axis of the foot and a straight
line of the progression of the body in walking, similar
to the Fick angle in adults. In-toeing is expressed as a
negative value, and out-toeing is expressed as a positive
value. During childhood and adult life, it shows little
change, with a mean of +10° and a normal range of −3°
to + 20°.24
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40)
Hip rotation is best measured in the prone position, and
clinicians examine the relationship between the femoral
head and the knee (or patella). If the head of the femur is
pointing anteriorly with the knee straight or parallel to the
table, the hip is anteverted, and in-toeing is most likely
evident. In retroversion, the femoral head is directed
posteriorly when the knee is parallel with the table, and
out-toeing is most likely present. This examination tech-
nique is a variation of the Craig test used in adults. Up
to 2 years of age, the total available hip internal rotation
(IR) and external rotation (ER) is 120°; over age 2 years
it is 95° to 110°.24
Tibial torsion is assessed by measuring the thigh-foot
axis, which is the angular difference between the longitu-
dinal axes of the thigh and foot, as measured in the prone
position with the knee flexed. An alternate position is to
have the child sit with the knee bent to 90°. Internal tibial
torsion is expressed as a negative value and is correlated
with in-toeing, and external tibial torsion, expressed as
a positive value, is correlated with out-toeing. Typically,
the tibia is internally rotated in infants because of intra-
uterine positioning, but spontaneous derotation occurs
during growth. During the first 6 months of life, the tibia
rotates into external tibial torsion. The normal thigh-foot
angle is between 0° and 30° of external tibial torsion,
with the average being 10°.24
Alignment of the foot involves assessing the foot for
metatarsus adductus, clubfoot, and calcaneovalgus. With
metatarsus adductus, the forefoot is curved medially and
the hind foot is in slight valgus. When the child walks,
there is dynamic forefoot varus with medial rotation of
the great toes. This condition is not present in non–
weight bearing. The condition is present from age 4 to 6
months, and mild cases typically resolve on their own.
Numerous differences of opinion exist on how to treat
torsional deformities, how to measure them, or if they
should be treated at all. Most treatment with shoes, braces,
or casts has no proven efficacy.24 Most conditions correct
themselves, and persistent deformity beyond skeletal matu-
rity is rare. However, the child with a torsional deformity
should be closely monitored for any changes.24
A number of children tend to toe-walk some of the
time when first walking independently. Idiopathic toe-
walking, when not related to other conditions such as
cerebral palsy, typically responds well to a conservative
treatment program consisting of gastrocnemius stretch-
ing.37,38 With severe contractures of the Achilles, children
may require serial casting; operative treatment is rarely
required.24,37,38
Childhood into Adolescence
(6 to 18 Years)
As any parent can report, children grow at an astonish-
ing rate. Childhood, the age range from approximately
295
6 years to 9 years, is marked by significant changes in
physical, emotional, and psychological organization.
Although generally linear, systems change at differing
rates, resulting in apparent mismatches between states at
times. However challenging it may be sometimes, most
children and their caregivers weather the storm to see
the end result of a healthy well-adjusted teenager and,
subsequently, adult.
While childhood is a time when young people grow
and develop at a somewhat predictable pace, adoles-
cence is a time of profound change. Most of us recall,
often with chagrin, the experiences of our adolescence.
Physical, emotional, and social changes come rapidly and
dramatically. While adults try to prepare their children
for adolescence, it is difficult to describe to children what
they might feel as these changes occur.
Adolescence is a chronological phase lasting roughly
6 to 7 years, from approximately age 10 to 16 years.
Although changes are occurring before and following this
period, the majority of changes take place during this 6-
or 7-year window.
As these changes take place, it is important to distin-
guish the concepts of growth and maturation. The term
growth is used to describe the actual changes in size that
occur over some period of time. Growth occurs at dif-
ferent rates throughout one’s lifetime, and one might
notice some body parts growing at a different rate than
others or different from the body as a whole.39,40 Progress
toward a state of biological maturity (not emotional or
psychological) is known as maturation. This is a relative
term, as biological maturity varies with the specific tissue,
organ, or system under consideration. For example, in
adolescence, one generally considers sexual, skeletal, and
somatic maturation.39,40 Both the timing of the matura-
tional events (i.e., progression to a different Tanner stage
of sexual maturity) and the rate of that system’s matura-
tion can vary greatly among and within individuals. This
is particularly important when matching pre- and young
adolescents for competitive sports.
Physical Growth/Physiological Development
Musculoskeletal Growth
Musculoskeletal growth throughout the lifetime is often
defined by measures of height, weight, and limb dimen-
sions. Changes in height are generally characterized by
four phases.41 The first phase is from age 0 to 2 years,
when significant longitudinal growth occurs. Phase 2 is
through childhood until just before puberty. During this
phase, changes in height are relatively linear, occurring at
approximately 5 cm/year.41 Just before puberty, height
accelerates (phase 3) until it tapers off in later adolescence
at near-adult height (phase 4). Throughout childhood,
girls and boys are of roughly equal body proportions,
and increases in weight follow increases in height.
296 SECTION I • Scientific Foundations
Phases of Changes in Height
● Phase 1: age 0 to 2 years
● Phase 2: childhood to just before puberty
● Phase 3: puberty
● Phase 4: late adolescence to adulthood
Musculoskeletal changes during adolescence are sig-
nificant. Unlike some other age groups, there are impor-
tant differences between males and females as they reach
puberty. The adolescent growth spurt generally occurs
between the ages of 13 and 15 years, although for girls, the
spurt can begin as much as 2 years before the boys, lasting
from age 11 to 13 years.42,43 The average standard devia-
tion around the onset of growth spurt is around 1 year.42
Height increases at a relatively steady rate through-
out childhood (phase 2) until just before puberty (phase
3). Just before puberty, the rate of change in height
increases significantly from approximately 5 cm/year to
10 to 12 cm/year.41 The rate of height increase for girls is
somewhat slower than it is boys, at approximately 8 cm/
year.42 The rate of change decreases over the next 4 to 5
years, and adult height is usually reached about age 16
years for girls and 18 years for boys.41 Most girls have
achieved 98% of their adult height by age 14.42 Height
growth occurs primarily through the trunk.43 A study of
Swedish adolescents and young adults found the boys
to be 5% taller than the girls at age 16 years.44 Changes
in weight parallel this pattern, following closely behind
increases in height. At age 16, a sample of boys was 11%
heavier than girls of the same chronological age (see
Figures 13-3 and 13-4).44 Within this time frame, growth
in height and weight is not linear. There are periods of
rapid growth and times when growth slows, and the rate
of growth of body parts may not be synchronous. The
phase of rapid growth in height during adolescence is
called peak height velocity (PHV) and refers to the age
at which the maximal rate of growth occurs. Generally,
PHV occurs approximately 1 to 2 years after the onset of
sexual maturation.41 Peak weight velocity occurs approxi-
mately 6 months after PHV.45
Body Composition
Body composition refers to the relative proportions of
lean body mass and fat mass. At birth, babies possess
about 10% to 12% body fat, which increases to approxi-
mately 20% during childhood.41 This proportion is the
same in boys and in girls, and it is consistent with the
many similarities between boys and girls prepubescence.
There are significant differences in body composition
as males and females pass through adolescence. These dif-
ferences are apparent in lean body mass (especially muscle
mass) and percent body fat. The average male is 4 inches
Changes Seen in the 6-to-18 Age Group
● Increased height
● Male and female differences
● Increased weight
● Body composition
● Changes in body mass
● Increased muscle mass
● Skeletal maturation
● Sexual maturation
● Improved motor skills
● Decreased heart rate
● Increased blood pressure
● Decreased respiratory rate
taller and 29 pounds heavier than the average female.46
The male skeleton weighs approximately 8 pounds
more and has approximately 25 more pounds of muscle
mass. During puberty, testosterone increases in boys cause
an increase in lean body mass, while estrogen increases in
girls cause increased fat deposition, breast development,
and widening of the hips. In general, postpubertal boys
exhibit approximately 15% to 17% body fat, while girls
have 25% to 27% body fat. However, female athletes
tend to have lower body fat compared with sedentary
controls.
Muscle accounts for only approximately 25% of total
body weight in childhood. Increases in muscle mass are
relatively linear as increases in weight occur. As boys pass
through adolescence, their muscle mass reaches about 40%
to 54% of their body mass at age 17 years, while in girls,
the muscle mass is about 40% to 45% of body mass at age
13 years and then declines relative to fat mass.41,47 By the
end of adolescence, girls have only about 79% of the lower
extremity muscle mass of their male counterparts.48
In terms of fiber distribution and size, there appears to
be no gender difference throughout childhood. However,
from childhood to adolescence, fiber size increases 3.5-
fold in girls and 4.5-fold in boys.48 The increase in muscle
cross-sectional size is nearly linear from infancy through
adolescence.49 These increases are the result of increases
in the muscle fiber size, not increases in the number of
fibers.41 Girls achieve peak fiber diameter during adoles-
cence, while boys reach their peak in early adulthood.49
Fiber type composition does not appear to differ between
the sexes at age 16, but total cross-sectional area in one
study was 13% greater in boys than in girls.44 Girls had
approximately 51% type I fibers and 48% type II fibers,
while boys had 55% type I fibers and 45% type II fibers.44
This is typical for adults, whose distribution of type I
muscle fibers averages 50% to 60%.49
In a longitudinal study of boys and girls from age 13
to 27 years, van Mechelen and Kemper found that there
was a significant increase in body mass index (BMI) for
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40) 297

both boys and girls from age 13 to 27 years.50 The longi-
tudinal pattern was different between boys and girls, with
the girls showing a higher BMI during adolescence and
boys showing a higher BMI at age 27 years. Skin-fold
measurements also followed a different pattern between
males and females, with a steady increase in the sum of
skin folds between ages 16 and 27 years for the boys,
while the girls showed a decrease between the ages of
21 and 27 years.50 In general, body fat averages around
20% through childhood until puberty. As estrogen levels
increase in girls, they deposit greater amounts of body
fat.41 Boys, while also continuing to deposit fat, coun-
terbalance this with a greater deposition of muscle mass,
thereby reducing the relative value of body fat.
There are some questions about the measurement
validity of BMI in children.51 Although correlations
between BMI and percent fat measured by dual photon
absorptiometry vary from 0.50 to 0.83, changes and dif-
ferences in BMI seem to have clinical significance. That is,
in children and adolescents, associations have been found
between BMI or BMI changes and increased blood pres-
sure, poor blood lipid profiles, non-insulin-dependent
diabetes mellitus, and early atherosclerotic lesions.51–53 A
study of adolescents with hypertension showed that train-
ing reduced both systolic and diastolic blood pressure,
although it never reached normal levels.54 Nine months
after the cessation of training, systolic BP had returned
to pretraining levels, while diastolic blood pressure was
still lower. There are also important ethnic variations.
The Third National Health and Nutrition Examination
Survey (NHANES) found that blood pressure levels were
higher for black girls than for white girls in every age
group.55 Glycosylated hemoglobin levels were higher for
black and Mexican American girls and boys than for white
girls and boys. All these ethnic differences remained after
accounting for socioeconomic status and age.55
Data from the Youth Risk Behavioral Surveillance
System (YRBS) suggest that there are disparities in adoles-
cents who are overweight. A greater percentage of females
who are black are overweight or at risk of becoming over-
weight than are whites (Table 13-1). Moreover, changes
in activity patterns, especially in females and blacks, are
already evident by the ninth grade.56 The NHANES found
that BMI levels were significantly higher for black and
Mexican American girls than for white girls.55 Moreover,
these differences were evident by the age of 6 to 9 years
and the differences widened further from age 18 to 24
years. This places these populations at risk for a multitude
of health problems in later years. Childhood obesity is
a strong predictor of obesity in adulthood, and rates of
obesity increase as children age. A study of overweight
adolescent boys found that those with a BMI greater
than the 75th percentile had increased the risk of death
from all causes and that overweight boys and girls had an
increased risk of obesity-associated morbidities compared
with their age-matched peer group.57
Much of this trend is due to insufficient activity in
youth today. Studies have consistently shown decreases in
activity, especially moderate or vigorous activity, beginning
early in youth.58 Tables 13-2, 13-3, and 13-4 highlight

Table 13-1
High School Students at Risk for Becoming Overweight
At Risk for Becoming Overweight* Overweight†

Category Female Male Total Female Male Total

% CI‡ (±) % CI (±) % CI (±) % CI (±) % CI (±) % CI (±)

Race/Ethnicity
White§ 13.8 3.0 14.3 1.8 14.1 1.9 7.8 3.1 16.2 4.9 12.2 4.0
Black§ 21.2 4.2 15.5 3.1 18.3 1.9 15.6 3.8 19.5 3.4 17.6 3.0
Hispanic 15.7 2.5 19.0 2.9 17.3 2.0 11.8 3.0 21.7 3.3 16.8 2.6
Grade
9 15.6 2.9 15.3 3.3 15.4 2.7 11.2 2.6 19.0 3.9 15.3 3.1
10 15.3 2.7 14.7 2.0 15.0 1.6 9.3 3.1 17.9 5.1 13.7 3.9
11 16.9 2.9 16.6 2.4 16.8 1.6 8.6 2.7 17.0 3.9 12.9 3.0
12 13.2 3.1 15.6 2.0 14.4 1.7 8.0 3.4 14.7 4.1 11.4 3.5
Total 15.3 2.0 15.5 1.3 15.4 1.3 9.4 2.6 17.4 3.7 13.5 3.1

From Grunbaum JA, Kann L, Kinchen S et al: Youth risk behavior surveillance—United States 2003, Morbidity and Mortality Weekly Report
Surveillance Summary 53(2):1–96, 2004.
*Students who were ≥85th percentile but <95th percentile for body mass index, by age and sex, based on reference data.
†
Students who were ≥95th percentile for body mass index, by age and sex, based on reference data.
‡
95% confidence interval.
§
Non-Hispanic.
298 SECTION I • Scientific Foundations

Table 13-2
High School Students’ Participation in Physical Education (PE) Class
Exercised or Played Sports
>20 Minutes during
Enrolled in PE Class* Attended PE Class Daily† an Average PE Class‡
Category
Female Male Total Female Male Total Female Male Total

CI§ CI CI CI CI CI CI CI CI
% (±) % (±) % (±) % (±) % (±) % (±) % (±) % (±) % (±)

Race/
Ethnicity
White¶ 51.5 10.4 55.9 9.3 53.7 9.7 23.1 7.3 26.8 7.1 24.9 7.0 76.6 5.4 85.8 4.0 81.5 4.4
Black¶ 49.3 8.8 63.1 4.8 56.0 6.2 29.0 7.5 37.1 6.0 33.0 6.3 66.7 5.8 80.0 4.0 74.0 4.3
Hispanic 56.1 5.7 61.4 6.3 58.8 5.0 34.0 8.5 39.5 9.0 36.7 8.0 73.5 4.9 82.5 4.5 78.2 3.9
Grade
9 71.2 7.1 70.8 7.5 71.0 6.9 38.0 9.7 37.7 8.5 37.9 8.6 75.7 5.0 84.8 3.3 80.3 3.6
10 58.3 10.8 63.0 7.9 60.7 9.0 29.1 8.8 33.5 7.9 31.3 8.0 77.0 4.3 83.2 4.3 80.3 4.0
11 40.8 9.8 50.5 8.8 45.7 8.8 19.2 4.8 26.0 5.0 22.6 4.6 71.6 6.7 83.7 5.7 78.4 5.4
12 34.6 9.8 44.5 9.3 39.5 8.9 15.2 4.0 21.4 4.9 18.2 4.0 74.9 5.4 87.2 4.4 81.8 4.5
Total 52.8 7.7 58.5 7.2 55.7 7.3 26.4 6.1 30.5 5.7 28.4 5.7 75.3 4.0 84.5 2.8 80.3 3.2

From Grunbaum JA, Kann L, Kinchen S et al: Youth risk behavior surveillance—United States 2003, Morbidity and Mortality Weekly Report
Surveillance Summary 53(2):1–96, 2004.
*
On one or more days in an average week when they were in school.
†
5 days in an average week when they were in school.
‡
Among the 55.7% of students enrolled in PE class
§
95% confidence interval
¶
Non-Hispanic

Table 13-3
High School Students’ Participation in Moderate or Vigorous Physical Activity
Participated in Sufficient Vigorous Participated in Sufficient Moderate
Physical Activity* Physical Activity†
Category
Female Male Total Female Male Total

% CI‡ (±) % CI (±) % CI (±) % CI (±) % CI (±) % CI (±)

Race/
Ethnicity
White§ 58.1 3.8 71.9 2.9 65.2 3.0 23.3 2.5 28.9 1.7 26.2 1.8
Black§ 44.9 4.6 65.0 3.5 54.8 3.5 17.5 2.4 25.8 2.7 21.7 2.1
Hispanic 51.8 4.1 66.7 4.3 59.3 2.9 20.6 2.9 23.3 3.6 22.0 2.6
Grade
9 63.6 4.2 73.1 3.2 68.5 3.0 22.3 2.5 28.3 2.6 25.4 2.1
10 58.2 4.0 71.5 4.0 64.9 3.5 25.3 2.7 26.2 1.9 25.7 1.7
11 49.4 3.5 70.4 2.8 60.1 2.7 20.0 2.6 28.1 2.9 24.2 2.3
12 46.4 3.6 63.7 3.8 55.0 2.5 20.0 2.6 26.3 3.2 23.2 2.4
Total 55.0 2.9 70.0 2.3 62.6 2.3 22.1 1.6 27.2 1.4 24.7 1.3

From Grunbaum JA, Kann L, Kinchen S et al: Youth risk behavior surveillance—United States 2003, Morbidity and Mortality Weekly Report
Surveillance Summary 53(2):1–96, 2004.
*Exercised or participated in physical activities that made students sweat and breathe hard for ≥20 minutes on ≥3 of the 7 days preceding the
survey (e.g., basketball, soccer, running, swimming laps, fast bicycling, fast dancing, or similar aerobic activities).
†
Physical activities that did not make students sweat and breathe hard for ≥30 minutes on ≥5 of the 7 days preceding the survey (e.g., fast walking,
slow bicycling, skating, pushing a lawn mower, or mopping floors).
‡
95% confidence interval.
§
Non-Hispanic.
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40) 299

Table 13-4
Percentage of High School Students with Insufficient Activity Participation
Participated in an Insufficient Amount No Vigorous or Moderate
of Physical Activity* Physical Activity†
Category
Female Male Total Female Male Total

% CI‡ (±) % CI (±) % CI (±) % CI (±) % CI (±) % CI (±)

Race/
Ethnicity
White§ 37.5 3.9 24.8 2.6 31.0 2.9 11.1 3.3 9.3 2.7 10.2 2.8
Black§ 50.4 4.6 31.8 3.9 41.2 3.6 20.0 3.2 12.6 2.6 16.3 2.3
Hispanic 42.6 4.5 30.3 3.8 36.5 2.8 15.4 3.1 10.6 2.8 13.0 2.0
Grade
9 32.7 4.0 23.8 2.9 28.1 2.9 9.7 3.2 8.4 2.3 9.1 2.5
10 35.9 3.7 25.6 3.6 30.8 3.2 10.2 2.4 10.0 2.7 10.1 2.2
11 46.2 3.7 27.0 2.8 36.5 2.7 16.7 4.0 10.8 2.7 13.7 2.8
12 48.4 3.5 32.1 3.3 40.2 2.7 17.0 4.3 10.9 2.6 14.0 3.2
Total 40.1 2.9 26.9 2.1 33.4 2.1 13.1 2.6 10.0 1.9 11.5 2.0

From Grunbaum JA, Kann L, Kinchen S et al: Youth risk behavior surveillance—United States 2003, Morbidity and Mortality Weekly Report
Surveillance Summary 53(2):1–96, 2004.
*Had not participated in sufficient vigorous physical activity and had not participated in sufficient moderate physical activity during the 7 days
preceding the survey.
†
Had not participated in either vigorous physical activity or moderate physical activity during the 7 days preceding the survey.
‡
95% confidence interval.
§
Non-Hispanic.

the low activity levels of high school students. One could
expect continued increases in chronic health problems
such as diabetes, hypertension, and elevated cholesterol
levels in a population with low activity levels.
Skeletal and Somatic Maturation
Somatic maturation, or maturation of the body as a whole,
is generally assessed by age at PHV and varies closely
with this musculoskeletal marker.39 Skeletal maturation
is usually assessed by evaluation the hand and wrist using
standardized radiographs.40 The child’s level of skeletal
maturation is referred to as the skeletal age as compared
to chronological age. Up until puberty, longitudinal
growth of the bone occurs through primary and second-
ary ossification centers. Primary ossification centers are
often located in the shaft or body of long bones, while
secondary centers exist at proximal and distal epiphyseal
plates. At puberty, these ossification centers begin to fuse
and longitudinal growth of the bone ceases. Most bones
have ossified by age 20 years, with girls generally com-
pleting growth before boys. Overall, girls have generally
completed skeletal maturation by age 18 years compared
with age 22 years in boys.
Puberty is a critical time for achieving peak bone
mass. Between the ages of 8 and 20 years, nearly 90%
of adult bone mineral content is deposited, with 30% of
that total occurring in the 3 years surrounding PHV.41
This is especially important for young females, who need
to maximize bone deposition in anticipation of bone
losses that occur later during menopause. The problem
of the female triad (disordered eating menstrual dysfunc-
tion-osteopenia) is especially troubling, as this condition
results in decreases in bone mineral content during the
critical adolescent period.
Sexual Maturation
Sexual maturation is influenced primarily by endocrine
and environmental factors. Although the mechanisms
contributing to the onset of puberty are not fully under-
stood, it is likely the release of gonadotrophin-releasing
hormone (GnRH) associated with bone age and body
composition.43 About 6 months after appropriate levels
of follicle stimulating hormone (FSH) and luteinizing
hormone (LH) are reached, the child should begin to
show outward signs of sexual maturation.43
Much of the work on classification of sexual matura-
tion was performed by James Tanner (Figures 13-7, 13-
8, and 13-9). Tanner classified sexual maturation into five
stages from prepubertal (stage 1) through the adult state
(stage 5). Each stage spans approximately 4.5 years. For
girls, the stages are defined by the development of pubic
hair and breasts, while the stages for boys are defined
by pubic hair and genitalia development. Progression
through the five stages should be linear and predictable.43
300 SECTION I • Scientific Foundations

Figure 13-7
Breast development in girls. The development of the mammae can be divided into five stages. In stage 1, only the nipple is raised above the level
of the breast (as in the child). In stage 2, the budding stage, there is bud-shaped elevation of the areola. On palpation, a fairly hard button can be
felt that is disk- or cherry-shaped. The areola increases in diameter, and the surrounding area elevates slightly. In stage 3, there is further elevation
of the mammae; the areolar diameter increases further, and the shape of mammae is visibly feminine. In stage 4, fat deposits increase, and the
areola forms a secondary elevation above that of the breast. This secondary mound occurs in approximately half of all girls and in some cases
persists in adulthood. In stage 5, the adult stage, the areola usually subsides to the level of the breast and is strongly pigmented. (From Halpern
B, Blackburn T, Incremona B et al: Preparticipation sports physicals. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 855, Philadelphia, 1996, WB Saunders.)

Figure 13-8
Pubic hair development in females. In the development of pubic hair, five stages can be distinguished. In stage 1, there is no growth of pubic hair.
In stage 2, initial, scarcely pigmented hair is present, especially along the labia (not visible on black-and-white photograph). In stage 3, sparse,
dark, visibly pigmented, curly pubic hair is present on the labia. In stage 4, hair that is adult in type but not in extent is present. In stage 5, there
is lateral spreading (type and spread of hair are adult). (From Halpern B, Blackburn T, Incremona B et al: Preparticipation sports physicals. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 855, Philadelphia, 1996, WB Saunders.)

It is incorrect to classify an individual into a single Tanner
stage, as boys and girls each have two distinct areas for
consideration. Proper classification for girls includes the
pubic hair stage and the breast development stage, while
classification for boys includes the pubic hair stage and
the genitalia development stage. The two stages are not
necessarily the same, evidence of the different rates of
maturation even within the same individual. This varia-
tion in maturation rates within and among individuals
can be a source of anxiety and frustration for teenagers
who do not understand why their peers may be more or
less developed than they are. It is within normal ranges
for adolescents of the same chronological age to differ by
as much as two Tanner stages.43
For boys, the onset of stage 1 is between ages 9 and
13 years, with PHV occurring between stages 3 and 4
and peak strength achieved between stages 4 and 5. For
girls, the onset of stage 1 is between ages 8 and 13 years,
with PHV occurring in stage 2 and menarche (onset of
menstruation) occurring at approximately age 12 years.43
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40) 301

Figure 13-9
Genital and pubic hair development in males. The development of external genitalia and pubic hair can be divided into five stages. In stage 1,
the testes, scrotum, and penis are the same size and shape as in the young child, and there is no growth of pubic hair (hair in the pubic area is no
different from that on the rest of the abdomen). In stage 2, there is enlargement of the scrotum and testes. The skin of scrotum becomes redder,
thinner, and wrinkled. The penis has not grown (or just slightly so). Pubic hair is slightly pigmented. In stage 3, there is enlargement of the penis,
especially in length, further enlargement of testes, and descent of scrotum. Dark, definitely pigmented, curly pubic hair is present around the
base of penis. Stage 3 can be photographed. In stage 4, there is continued enlargement of the penis and sculpturing of the glans, with increased
pigmentation of the scrotum. This stage is sometimes best described as not quite adult. Pubic hair is definitely adult in type but not in extent (no
further than the inguinal fold). In stage 5, the adult stage, the scrotum is ample, and the penis reaches almost to the bottom of the scrotum. Pubic
hair spreads to the medial surface of the thighs but not upward. In 80% of men, hair spreads along the linea alba. (From Halpern B, Blackburn
T, Incremona B et al: Preparticipation sports physicals. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p
855, Philadelphia, 1996, WB Saunders.)

Performance Development compensated by an increased heart rate. Because blood

As with most aspects of growth and development, the
timing and tempo of performance development vary
as well. Children generally lack the motor skills in the
major physical performance domains of running, catch-
ing, and throwing.59 These skills are developing as the
neurological and musculoskeletal systems are maturing
and growing. Somewhere between the ages of 6 and
10 years, children will acquire the adult forms of these
skills.59 Skill is quite dependent on the nervous system.
Nerve cells can increase in mass up to 200,000 times,
and the diameter of myelinated nerve cells increases
significantly during growth.60 The nervous system has
reached about 90% of its adult size by age 6 years, and
by puberty, it is nearly fully matured.60 At this point,
the ultimate development of skills depends on practice
and training. There are also differences between males
and females that begin to widen in adolescence. These
differences will be explored relative to the various body
systems.
Cardiorespiratory Fitness
Measures of cardiorespiratory fitness generally include
performance measures during endurance activities and
other baseline measures such as blood pressure, respira-
tory rate, heart rate, and cholesterol levels. In general, as
children pass from infancy through to adulthood, their
heart rate drops from an average of 120 bpm to the adult
norm of approximately 80 bpm. The decrease in heart
rate to adult levels occurs at roughly age 16 years and
is partially the result of increased efficiency and greater
stroke volume. The smaller heart and lower blood vol-
ume of a child result in a lower stroke volume, which is
pressure is directly related to body size, it is lower in
children than in adults. It increases with growth from
approximately 90/60 mmHg in children to approxi-
mately 110/70 mmHg by age 18 years.41 The respira-
tory rate decreases from 20 breaths/minute in infancy to
adult levels of 12 breaths/minute. The heart and lungs
grow in a linear fashion along with the growth of other
body organs and systems.
Because resting metabolic activity is related to muscle
mass, women have a 5% to 10% lower resting metabolic
rate than men.61 When expressed relative to fat-free mass,
gender differences generally disappear. As expected,
women with greater muscle mass have a higher resting
metabolic rate than untrained women. Like metabolic
activity, cardiorespiratory capacity is related to body size
and composition. Much of the difference between males
and females can be explained by sex. Before puberty,
maximum oxygen consumption (VO2max) is equal
between boys and girls. After puberty, when VO2max is
described in terms of ml/kg fat-free/min, male/female
differences decrease to about 15%.61
During puberty, VO2max increases linearly with increases
in body weight, with boys peaking at about age 16 years.
In contrast, VO2max peaks at approximately age 13 to 15
years in girls and then declines gradually.41 Again, when
normalized for body weight or lean body mass, the boys
show little change between the ages of 6 years and young
adulthood, while girls show a gradual decrease across
the adolescent period, likely a reflection of decreases in
activity levels.41 Although the absolute VO2max changes
little throughout childhood into puberty, performance in
endurance events obviously increases substantially. This
likely is the result of improvements in muscular strength,
302 SECTION I • Scientific Foundations
endurance, and efficiency. Studies of children and adults
performing similar activities have shown the adults to be
30% to 42% efficient, while the children were only 15%
to 22% efficient.62
Anaerobic Power
Anaerobic power is often used as another measure of
cardiorespiratory fitness. The direct measurement of
anaerobic power in children and adolescents is not
currently possible because the techniques are too inva-
sive, so most research focuses on determining short-term
power output. Most studies use the Wingate anaerobic
test to assess peak power (PP) and mean power (MP)
over a specified period of time. Unfortunately, the data
are conflicting, with some studies finding that MP
is higher in boys, others finding that MP and PP are
higher in girls, and others detecting no difference by
sex.48,63,64 This may be the result of differences in meth-
ods, with most studies being cross-sectional in nature.
Longitudinal studies looking at changes with age also
have provided conflicting results, perhaps because of
how body mass was controlled.47,65 Armstrong et al.
measured short-term power output longitudinally in
boys and girls while controlling for body mass, stature,
and age.48 They found that the values for girls were sig-
nificantly lower than values for boys, with progressive
divergence as age increased. Both body mass and skin-
fold thicknesses had significant influences on MP and
PP, but age continued to have a strong effect indepen-
dent of these two variables. Additionally, the authors
noted that higher oxygen uptake kinetics in children
may denote a lesser reliance on anaerobic metabolism
than shown in adults. Even during the 30-second bout
of exercise, aerobic metabolism provided extensive sup-
port for MP in children. This contribution has been
shown to vary from 18% to 44%.66 Because power is
related to the cross-sectional areas of the muscle and the
length of the muscle, it has been speculated that mus-
cle volume may be an important predictor of MP and
PP in this age group.48,67 It has been found that girls
were exercising at a higher resistance than boys during
Wingate testing when resistance is expressed relative to
thigh muscle volume.68
Expanding on these results, Martin et al. looked at
the effects of age, body mass, and lean leg volume on
short-term peak power in boys and girls from 7.5 to 17.5
years of age.69 They also controlled for the optimal force
and pedaling frequency during the test. The authors
found that PP does not depend on age until age 14 years.
Thereafter, PP is significantly lower in girls, with lean leg
volume being the greatest predictor of PP, accounting
for 68% of the variance in PP. In contrast, the greatest
predictor of PP in boys is age, accounting for 57% of the
variance in PP values. The authors felt that qualitative
muscular factors such as muscle fiber type, motor coordi-
nation, and motor unit activation might account for the
greater values seen in boys compared with girls.69 Motor
unit activation may be a significant factor in peak power
values, because research has shown that 16-year-olds can
activate their quadriceps to a greater extent than can 10-
year-olds. This may be a function of skill development
and of maturation of the nervous system.48
Muscle Strength
Muscle strength performance is the complex inter-
play of muscle fiber type, neurological recruitment,
and cross-sectional size. The last two factors are quite
dependent on training. Studies of muscle performance
in adolescents have generally shown greater strength
performance in males than in females. A study of 16-
year-olds showed that males performed 26% better
in the Sargent jump test and 60% better in the two-
hand lift than females.44 When the data were adjusted
for height and weight, the males still outperformed
the females, 13% in the Sargent jump and 42% in the
two-hand lift. Strength was correlated with an activ-
ity index (questionnaire about physical activity during
leisure time) in females but was correlated with height
and body mass in the males.44
Studies of other strength performance activities have
shown that the young males (age 13 to 27 years) con-
sistently outperform the females in activities such as
the standing high jump, sprint running speed, arm pull
(relative to body weight), bent-arm hang, and leg lifts.50
In most cases, the males continued to show improve-
ments throughout the adolescent period (measured
ages 13 to 16 years), while females improved slightly
or remained unchanged.
The female’s unique body composition contributes
to, but does not fully explain, differences in strength
between males and females. The total cross-sectional
area of women’s muscle averages 60% to 85% of their
male counterparts.61 Peak strength gain occurs approxi-
mately 14 months after peak height velocity (approx-
imately 1 to 2 years after onset of sexual maturation)
and 9 months after peak weight velocity (approximately
6 months after peak height velocity). For girls, mus-
cle strength increases linearly throughout childhood
until approximately age 15 years. There is no apparent
strength increase with puberty as is seen with their male
counterparts. At age 15 to 16 years, a girl’s strength is
approximately 75% of a boy’s strength.61 The strength
differences are more apparent in the upper body than in
the lower extremities.
Motor Performance
Motor performance on a variety of tasks increases
throughout childhood into early adulthood. Overall,
boys outperform girls on many physical tasks includ-
ing running, jumping, and throwing. Boys continue to
 CHAPTER 13 • Effects of Aging-Growth Changes and Life Span Concerns (0–40)
demonstrate improvements in motor performance until
the late teens or even early 20s.59 In contrast, motor
performance increases in girls as a population tends to
slow by age 14 years, perhaps because of changes in
the level of physical activity of many girls.59 A study of
activity levels in children and adolescents from grades
1 through 12 showed that boys were consistently more
active than girls across all age groups.58 Most of the
difference was related to time spent in vigorous physi-
cal activity (VPA) (a difference of 45% between boys
and girls) compared to moderate-to-vigorous physical
activity (MVPA) (an 11% difference). These findings
are consistent with other studies of physical activity.70
More important, all activity decreased as the students
aged, and participation in continuous 20-minute bouts
of physical activity was nearly nonexistent.58 The great-
est decreases were between grades 1 to 3 and 4 to 6.
These significant activity decreases may affect the per-
formance of girls in many motor skills. The one area
where girls tend to outperform boys is in fine-motor
skills. In a study of plate tapping, the girls had consis-
tently faster scores than the boys, although these were
not significantly different.50
Muscle performance characteristics seem to differ
between males and females and may be significant in
the epidemiology of injuries. While there does not
appear to be a difference in muscle reaction time,
some female athletes seem to have different activation
patterns compared with their male counterparts.45 In
response to an anterior tibial perturbation, female ath-
letes preferentially contracted their quadriceps in com-
parison to males and female nonathlete controls who
first contracted their hamstring muscles.71 Additionally,
differences in muscle stiffness exist. After normalizing
for body weight and height, women were less able to
voluntarily stiffen the knee joint in the anterior-poste-
rior plane. Men were able to increase their knee stiff-
ness by an average of fourfold, while women were only
able to double their knee joint stiffness.45 These dif-
ferences in motor performance may have significant
implications in the incidence of anterior cruciate liga-
ment injuries.
Early Adulthood (19 to 40) Years
Early adulthood is the phase from approximately age
19 to 40 years. By this time, physical growth has ceased,
although skeletal maturation may still occur at selected
sites in some individuals. Thus, any changes in this age
group are generally the result of lifestyle choices and not
normal physiological processes.
Some of the greatest concerns in this age group
relate to lifestyle choices that impact the health of
the individual for many years to come. For example,
the prevalence of diabetes in the 20- to 39-year-old
303
age group increased from 1.6% of the population in
1988 to 1994 to 2.2% of the population in 1999 to
2000.72 For those aged 18 to 44 years, the percentage
with limited activity caused by chronic conditions was
6.3% of the population and was similar for both sexes.
However, there were differences by socioeconomic sta-
tus, as 23% of the poor and only 10% of the nonpoor
had these activity limitations.72 Approximately 25% of
the population aged 20 to 74 years has hypertension,
a significant increase from the last reporting period
of 1988 to 1994.72 The percentage of the population
with hypertension is also significantly higher in black
males and females, at 37% and 39%, respectively.72
Crude measures for the age range of early adulthood
show lower levels of hypertension, with only 8.1% of
the males aged 20 to 34 years with diagnosed hyper-
tension. However, this number increases to 17.1% in
the 35-to-44-year-old range. A similar trend is seen
in females, with a prevalence of 2.7% in the 20-to-34-
year-old group, and 15.1% in the 35-to-44-year-old
group.72
Overweight and obesity continue to be significant
factors in early adulthood, with increasing prevalence
of being overweight in our population. The percentage
of people who were overweight (aged 20 to 74 years,
age-adjusted) in 1999 to 2002 varied by gender and
race. Age-adjusted percentages were 69% for the males
and 62% for the females.72 When controlling for race,
nearly 78% of black females were overweight, and 73%
of Mexican males and 71% of Mexican females were
considered to be overweight. When examining data by
gender and age group, 57% of males aged 20 to 34
years were overweight (up from 48% in 1988 to 1994),
and 71% of males from 35 to 44 years were overweight
(up from 66%).72 The same trend is seen in females,
with 53% of those aged 20 to 34 years overweight (up
from 37%), and 61% of females aged 35 to 44 years
overweight (up from 50%).72
These findings are all consistent with Winkleby et
al.,55 who found that the ethnic difference in body mass
index, percentage of energy consumed in the form of
fat, blood pressure, and glycosylated hemoglobin levels
were higher in Mexican American and black boys as
compared with white boys and girls. These differences
found in adolescence persisted into the 25-to-34-year-
old age group.
These trends are all disturbing and reinforce the
importance of regular physical exercise. As noted ear-
lier, the decreases in physical activity begin in early
childhood and expand as children go through ado-
lescence. Poor habits are established young and car-
ried into young adulthood, creating a serious health
problem for our country as these individuals age. It
is imperative that health care providers take proactive
action to reverse this alarming trend. Getting involved
304 SECTION I • Scientific Foundations
in prevention and wellness at the school or community
level is an important charge for health care providers.
Summary
The chapter explored the normal, yet numerous,
changes that occur to the human body throughout the
life span. The specific milestones, issues, and concerns
that the musculoskeletal physical therapist should be
aware of were highlighted. Changes in muscle strength,
balance, motor control, power, and flexibility are nor-
mal throughout development. The accomplishment of
new motor skills and tasks is highly variable. Clinicians
involved in musculoskeletal rehabilitation should have
a good general understanding of life span accomplish-
ments and issues in order to most effectively examine
and treat the patient/client from birth to the age of
40 years.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 72 references for this chapter.

E FFECTS OF A GING -G ROWTH C HANGES
AND L IFE S PAN C ONCERNS (40+)
Marybeth Brown
Physical Changes with Aging:
Middle Age through Old Age
Aging is not one of those events that occurs upon retire-
ment. The process actually begins in the third decade and
continues inexorably until death. The decline that occurs
between the ages of 25 and 55 years is modest, amount-
ing to about 15% to 20% of the total decline, but after age
55, the pace of loss accelerates.1–25 Thus, evaluation and
treatment considerations for the older adult vary tremen-
dously, just on the basis of chronological age. Humans
spend about 70% of their lifetimes undergoing age-
related decline. As the following pages explain, systems
can decline at varying rates, which makes the proper
selection of evaluation tools and treatment design more
challenging for this population than any other group of
patients clinicians treat. Coincident with varying rates of
system decline with aging is the emergence of disease,
which further complicates the issue of proper care.20,26–32
Aging Process
● Aging begins in the third decade of life
● Between the ages of 25 and 55 the decline is approximately 15%
to 20% of total decline
● After the age of 55, decline accelerates
To clarify “older adult,” the following terms from the
National Institute on Aging are used throughout this
chapter: middle age, 45 to 55 years; older middle age,
55 to 65 years; young-old, 65 to 75 years; old, 75 to 85
years; and old-old, 85 years and over. Exercise concerns
14
C H A P T E R
generally differ for each of these age categories, so to
simply treat someone over 50 years as “old” will not suf-
fice. Treatment expectations and design for a 55-year-old
who is deconditioned should not be the same as those
for an 85-year-old who is also deconditioned but has bal-
ance, strength, sensory, visual, and range of motion defi-
cits in addition to diabetes and coronary heart disease.
Age Classifications of the National Institute of Aging
● Middle age: 45–55 years
● Older age: 55–65 years
● Young-old: 65–75 years
● Old: 75–85 years
● Old-old: 85+ years
Skeletal and Articular Changes
Osteoporosis
Loss of bone mass (osteoporosis) with aging is inevitable,
and loss occurs in both men and women beginning in
middle age (Figure 14-1). The rate of bone loss is about
1% per year, and because women have less bone than men
at all times of life, they are more at risk for osteoporo-
sis than are men.9,20,23–25,33,34 Women have an accelerated
phase of bone loss during the menopausal years when the
rate of loss is about 2% per year for about 5 years. Thus,
the overall bone loss in women typically exceeds that of
men, putting women at greater risk for bone failure than
men. It has been determined that half of all women over
the age of 50 years are osteopenic, an appalling statistic, as
it indicates that North Americans are not doing things to
optimize bone mass during the growing years (according
305
306 SECTION I • Scientific Foundations
Figure 14-1
Bone mass changes with age as measured by DEXA in men and
women. Bone declines at a rate of ∼1% per year in both men and
women, starting in the 5th decade. An accelerated decline in bone is
observed during the menopause in women. (Data from Smith DM,
Khairi MR, Norton J, Johnston CC Jr: Age and activity effects on rate
of bone mineral loss, J Clin Invest 58(3): 716-721, 1976.)
to the National Osteoporosis Foundation). Young people,
particularly women and girls, are far more likely to reach
for a soda than a glass of milk, and thus daily intake of
calcium for today’s youth is less than what is required. The
majority of bone loss occurs from the trabecular sites such
as the vertebrae and the head/neck of the femur.35 Thus,
there is a higher prevalence of vertebral and femoral neck
of the hip fractures in osteoporotic individuals.
Although, as mentioned earlier, bone loss typically
begins in middle age (about 40 years), bone loss can
occur at any time of life. Children and teenagers who
do not get sufficient calcium fail to develop a complete
bone framework. Young adults who fail to meet daily
calcium demands lose bone needed to provide sufficient
calcium for muscle contraction and other vital functions.
Bone is a calcium reservoir, and if dietary calcium intake
is inadequate, the needed calcium is taken from the bone.
This then leads to an overall loss in bone tissue. Stories
abound of young women, mostly track athletes, who
train so hard they become amenorrheic, secondary to
low estrogen values (the female athlete triad). The lack of
estrogen effect on bone, coupled with inadequate calcium
intake (about 1500 mg/day required) in these female
athletes, ultimately results in profound bone loss. It is not
uncommon to find the skeletal framework of a 70-year-old
woman in a 20-year-old body under these conditions.36
This magnitude of skeletal decline can occur within 1 or 2
years. What is sad is that recovery of bone seldom occurs
in the young female athlete. Preventing bone loss is the
key to healthy aging.
Rate of Bone Loss
● 1% per year starting in middle age (about 40 years of age)
● 2% per year in women (postmenopausal) for 5 years
● Bone loss may be seen in children and young adults if daily
calcium demands are not maintained
Osteoarthritis
Joint changes also occur as a natural part of aging; what
is not due to natural aging is due to the development of
osteoarthritis. Over the years there is a subtle alteration of
the glycosaminoglycan (GAG) content of cartilage (chon-
droitin sulfate to keratin sulfate) within articular cartilage.
This results in articular cartilage that is less resilient and tol-
erant of stress placed on it. Chondroitin sulfate holds water,
and it is the water content that provides articular cartilage
(and intervertebral discs) with its “give” or resilience. The
loss of water from cartilage and discs is particularly pro-
nounced between ages 60 to 70 years and accounts for the
loss in height that older adults experience. This height loss
is between 2 to 2.5 inches for both men and women.37,38
Loss in height of more than 2.5 inches may indicate
osteoporosis, and excessive height loss should be probed
further during a clinical evaluation. Osteoporosis must be
considered in the design and execution of an appropriate
treatment program (see the Management of Osteoarthritis
and Rheumatoid Arthritis chapter of the Pathology and
Intervention book of this series).
The shift in GAG content and loss of water from
articular cartilage are major factors that predispose car-
tilage to breakdown, a process referred to as osteoar-
throsis or osteoarthritis (OA). OA causes joint surfaces
to erode, and thus the articular surfaces, which normally
are smoother and more friction-free than ice, become
uneven. Fissures may develop, and cartilage material
can be worn down to the point where bone is interfac-
ing with bone, a painful situation. Loose cartilage mate-
rial interacting with the synovial membrane or the joint
capsule may set up additional inflammation, pain, and
swelling (Figure 14-2). OA is the most prevalent clini-
cal condition in seniors, affecting about three quarters
of the entire older adult population, most often at the
knee, followed by the hip.13,20,28,29,34,39–45 Pain, loss of
motion, muscle weakness around the joint, and swelling
are common complaints and ample justification for treat-
ment. In addition to the clinical symptoms mentioned
previously, a joint eroded by OA experiences a large
increase in the coefficient of friction, which contributes
to the slowing observed with age and a reduction in end
range of motion.
Soft tissues surrounding joints (e.g., tendons, liga-
ments, capsule) also undergo changes that include a shift
in GAG content, a loss of water, and an increase in colla-
gen cross-links. These age-related changes result in joint
tissues that are stiffer, less pliant, and more susceptible to
injury. Stiffness is the most ubiquitous complaint of older
adults, and it is probable that the shift in GAG content,
resulting in a loss of water, and the increase in collagen
cross-linking contribute substantially to the significant
reduction in joint range of motion seen in all major joints
with age and to the complaints of difficulty with initia-
tion of movement.
 CHAPTER 14 • Effects of Aging-Growth Changes and Life Span Concerns (40+) 307

NORMAL JOINT

Bone Muscle

Bursa
Synovial
membrane
Tendon
Synovial
fluid

Joint capsule
(ligaments) Cartilage

OSTEOARTHRITIS RHEUMATOID ARTHRITIS

Swollen,
thickened, Bone
inflamed loss
synovial
membrane Bone
erosion
Osteophyte
Thinned
cartilage

Bone ends Cartilage

rub together thinning
Deformity

Figure 14-2
Typical osteoarthritic changes that may occur with advancing age. Severe erosion of articular cartilage results in bone on bone, altered
biomechanics at the joint, an increase in joint friction or resistance to movement, and frequently pain and swelling.

Skeletal Muscle in those who are sedentary.56–65 Atrophy is evident in

Most texts that describe the aging of skeletal muscle
indicate that after the age of about 30 years muscle mass
declines at a rate of 1% per year.1,36,46–55 Thus, by age 80,
elders have half the muscle mass they started with as a
young adult. As indicated above, muscle loss does not sud-
denly occur at age 65; rather the process begins in young
adults. Even though the change in muscle during the 20s
and 30s is modest, the consequence of muscle decline is
evident in athletes such as Kareem Abdul Jabbar, who
is still a spectacular athlete, but simply cannot perform
at the level he once did. His decline in performance is
not exclusively the result of age-related decline in muscle
tissue; but muscle loss is a large contributor to the fact
he cannot jump as high or run as fast. With aging, these
changes in performance, although slowed because of his
original, excellent conditioning, are irreversible.
Loss in muscle mass is the consequence of two phe-
nomena: an actual decline in the number of muscle
fibers present and atrophy of many of the remaining
fibers, particularly among the fast-twitch or type II fiber
population.1,52–54 Modest muscle fiber loss occurs between
the ages of 25 and 50 years secondary to denervation
(the primary cause) and possibly as well to cell death
(apoptosis). Fiber loss occurs in all people regardless of
their level of fitness or adherence to training. However,
the magnitude of muscle mass loss seems to be far greater
middle age, particularly among men and women with a
long history of inactivity. It is not clear if atrophy begins
to occur before about 50 years of age as most studies
include as subjects individuals who are nonexercisers.
Anecdotally, power lifters who are in their 40s and 50s
do not give the appearance of being atrophic.
Muscle Mass Decline
● 1% per year after age 30
● Decline in number of muscle fibers
● Atrophy, especially of fast-twitch (type II) fibers
Interestingly, in a study of master athletes, lifters who
ranged from 18 to 82 years, fiber atrophy emerged as
a failure to maintain hypertrophy.66 Whether failure to
maintain hypertrophy involves the same molecular pro-
cess as the atrophy that occurs secondary to immobiliza-
tion or bed rest is unclear. In Figure 14-3, loss in fiber
area is plotted against age in 22 Olympic and power lifters.
It is apparent that after age 50, there is a consistent loss
of muscle fiber size. Of note is the oldest lifter, who had
fiber areas that were comparable to those of five physical
therapy students who were biopsied as controls. These
data suggest that the majority of fiber atrophy with old
308 SECTION I • Scientific Foundations
Figure 14-3
Muscle fiber area in master lifters. Muscle biopsies from the vastus
lateralis muscle of 22 master athletes aged 18 to 82 years and 5
physical therapy students who exercise recreationally. Only type IIa
fiber areas are presented as this fiber type represented approximately
75% of the total in the lifters.
age is due to inactivity. Data also provoke the question of
why these men cannot maintain fiber hypertrophy with
advancing age even though they are training rigorously.
Hormonal effects on skeletal muscle with aging are
minimally understood. Starting in middle age, a reduction
in serum values of sex hormones (testosterone and estro-
gen) is evident. The decline in both male and female sex
hormones is associated with the age-related loss in skel-
etal muscle mass and strength. Hypogonadal men show
a remarkably rapid increase in muscle mass and strength
when testosterone values are returned to physiologically
normal.6,7,18,19,27,67 Women given hormone replacement
therapy do not show the dramatic improvement in
muscle mass that men do, but there are not enough stud-
ies on women to draw meaningful conclusions. There is
evidence to suggest that estrogen directly or indirectly
affects muscle mass and contractile function.6,7,23,28,68
Another hormone that may affect skeletal muscle mass
and function with advancing age is thyroid hormone. Nearly
one third of the older adults in our senior exercise program
are taking Synthroid or some other brand of thyroid hor-
mone, suggesting that many elders are regarded by their
physicians as hypothyroid.39,47,67,69–71 Hypothyroidism is
associated in young men and women with profound fatigue
and atrophy of type II (fast) fibers. Given the preferential
atrophy of type II fibers in older adults, it is tempting to
speculate that one cause of the atrophic change with aging is
hypothyroidism. That being said, it is likely that the majority
of the atrophic change in older adults is due to inactivity.
Cardiovascular
The fundamental change that occurs with age that markedly
affects human performance is the decline in maximum heart
rate (HR). HR declines about 1 beat/year starting in the
third decade, regardless of level of fitness.53,72–77 Because
of the drop in maximum HR with age, exercise intensity
(HR training zone) can be estimated using the formula
220-age. Other cardiovascular changes occur with age, but
it is the drop in HR that contributes the most to the reduc-
tion in exercise capacity as one gets older.
The key indicator of exercise capacity is VO2max, which
translates to the capacity of the cardiovascular system
to provide oxygen to active muscles and to the organs.
Another aspect of VO2max is the amount of oxygen that
can be taken up by working tissues, primarily muscle
mass. Thus, the decline in maximum HR coupled with
the reduction in muscle mass results in a loss of maxi-
mum aerobic capacity of about 50% between 30 and 80
years. While jogging and intensive cycling constitute an
aerobic workout for young adults in their 20s, walking
at a preferred rate of speed may constitute an aerobic
workout for an 80-year-old, particularly if the individual
is unfit. The decline in VO2max with aging is depicted in
Figure 14-4 for both men and women. Note that men
start with a higher maximum oxygen capacity, and thus
loss of VO2max in men with age may not have the same
functional impact as it does in women. Women are more
susceptible to losing independence in society secondary
to the loss in aerobic capacity than men.53,74–77
The values depicted on the graph in Figure 14-4 are rep-
resentative for men and women who are sedentary, which
is the majority of people in North American society. If one
maintains an active aerobic training program throughout
the course of a lifetime, VO2max values will be about 25%
higher than those depicted in Figure 14-4 at all ages.74,75
Thus, exercise is a powerful option for maximizing inde-
pendence and functional capacity throughout the lifetime,
but particularly in the older years.
Small changes occur within the heart with advancing
years such as the rate of ventricular filling, which decreases
about 50% between the ages of 20 and 75 years.68 Left
Figure 14-4
Decline in VO2max with age. Maximal oxygen uptake declines with
age in men and women, at approximately the same rate of loss for
both sexes. Men have a significantly higher aerobic capacity than
women at all ages. (Data from Hawkins SA, Marcell TJ, Victoria
Jaque S, Wiswell RA: A longitudinal assessment of change in VO2
max and maximal heart rate in master athletes, Med Sci Sport Exerc
33(10): 1744-1750, 2001.)
 CHAPTER 14 • Effects of Aging-Growth Changes and Life Span Concerns (40+)
ventricular wall thickness increases because of the increase
in peripheral resistance that also occurs with age.75 These
changes do not meaningfully affect overall heart func-
tion. The pathological changes secondary to disease and
inactivity are what markedly affect heart function and
competence in the older adult.
Total peripheral resistance increases at a rate of
about 1% per year, which has a significant impact on the
heart.53,75–77 Resistance increases because the compliance
of peripheral vessels decreases. Arteries and arterioles
stiffen with age, thus the heart has to pump harder to
overcome the increase in peripheral resistance. In con-
junction with an increase in peripheral resistance is an
increase in aortic resistance. The increase in workload
(demand) on the heart causes the increase in left ven-
tricular wall thickness. Because of increased aortic and
peripheral resistance, resting systolic blood pressure goes
up with aging and may lead to hypertension.
Effect of Aging in Heart and Circulation
● Maximum heart rate decreases
● Maximum aerobic capacity decreases
● Rate of ventricular filling decreases
● Peripheral resistance increases
Nervous System
Nervous system changes are fairly extensive, and this seg-
ment of the chapter addresses changes that affect skeletal
muscle. The primary event impacting muscle function
with advancing age is the loss of axons. Axonal death
leaves muscle fibers without innervation; some of the
remaining fibers die and some are “adopted” by adja-
cent neurons. Thus, the end result is fewer muscle fibers
(and less strength) and fewer motor units. Remaining
motor units contain more muscle fibers than they did
at younger ages, which suggests that recruitment is not
as finely tuned or graded as it was in earlier years. Thus,
the muscles of older adults have fewer fibers secondary
to denervation, and fewer motor units, but remaining
motor units are quite large.
Effect of Aging on Nervous System
● Number of axons decrease
● Fewer motor units
Body Composition
In our relatively sedentary society, it is typical to gain
about a pound a year between the ages of 25 and 65 years.
309
Thereafter body weight stabilizes in most individuals. The
increase in girth is fat mass. Occurring concomitantly
beginning in middle age, along with the expansion of the
waistline, is a reduction in lean mass, primarily skeletal
muscle and bone. Even in those individuals who do not
gain weight with age there is a shift in body composition
to one that has less skeletal muscle and bone and more
fat. This loss of lean mass or fat-free mass is depicted in
Figure 14-5. In this hypothetical case, body weight has
remained unchanged over the course of 50 years.
Even in men and women who are rigorously active
throughout the course of a lifetime (e.g., master’s ath-
letes), there is a change in body composition, reflecting
the expected increase in fat mass and the concomitant loss
of lean mass.70,78–81 Master athletes do not gain as much fat
mass as sedentary individuals, but the pattern is the same:
increased central adiposity. Unfortunately, the majority of
the increase in fat occurs in the peritoneum, which puts
older adults at greater risk for diabetes and heart disease.
Effect of Aging on Body Composition
● Weight gain
● Decreased lean body mass
● Increased fat
Performance Declines with Aging
Skeletal Muscle
Figure 14-6 represents the decline in physical perfor-
mance that is typically observed with advancing age. Even
though the men and women representing the data points
Figure 14-5
Body composition changes with aging in men. With advancing years,
the proportion of lean mass to fat mass changes. Reasonably fit men
and women in their 20s have a body mass composed of approximately
15% to 22% fat with the remainder lean mass (mostly muscle and
bone). The ratio of fat to lean mass gets larger and larger with each
decade. It is not uncommon to find a 50/50 ratio in men and women
in their 80s. (Adapted from Nuti R, Martini G, Gennari C: Age-
related changes of whole skeleton and body composition in healthy
men, Caleif Tissue Int 57(5): 336-339, 1995.)
310 SECTION I • Scientific Foundations
Figure 14-6
Shot put distance performance changes with age. (Redrawn from
Spirduso WW: Physical dimensions of aging, Chicago, 1995, Human
Kinetics.)
on this graph were likely well trained and in good physical
condition, the drop in performance reflects the probable
age-related decline in muscle mass, strength, and power
that was occurring in these individuals.82–90 It should be
noted, however, that there are men and women up to
the age of 100 years who are capable of performing shot
putting, which suggests that our perceptions of what older
men and women can do are skewed toward inactivity.
Probably the most remarkable aspect of skeletal muscle
change with age is its phenomenal variability. Figure 14-7 rep-
resents handgrip as a reflection of general body strength.
Several aspects of this graph are striking. First, there is an
enormous amount of difference in grip strength at any
age. At the age of 35, for example, grip in some men was
Figure 14-7
Handgrip strength in 874 men. (From Kullman DA, Plato CC,
Tobin JD: The role of muscle loss in the age-related decline of grip
strength: cross-sectional and longitudinal perspectives, J Gerontol 45:
M83, 1990.)
a low as 60 kg and as high as 150 kg. Second, the low
values for grip in 35-year-old men are equivalent to those
for some of the 80- and 90-year-olds. Even data for a
muscle group (the quadriceps), which is more critical to
lower extremity function, show the same variability. Data
from the Baltimore Longitudinal Study on Aging (www.
grc.nia.nih.gov/branches/blsa/blsa.htm) indicate that
quadriceps torque output (Cybex test) at 180°/s ranges
from 101 to 248 ft/lbs for men 20 to 29 years and from
16 to 239 ft/lbs for men 80 to 96 years of age. Why are
some men prone to so much strength loss with age while
others are spared? Lifestyle is a major contributor to the
health and well-being of any body system with advancing
age. The old adage of “use it or lose it” certainly applies
to muscle tissue. Nonetheless, there are factors other than
lifestyle that impact the quality and quantity of skeletal
muscle in an aging and aged organism.
Factors Impacting Quality and Quantity of Skeletal
Muscle with Aging
● Lifestyle
● Genetic inheritance
● Muscle group
● Contractile function
● Type of muscle action
● Loss of strength (i.e., the amount of torque produced/unit muscle)
● Speed of movement
● Susceptibility to injury (decreased extensibility)
● Susceptibility to fatigue
Genetic inheritance accounts for 50% to 60% of the
total muscle mass (and strength) an individual possesses,
which leaves great latitude for improvement. There is
ample evidence to indicate that even individuals who are
not genetically gifted with a great deal of muscle mass can
gain substantial (25% to 30%) strength and enhance mus-
cle mass by 10% with strength training.36,47–51, 69,78,82,87,91–110
Regardless of body size or initial muscle size, individuals
have ample muscle mass to remain independent through-
out their lifetimes, if they choose to use it. This subject is
covered more thoroughly later in the chapter.
Interestingly, the rate and magnitude of decline in
skeletal muscle mass and strength differ from muscle
group to muscle group. Upper extremity and fast-twitch-
dominant muscles tend to be spared to a greater extent
than lower extremity muscles. To put this thought a dif-
ferent way, individuals lose muscle mass and strength at
a greater rate in the lower extremities than in the upper
extremities.33,66,111–126 The muscles needed the most
(postural gluteus maximus, quadriceps, erector spinae,
triceps surae) are the ones that tend to show the greatest
magnitude of decline,127–145 a facet of aging that is not
 CHAPTER 14 • Effects of Aging-Growth Changes and Life Span Concerns (40+)
well understood. One would expect the muscles one
needs the most to undergo the least amount of change
with age, but given our sedentary lifestyles, individuals
may not be using these muscles sufficiently to maintain
them. Postural muscles are highly susceptible to atrophy
and need routine mechanical stimulation (e.g., gravity
and body weight) to prevent decline. Astronauts, for
example, lose up to 1% of calf muscle strength per day in
the space station, whereas the nonpostural muscles such
as the toe extensors are relatively impervious to atrophic
change.
One interesting aspect of muscle aging is the change
that occurs in contractile function. Age-related reduc-
tions in muscle mass obviously lead to a concomitant
reduction in strength. As with the decline in muscle
mass, the magnitude and rate of strength change are not
uniform. As expected, lower extremity strength loss is
greater than upper extremity strength loss, at least in the
early years of older age.1,6 For some muscles, strength loss
is commensurate with the loss in muscle mass. In other
instances, the loss in strength exceeds the loss in mass.
Several reports indicate that muscle quality (force/mass
relationship) is diminished in older adults3,33,50,51,66,86,88,11
3,146–150
because of a reduction in calcium delivery from
the sarcoplasmic reticulum, a breakdown of structural
or supporting proteins in the Z line, and an inability to
neurologically “drive” a muscle. Increasing quadriceps
strength by 200% in response to a weight-training pro-
gram is evidence of “neural factors” driving change in
older muscle.47–49,97
Not all forms of “strength” are equally affected by
aging. There is evidence that eccentric strength is main-
tained to a greater extent than isometric or isotonic
strength, which is curious given the tendency of older
adults to eliminate eccentric contractions from their rep-
ertoire. It is common to observe older men and women
plopping into chairs, for example, instead of slowly low-
ering themselves eccentrically onto the furniture, and
dropping from one stair step to the next. Eccentric con-
tractions are more likely to produce damage in old mus-
cle than young muscle and, as a protective mechanism,
elders may not generate eccentric force or torque. In
summary, eccentric strength is best maintained followed
by isometric and then concentric strength. Thus, a com-
prehensive strength evaluation for older adults should
include an assessment of concentric, isometric, and
eccentric capabilities.
Loss of specific strength is another aspect of aging that
has been identified.3,6,7,10,49,92,112,113,127 Specific strength
refers to the amount of torque or force produced per
unit of muscle. As young adults, the relationship between
strength and muscle mass is very close. Equations exist
to determine the amount of force or torque that can be
produced on the basis of available lean muscle mass.113 In
many older adults, loss of strength exceeds the decline in
311
mass, altering the specific strength ratio.3,6,7,10,16,49,92,112,11
3,127
Some of the decline in strength may be due to the
reduction of calcium being delivered to the muscle cell
from the sarcoplasmic reticulum. Although a reduction
in calcium delivery may be part of the problem, it is not
the entire explanation. Single muscle cells that have been
isolated from old and old-old adults also show a deficit in
specific tension, and these cells have all the calcium they
require to generate peak force. Thus, loss of specific mus-
cle strength is a complicated event that is exacerbated by
inactivity. It is not uncommon to see an improvement in
specific strength with a resistance type of exercise pro-
gram.47,78,86,92,95,96,106,108,151,152
The speed of muscle movement also declines (gets
slower) with age.86,153–168 Slowing of movement is a
natural outgrowth of several physiological phenomena:
a greater reduction in type II (fast) fiber size with age
than type I (slow) muscle fibers, possible neuromus-
cular junction remodeling, loss of motor units with an
increase in the size of remaining motor units, and slower
axonal transmission. Slowing of movement is evident in
functional tasks such as picking up an object or walking
quickly. Muscle changes are not exclusively responsible
for slowing of movement. Stiffening of soft tissues, joint
changes, slower axonal transmission, slower central pro-
cessing and motor time, sensory loss,169–171 and strength
loss all contribute to the inevitable slowing of movement
that occurs with aging.
Old muscles are more susceptible to injury than
young muscles are, and the consequences are far more
severe. Muscle tearing with seemingly trivial tasks such
as bending over to pick up an object is not uncommon
because of the reduced extensibility of connective tis-
sues and the increased demand on remaining muscula-
ture. Once an injury occurs, older adults do not repair
as well or as quickly as young adults. In a series of classic
studies, Brooks and Faulkner injured the extensor digi-
torum longus muscle (EDL) in young and old mice and
followed the recovery of muscle mass and function for
up to 60 days post injury.172 Muscle injury was accom-
plished through the imposition of eccentric contrac-
tions on the EDL. As expected, the decline in muscle
force with injury was about 60% in young and old mice,
but the recovery in force occurred much more slowly
in the old animals. Young rats had recovered almost
100% of their EDL muscle strength by 30 days post
injury whereas the old mice had recovered only 80% of
normal muscle force at the end of 60 days. No further
improvement occurred thereafter (up to 120 days), sug-
gesting that once old muscle is injured, force may never
return to the same level. Additional mechanistic stud-
ies revealed that satellite cell activation in old muscle is
insufficient to restore muscle function.173 When satellite
cells are isolated from muscles of old rats or mice and
placed in growth medium, young cells differentiate and
312 SECTION I • Scientific Foundations
proliferate rapidly but old cells are slow to differentiate
and initiate replication.
Another common complaint of old age is muscle
fatigue. In a rehabilitation setting, one often sees older
adults who are attempting to reach a target or lift a small
weight a certain distance; they may show muscle quiv-
ering and what appear to be physical signs of fatigue.
Curiously, the few studies on fatigue that have been
done with middle-aged and older adults do not show
an increased susceptibility to fatigue with advancing age.
One paradigm to induce muscle fatigue is to have a sub-
ject squeeze a hand dynamometer and hold the maximal
contraction as long as possible. The test ends when grip
strength falls to 50% of maximum and time is recorded.
Another protocol involves multiple maximal repeated
contractions of the quadriceps at 180°/s, and when force
reaches 50% of maximum, the test is stopped.156 In both
of these tests, older adults perform as well as young adults,
when strength loss is normalized to differences in start-
ing point (young adults typically have more strength).
What then accounts for the observed fatigue in older
men and women? Central (neural) fatigue is one possibil-
ity, particularly when superimposed on muscles that have
a long history of inactivity. Most individuals in a reha-
bilitation and hospital setting have been quite inactive
before coming for treatment.
Cardiovascular Endurance
The drop with age in VO2max is highly significant, and
the impact of the loss in aerobic capacity is reflected in
routine activity as well as in leisure time activities. It is
not aerobically feasible for most old adults to climb high
mountains or perform a triathlon. For many older adults,
the process of walking only half a mile is beyond their
means. In an earlier study of older women, aerobic test-
ing was done to determine the energy cost of walking.72
Preferred gait speed, which was about 1 mph slower
than gait speed in young adults, required about 70% of
maximum aerobic capacity. Thus, the process of walking
for these women was an aerobic challenge. By contrast,
walking at 3.5 mph as a 20-year-old requires between
20% and 40% of maximum aerobic capacity.174 Any activ-
ity that can be accomplished at less than half of aerobic
maximum can be performed for many hours, and walk-
ing is usually one of those activities. By contrast, walking
at 70% of maximum aerobic capacity results in fatigue
within 20 to 30 minutes. Because the energy cost of
walking is so high, it is rare to see older adults in venues
that require walking long distances such as in a mall.
It must be emphasized that aerobic capacity can be
optimized at any point in life with exercise. A sedentary
individual can increase aerobic capacity by about 25%
with training.75,76,80,85,146,152,163,175 To provide an example
of the importance of aerobic training, the older women
in the aforementioned study had a VO2max of about
12.5 ml O2/kg/min and walking at 2.5 mph required
70% of their available aerobic capacity. If these women
trained (and training is feasible in older adults, even with
heart disease) and raised their VO2max to 16 ml O2/kg/
min, walking at 2.5 mph would now require 55% of avail-
able reserves. After training, sustained walking would be
far more comfortable and reasonable and would result in
less fatigue.
Balance/Coordination
Balance is a complex event, and “good” balance requires
information from the periphery (muscle spindles and
joint receptors), the vestibular apparatus, and the eyes
to be then integrated and refined quickly by the ner-
vous system. Because of changes in central processing
(delays), changes in the vestibular system, the loss of
muscle spindles, and changes in peripheral joint recep-
tors (particularly when vascular disease or neuropathy
is present), balance declines with age. A complete dis-
cussion of balance changes with age is outside the scope
of this chapter. The reader is referred to the special
balance issue of Physical Therapy published in 1997, the
website of the Geriatric Section of the American Physical
Therapy Association, and Hooked on Evidence from the
American Physical Therapy Association. Information
from these resources may be accessed through the Web
at www.apta.org.
Special Issues
Frailty/Sarcopenia
The incidence of sarcopenia (loss in muscle mass) is
increasing as we as a society are living longer.19,54
Sarcopenia is currently defined as two standard
deviations below the mean muscle mass for young
adults. Roughly 20% of men and women in their
70s are sarcopenic, but the percentage increases
exponentially after the age of 80 years, especially for
women. Sarcopenia is a major risk factor for physical
frailty.28,32,176–178 Not all frail elders have sarcopenia, but
a large proportion have muscle weakness as a major
impairment.90,179 Because so many older adults have
weakness and the incidence of sarcopenia and frailty
are increasing, strength training should be included
as a fundamental treatment approach in almost all
conditions.11,15,36,47–49,51,52,82, 85,86,91,97,104,180–186
Predisposition to Disease
Body composition changes that occur with aging include
an increase in fat mass, particularly in the abdomen, and
the obvious decline in lean mass such that the proportion
 CHAPTER 14 • Effects of Aging-Growth Changes and Life Span Concerns (40+)
of fat-free mass to fat mass goes from about 80/20 in
young adults to about 50/50 in old-old adults.23,112,154,187
The increase in abdominal fat predisposes many older
adults to diabetes, and a high percentage of patients
have this condition. Muscle activation is the best tool
in our treatment cache for the modification of glucose
intolerance.56 Indeed, optimal diabetic management for
the majority of adult-onset diabetics is exercise, and for
many patients, minimal to no insulin or other diabetic
medication is required if physical activity is part of the
daily routine.
Diabetes and peripheral vascular disease both result in
reduced circulation to the extremities.1,27,36 The loss in
blood flow predisposes muscle to additional loss in fibers
and to additional loss in muscle spindles and other sensory
fibers. Associated with nerve loss is reduced sensation on
the bottom of the feet.170,188 With or without diabetes,
about two thirds of all the elders who enter our clinic
have diminished sensation in their feet, which probably
plays a role in diminished balance. Reduced sensation,
slower reaction times, and muscle weakness combine to
predispose older adults to falling. Activities to improve
muscle strength have obvious implications for enhancing
balance and decreasing the likelihood of falls.
Drug Effects
A number of drugs for medical conditions have adverse
effects on skeletal muscle. Beta-blockers and statin
313
drugs, for example, have muscle weakness as a secondary
consequence. Any medication that contains a cortisone-
like substance will result in muscle wasting. More definitive
texts that delve into the interaction of performance, muscle
mass and strength, endurance, and speed of performance do
exist (e.g., Guccione, Bottomley and Lewis, and Ciccone).
The reader is referred to these excellent resources as well
as Chapter 12 of this text.
Summary
Age-related decline is evident in all tissues that have a
direct effect on performance. Frequently, slowing of
movement, diminished activity of daily living (ADL)
function, an inability to complete shopping tasks,
exhaustion, and imbalance are evident. Not all of these
declines are present in all people, but the majority of
older adults do show compromise. Exercise is highly
beneficial for the modification of all of the changes
that occur with age as much of what clinicians see is
due to inactivity superimposed on age-related decline.
Clinicians have the potential to affect the well-being of
nearly all older adults.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 229 references for this chapter.

SECTION II PRINCIPLES OF PRACTICE
R EHABILITATION P ROGRAM
D EVELOPMENT : C LINICAL D ECISION
M AKING , P RIORITIZATION ,
AND P ROGRAM I NTEGRATION
Patricia E. Sullivan, Michael S. Puniello, and Poonam K. Pardasaney
Introduction
Effective and efficient decision making is critical to
patient care. Decision making encompasses selection of
tests in the examination process, interpretation of data
from the detailed history and examination, establishment
of the diagnosis, estimation of the prognosis, determina-
tion of intervention strategies, sequence of therapeutic
procedures, and establishment of discharge criteria.1 By
analyzing the actual decision-making processes used in
clinical practice and reflecting on our clinical decisions
and consequences, we evolve in our understanding of
this complex process.2–4 Understanding the components
of clinical reasoning and decision-making processes and
using the strategies employed by expert practitioners can
improve clinical effectiveness.2,5,6 Integrating decision-
making concepts with content knowledge and evidence-
based practice in professional, post-professional, and
continuing education programs is essential to continued
growth of the physical therapy profession.7,8
This chapter describes the application of decision-
making strategies to enhance patient care outcomes, in
addition to common decision-making errors and ways
to avoid them. As health care providers, clinicians are
accountable for clinical decisions to patients, other health
care providers, payers, and society.9 Therefore enhancing
314
151
C HCAHPAT PE TRE R
clinical skill in decision making is as critical to improved
patient care as is enhancing skill in examination and
treatment. Decision making is not a static process. As the
breadth of content knowledge expands, so will clinical
decision making change. Future advances in genetics and
availability of such information in clinical settings may
enable clinicians to identify persons with a genetic predis-
position for particular dysfunctions, which increases the
clinician’s decision-making role in preventative interven-
tion. Knowledge of a person’s genetic composition may
help clinicians identify patients with a hereditary predis-
position for joint laxity or osteoporosis and thereby pro-
vide preventative exercise and education.
This chapter follows the sequence of the patient-client
management model.1 During the examination phase, the
clinician hypothesizes the clinical problem then chooses
and implements measures to test the hypotheses. In the
evaluation phase, the clinician clusters the examination
findings and develops the diagnosis, prognosis, and
treatment plan. The intervention phase combines imple-
mentation of various treatment strategies with continual
reexamination to assess effectiveness of the plan.
Decision making is multifaceted, with many cognitive,
affective, and psychomotor factors considered simultane-
ously in a parallel-processing manner. Decision making
CHAPTER 15 • Rehabilitation Program Development : Clinical Decision Making, Prioritization, and Program Integration
is a fluid process that takes place neither in a lock-step
manner nor with use of a single method of analysis.
Writing, however, occurs in a linear format and cannot
duplicate the complex integration that occurs in the clini-
cal environment. Within this caveat, this chapter applies
decision-making strategies to patient care decisions.
Hallmarks of Expertise and Processes
of Decision Making
Clinicians involved in rehabilitation continually are
improving their practice, which requires expansion of
factual knowledge of anatomy, physiology, pathology,
and intervention procedures and an optimal applica-
tion of that knowledge.2,5 Experts apply factual or con-
tent knowledge using a collaborative, client-centered
decision-making process to make efficient and effective
clinical decisions.3,10
Knowledge Organization
Systematic organization of diagnostic and intervention
knowledge into a well-structured memory with easily
accessible associations is key to accurate recall and use.6
Knowledge used to diagnose a condition differs from
knowledge used to determine and implement the inter-
vention plan. Diagnostic information encompassing the
examination and evaluation processes seems best orga-
nized into systems categories, including environmental,
social, and cultural factors; medical and psychological fac-
tors; and factors related to the physical systems. Diagnostic
knowledge within the physical systems encompasses nor-
mal and pathological anatomy and biomechanics, com-
ponents of movement control, parameters of movement
capacity, and an understanding of subjective reports and
objective tests and measures to assess these factors.11 The
clinician’s diagnostic knowledge base includes interrela-
tionships between clusters of physical impairments, social,
cultural, and environmental factors, medical and psycho-
logical factors, occupational and recreational stresses, and
physical strains that result in that combine that common
pathologies or dysfunctions.
Diagnostic Systems Categories
● Environmental, social, and cultural factors
● Medical and psychological factors
● Factors related to physical systems
Different knowledge is used to determine and imple-
ment intervention. Interventional knowledge includes (1)
temporal phases of tissue healing, common impairments
in each phase, and stresses that tissues can safely tolerate
315
during each phase; (2) movement characteristics includ-
ing amount of range, control, and capacity required for
various functional activities; (3) the range of available
intervention strategies and procedures to promote these
movement characteristics, and corresponding outcomes in
varied patient populations; (4) sequencing of various inter-
ventions to challenge appropriately involved tissues and the
whole patient; and (5) intervention strategies to promote
health and prevent secondary dysfunction. The systems
categories of diagnostic knowledge and the classification of
interventional knowledge are depicted in the two models
of the Framework of Clinical Practice (Figure 15-1).11
Improvement of knowledge organization can be
accomplished by analysis of expected similarities and
differences among similar problems and development
of an analytical assessment of aspects of treatment.
During examination, the clinician may have difficulty in
differentiation of dysfunction that is anatomically close
in origin. During intervention, novice clinicians may
have difficulty relating the amount of change needed
in each impairment to the functional needs of the client
and also to expectations of the amount of impairment
change to specific treatment procedures. Completing
tables such as Table 15-1 with expected and observed
findings can assist in clarification and organization of
this knowledge. The question to be asked during this
exercise is, “What are expected findings in two differ-
ent pathological diagnoses, and what are intervention
expectations?”
Whole Patient
As practicing clinicians gain expertise and develop skills
regarding what they “see” in the patient, identification
of the uncertain “gray” findings in addition to the obvi-
ous “black and white” ones becomes easier. The expert
clinician examines the patient as a whole rather than only
the specific structure or function that appears to be the
direct source of presenting complaints. Seeing the whole
patient in his or her life context implies incorporation
of the influence of environmental, cultural, and psycho-
logical factors on natural tissue healing and the patient’s
signs and symptoms.12
The expert clinician recognizes the implication of psy-
chological stress from unemployment or ergonomic stress
from poor workstation positioning or body mechanics and
the resultant physical strain on somatic tissues.13 In addi-
tion to direct treatment of pain or other symptoms, the
expert clinician treats the whole patient by providing
a multifaceted intervention that modifies environmental
and ergonomic irritants and provides education to prevent
or diminish repetitive strain injury. Examples of treating
the whole patient include recognition of the underlying
tissue healing and balance disorders in a patient status post
tibial fracture with diabetes mellitus, the need for aerobic
316 SECTION II • Principles of Practice

EVALUATION MODEL

Environmental/Social/
Functional capability Cultural
Medical
Psychological Physical

Functional limitations

ity INTERVENTION MODEL

s of pac
er a
et nt c speed
m
a ra eme duration
P ov frequency
m
intensity

Mobility Stability Controlled Skill

postures and movements

Mobility
A. Supine, A. sidelying; scap
scap motion add
T. Jt. Mob; hold relax T. SHRC

A. Mod. Plant
T. AI, RS
Activities:

Figure 15-1
The two clinical models of the Framework
of Clinical Practice. The Evaluation Model
highlights the factors to be considered during the
examination and evaluation. The Intervention Functional outcome
Model guides treatment planning and the
development of intervention procedures. Stages of movement control

conditioning in a sedentary patient with low back dys-
function, the importance of body mechanics education in
prenatal and postnatal exercise classes, and the incentive
of athletes’ premature return to full activity before tissues
can tolerate the stress. Treating the whole patient includes
education to prevent further dysfunction and to promote
optimal health and performance.
For example, Mr. B. is a right-handed male who
recently has completed 6 weeks of therapy for a right
shoulder impingement syndrome and is transitioning to
playing competitive tennis. Working as a letter carrier for
the postal service, Mr. B. carries a mailbag over his right
shoulder and repetitively reaches to different level bins
while sorting mail. He reports mild to moderate shoulder
soreness after work that subsides within 1 hour with use of
ice and over-the-counter NSAIDs. On some days, Mr. B.
can practice tennis for 1 hour without symptom exacerba-
tion, whereas on other days, pain is aggravated for 4 hours
after practice. Considering that cumulative work-related
stresses combined with return to tennis can cause increased
stress to connective tissues of the shoulder complex, the
clinician must make recommendations to minimize work-
related stresses, in addition to recommendations for safer
tennis training. Recommendations to Mr. B. may include
using a pushcart instead of carrying a mailbag, using his
left hand or a stool to reach high bins at work, and limit-
ing tennis practice when shoulder pain is aggravated. The
patient should be educated regarding recovery time of
“pathological” pain from work or tennis, as pain persist-
ing longer than 1 hour is suggestive of increased tissue
stress resulting in microtrauma and tissue inflammation.14
The patient also should be advised to grade training inten-
sity based on pain recovery time. He may be able to con-
tinue tennis training with low-level pain if recovery time
is within acceptable limits and if he does not experience
increased rest or activity pain the following day. Teaching
the patient to correctly identify an acceptable pain level
to work through and the need for activity modification
or limitation as a result of symptoms is important for safe
return to work and sports.
CHAPTER 15 • Rehabilitation Program Development : Clinical Decision Making, Prioritization, and Program Integration 317

Table 15-1
Example of Using Expected and Observed Findings to Organize Knowledge to Differentially Diagnose and Delineate
Intervention Expectations
Expected Examination L4, L5 S1 Similar/Different
Findings

Mobility
Strength
Pain
Impairments to Needed Change Treatment During Expected Observed
Rectify to Achieve Procedures Treatment Treatment Effect Treatment Effect
Functional Measure with Each Session
Outcome
Pain Diminish pain Asking for report Immediate
reports from of pain on the response in the
6/10 to 2/10 1–10 scale reduction of pain
by 2 points
Joint mobility Full mobility Soft tissue Assess glide Less discomfort
mobilization, mobility with motion,
joint mobility
mobilization improves sooner
in treatment over
time

Examination Decision Processes In addition to decisions regarding assessment tools,

During examination, the clinician conducts a compre-
hensive screen and implements tests to gather suffi-
cient information to develop a diagnosis and design an
intervention plan.1 A goal of examination is to narrow
the range of probable conditions, termed narrow-
ing the problem space. The clinician continually makes
decisions regarding what questions to ask in taking
the history, which tests to use, and how thoroughly
to conduct different aspects of assessment. Some of
these decisions can be considered before actual patient
interaction. For example, clinicians can examine the
range of available measures for assessment of low back
dysfunction to determine the set of tests and measures
that provide the most reliable, valid, sensitive, and
specific information to establish a diagnosis and plan
the intervention.15 A specific example is to explore the
various measurement tools designed to assess pain or
those that assess function. In addition to analyzing
measurement properties, clinicians may consider those
tools that assess the characteristics of the patient mix
most commonly seen in their practice. The analysis of
examination tools also considers performance-based
versus self-report, and generic versus diagnosis-spe-
cific measures. Standardized use of measurement tools
allows comparison of data within the practice, and
with the literature.
diagnostic decisions are made at various points in the
process with varying amounts of information or in con-
ditions of uncertainty.15–17 Examination strategies have
been described that may improve diagnostic effectiveness
and efficiency and reduce error.
Determining Tests and Measures
Examination tools can be divided into performance-
based or self-report measures and generic or disease-
specific measures. Performance-based (PB) measures
involve the clinician’s performance of the test or observa-
tion of patient performance. The test commonly may be
performed only once or twice in a clinical environment.
Examples of PB tests include assessment of joint mobil-
ity, muscle strength, balance, walking speed, stair climb-
ing, or characteristics of a tennis serve. In self-report
(SR) measures, the patient rates performance during
activities such as walking, stair climbing, or recreational
sports. Rating of SR measures includes the ability to per-
form a task, difficulty with the task, pain during perfor-
mance, or need for assistance. Self-report measures have
been found related to psychological factors to a greater
extent than PB measures. Performance-based measures
are more sensitive to physical change and are related to
physical function to a greater extent than SR measures.18
In the decision-making process, the clinician chooses
318 SECTION II • Principles of Practice
measures that reflect the patient’s current impairment
and functional ability and measures that are sensitive to
changes that may occur with the natural course of the
condition and therapy. Tests are chosen to examine the
performance of activities, function, and of impairments.
Examination Strategies
Different examination strategies including pattern recog-
nition, updating from an anchor, and hypothetico-deduc-
tive reasoning are useful to improve clinicians’ diagnostic
ability. Each strategy is discussed with suggestions to
reduce the chance of error.19
Pattern Recognition
Pattern recognition is the process of relating a series of
signs and symptoms to a particular observed phenom-
enon.6,20,21 A pattern may be identified by perception of
a cluster of symptoms or by observation of a patient’s
static postures and movement patterns. An experienced
clinician quickly recognizes these patterns and thereby
improves time-efficiency of examination and effective-
ness of intervention. Pattern recognition is a highly
theory-laden strategy.20 Theory describes the pattern
or cluster of impairments common in a particular diag-
nosis or condition. The clinician tends to see, observe,
or interpret findings in accordance with theoretical
descriptions.
Exclusive use of pattern recognition may lead to
errors resulting from failure to examine for other diag-
nostic probabilities, or explore other intervention strat-
egies that for a particular patient may be more effective.
A common error is for the practitioner to test only for
what is expected, termed positive testing or confirma-
tion bias, and to interpret test results as theory directs.22
The practitioner’s inherent observation and interpre-
tation skills are overridden by reliance on theoretical
descriptions. Although knowledge of common patterns
among patients is essential to develop expertise in an
area, the clinician must be cautious not to rely solely
on pattern recognition. The individual patient always
is different from the textbook example, and the general
description is different from the particular manifesta-
tion.23 The clinician must identify similarities among
patients and recognize differences that make a par-
ticular patient unique. In addition to recognizing the
pattern, the clinician must examine for other probable
differential diagnoses or impairments that may exist in
the patient. The expert considers all probable and not all
possible conditions.
Updating from an Anchor
The pattern recognized during initial observation usually
sets an “anchor” in the examination process. The first
estimation of the problem anchors the clinician to an
initial hypothesis. Based on the relative strength of the
clinicians’ belief that the initial hypothesis is correct, they
choose tests and measures to examine the accuracy of the
hypothesis and generate a diagnosis. As data are gathered,
clinicians continually weigh the value of emerging find-
ings to confirm or disconfirm the initial hypothesis.4,16
Clinicians may have a tendency to persist with the original
idea despite the presence of data refuting it or to exces-
sively waver despite the presence of data consistent with
one diagnosis. Each clinician should become aware of his
or her tendency to excessively persist or waver because it
may lead to diagnostic errors. The process of continu-
ally applying results of each test or measure to confirm
or disconfirm the initial opinion or “anchor” is termed
updating from an anchor. The relative importance of
each finding is compared with the relative strength of the
initial belief.
For example, a clinician observing a 35-year-old
patient walk into the examination area notes that he
has an antalgic gait with a slight lateral shift of his
upper trunk. The clinician may hypothesize the pattern
as discal in origin. The results of all tests are examined
relative to whether they support or refute this initial
hypothesis. The patient then states that pain is primar-
ily in the hip area resulting from a fall. This finding does
not conform to the initial hypothesis. Three options
are available as the clinician continues the examina-
tion. The clinician may persist with the opinion that
the problem is discal, believe that one negative finding
does not disconfirm the initial hypothesis, and con-
tinue examination with the initial hypothesis anchoring
the process. Alternatively, the clinician may choose to
drop the initial hypothesis and believe it was based on a
false premise and focus further examination on the hip.
Finally, the clinician may explore the possibility that the
two problems coexist.
Hypothetico-Deductive Reasoning
The hypothetico-deductive reasoning process is a widely
described process of diagnostic decision making.6,24,25
According to this concept, the clinician makes an ini-
tial assumption of the problem, possibly using pat-
tern recognition, and develops a list of five to seven
hypotheses, reasons, causes, or impairments likely to
be associated with, or causative of, the patient’s condi-
tion. For any clinician who is the initial point of contact
with the health care system, it is important that red
and yellow flags be identified as probable hypotheses
for the condition when applicable. The hypothesized
differential diagnoses and red and yellow flags are
based on existing background evidence relative to the
patient’s age, gender, body region involved, comor-
bidities, and medications.26 The clinician refines the
hypotheses during history-taking and chooses objec-
tive tests and measures to rule out (challenge) or rule
CHAPTER 15 • Rehabilitation Program Development : Clinical Decision Making, Prioritization, and Program Integration 319

in (confirm) these hypotheses. In many instances, the

clinician hypothesizes the cause of the presenting con-
dition: for example, the reason the patient had a fall as
well as the consequences of the condition (i.e., physi-
cal sequelae of the fall or injury). Effective use of this
reasoning methodology generates a maximum of five
to seven hypotheses, . . . If a longer list of hypotheses is
generated, the clinician should cluster them to facilitate
the ruling in/ruling out process. For example, under
the phrase impaired mobility the clinician may clus-
ter all tissues and conditions that contribute to limited
ROM.
For example, based on a patient’s initial statement, “I
hurt my ankle when I fell,” the clinician generates initial
hypotheses regarding the potential problems that may
exist. The musculoskeletal problems may range from mus-
cle strain, to ligament sprain, to ankle-foot fracture based
on the nature, intensity, and circumstances of the fall; age
of the patient; previous injuries; and comorbidities. The
fall may have been “caused” by externally applied forces,
diminished balance responses as a result of poor proprio-
ception or weak ankle stabilizers, poorly fitting shoes, or
environmental hazards. During examination, the clini-
cian selects questions, tests, and measures to adequately
address and rule in or rule out each hypothesis.
Combining Hypothetico-Deductive Reasoning
with Multiple Subsystems
An expert clinician examines for multiple factors asso-
ciated with physical dysfunction and provides multi-
ple intervention strategies to remediate these factors.
The multiple factors associated with musculoskeletal
dysfunction can be classified into three subgroups,
including environmental, social, and cultural factors;
medical and psychological factors; and physical factors
(Figure 15-2).
Examples of examining multiple subsystems during
hypothesis-generation include evaluation of the
following:
● The extent to which a patient’s occupation, recreation, and socio-
economic status influence his/her general well-being, presenting
condition, and overall physical functioning
● The likelihood that a patient’s depression and anxiety related to
recent unemployment could affect autonomic system activ-
ity including pain threshold, tissue circulation, vital signs, and
exercise responses
● The extent to which a patient’s diabetes mellitus, lack of exercise,
and aerobic conditioning may influence tissue healing
● The likelihood that a young female patient with a Latino back-
ground speaking limited English can accurately report symptoms
to an older male clinician with an Asian background
● The effects of sleep deprivation, psychological fatigue, and
physical fatigue on a young mother’s musculoskeletal structures,
overall physical well-being, and ability to lift and hold her
20-pound child for extended periods
● The effects of excessive motivation, limited nutritional intake, and
anorexia on the musculoskeletal system of a young female gymnast
Examining the physical factors (Figure 15-3) involves
examination of systems commonly associated with move-
ment dysfunction including the musculoskeletal system,
movement control, and movement capacity. Within these
overlapping areas, the clinician considers the connective
tissues in the affected, proximal, and distal regions most
likely involved including skin, fascia, muscle, tendon,
nerve, ligament, capsule, and bone. The pathologies affect-
ing these connective tissues such as inflammation, edema,
sprain, strain, stiffness, and pain (pain would be a symptom,
not pathology) are clustered into the common impairment
classifications including hypo/hypermobility, impaired

Environmental Physical Psychological

Social Depression
Cultural Anxiety
Socioeconomic status Motivation
Cultural and educational N CVP Locus of control
background
Health beliefs Figure 15-2
Nutrition
The examination/evaluation model and the
Community and
family involvement MS factors that commonly must be considered
Home environment during the examination and evaluation. N,
central nervous (proprioception) system;
Medical CVP, cardiovascular and pulmonary systems;
Diabetes mellitus MS, musculoskeletal system (includes PROM:
Number and type of medications capsular, joint mobility, segmental/regional
Comorbidities common for that joint/muscle ROM; pain; and, postural
age and gender alignment)
320 SECTION II • Principles of Practice
Figure 15-3
The physical systems of the evaluation model. ANS,
autonomic (sympathetic) nervous system; N, central nervous
(proprioception) system; CVP, cardiovascular and pulmonary
systems; MS, musculoskeletal system (includes PROM:
capsular, joint mobility, segmental/regional joint/muscle
ROM; pain; and, postural alignment)
stability and alignment, weakness, impaired movement
control in weight-bearing and non–weight-bearing posi-
tions, and diminished aerobic or anaerobic capacity.
Interrelationships of multiple physical subsystems
may include the following:
● Muscle weakness resulting from edema and inflammation and
reflexive inhibition from pain
● Decreased passive range of motion (PROM) resulting from swell-
ing, capsular restrictions, and muscle tightness
● Decreased postural stability resulting from ligamentous laxity,
muscle inhibition, and diminished proprioception
● Diminished static and dynamic movement control in weight-bear-
ing postures associated with abnormal alignment and decreased
muscle endurance, that is, ability to effectively perform repetitive
movements
The majority of patients present with clusters of
impairments more commonly than isolated dysfunc-
tion, and many patients have more than one diagnosis
or condition. Therefore, in development of probable
hypotheses, consideration of multiple subsystem clusters
is important. The following is an example of the inter-
relationship between multiple subsystems, extrinsic and
intrinsic hypotheses during examination.
A clinician examining a 45-year-old female patient
with a chief complaint of low back pain generates five
probable hypotheses as follows:
1. Repetitive stress related to the patient’s daily,
occupational, or recreational activities, resulting in
a cycle of musculoskeletal strain causing impaired
flexibility, joint kinematics, and muscle perfor-
mance, further sustaining abnormal tissue strains
2. Inflammatory process in deep tissues that reflex-
ively inhibits superficial muscular tissues, reducing
local stability
3. Altered soft-tissue flexibility, including muscle, fas-
cia, and nerve, or joint mobility in the thoracic,
lumbar, sacroiliac, or hip regions
4. Impaired muscle stability in the abdominal and/
or lumbar regions, or ligament laxity resulting
N CVP
ANS
Movement Movement
Control Capacity
Initiation of movement MS Decreased muscle and
Muscle and postural stability general body endurance
Static and dynamic controlled movement
Timing/sequencing
from multiple pregnancies that contribute to joint
dysfunction
5. Pain referred from visceral structures to the low
back region, history of cancer, or long-term steroid
use that warrants ruling out red and yellow flags,
with consideration of referral to other practitioners
If the problem is long-standing or recurrent, the
clinician more likely will have confirmed a number of
the above tissue pathology/impairment clusters. A
syndrome of interrelated movement control and capacity
impairments may be a better description of the patient’s
problem than a single pathological or anatomical term.
A common error is to merge all examination findings
into one diagnosis and disregard findings that do not
cluster. Findings that do not cluster frequently reflect
red or yellow flags that require special consideration.
For example, a client with a diagnosis of fractured ankle
has persistent swelling and pain beyond expectations.
These symptoms may reflect deep vein thrombosis even
in people not at risk for that condition in addition to
other possible diagnoses. These signs or symptoms can-
not be disregarded just because they do not cluster into
expected findings.
Functional Relationship
Functional relationship is a strategy that highlights the
relationship among pathology, impairment, and func-
tional status/limitation. Using the strategy of functional
relationship, the clinician estimates the proportional
contribution of tissue pathology and impairment clus-
ters to the patient’s functional limitations.11 For example,
a commonly reported functional limitation is decreased
sitting tolerance at a workstation associated with pain.
Pathology/impairment clusters that contribute to this
functional limitation include lumbar facet inflammation,
hip and lumbar hypomobility, diminished proprioception
and decreased muscle, and postural stability in sitting.
The clinician estimates the relative contribution of these
factors to the patient’s decreased sitting tolerance, incor-
porating ergonomic and environmental influences into
the estimate (Figure 15-4). Estimating the functional
relationship assists in establishment of a diagnosis and
determination of intervention priorities. The literature
CHAPTER 15 • Rehabilitation Program Development : Clinical Decision Making, Prioritization, and Program Integration
Figure 15-4
Estimated proportional contribution of physical impairments to the
functional limitation of limited sitting tolerance.
provides guidance regarding the relative contribution of
impairment clusters to functional limitations.
Competing Formulation
Competing formulation is an examination strategy that
helps avoid errors of omission. Opposite, contrasting,
or dissimilar reasons for a problem are paired and with
estimation of their relative contribution to the activity
limitation. Contrasting pairs may be involvement of con-
tractile or noncontractile tissues, occurrence of pain at
rest or during activity, source of pain as mechanical or
nonmechanical, or “cause” of the problem as physical
dysfunction or environmental strain. Use of the com-
peting formulation strategy helps avoid pattern recog-
nition assumptions. Many competing formulations are
not exclusive; the patient is likely to have involvement
of contractile and noncontractile tissues. By considering
dual pairs such as the ones listed above, the clinician is
less likely to omit findings.
Error of Premature Closure
The most common diagnostic error that can be avoided
by use of these examination strategies is premature clo-
sure.4,27,28 This error describes the practice of concluding
inquiry or completing the examination once a positive
result has been found or accepting a hypothesis based on
minimal data. Concurrent with premature closure is the
error of positive testing, for example, testing only for what
is expected.22
For example, a patient is referred for treatment with
a chief complaint of right knee pain. As the patient rises
from a chair, the clinician observes an antalgic posture
with a shift in weight bearing toward the uninvolved
left lower extremity. The patient describes generalized
anterior patellar discomfort, particularly when descending
321
stairs. These symptoms conform to a pattern of patello-
femoral syndrome. The clinician knows that compression
of the patella is likely to cause pain and applies the patel-
lofemoral compression test. Based on a positive finding,
the clinician concludes the examination, establishes a
diagnosis of patellofemoral dysfunction, and designs a
treatment plan to improve patellar alignment.
Recognizing the pattern of patellofemoral dysfunc-
tion is an efficient decision. However, errors made in
this example include positive testing, or examining for
positive results only, and premature closure, or conclud-
ing the examination after one positive finding. Although
the patient may have patellofemoral syndrome, he or
she also may have other concurrent lower extremity
musculoskeletal dysfunctions and abnormal distal or
proximal alignment that contributes to the problem.
To adequately consider all probable findings, the cli-
nician needs to assess the involved area, and regions
above and below, assess the multiple tissue subsystems,
compare findings to the contralateral limb, and refer-
ence findings to age-appropriate and gender-appropri-
ate norms.
Throughout the examination process, the clinician
compares what was expected to what is observed.29
The hypothesis or pattern provides the clinician with
an expectation of the results of functional and move-
ment characteristic analysis. If the expectations are met,
then the likelihood of confirming the hypothesis is high.
However, if the observed examination findings do not
match the expected range of limitations considering age,
gender, and number of comorbidities, or if the findings
do not cluster into meaningful impairments, then the
diagnostic hypothesis has to be reconsidered.
Evaluation
During evaluation, the clinician puts a value on exami-
nation findings, considering relevant environmental,
social, cultural, psychological, medical, and physical find-
ings. In the majority of patients, the findings cluster into
recognizable, understandable, or identifiable diagnoses,
dysfunctions, or classification syndromes. Findings that
do not cluster may represent comorbidities, indirect
problems such as physiological changes from sedentary
behavior, or red and yellow flags; these need careful con-
sideration. Pain patterns that do not appear mechanical
in nature or sensory deficits that are not consistent with
other findings may require referral to a physician for
further investigation.
Examination findings are clustered into impairment
classifications including mobility, stability, controlled
mobility, and skill to effectively apply the information
to determination of the diagnosis, prognosis, and inter-
vention plan.11 Mobility includes PROM (osteokine-
matic and arthokinematic) and active range of motion
322 SECTION II • Principles of Practice
(AROM). Mobility impairments can be hypermobility or
hypomobility. Passive and active mobility may be limited
by factors such as pain on movement, edema, capsular
restrictions, muscle tightness, and weakness.30 The above
information, incorporated with the degree of restriction
and probable tissue involvement, contributes to formula-
tion of a diagnosis and treatment plan. If the mobility
restriction is not significant and if tissues limiting mobility
are amenable to change, then the prognosis for improved
mobility and subsequent improvement in function rela-
tive to that impairment is considered good. However,
significant tissue restriction with limited modification
potential resulting from factors such as age-related
changes or chronicity may necessitate alternative strate-
gies such as providing compensatory aids or modifying
the environment. Stability includes muscle holding in
shortened ranges and maintaining alignment in closed-
chain, weight-bearing postures. Stability may be affected
by and associated with factors such as diminished pro-
prioception, edema, muscle weakness, active lag, poor
co-contraction of intrinsic muscle stabilizers, and pain on
weight bearing. Muscle strength less than 3/5 is insuffi-
cient to provide joint support in weight-bearing postures
and may necessitate use of compensatory aids or orthot-
ics until muscle strength increases sufficiently to provide
postural stability. Interrelated with stability is muscle
endurance, the ability to maintain a low intensity-long
duration muscle contraction or position. Controlled
mobility, also termed dynamic stability, includes through
range movement and weight shifting in weight-bearing
postures. Examples of controlled mobility include con-
trol of scapulohumeral rhythm and dynamic balance in
standing. Skill encompasses proximal dynamic stability
and distal dexterity to perform activities such as ADLs,
locomotion, recreation, and sport.
By clustering examination findings into the above
impairment classifications, the clinician can identify inter-
relationships and develop more appropriate intervention
strategies.
Evidence Proportionalism
Evidence proportionalism is a concept that states that no
diagnosis should be more general or specific than the
data support. The strength of the clinician’s belief in
the accuracy of the diagnosis or in the appropriateness of
the intervention should be proportional to the strength
of existing evidence.31,32 Knowledge of the reliability,
validity, sensitivity, and specificity of common tests and
measures allows the clinician to estimate more accurately
the value of examination findings in diagnosis of specific
conditions.33 In addition, clinicians must consider indi-
vidual skill in performance or interpretation of a proce-
dure when determining strength of their beliefs in the
findings.
For example, a 20-year-old male patient presents with
poor balance after multiple lower extremity fractures sus-
tained in a motorcycle accident. The clinician may choose
the Berg Balance Scale (BBS)34 to assess the patient’s bal-
ance and estimate his likelihood of falling. The clinician
should recognize that normative threshold scores vali-
dated in elderly patients and in patients with neurological
involvement34 may not translate to a young adult. Thus,
in accordance with the concept of evidence proportional-
ism, the clinician should acknowledge that the BBS may
not provide accurate information about fall risk in this
20-year-old patient and put limited belief in the finding.
Two classic examples of evidence proportionalism in
musculoskeletal assessment include use of the six-point
scale for assessment of joint mobility35 and the six descrip-
tors of end-feel assessment to implicate tissues limiting
mobility.36,37 Reliability of joint mobility assessment may
be improved by reducing the six-point scale to three
categories, namely, hypomobility, normal, and hyper-
mobility. Likewise, limiting end-feel descriptors to more
discernible categories may enhance reliability and valid-
ity.38 Therefore, when using results of the above tests in
development of a diagnosis and treatment planning, the
clinician must consider measurement properties of the
test, in addition to individual skill in performance.
Culmination of the evaluation phase includes the clini-
cian’s determination of the patient’s diagnosis, prognosis,
and comprehensive plan of care.
The diagnosis may comprise the pathology and impair-
ments, including tissue structures and body segments
involved, and resultant function, activity, limitations,
disability, and handicap as applicable.39 A diagnosis may
describe the cluster of impairments and activity limita-
tions associated with the syndrome. A diagnosis compre-
hensively identifies the problem areas to plan the overall
intervention. The diagnosis may state the precursors and
consequences of the pathology.
For example, Mr. K. is referred for treatment with a
medical diagnosis of L4-L5 disc herniation and a chief
complaint of inability to sit for longer than 1 hour because
of pain. Examination findings include low back pain with
radiation to the knee, hypomobility of L4-L5 vertebral
segments and bilateral hip joints, decreased stability and
endurance of the abdominals and back extensors, and
diminished proprioceptive awareness in the lumbopelvic
region. One example of a diagnostic statement is “lim-
ited sitting tolerance associated with discal pathology,
impaired mobility of L4-L5 vertebral segments and hips,
and decreased trunk muscle performance.”
Clinicians increasingly are developing classification
systems that describe diagnostic groups.40–44 Although
such classification assists in delineating the underlying
pathology, it reinforces the assumption that determining
pathological classification is the goal of the diagnostic
process and forms the basis for its closure. Pathology-
CHAPTER 15 • Rehabilitation Program Development : Clinical Decision Making, Prioritization, and Program Integration
based classification presupposes that a particular pathol-
ogy results in similar levels of dysfunction among different
patients and justifies equivalent therapeutic prescriptions
in different patients based on pathological diagnoses.
This assumption neither accounts for varied manifesta-
tions of pathology in different patients because of the
influence of age, gender, comorbidities, race, recurrence,
and external and internal factors, nor accounts for the
variety of intervention strategies that can be employed to
address dysfunction.
Prognostic Estimate
As clinicians improve and standardize diagnostic pro-
cesses, prognoses, and therapeutic prescriptions, the
need is increasing to account for the “person behind
the patient.” The prognostic estimate takes into account
the patient’s age, extent of pathology, ability of surround-
ing tissue structures to compensate in the short or long
term, premorbid conditions, functional requirements,
and motivation. Basic research45 and population studies
provide evidence of estimated time frames of healing and
improvement in muscle strength in different pathological
conditions,46 in addition to expected changes during the
natural course of recovery with or without intervention.47
Case studies and prediction research provide evidence in
particular patients of various clusters of impairments and
their outcome trajectory.48–51
The prognosis includes the estimated functional
outcome achievable in an estimated time frame. The
following are some examples of estimated prognostic
statements:
● “In 8 weeks, the patient will be able to sit for ≥2
hours without a significant increase in pain.”
● “In 3 months, the patient will be able to lift 15
pounds from the floor.”
“In 4 months, a patient with central canal stenosis
●
will be independent in pain control and self-man-
agement of ADL.”
● “In 2 months a patient recovering from a hip frac-
ture will be able to walk 100 feet in 30 seconds using
a J cane.”
The above statements are prognostications about the
patient’s physical capacity and functional outcomes at the
end of a course of treatment, and they assume a favor-
able change in impairments. Understanding the amount
of change needed at the impairment level to achieve the
functional outcome is critical to determination of the
prognosis and intervention plan.
For example, Mr. K. has limited sitting tolerance as
a result of discal pathology, restricted mobility of the
lumbar spine and hips (stiffness noted at 80 degrees of
flexion), and decreased trunk muscle stability and endur-
ance. To maintain upright sitting with the lumbar spine
in a neural position, he needs at least 100-degree hip
323
flexion, improved proprioception and postural aware-
ness, and improved muscle stability to maintain neutral
positioning. Based on assessment of hip joint mobility
and endfeel, the clinician can estimate the time and types
of interventions required to achieve a 20-degree increase
in hip flexion. Knowledge of the amount of increase in
muscle and postural stability required to achieve the
patient’s sitting requirements without increase in pain
allows the clinician to estimate the time needed to achieve
the functional outcome.
The clinician should limit prognostic expectations
and estimated functional outcomes to statements regard-
ing the patient’s physical status. The scope of practice
is to enable the patient to achieve the physical capacity
for various functional activities. Clinicians, however, may
not be able to predict or ensure actual patient partici-
pation and adherence. Returning to premorbid function
such as working full time, playing on a sports team, or
participating in community activities incorporates many
psychological, manpower, and satisfaction factors beyond
the scope of clinical practice.
In determining the plan of care, the clinician con-
siders the combination of intervention strategies that
best treats the cluster of impairments, the sequence of
particular intervention procedures, and the frequency
and duration of treatment. The plan of care includes
the interim outcome assessments to determine if
treatment goals and functional prognostic outcomes
are being met. Choosing tests that are sensitive to
change and that validly assess the physical character-
istics being addressed by therapy may best reflect the
actual therapeutic effect.
Achievable changes in a patient’s impairments translate
into treatment goals, and realistic changes in functional
limitations translate into functional outcomes.
Intervention Strategies
The goal of the intervention process is to achieve desired
functional outcomes by reduction of existing impairments,
prevention of secondary impairments, enhancement
of functional ability, promotion of optimal health, and
reduction of environmental challenges.12 Determination
of the most effective and efficient treatment plan requires
interrelating the examination findings and the diagnos-
tic and prognostic evaluation outcomes with the range
of available intervention strategies. Intervention strat-
egies most likely to be effective are considered relative
to the cost benefit to individual patients or groups of
patients. Short-term and longer-term treatment goals are
sequenced according to the expected change in impair-
ments needed to achieve functional outcomes. Treatment
procedures are developed, sequenced, and implemented
to achieve treatment goals and functional outcomes (see
Figure 15-1).
324 SECTION II • Principles of Practice
In this portion of the decision-making process, the cli-
nician translates examination findings and clinical assess-
ments into a comprehensive intervention plan. Having
estimated the proportional contribution of environmen-
tal barriers as a causative influence in the patient’s condi-
tion, the clinician estimates the proportion of functional
outcome that can be achieved by environmental modi-
fication. Assessment of patient insight into his or her
condition, safety precautions, and preventive measures
determines the extent of patient education needed and
the appropriate time to impart education in the treat-
ment process. The clinician’s sense of the patient’s moti-
vation, anxiety, fear, and depression is used to determine
motivational strategies. The potential benefit from incor-
poration of individual treatment and group exercises, and
the extent of treatment challenge and progression appro-
priate for the patient are estimated to determine direct
treatment. Concerns beyond the scope of practice reflect
the need for referral for other professional services.
Theory of Medical Fallibility
The theory of medical fallibility states a universal differ-
ence between the general understanding of a condition
and its particular expression in a patient.24 Although gen-
eralization among patients is critical, the clinician must
realize that the specific treatment warranted in a partic-
ular patient and his or her response to treatment may
not correspond to general understanding. The follow-
ing decision-making questions assist in merging general
understanding with needs of a particular patient:
1. Is the patient capable of change, and within what
timeframe? Would environmental modification or
compensatory aids in addition to, or instead of, direct
treatment assist in achieving functional outcomes with
greater time-efficiency and less cost?
2. What is the cluster of impairment changes needed,
and what is the amount of change required in each
impairment before a functional change is noted and
the overall outcome achieved? For example, a patient
post total-knee-arthroplasty may have impaired
mobility, proprioception, muscle stability, balance,
and aerobic capacity. For this patient to return to
required walking speed and playing golf, how much
change is needed in each of the above impairments?
Because the recovery of movement characteristics and
impairments progress over time and with interven-
tion, it is important to determine the least restrictive
compensatory aids that can be used until propriocep-
tion, stability, and balance are within safe and func-
tional limits.
3. Is producing a change in the patient’s impairments
the most effective and efficient strategy to choose? Is
it likely that many people may present with a similar
condition, requiring similar types of intervention? If
so, could effectiveness be improved by changing the
environment rather than or in addition to providing
individual therapy to rectify a particular impairment?
For example, if a number of runners are diagnosed
with shin splints, then changing the track, footwear,
or training regimen may be considered a more effec-
tive and longer-lasting strategy to prevent repetitive
injury than individual therapy.
A hallmark of an expert is to integrate backward rea-
soning with forward reasoning.6 Forward reasoning,
common among novice clinicians, follows a sequence of
examination, evaluation, treatment planning, and inter-
vention. Experts incorporate backward reasoning into
this sequence. The expert has knowledge of the range of
available and appropriate interventions and uses exami-
nation data to narrow the range of interventions. The
effectiveness of various intervention options is assessed
as part of examination. Integration of forward and back-
ward reasoning is more time efficient and may result in a
better match between impairments and interventions.
Intervention strategies include the following:
● Direct treatment
● Environmental modification
● Compensatory assistance
● Patient education
Direct Treatment
Direct treatment aims at improving movement control
and capacity characteristics using modalities such as ther-
mal agents, pain relief, joint mobilization/manipulation,
manual and mechanical exercise, functional retraining,
and aerobic conditioning. The clinician may be providing
hands-on, manual therapy, as well as providing instruc-
tion in home or independent exercises and programs.
Environmental Modification
Environmental modification may be an interim, short-
term treatment, or a permanent, long-term functional
adaptation. The following are some examples of environ-
mental modifications that may be addressed for an indi-
vidual patient, or a group of clients:
1. Adding a ramp or banister to ease home access
2. Providing ergonomic workstation alterations such
as dental chairs to reduce back strain
3. Increasing lighting for persons who have poor bal-
ance in darkened areas
4. Raising the height of commonly used chairs and
toilet seats for persons with range of motion
(ROM) limitations or decreased lower extremity
extensor strength
CHAPTER 15 • Rehabilitation Program Development : Clinical Decision Making, Prioritization, and Program Integration
5. Altering the running surface for a track team whose
members commonly have lower leg, ankle, or foot
dysfunction
6. Changing the timing of the walk cycle of a town’s
street crossings
7. Changing car seats to provide better back support
8. Changing competitive sports scoring to reduce
maneuvers that can lead to long-term instability
9. Requiring head and facial protection for contact or
potentially dangerous sports
Compensatory Assistance
Compensatory assistance may be temporary or perma-
nent based on degree of reversibility of existing impair-
ments and includes orthotics to provide joint stability
until sufficient muscle stability is regained, external sup-
ports such as lumbar corsets, and walking aids.
Education of the Individual, Family, And Community
Education of the individual, family, and community may
include educational material regarding pathological and
healing processes, suggestions to improve body mechan-
ics and protect musculoskeletal structures, ways to prog-
ress parameters of a home exercise program, effective
use of gym equipment, and community resources such
as prenatal, senior citizen, or council of aging exercise
groups. Education also can be provided to equipment
manufacturers to design gym equipment to meet the
needs of a more varied population. For example, many
patients including those with patellofemoral dysfunc-
tion or post-hip fracture/arthroplasty need abductor
strengthening with the hip in extension. However, the
majority of devices strengthen the hip abductors with the
hips in 90 degrees of flexion.
In applied sciences such as rehabilitation, absolute
rules cannot be established. However, intervention
guided by general heuristics or decision-making prin-
ciples allows application of general concepts to specific
situations. Discussion of principles and ways of imple-
mentation in treatment assists clinicians in determining
best practice guidelines.
Formulation Principles for an Intervention Plan
The following principles may guide clinicians in formula-
tion of an intervention plan:
Principle 1: Protect and position injured tissue to
allow early healing in an appropriate resting length. After
positioning in the most appropriate position, gradually
introduce tissue stress to promote healing with organized
collagen formation, maximize strength of scar tissue, and
reproduce functional challenges in a controlled environ-
ment. While involved tissues are protected, treatment
325
also is provided to reduce existing impairments, prevent
anticipated impairments, and promote optimal health.
Critical questions that the clinician must consider in this
first principle are as follows:
1. Does the involved tissue need to be protected from
stress to allow healing? Does the tissue need to be
protected from all movement, including weight-
bearing and non–weight-bearing forces?
Then immobilization and non-weightbearing
status is initiated.
2. During the complete or partial immobilization
phase, can the contralateral limb and regions proxi-
mal and distal to the involved area be exercised?
What are the goals of exercise?
If the lower extremity is involved, then balance
impairments may be anticipated. Noninvolved
muscles essential to weight-bearing balance activi-
ties such as gluteus medius, gluteus maximus, quad-
riceps, and ankle plantarflexors and everters are
strengthened bilaterally.
If the upper extremity is involved, then scapu-
lohumeral rhythm impairments may be anticipated
and stability of the scapular adductors and depres-
sors promoted.
3. If the primarily involved tissue is articular, capsu-
lar, or ligamentous, do the surrounding intrinsic
muscles provide sufficient stability?
If intrinsic muscles are inhibited by pain and
swelling, or have been involved in the insult or sur-
gery, then compensatory external supports includ-
ing orthotics may be necessary.
A low-intensity isometric exercise program is
initiated to enhance the muscle’s ability to provide
stability to underlying joint structures.
Principle 2: Functional movement requires a balance
of connective tissue mobility, muscle and postural stability
to support weight-bearing segments and reduce stress on
joint structures, and controlled movement through range
across all involved regions to dissipate stress and ensure
smooth, coordinated motion. Critical issues that the clini-
cian must consider in this principle are the following:
1. Does the involved area present with decreased
mobility, is increasing mobility indicated at this
time, and how much mobility is needed for func-
tion?
If pain is limiting mobility, then pain-relieving
modalities and medications are considered.
What combination of tissues and findings is
limiting mobility?
2. Is there swelling and stiffness in superficial tissues?
If so, then compression, elevation, and tissue-spe-
cific procedures such as soft-tissue mobilization
and hold relax are considered.
3. If joint hypomobility is present, then joint mobili-
zation procedures are considered.
326 SECTION II • Principles of Practice
Principle 3: Activity tolerance requires an integration
of aerobic capacity, peripheral circulation, and anaerobic
power. Critical issues that the clinician must consider in
this principle are the following:
1. During the healing process, is the person going to
be more sedentary than his or her usual lifestyle?
2. If the person needs more aerobic exercise, then
aerobic exercise education and prescription must
be included in the overall plan to achieve the out-
come of health promotion.
3. Does the person have the strength or power to
perform activities such as stair climbing, getting
on/off a bus, or performing a push-up or chin-
up? Then anaerobic power exercises need to be
incorporated into the program.
Principle 4
1. Foundational muscle stability is necessary for
all subsequent postural stability and controlled
through range movements.
Principle-based decision making allows individ-
ual expression of general understanding.
The concept of multiple subsystems, which was applied
during the discussion of examination strategies, also
applies to the intervention process. A patient with low
back dysfunction is used as an example. An office man-
ager may report inability to work at a computer longer
than two hours due to increased low back pain in sitting.
Although the problem has been ongoing, it was aggra-
vated 3 weeks ago while gardening. A brief summary of
the examination includes poor workstation ergonomics
putting undue strain on the low back, sedentary lifestyle
without patient participation in a regular aerobic or exer-
cise program, weakness of abdominals and back extensors,
and hypomobility in the lower lumbar region and hips.
A multisystem approach may include modification of the
workstation, an aerobic exercise program encouraging
the patient to walk at least 20 minutes a day after a gen-
eral cardiovascular screen, an exercise program consisting
of exercises to improve the endurance of abdominals and
back extensors, and manual mobilization and hold relax
to improve lumbar and hip mobility. When providing
this type of multisystem intervention, the clinician can-
not determine accurately the effectiveness of individual
aspects of intervention. However, most patients do not
present with single-system involvement or with just one
impairment. Environmental strains compound cultural,
social, and psychological influences on physical systems
with imbalanced flexibility, strength, endurance, nutri-
tion, or hydration. Assuming that one type of treatment
procedure will result in long-lasting benefits does not
account for the multiple examination findings of most
patients. The vast number of patients who present with
recurrent low back dysfunction, chronic sprained ankles,
or recurrent shoulder involvement may attest to the need
for comprehensive multisystem interventions.
Clinician interaction time with each patient is limited.
Developing decision-making algorithms or clinical path-
ways for patients commonly seen in a particular practice
can assist decision making when actually working with
a patient, as long as the clinician keeps in mind that all
patients have differences and is prepared to modify the
treatment accordingly. Modifying the clinical pathways
concept by sequencing the range of intervention strate-
gies across treatment sessions can improve the delivery of
intervention procedures, patient compliance, and under-
standing. Providing the range of intervention strategies
including educational materials that parallel and reinforce
direct treatment procedures implemented by clinicians
may improve compliance. A table such as the one below
can be completed to provide a general guide to interven-
tion that then can be adapted to the individual patient
(Table 15-2).
When using this type of table, the clinician determines
when across treatment sessions various combinations of
intervention strategies would be indicated. Clinicians also
can indicate who will provide that care, what the specific
care will be, and the outcomes expected. These a priori,
prior to the treatment of individual patients, decision-
making guides are based on the evidence, on experience,
and on the common trajectory of the condition. They
can help ensure best practice.
Reflection is an effective way to improve practice.
Reflecting on patients with whom one has been successful
can be as good a learning experience as reflecting on those
whose outcome was not anticipated or deemed unsuccess-
ful. Adapting Tables 15-3 and 15-4 to the particular needs
of an individual practice setting may assist with organized
and systematic reflection. When utilizing Tables 15-3 and
15-4, the clinician should ask, “If observations did not
match expectations what could have been the reasons?
What about the patient, the insult-injury, the cluster of
Table 15-2
Modified Clinical Pathway Describing Interventions Across
Groups of Treatment Sessions
Tx 1–3 Tx 4–8 Tx 9–12
Direct treatment
to increase:
ROM
Stability
Strength
Balance
Educational
materials
Compensatory
aids
Environmental
modification
CHAPTER 15 • Rehabilitation Program Development : Clinical Decision Making, Prioritization, and Program Integration 327

Table 15-3
Comparison of Expectations to Observations
Primary Insult Comorbidities

Expected Observed Expected Observed

impairments impairments impairments impairments

Table 15-4
Delineating Expectations and Observations Across a Common Patient Condition
Impairment Test/Measure Goal Treatment Performed Actual Treatment Results

Expected
finding
Observed
finding

comorbidities, the level of irritability could have contrib-
uted to the unexpected results?” In addition, reflecting
on the outcomes of the examination and intervention can
assist the clinician in understanding clinical decisions so
that future decisions can be more deliberate.
The goal of clinical practice is to provide the most
effective and efficient care possible. Best practice requires
practitioners to make clinical decisions regarding the
choice of examination procedures, the interpretation of
examination findings, the determination of the interven-
tion strategies, and implementation of those strategies.
This chapter has applied decision-making concepts within
the patient care process so that clinicians integrate how
information is used with what the information means.
References
To enhance this text and add value for the reader, all reference have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever pos-
sible. There are total of 51 reference for this chapter.

C LINICIANS ’ R OLES IN H EALTH
P ROMOTION , W ELLNESS ,
AND P HYSICAL F ITNESS
Marilyn Moffat
History
The evolution of health promotion, prevention, well-
ness, and physical fitness activity has been inextricably
woven into the fabric of life and the culture of the times.
The impacts of the necessities of life, war, and technol-
ogy have all had both positive and negative effects on
the health, wellness, and fitness of humankind over the
centuries. Landmarks in the history of activity parallel
both social and political conditions existing at that time.
From prehistoric times to the present, the pursuit of fit-
ness has been an up-and-down part of the life of human
beings. Primitive people needed to hunt to provide
food for daily subsistence and then often shared the suc-
cess of the hunt with adjoining tribal communities.1,2 In
contrast with the need for activity of prehistoric people
came the domestication of animals and the inventions
of farming implements, which led to more sedentary
forms of life.3
In looking at the great civilizations, one sees many
approaches that recognized the importance of fitness and
wellness. Confucius encouraged regular physical activity
as a part of life.4 The practice of yoga, developed origi-
nally by Hindu priests, has been in existence for more
than 5000 years and has been recognized for its impact
on total well-being.5 Leaders in the Persian Empire
demanded high levels of physical fitness for military pur-
poses.6 The citizens of ancient Greece not only regarded
the beauty and physical perfection of the body, but they
328
161
C H AC PH TA EP RT E R
also held the importance of the development of the mind
and body in high regard. Fitness for the sake of fitness
characterized the Athenians in ancient Greece, while fit-
ness for military purposes characterized the Spartans.7
At its peak, the Roman civilization required fitness
conditioning for all eligible men for military service.8
With the demise of the Roman Empire, the barbarians
of the Dark and Middle Ages needed again to be fit for
survival, which required performing the activities of food
gathering and hunting.9
The Renaissance purported increased intellectual abil-
ities with increased fitness levels.10 In the 18th and 19th
centuries, the people of Europe continued to recognize
the importance of fitness as many physical education and
gymnasia programs evolved.4 These programs served as
the basis of physical therapy educational programs and
practice in the early 1900s in Europe and the United
States.
Health-related fitness—as opposed to fitness for hunt-
ing and food gathering, for participation in sport activ-
ity, or for military service—has been an area of changing
focus influenced by the societal changes of the 20th cen-
tury in the United States. The great wars led to the real-
ization that individuals had to be fit for combat.11,12
After World War II, people became increasingly aware
of the negative effects of the lack of fitness as well as
the health-related benefits of regular exercise, as a grow-
ing body of research data supported the relationships
between a level of physical activity and health.13,14
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
Concepts of Health Promotion,
Wellness, and Fitness
Health Promotion
Health promotion has been defined in several ways, but
in each case its aim is to improve the human condition
by achieving the best possible condition of the body as
evidenced by the absence of illness or disease, injury,
impairment, or disability. The World Health Organization
(WHO) has defined health promotion as the “process of
enabling people to increase control over their health and
its determinants, and thereby improve their health.”15
Green and Kreuter defined health promotion as “the
combination of educational and ecological supports for
actions and conditions of living conducive to health.”16
O’Donnell expanded the definition of health
promotion as
the science and art of helping people change their life-
style to move toward a state of optimal health. Optimal
health is defined as a balance of physical, emotional, social,
spiritual, and intellectual health. Lifestyle change can be
facilitated through a combination of efforts to enhance
awareness, change behavior and create environments that
support good health practices. Of the three, supportive
environments will probably have the greatest impact in
producing lasting change.17
Wellness
Definition of Wellness
Wellness has been defined as “a healthy state of well-being free
from disease”18 and further defined as an active process of becoming
aware of and making choices toward a more successful existence.19
To participate in and enhance wellness, we must provide
opportunities for our patients and clients to adopt healthy
choices and embrace lifelong wellness lifestyles through
education, modeling, and mentoring, thus leading to a
successful lifestyle. The National Wellness Institute has
delineated six components of wellness: social (contribut-
ing to one’s environment and community, emphasizing
the interdependence between others and nature), occu-
pational (satisfaction and enriching life through work),
spiritual (appreciation of the depth and expanse of life,
having meaning in one’s life), physical (awareness of the
need for regular physical activity, good diet and nutri-
tion, and avoiding habits that are harmful to wellness),
intellectual (being able to problem-solve, expand knowl-
edge and skill, openness to new ideas), and emotional
(awareness and acceptance of one’s feelings, thinking of
oneself positively).20
329
Components of Wellness20
● Social
● Occupational
● Spiritual
● Physical
● Intellectual
● Emotional
Fitness
For the purposes of this chapter, fitness is defined as
physical fitness. According to the Department of Health
and Human Services, physical fitness is a set of attri-
butes a person has in regards to a person’s ability to
perform physical activities that require aerobic fitness,
endurance, strength, or flexibility and is determined by
a combination of regular activity and genetically inher-
ited ability.21
Physical fitness encompasses aerobic capacity/endur-
ance (the ability to perform work or participate in activity
over time using the body’s oxygen uptake, delivery, and
energy release mechanisms),22 muscle strength (the ability
of muscles to exert or resist a force), muscle endurance
(the ability of the muscle to perform sustained work),
power (the ability of a muscle to exert high force at high
speed), balance (the ability to maintain equilibrium when
the body is static or moving), agility (the ability to per-
form power movements in opposite directions), and flex-
ibility (the ability to be stretched, easily bent, or pliable).
Components of Physical Fitness
● Aerobic capacity/endurance
● Muscle strength
● Muscle endurance
● Power
● Balance
● Agility
● Flexibility
Health promotion, wellness, and fitness activities pro-
vided by the clinician for patients or clients may span
all six domains of wellness, all seven aspects of physical
fitness, and may include many of the following activi-
ties: physical fitness activities across the life span, weight
management, safety in the work environment, elimina-
tion of unhealthy behaviors such as smoking and stress,
prepartum care, and knowledge of appropriate referral
sources related to spiritual health, environmental health,
substance abuse, and social health.
330 SECTION II • Principles of Practice
Economic Costs of Lack of Health
Promotion, Wellness, and Fitness
The staggering statistics related to both the incidence
and the cost of our lack of health or ill health provide
strong data for the important role that clinicians have
to play in promoting health, wellness, and fitness. It has
been estimated that between 50% and as much as 70%
of all disease is preventable and that the risk of major
diseases may be reduced by between 25% and 50% with
improved fitness alone, without any other intervening
health interventions.23,24
The American College of Sports Medicine has indi-
cated that by the year 2030, the number of individuals
in the United States who are 65 years of age and older
will reach 70 million and that the fastest growing age
segment of this population will be in those 85 years of
age and older.25
Frailty—defined as a clinical syndrome in which
the individual has difficulty in two or more functional
domains (physical, nutritive, cognitive, and sensory) or
has three or more criteria (unintentional weight loss [10
pounds in past year], self-reported exhaustion, weak-
ness [grip strength], slow walking speed, and low physi-
cal activity)—also increases with our increasingly older
populations. By modifying the risk factors (physical
inactivity, fairly or poorly perceived health, prevalence
of chronic symptoms, prevalence of chronic conditions,
cigarette smoking, drinking, depression, and social isola-
tion), it may be possible to postpone the onset of frailty
or ameliorate its further development.26,27
Risk Factors of Frailty
● Physical inactivity
● Perceived poor health
● Prevalence of chronic symptoms
● Prevalence of chronic conditions
● Cigarette smoking
● Drinking
● Depression
● Social isolation
The Centers for Disease Control and Prevention
(CDC) has estimated that more than half of all prema-
ture adult deaths in the United States and in other devel-
oped countries are from lifestyle-related causes that could
be altered with adherence to a healthy lifestyle.28 Many of
these deaths actually could be prevented and lives could be
enhanced if individuals could be made to “exercise regu-
larly, eat nutritious foods, avoid tobacco and excess alco-
hol, learn to manage stress, enhance social networks and
economic conditions, clarify lifestyle values, and achieve a
sense of fulfillment in their intellectual pursuits.”29
Evidence also exists that individual behavior and life-
style choices influence the development and course of
chronic conditions, such as cardiovascular disease, diabe-
tes, and obesity. Unhealthy behaviors, including a lack of
physical activity, a poor diet, and tobacco use, are risk fac-
tors for many chronic conditions and diseases. Adopting
healthy habits and practices will be essential in easing the
many burdens of chronic disease on society.30
Exercise and physical activity are increasingly impor-
tant in maintaining or improving health, wellness, fitness,
functional capacity, quality of life, and independence and
are equally important in preventing diseases, impair-
ments, functional limitations, and disability. This will be
especially true as the population ages substantially, as the
potential prevalence of chronic diseases and their impact
on health care costs increases if remedial steps are not
taken, and as the frail segments of our population con-
tinue to live longer.
Over the past decades, the United States has witnessed
increasing costs of health care services borne by payers at
all levels, by employers, and by individuals.
Health care spending is growing faster than the gross
domestic product (GDP) and is projected to account for
17.7 percent of the GDP by 2012, up from 14.1 percent
in 2001. A small number of chronic disorders-such as dia-
betes and cardiovascular diseases-account for the majority
of deaths each year, and the medical care costs of people
with chronic diseases account for more than 75 percent of
the nation’s medical care costs.31
The National Center for Health Statistics (NCHS)
found that “less than a third of U.S. adults engage in
regular leisure-time physical activity, and only about one-
fifth of adults engage in a high level of overall physical
activity.”32
The Department of Health and Human Services
(HHS) recognized that prevention makes “common
cents” and noted the facts detailed in Table 16–1 about
health promotion that provide solid evidence for the
need to alter health behaviors through health promotion,
wellness, and fitness programs. Further, HHS estimated
that health promotion and disease prevention programs
result in median savings of $3.14 for each dollar spent.30
Health care reform came to the forefront of legislative
priorities, and that has led to increasing interest in health
promotion and wellness on the part of the American
population. “Healthy People 2010” became the nation’s
foremost public health document, with its goals to
increase the quantity and quality of life and to eliminate
disparities in health among the American population.33
However, the interest in health promotion, wellness,
and fitness and the goals of Healthy People 2010 must
be converted into action, and that action will require a
paradigm shift on the part of consumers who have been
immersed in the sickness model of health service delivery
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness 331

Table 16-1
Health Promotion Facts and “Common Sense”
The United States spends $1 trillion on health care costs; 95% of that is directed toward diagnosing and treating illness and
disease. This number could jump to $2 trillion in 10 years.
At least 50% and up to 70% of all disease is preventable, but only a small fraction of the health care budget is dedicated to health
promotion, prevention, or research.
“We’re mopping up the floor but neglecting to turn off the sink.” Medical costs can consume 50% of a company’s profit.
High health risks are associated with increased medical expenditures in an otherwise healthy working population.
Changes in costs follow changes in risk.
Studies consistently show that healthy people make healthy companies.
Health promotion programs cost less than medical interventions.
Employee health promotion programs have been shown to be both effective and cost effective in the following areas:
Increased productivity (just a 1% increase in productivity equals at least a $150 to $200 cost savings for most employers)
Improved health status
Improved job satisfaction/appreciation for employer
Improved morale/personal satisfaction
Decreased health care costs
Decreased workers’ compensation claims
Decreased life insurance claims
Decreased disability claims
Decreased absenteeism
Health promotion/disease management programs return an average of $4 for every $1 invested (up to $12).

Adapted from US Department of Health and Human Services: Prevention makes common “cents,” September 2003, http://aspe.hhs.gov/
health/prevention; accessed July 2005.

rather than the wellness, prevention, and fitness model of
service delivery. This latter model will require thorough
knowledge of the impact of race, class, and gender on
health promotion, since they all have a potential impact
on the achievement of a healthy citizenry.
Many disease entities, some of which have been
referred to as “diseases of civilization,” have had a mor-
bidity, mortality, and cost effect on the health resources
throughout the country. A brief review of the impact of
these conditions is provided.
Cardiovascular Disease
The first and third leading causes of death in the
United States in both men and women are heart dis-
ease and stroke. The 2000 age-adjusted death rate
from cardiovascular disease (CVD) among the gen-
eral population was 343.1 per 100,000 people with
prevalence rates varying by race and ethnicity. 34,35
Almost one fourth of the general population in the
United States, or about 61 million persons, live with
some form of CVD, including coronary heart disease,
stroke, high blood pressure, congestive heart failure,
congenital heart defects, and other diseases of the cir-
culatory system.36
Cardiovascular disease, including heart disease and
stroke, results in about 6 million hospitalizations each
year and significant disability among working adults.
Victims of a stroke make up more than half of those
patients who are hospitalized for a neurological disease,
although this hospitalization should rightly be attrib-
uted to vascular disease rather than neurological disease.
Approximately 1 million of the 4.5 million Americans
who have had sustained a stroke have some form of
long-term disability.37
The American Heart Association conducted the first
major economic analysis of the costs of CVD in 2000–
2001. These costs have risen steadily and are approach-
ing the $400 billion mark.38–40
The CDC have identified five key risk factors for
cardiovascular disease. These are lack of physical activ-
ity, use of tobacco, high cholesterol levels, high blood
pressure, and poor nutrition. Of interest, they found
that the relative risk of coronary heart disease that was
associated with a lack of physical activity ranged from
1.5 to 2.4. This increase in risk was comparable to that
observed for high blood cholesterol, high blood pres-
sure, and smoking.41
Risk Factors for Cardiovascular Disease41
● Lack of physical activity
● Use of tobacco
● High cholesterol levels
● High blood pressure
● Poor nutrition
332 SECTION II • Principles of Practice
Obesity
Obesity in the United States has reached epidemic pro-
portions and is a major contributor to the rising health
care costs. The CDC now sees obesity as one of the
top threats to the health of the United States.42 Most
obesity is the result of faulty diets and a lack of physi-
cal activity. Although genetic factors sometimes play a
role in obesity, most incidents of obesity result from
an imbalance between the calories consumed and the
calories expended.42
It is estimated that approximately 129 million adults
are overweight or obese, and the costs associated with
obesity range from $69 billion to $117 billion per year.30
The direct health care costs of overweight and obesity
range from 4.3% to 9.1% of the total annual health care
expenditures in the United States.43,44 Grossman noted
that for morbidly obese individuals, health care costs
are 36% higher and medicines cost 77% more than they
do for people who are not obese.45 Finkelstein and his
associates noted that obese people who reach 65 years of
age have much larger annual Medicare expenditures than
non-obese people.44
Diabetes
One in three Americans overall, two in five blacks and
Hispanics, and one in two Hispanic females born in the
United States in 2000 are estimated to have a lifetime
risk of developing diabetes unless significant changes
occur in patterns of eating and exercising. By 2050, an
estimated 39 million people in the United States could
have diabetes.46
The American Diabetes Association (ADA) has
indicated that the national cost of diabetes for the
year 2002 was approximately $132 billion. This total
included the following: $91.8 billion in direct medical
expenditures ($23.2 billion for diabetes care, $24.6
billion for chronic complications attributable to dia-
betes, and $44.1 billion for excess prevalence of gen-
eral medical conditions.), with inpatient days, nursing
home care, and office visits making up the biggest
expenditure categories by service setting. Indirect
expenditures totaled $39.8 billion and resulted from
lost workdays, restricted activity days, mortality, and
permanent disability due to diabetes.47
Adjusting for differences in age, sex, and race/
ethnicity, the ADA further noted that medical costs
for those with diabetes were 2.4 times higher than
the costs that would have been incurred by the same
group if they did not have diabetes.47 CDC research
has shown that people with diabetes lost 8.3 days
per year from work, accounting for 14 million dis-
ability days, compared to 1.7 days for people without
diabetes.46
Sarcopenia
As the number of older Americans increases, the eco-
nomic costs of sarcopenia (loss of muscle mass) will
also continue to increase unless effective public health
programs aimed at reducing the occurrence of sarcope-
nia are instituted. The estimated direct health care cost
attributable to sarcopenia in the United States in 2000
was $18.5 billion ($10.8 billion for men, $7.7 billion for
women), which represented about 1.5% of total health
care expenditures for that year.48
Osteoporosis
As the population ages, postmenopausal osteoporo-
sis (loss of bone mass) is increasingly associated with
significant morbidity, mortality, reduction in one’s
quality of life, and increasing health care costs. In
the United States, an estimated 1.5 million women
will have one or more osteoporosis-related fractures
annually. Although fractures may occur at any site,
vertebral and hip fractures are the most common.49
The National Institutes of Health no longer considers
osteoporosis to be age or gender dependent. Whereas
previous studies focused on the postmenopausal
female population, increasing research on men has
been published. One in eight men over age 50 experi-
ences an osteoporosis-related fracture in his lifetime.
Men account for 30% of all hip fractures, and they
lose bone mineral density (BMD) at a rate of up to
1% per year with advancing age. 50
Kyphotic postural change is not only physical disfig-
uring, but also psychologically damaging. Progressive
kyphotic postural changes may predispose an individ-
ual to back pain, increased risk of falls, altered balance,
increased chance of vertebral fractures, altered respiratory
function, anxiety, depression, and social isolation.51–53
Murphy and associates reported that longitudinal stud-
ies have demonstrated a decreased life expectancy asso-
ciated with both vertebral and nonvertebral fractures.49
Once an initial fracture occurs, the risk of a second frac-
ture within 1 year increases fivefold. The management of
osteoporosis is aimed at preventing the first fracture from
occurring and includes early detection through bone
density studies, patient education, both weight bearing
and strengthening exercises, nutritional supplementa-
tion, and drug therapies.49
Physiological Changes Associated
with Aging
This section reviews the myriad changes that occur as the
human body ages. Many of these changes may be less-
ened with a lifelong commitment to a program of health
promotion, wellness, and fitness.
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
Cardiovascular/Pulmonary Systems
Cardiac Changes
Many changes may occur with the aging heart. Since
the heart is a muscle, its strength decreases with age,
resulting in less intensive muscular activity. Its size also
decreases anywhere up to 30% to 40% unless an individual
has continued to engage in heavy physical training. The
left ventricular mass and wall thickness increase, resulting
in reduced early diastolic filling, and the left ventricu-
lar internal diastolic and systolic dimensions decrease
slightly. Thus, end-diastolic volumes also are likely to
decrease. The left atrium and aortic root become some-
what dilated. The atrial septum becomes thicker and
stiffer. The leaflets of the valvular structures thicken. The
pacemaker cells in the sinus node decrease. The epicar-
dial fat increases.54–56 The compliance of the large arteries
in the cardiothoracic circulation declines.57
Cardiac function declines with age, which means
that cardiac output, stroke volume, peak heart rate,
and maximum oxygen consumption will decrease.58
Maximal oxygen intake values decline from young
adult values of 42 to 50 ml/kg.min in males and 35
to 40 ml/kg.min in females to 25 to 30 ml/kg.min in
both sexes by 65 years of age.59 The decrease of peak
stroke volume is the result of the progressive change in
the chemical composition of the myocardium result-
ing in slower and less forceful ventricular contractions.
Ventricular filling slows, and ventricular afterload-
ing increases. There is a decrease in the secretion and
release of catecholamines, in sympathetic nerve activa-
tion, and in receptor sensitivity.55,56
Tonic vagal modulation of the cardiac period and
cardiovagal baroreflex sensitivity decrease. While tonic
(basal) sympathetic nervous system activity increases,
sympathetic nervous system beta-adrenergic support of
the resting metabolic rate decreases.60
Overall, the increase in heart rate during exercise
becomes smaller with aging, probably because of both
less withdrawal of cardiac vagal tone and diminished
beta-adrenergic responsiveness.61
Vascular Changes
Changes in the amount and nature of elastin and col-
lagen in the arterial walls with aging cause blood ves-
sels to become stiffer, thicker, tougher, and dilated and
therefore less compliant. These changes lead to a loss in
the ability to adjust to sudden changes in blood pressure.
The smooth linings of the vessels become roughened
with age. Peripheral vascular resistance increases, result-
ing in an increase in afterload. The walls of the veins also
weaken and stretch, leading to decreased competence of
the valves, which in turn may result in the development
of varicose veins. The important baroreceptors, located
in the aortic arch and carotid sinus, become less sensitive,
333
thus decreasing the body’s responses to blood pressure
changes.62
Pulmonary Changes
During aging, the lungs undergo changes that decrease
the gas exchange of oxygen and carbon dioxide. The
chest wall becomes stiffer and more rigid as a result
of changes in the shape of the thoracic cage and the
decreased range of motion of the articulations of the rib
cage. The respiratory muscles tend to weaken, probably
because of the aging changes that occur in the muscles
themselves and the impact of the changes in the chest
wall (more barrel-like) that affect the force generation
capacity of the diaphragm.63
A decrease in elastic fibers and an increase in type
III collagen occur in the lungs with aging. Cross-linking
and fiber orientation changes also occur.64–66 With the
decrease in elastic properties of the lung parenchyma and
the airways, elastic recoil diminishes. The overall surface
area of the alveoli is reduced as a result of a decrease
in the number of alveoli and an increase in the size of
the alveolar ducts.67 Alveolar vascularity also decreases,
which, when accompanied by the decrease in the num-
ber of alveoli, reduces both the rate and quantity of gas
exchange.64
The vital capacity declines as residual volume increases
and ventilation-perfusion imbalance increases.58 Smaller
tidal volumes and higher frequencies of breathing are
observed.63 Peak airflow and gas exchange decrease.68
The reserve capacity capable of adapting to increased
ventilatory demands is reduced.69
Therefore, the alterations associated with age-related
changes result in reduced capacity for exercise and in
increased oxygen demand by the respiratory muscles at
any given level of exercise.63
Musculoskeletal System
Muscle Changes
Muscles atrophy and weaken with age. The onset of
strength decline varies, but in general, muscle strength
is adequately maintained through the 40s and 50s.70,71
Beyond the sixth decade, muscle strength steadily
declines, with the total decrement in voluntary muscle
strength ranging from 30% to 45%.72 Muscle area is
reduced approximately 40% between the second and sev-
enth decades of life.73 The contractile strength of muscle
reduces with advancing age and is believed to be the
result primarily of motor unit losses leading to a quanti-
tative loss in muscle cross-sectional area.74,75
Sacropenia (reduced relative skeletal muscle mass) is a
common occurrence in older persons.76 The loss of mus-
cle mass with aging appears to be the major factor in the
age-related loss of muscle strength. The loss of muscle
mass is partially the result of a significant decline in the
334 SECTION II • Principles of Practice
numbers of both type I and type II muscle fibers plus a
decrease in the size of the muscle cells, with the type II
fibers showing a preferential atrophy. Muscle oxidative
enzyme activity and muscle capillarization decrease by
about 25%.73
Extremity muscles of older men and women were
noted to be 25% to 35% smaller and had significantly
more fat and connective tissue than those from younger
individuals. Type II (fast-twitch) fibers were found to
be smaller in older persons. While the size of the type I
(slow-twitch) fibers was less affected, nonetheless reduc-
tions were also observed in aging muscle in the percent-
age of type I fibers and the capillary-to-fiber ratio. Type
II fiber area decreased and fiber type grouping increased
with age. A slowly progressive neurogenic process may
also be responsible for the decrease in muscle mass.75,77
The fasting rate of mixed and myosin-heavy chain pro-
tein synthesis reduces with age and is a contributory
factor in muscle protein wasting.78 With age, the rates
of whole body and muscle protein metabolism decline,
indicating a progressive decline in the remodeling pro-
cesses of the body.79
Peak anaerobic muscular power in both upper and
lower extremities decreases progressively with age, and
this decrease is more evident when a person performs
tasks that require complex and powerful movements. This
decrease is greater in women than in men in the complex
and explosive power movements.80 Maximum isometric,
concentric, and eccentric forces also decrease. Isometric
muscle strength appears to be lost at approximately
1% to 1.5% per annum after the sixth decade. Concentric
strength can decline as much as 56% by the ninth decade.
Eccentric muscle strength appears to be less affected by
aging than either isometric or concentric strength.81–87
“Age and body fat also had significant inverse associa-
tions with strength and muscle quality. Both preserva-
tion of lean mass and prevention of gain in fat may be
important in maintaining strength and muscle quality in
old age.”88
Schwendner and colleagues noted that older women,
especially those with a history of falls, demonstrated
decreased muscular endurance and required increased
time to recover from fatiguing exercise as compared to
young women.89
Flexibility Changes
A decrease in range of motion with a loss of flexibility
is omnipresent in older adults and is directly related
to declines in function.90–92 Muscle atrophy results in
decreased range of motion and therefore decreased flex-
ibility. Changes in the collagen structures of the body
and inactivity are the two main reasons for decreased
flexibility in joints, ligaments, and surrounding tissues.
Collagen fibers normally have a parallel formation, but
with aging, this parallel formation deceases.93 Thus, the
viscoelastic properties of collagen tissue change, causing
them to become less elastic and less flexible.
The lining of the joints thickens with age. Degeneration
in the ligaments surrounding the joints also occurs.
A further age-related change that affects flexibility relates
to the increase in fibrous tissue surrounding the joints,
resulting in a loss of elasticity and flexibility, less precise
movement, a loss of ability to produce smooth flowing
motions, a decrease in joint range of motion, and pos-
sibly even contractures or ankylosis of the joints. Of note
is the fact that the joint capsule contributes to approxi-
mately 47% of the resistance to joint motion, muscle and
fascia contribute 41%, ligaments and tendons contribute
10%, and skin contributes 10%.94
Spinal and peripheral joint mobility decreases with
advancing age.95–98 Flexibility generally decreases 20% to
30% from the ages of 30 to 70 years, but this decline
varies significantly with body area. Spinal mobility may
decrease up to 50% in individuals in their late 70s,94,99
while upper extremity flexibility declines at a lesser rate
than does lower extremity flexibility.88
Bone Changes
With age, bones become demineralized. Bone resorption
slowly begins to exceed bone formation regardless of sex
after the age of 30, leading to loss of bone mass with
age. Previous studies had concentrated on the female
population and found that bone loss is most rapid in
the first few years after menopause but persists into the
postmenopausal years.100 However, increasing research
on men found that one in eight men over the age of
50 years experiences an osteoporosis-related fracture and
loses bone mineral density (BMD) at a rate of up to 1%
per year with advancing age.101
Changes in the hormonal and age-related activity of
the cells that are responsible for maintaining the physiol-
ogy of bone result in thinning of the bone matrix. In type
I, or postmenopausal osteoporosis (15 to 20 years after
menopause), the decrease in estrogen levels increases
osteoclastic activity, resulting in decreased matrix thick-
ness and calcification, especially in cancellous bone. Sites
of trabecular bone loss include the vertebral body, distal
forearm, ankle, mandible, and maxilla.102
Type II or age-related (senile, above the age of 70)
osteoporosis begins in the third decade with bone density
changes usually occurring at osteopenic/osteoporotic
levels.103 While type II osteoporosis is twice as common
in women, it also occurs in men.102 The gradual loss of
bone in this type of osteoporosis is due to the decrease
in vitamin D synthesis (which leads to a lack of calcium
absorption) or to the increase in parathyroid activity
(which increases osteoclastic activity).104 Bone loss occurs
in both cortical and cancellous bone.102 Common frac-
ture sites associated with type II osteoporosis occur at
the hip, pelvis, proximal humerus, or proximal tibia.102
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
Types of Osteoporosis
● Type I: postmenopausal
● Type II: age related (senile type)
Body Fat Changes
As one ages between the mid-20s and the mid-50s, a
gradual increase in gross body weight occurs because of
the accumulation and increased deposition of adipose tis-
sue. From the mid-50s and on, gross body weight gen-
erally begins to decline slowly. The average percentage
increase of body fat in men from almost 20 to 60 years of
age is from 15% to 28%, while in women it is from 25%
to 39%.69
With this absolute increase in body fat, a decline
occurs in the body’s fat-free mass or lean body mass. In
addition, with aging, a change also occurs in the body’s
fat distribution, leading to an increase in intra-abdomi-
nal fat and a decrease in the subcutaneous fat of the
extremities.
The increase in body fat with aging is attributed to the
decline in metabolic rate that also occurs with aging. The
metabolic rate decreases approximately 10% between
the ages of 20 and 65 years, and from then on, there is
another approximate 10% decrease.69 Several factors have
an impact on the decline in metabolic rate, including
endocrine changes, cardiovascular changes, a decrease in
physical activity, and most importantly increasing sarco-
penia. This latter reduced relative skeletal muscle mass
means that metabolically active muscle—which normally
helps to increases the lean body mass, increase caloric
consumption, and increase metabolic rate—is lost, lead-
ing to an increase in body fat. The age-related increase in
abdominal fat is also associated with an age-related rise
in plasma free fatty acid concentrations, which in turn is
related to age-related insulin resistance.105
Nervous System
Age changes in the nervous system begin at about the
age of 30 with a decrease in the number of neurons. As
with all other systems, changes in the nervous system
vary greatly from person to person both in terms of the
type of changes that occur and the degree or severity of
those changes.
Brain and Spinal Cord Changes
A decrease in the number of nerve cells in the brain
occurs. While minimal loss takes place in some areas of
the brain (e.g., brain stem nuclei and supraoptic and
paraventricular nuclei), loss in other areas may range sig-
nificantly between 10% to 60% (e.g., hippocampus). The
335
superior temporal gyrus of the cortex also undergoes a
loss of nerve cells of about 55%, while the tip of the tem-
poral lobe only undergoes a loss of about 10% to 35%.
The brain weight decreases by about 10% between the
ages of approximately 20 and 90. The cerebral ventricles
may increase three to four times. Cerebral blood flow
decreases by about 20%.106
Atrophy of the brain and spinal cord occurs as a result
of a loss of nerve cell mass. Transmission of impulses
slows down because of the decrease in the number of
nerve cells and dendrites. The latency period in impulse
transmission increases. Demyelinization may also occur.
Plaque formation and neurofibrillary tangles may be
noted in the brain. With degeneration of the nerves,
there may be an accompanying involvement of the senses.
Reflexes may be reduced.107
Changes occur in the neurotransmitter systems, par-
ticularly in the levels of enzymes, receptors, and neu-
rotransmitters. Those enzymes that decrease include
acetylcholinesterase, carbonic anhydrase, and choline
O-acetyltransferase. Those that increase include catechol
O-methyltransferase and monoamine oxidase. The recep-
tor dopamine 2 increases, while muscarinic and serotonin
receptors decrease. The neurotransmitters neurotensin
and substance P decrease, while vasoactive intestinal
polypeptides increase.108
Sensory Organ Changes
The sensory systems become less acute. Hearing is
altered by the cumulative damage to hair cells in the
organ of Corti in the ear after the age of 60 that leads
to a loss in the ability to hear high-pitched sounds
and certain consonants. Visual changes include a loss
of lens elasticity, formation of cataracts, a gradual loss
in the number of rods, and the development of macu-
lar degeneration. Pupil size and reactivity decrease as
a result of the decreased autonomic nervous system
activity. Tactile sensation, touch, and pain receptors
decrease in number and sensitivity. Smell is altered with
a decline in function of the cranial nerves and a decrease
in the olfactory receptor cells. Taste is also altered with
a decline in function of the cranial nerves, a decrease in
the sensitivity and number of taste buds, and a thinning
of the mucous membranes.109
Peripheral Nerve Changes
Studies have shown that with age, there is some loss of
peripheral motor neurons, reduction in the number of
motor units, alterations in the neuromuscular junctions,
and selective denervation of type II muscle fibers.110
Reaction time and balance decrease.96 Research sug-
gests that older adults experience some breakdown in
the timing and sequencing of muscle activity and in the
functional coordination of their postural reflexes, with
voluntary sway.111
336 SECTION II • Principles of Practice
Mental Function Changes
It is interesting that this is one area where the aging
changes seem to present fewer problems than they do
with other bodily changes. Most older individuals do
cope with the cognitive changes and other mental and
psychological stressors that confront them. These stress-
ors include the medical stressors occurring in older ages
and the often co-morbid conditions,112 the psychologi-
cal stressors including isolation and bereavement, and
the drug-related stressors that result from the often large
number of medications that they may be taking.113
While most aging individuals do cope with these stress-
ors, about one third of older adults do experience mild
cognitive impairment. This impairment does not inter-
fere with the individual’s daily living but may include a
decrease in the speed of cognitive processing, impaired
memory, and a decrease in the ability to learn.114,115 Mild
cognitive impairment may be related to the physical
changes occurring in the brain, including the decreases
in the number of nerve cells, nerve impulses, and levels
of acetylcholine (a primary neurotransmitter for memory
and learning) and serotonin.116
However, it has been estimated that minor depres-
sion, which may have a major impact on the lives of older
adults, occurs in 8% to 20% of community-dwelling
adults.117,118
Endocrine Changes
Age-related changes to the hormone system are gener-
ally not sufficient to prevent it from functioning ade-
quately. The most serious hormone deficiencies tend
to be pathological rather than age related. Few signifi-
cant hormonal changes occur with age. Of those that
do change, the sex hormones, pancreas, urinary system,
and growth hormone changes are perhaps the most
important clinically.
A decline occurs in the levels of the female sex hor-
mones estrogen and progesterone and the male hormone
testosterone. In terms of the pancreas and the islets of
Langerhans, insulin concentration increases, while glu-
cose tolerance decreases. The urinary endocrine changes
that occur include a decline in the levels of vasopressin
and a rise in the levels of atrial natriuretic peptide. The
latter may increasingly cause nocturia, since the peptide
tends to increase urine production. Growth hormone,
which interestingly may reverse the decline in muscle
mass observed with increasing age, declines.119
Clinicians’ Roles in Health Promotion,
Wellness, and Fitness
Clinicians, especially physical therapists, are in a unique
position to serve as major providers in the realm of health
promotion, wellness, and fitness. To do this, profession-
als must embrace the concepts of health promotion,
wellness, and fitness and then impart these concepts to
their patients and clients. Professionals can make patients
and clients more aware of the importance of lifestyle
changes, particularly in the physical activity areas; they
can help patients and clients to make behavioral changes,
especially in the adoption of lifelong health promotion,
wellness, and fitness programs; and they can create an
environment that will support health practices leading to
a healthy lifestyle.
Health promotion or prevention of ill health may
complement the aspects of health services that have
traditionally emphasized treatment. 120 The difference
between the promotion and prevention approach
and the treatment approach is that the former seeks
to decrease disease risk factors and promote healthy
behaviors while the latter does not. Equally impor-
tant is that the promotion and prevention approach
shifts a great deal of the responsibility for good health
from the provider to the client.120 Evidence exists that
when health care professionals counsel their patients
about risk reduction, those patients are more likely to
change poor health habits, thus enhancing a healthier
lifestyle. 121 In addition, the simultaneous and bal-
anced satisfaction of personal, interpersonal, and col-
lective needs also facilitates the adoption of healthy
lifestyles. 122
Goals of Health Promotion
● Decrease risk factors
● Promote healing endeavors
● Make client responsible for his/her good health
The Guide to Physical Therapist Practice recognized
these roles of promotion, wellness, and fitness and the
effect of these services in decreasing costs
by helping patients/clients (1) achieve and restore optimal
functional capacity; (2) minimize impairments, functional
limitations, and disabilities; (3) maintain health (thereby
preventing further deterioration or future illness); and (4)
create appropriate environmental adaptations to enhance
independent function.22
Primary, secondary, and tertiary prevention roles are
inherent aspects of practice in which physical thera-
pists are involved.22 Table 16–2 describes prevention
screening activities and possible intervention pro-
grams to address wellness issues. Whenever possible,
health promotion, wellness, and fitness programs
should be based on measurable results and supported
by research.
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
Table 16-2
Prevention Screening and Intervention Strategies for Wellness Concerns
Prevention Screening
Identification of lifestyle factors (e.g., amount of
exercise, stress, weight) that may lead to increased
risk for serious health problems
Identification of children who may need an examination
for idiopathic scoliosis
Identification of elderly individuals in a community center
or nursing home who are at high risk for falls
Identification of risk factors for neuromuscular injuries
in the workplace
Preperformance testing of individuals who are active
in sports
Adapted from American Physical Therapy Association: Guide to physical therapist practice, Phys Ther 81(1):9-746, 2001.
Benefits of Health Promotion,
Wellness, and Fitness
The benefits of a regular exercise program apply to almost
every body system and to every age from childhood to
senescence. As Menard and Stanish have pointed out,
not too long ago we perceived our grandparents as being
inactive and sitting in rockingchairs.119 Fortunately that
image has changed drastically, and we now know that the
body that is engaged in regular physical activity under-
goes changes to preclude the negative atrophic changes
that take place with disuse. Regular exercise, which they
noted “is truly a fountain of youth from which we can
all rejuvenate ourselves,” may slow down or retard the
age-related physiological declines noted previously by as
much as 50%. Thus, while life does not begin at 40, it has
does not have to end there or at 70 or 80 or 90.123
Traditionally one has been advised to consult with a
physician before embarking on an exercise program. This
337
Intervention Strategies
Back schools, workplace redesign, strengthening, stretching,
endurance exercise programs, and postural training to
prevent and manage low back pain
Ergonomic redesign; strengthening, stretching, and endurance
exercise programs; postural training to prevent job-related
disabilities, including trauma and repetitive stress injuries
Exercise programs, including weight bearing and weight
training, to increase bone mass and bone density (especially
in older adults with osteoporosis)
Exercise programs, gait training, and balance and coordination
activities to reduce the risk of falls—and the risk of fractures
from falls—in older adults
Exercise programs and instruction in activities of daily living
(ADL) (self-care, communication, and mobility skills
required for independence in daily living) and instrumental
activities of daily living (IADL) (activities that are important
components of maintaining independent living, such as
shopping and cooking) to decrease utilization of health care
services and enhance function in patients with cardiovascular/
pulmonary disorders
Exercise programs, cardiovascular conditioning, postural
training, and instructions in ADL and IADL to prevent
disability and dysfunction in women who are pregnant
Broad-based consumer education and advocacy programs to
prevent problems (e.g., prevent head injury by promoting
the use of helmets, prevent pulmonary disease by
encouraging smoking cessation)
Exercise programs to prevent or reduce the development of
sequelae in individuals with lifelong conditions
notion creates an image that exercise may be potentially
harmful, an image that negates the roles of health profes-
sionals in health promotion, wellness, and fitness. While
this advice may be warranted especially for at-risk individ-
uals, clinicians, especially physical therapists, must recast
their roles as physical activity and exercise advocates.124
The health benefits of regular exercise are countless,
including a decrease in mortality and age-related mor-
bidity, an enhancement of function and quality of life,
and improvements in the cardiovascular/pulmonary,
musculoskeletal, neuromuscular, including neurocog-
nitive function and endocrine systems. However, it has
been estimated that up to 75% of older Americans are not
active enough to achieve these health benefits.58 They
suffer from hypokinesis, or what has been called the dis-
ease of inactivity.125
Thus, the challenge to clinicians is to teach clients and
patients, regardless of their age or presenting diagnosis,
the benefits of regular physical activity and to incorporate
338 SECTION II • Principles of Practice
into all interventions those strategies that increase partic-
ipation in and adherence to lifelong physical activity and
exercise.126 Such physical activity and exercise programs
are essential to prevent the decline in physiological func-
tion and in functional performance that too often leads
to a loss of autonomy and to increasing burdens on the
health services delivery system. Ample evidence exists of
the manifold benefits of exercise, and they are reviewed
in the following sections.
Effects on Mortality and Morbidity
While the health benefits of regular physical activity and
exercise are abundantly clear, it is important to note that
such activity is inversely associated with decreased mor-
tality and age-related morbidity.127–129 Blair and associ-
ates, in their prospective study, found that higher levels
of physical fitness appeared to delay mortality, regardless
of cause, primarily as a result of lowered cardiovascular
disease and cancer rates,130 while low levels of fitness were
antecedents of mortality.131
Adopting healthy lifestyles—such as engaging in mod-
erately intense physical activity, quitting smoking, being
normotensive, and avoiding obesity—was associated
with lower rates of death from all causes.132 However,
the protective effect of moderate levels of physical fit-
ness appeared to decrease the risk of premature mor-
tality regardless of whether individuals were unhealthy,
smoked, or had elevated cholesterol or blood pressure
levels.133 Even individuals with chronic diseases have
been shown to have a long-term beneficial mortality
effect from regular aerobic, strength, flexibility, and bal-
ance exercise programs.133
The reduction in mortality associated with regular exer-
cise has been attributed to the ability of exercise to pro-
vide physiological and functional reserves through early
muscle strengthening;134 reverse sarcopenia, since strength
and its decline have an impact on mortality;135,136 increase
parasympathetic tone at rest;137 enhance aerobic capacity,
which is an independent predictor of all-cause mortality;
and reduce mortality approximately 10% with each 1 met-
abolic equivalent increase in cardiovascular fitness.138
Effects on Functional Abilities/Quality of Life
Evidence supports the regular participation in exercise
programs consisting of aerobic conditioning and strength
training to help increase functional capabilities, maintain
independence, and therefore improve one’s quality of
life.139 Quality of life comprises the psychological con-
struct of life satisfaction and the dimensions of health sta-
tus or health-related quality of life.140 The public health
benefits of these functional and quality-of-life improve-
ments with physical activity and exercise are especially
important for our increasingly elderly populations.141
Functional decline that had traditionally been accepted
as part of the aging process can be retarded,54 thus reduc-
ing the burden of impairments on aging individuals and
its resultant cost to society.142,143
Mazzeo noted that in older individuals both the
quality and the quantity of exercise that is needed to
enhance the quality of life differ from those needed to
significantly increase fitness.126 Studies have shown that
function, quality of life, and independence through mul-
tidimensional programs of strength, endurance, and bal-
ance training may be improved at any age as long as the
intensity, duration, and frequency of the exercise are suf-
ficient to consistently overload the system. In addition
to exercise training, promoting a physically active life-
style further prevents or treats functional disability.144–146
Long-term high and low progressive resistance strength
training results not only in improved morale and quality
of life147 but also in substantial improvements in walk-
ing speed, stair-climbing ability, the ability to rise from a
chair,148–151 and the ability to carry groceries.148
Power training (or high-velocity resistance training)
improved physical function even more effectively than
strength training in community-dwelling adults152 and is
thought to exert greater influence than other types of
exercise in improving age-related reductions in physical
functioning.153 Lower extremity power in older women
has been shown to be a strong predictor of self-reported
functional status.154 Aerobic conditioning exercises have
been shown to enhance overall health, protect against dis-
ability, and extend the time of a disability-free life.155,156
Functional capacity (as measured by muscle strength,
range of motion, muscle endurance, speed of muscle con-
traction, walking speed, and standing balance) improves
with exercise training consisting of low-intensity strength-
ening and flexibility exercise and moderate-intensity
aerobic capacity/endurance exercise.157 Programs that
combine functional strength training (i.e., the use of resis-
tive weights while stair climbing) and aerobic condition-
ing also result in improved muscle performance, especially
of the lower extremities, and enhanced function.158
The effects of a 12-month tai chi exercise program
resulted in an overall improvement in fitness in the
elderly,159 as well as in increases in range of motion and
balance, improved mood, and a decreased perception of
pain. These changes are purported to potentially affect
the incidence of falls and quality of life.160
A moderate-intensity exercise program consisting
of low-impact aerobics and brisk walking resulted in
improved quality of sleep in older adults.161 Resistance
exercises were also shown to improve sleep quality.162
Effects on the Old-Old
The increasing number of studies done with oldest-old
and frail subjects and with subjects with chronic diseases
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
further support the role of physical activity throughout
life. Disability is postponed and independent living is
maintained.163 Older adults with physical function impair-
ments and with oxygen uptake impairment have been
shown to improve their physical function with intensive
exercise.164
Eighty-five-year-old individuals who underwent 8
months of physical reactivation and regular training
appeared to have increases in walking speed and maxi-
mal oxygen uptake and a decrease in blood pressure
leading to risk reduction and improved independence.165
Individuals in the 10th decade of life improved their
functional activity performance with simple progressive
muscle power exercise training.166 A 10-week moderate-
intensity exercise program of well-rounded, low-impact
training for older adults enhanced aerobic capacity, lower
extremity strength, and feelings of vigor.167
Meuleman and associates found that debilitated
elderly patients who underwent resistance training had
increased function.168 Of particular interest was the find-
ing that those who were most impaired gained the most
function.
Independent living and adequate functional perfor-
mance and strength may result from the carrying out of
everyday functional training (e.g., walking, gardening,
performing household chores) in 75-to-80-year olds.169
Effects on Frail Elders
Data suggest that frailty can be minimized or even
reversed through low-intensity exercise.170,171 Evans
indicated that no segment of the population can benefit
more from exercise than the frail elderly.171 Frail elders
who have low functional abilities and high incidences
of chronic disease have been shown to make improve-
ments in multiple arenas of physical health through exer-
cise programs. Comprehensive exercise programs can
enhance fitness and physical performance in this popula-
tion.172 Gains made by frail elders are influenced by their
level of frailty before exercise training and the specificity
of the exercise program. Chandler and associates demon-
strated that a lower extremity strengthening program led
to increases in gait and gait speed and in the ability to rise
from a chair, perform transfers, and climb stairs.173 Those
frail elderly with limited exercise tolerance have been
shown to improve their function with lower extremity
eccentric exercises.174
In spite of the data supporting the use of therapeutic
exercise with frail elders, it is an underused intervention
according to Heath and Stuart,175 who attributed this
underuse to barriers created by patients, caregivers, and
health care providers. They proposed that these barriers
may be overcome with a safe and sustainable exercise pro-
gram designed to meet the functional needs of the frail
elderly as well as their preferences. In addition, providing
339
this population with the appropriate motivation and an
awareness of the benefits of the exercise program should
be part of the total approach to participation.175
Effects on the Cardiovascular/Pulmonary Systems
Research has shown that the adaptations of the cardio-
vascular system to prolonged endurance training are
similar in individuals whether they are young or old.176
Engels and associates showed that even low-impact,
well-rounded, moderate-intensity exercise training will
enhance aerobic fitness.167
Cardiovascular exercise training results in increases in
cardiac output, stroke volume, maximum heart rate,58
VO2max, maximal O2 pulse, systolic blood pressure,176,177
endurance,126 anaerobic threshold,178 arterial flow capacity
as a result of enlarged caliber of the arterial supply vessels,179
and central arterial compliance.57 Cardiovascular exer-
cise training results in decreases in heart rate, perceived
exertion during submaximal exercise,176 hypertension,
arterial compliance, energy metabolism,126 and levels of
plasma catecholamines at the same absolute submaximal
workload.61
Cardiovascular exercise training results in improve-
ments in left ventricular performance during peak exer-
cise in men61 and in lipid profile,128 although the time
required to achieve an HDL cholesterol change (2 years)
may be longer in older populations.180 Cardiovascular
exercise significantly reduces the risk of coronary heart
disease.126 Aerobic conditioning activities (running,
rowing, and walking) and resistance exercises (weight
training) were shown to be inversely associated with risk
of coronary heart disease.181
Responses of the autonomic nervous system are
enhanced with regular aerobic exercise. These include
increasing the tonic vagal modulation of the cardiac
period, lessening the decline of cardiovagal baroreflex sen-
sitivity, and maintaining the sympathetic nervous system
beta-adrenergic support of the resting metabolic rate.60
Of interest are the studies of older athletes who do not
show the declines in maximum stroke volume and aVO2
difference that are seen in aging sedentary individuals.182
Strength training programs have also been shown
to increase endurance performance and decrease blood
pressure in hypertensive individuals.183,184 A high-
intensity resistance training program (85% to 90% 1RM)
two times per week, three sets to failure (leg press, half
squat, leg extension) resulted in increased maximal work
capacity, VO2max, and serum lipid profiles.185 Exercises
using an eccentric overload in elderly individuals were
significantly less stressful on the cardiovascular system in
terms of heart rate, mean arterial pressure, rate pressure
product, and perceived exertion.186
An aquatic exercise program of 70 minutes per day and
3 days per week has been shown to significantly improve
340 SECTION II • Principles of Practice
cardiorespiratory fitness and cholesterol levels in women.
The program consisted of 20 minutes of warmup and
stretching, 10 minutes of resistance exercise, 30 min-
utes of aerobic conditioning (walking and dancing), and
10 minutes of cooldown.187 D’Acquisto and associates
also showed the cardiovascular benefits of shallow-water
exercise.188
Prolonged participation in regular tai chi exercise has
been shown to produce significant cardiovascular changes
in resting heart rate and 3-minute step test heart rate in
older adults (65+ years).189
Age is no barrier to enhancing the cardiovascular sys-
tem through exercise. Individuals 80 years and older who
participated in a moderate-intensity exercise program (at
a frequency of two to three times per week, a duration of
20 to 30 minutes per session, and a mode of treadmill or
stationary bicycle) had an increase in their VO2peak and
a decrease in their systolic blood pressure.190
Studies show that the changes in respiratory function
are less profound than they are for cardiac function.58
However, exercise training increases ventilation.176
Cardiac Pathology
Research indicates that physical activity (1600 kcal per
week) may halt the progression of coronary artery dis-
ease. Actual regression of coronary artery disease may be
achieved with physical activity requiring a gross energy
expenditure of 2200 kcal per week.138
Congestive Heart Failure. The benefits of exercise
training and enhanced physical fitness in patients with
congestive heart failure (CHF) are increasingly supported
by data. Twelve weeks of exercise training in patients with
CHF produced significant improvements in maximal,
submaximal, and endurance exercise capacity.191 Systemic
arterial compliance was also shown to improve with exer-
cise training.192 Exercise for these patients also increases
their quality of life and decreases mortality.193
Maiorana and associates found that a combination of
aerobic exercise and circuit weight training for patients
with CHF resulted in increased muscle strength, peak
exercise oxygen uptake, exercise test duration, and ven-
tilatory threshold.194 They also found decreases in the
patients’ submaximal exercise heart rate and rate pres-
sure product.194
The significant changes in exercise capacity that are
observed in patients with CHF may be the result of
the cardiac output increase, skeletal muscle metabolism
improvement, peak blood flow increase to the exercising
limb because of the vascular resistance reduction,195 and
in part of arterial function improvement.192
Intermittent Claudication. Research has shown
the benefits of physical activity for patients with moder-
ate to severe intermittent claudication. Walking ability,
6-minute walk distance, walking economy, and claudica-
tion distances are enhanced.196–198 Gardner and associates
showed that after 6 months of exercise, the improvements
in walking ability, in physical activity level, and in periph-
eral circulation in patients with intermittent claudication
were sustained for an additional 12 months.198 Langbein
and associates used a technique called polestriding
(24 weeks of walking with modified ski poles) to train
individuals with intermittent claudication and found
significant quantitative and qualitative improvements in
exercise tolerance.199
Hypertension. Exercise is an effective means of
reducing blood pressure in hypertensive individuals.200
Using the American College of Sports Medicine and the
Centers for Disease Control and Prevention (ACSM-
CDC) physical activity recommendation of 30 minutes
of daily moderate-intensity physical activity, Moreau and
associates found that a 24-week walking program effec-
tively lowered systolic blood pressure in borderline to
stage 1 hypertensive individuals.201
Stroke. Data support the use of physical activity,
including moderate-intensity exercise such as walking, to
decrease the risk of stroke and also as a means of interven-
tion to increase blood flow and reduce brain injury during
cerebral ischemia.202 Strength training alone improved
the quality of physical function in stroke survivors.203
Combining aerobic conditioning exercises and muscle
strength training at a frequency of three days per week
over 10 weeks for patients with chronic stroke produced
gains in all measures of impairment and disability.204 Even
a year after onset of a stroke, exercise and endurance
training can improve sit-to-stand performance and can
increase walking speed.205
Ouellette and associates showed the effects of high-
intensity progressive resistance training (consisting of
12 weeks of bilateral leg press, unilateral paretic and
nonparetic knee extension, ankle dorsiflexion, and ankle
plantar flexion exercises) on individuals who sustained a
mild to moderate stroke anywhere from 6 months prior
up to 6 years after.206 They found improved strength
in both the paretic and nonparetic lower extremities,
an increase in reductions in functional abilities, and a
decrease in disability.206
Pulmonary Pathology
Chronic Obstructive Pulmonary Disease. Data sup-
port the use of increasing exercise training and physical
activity in patients with chronic obstructive pulmonary
disease (COPD) as means of not only improving exer-
cise tolerance and decreasing dyspnea but also enhancing
functional improvements in activities of daily living and
health-related quality of life.207
Ortega and associates studied the effects of strength
training, endurance training, and both in patients with
COPD.208 The strength group significantly increased
their strength, the endurance group significantly
increased their submaximal exercise capacity, and the
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
combined group increased significantly in both param-
eters. Improvements in breathlessness scores and in dys-
pnea were also significant.208
Patients with COPD who were on an aerobic capacity
training program and were trained with progressive resis-
tance strengthening exercises showed improvements in
their functional outcomes,209 their muscle function, and
their treadmill walking endurance.210
Effects on the Musculoskeletal System
Muscle Strength
Skeletal muscle has the amazing ability to adapt, and the
extent of the change in muscle depends on several fac-
tors, including the specificity and type of activity, age, and
muscle fiber type composition. The adaptations include
modifications of morphological, biochemical, and molec-
ular variables. These modifications lead to alterations in
the functional attributes of the muscle fiber types.211 Data
now support the fact that the once thought inevitable
decline in the muscle’s metabolic and force-producing
capacity can no longer be considered as an inevitable con-
sequence of the aging process.73 Even in aging skeletal
muscle, a high degree of residual plasticity remains.212
Muscle Strength with Aerobic Capacity/Endurance
Training. Using an aerobic capacity/endurance train-
ing program of walking or jogging at an intensity of 80%
of maximal heart rate, a duration of 45 minutes per day,
and a frequency of 4 days per week over a 9-to-12-month
period resulted in significant skeletal muscle adaptations.
These included increases in type IIa fibers, cross-sec-
tional area of type I and type IIa fibers, capillary density,
and mitochondrial enzymes (succinate dehydrogenase,
citrate synthase, and beta-hydroxyacyl-CoA dehydroge-
nase). Decreases were found in type IIb fibers and lactate
dehydrogenase activity.213
Vigorous and progressive aerobic capacity/endurance
training resulted in a proliferation of muscle capillaries
and an increase in oxidative enzyme activity in skeletal
muscle.73 Muscle protein synthesis regardless of age is
enhanced with aerobic exercise.79
Muscle Strength with Resistance Exercise Train-
ing. Resistance exercise training results in increases in oxida-
tive capacity, mitochondrial volume density, muscle size,214
and myofibrillar protein turnover.215 Progressive resistive
strength training consisting of high- and low-intensity
and high- and low-velocity significantly increases strength,
power, and endurance and results in muscle hypertrophy as
long as the training consistently overloads the muscle and
the intensity and duration are sufficient.73,149,151,215–219 As
muscle strength improves with strength training exercises,
fat may be replaced by lean muscle mass.58
The DeLorme (10 reps of 10 repetitions maximum
(RM) at 50%, 75%, 100%) and Oxford (using the reverse
protocol of 10 reps of 10 RM at 100%, 75%, 50%)
341
protocols for progressive resistive exercises were equiva-
lent in improving strength.220, 221 Progressive heavy resis-
tance strength training results in increases in functional
strength that appear to be specific to the type of exer-
cise, thus supporting the specificity principle for design-
ing interventions. Resistance exercise training, which
improves strength, was found to not significantly alter
habitual activity, especially sleep.162
Muscle Strength in Elder Persons. Young and old
men have the same capacity to increase muscle strength
and power with a periodized training program including
rapid, high-power strength exercises.222 However, high-
velocity resistance training was found to increase strength
and peak power more than low-velocity resistance training
in older women.153 Since resistance training in the elderly
increases strength, hypertrophy, and thus power of both
type I and type II muscle fibers, muscle mass, power,
endurance, contractile velocity, quality of skeletal muscle,
synthesis rate of heavy chain myosin, and transcript levels
of the slow myosin heavy chain isoform, it is an effec-
tive intervention against sarcopenia.78,144,150,167,183,23–225
High-intensity resistance training (above 60% of the one
repetition maximum) for the elderly has also been shown
to significantly increase insulin action.226
Both resistance exercise training and aerobic capacity/
endurance training increased the energetic pathways (oxida-
tive capacity, contractile ATP demand, and glycolytic ATP
supply) of muscle in the elderly (69.2 +/− 0.6 years).214
A low-intensity resistance exercise program resulted in
gains in muscle strength and muscle endurance, while sig-
nificant improvements in speed of muscular contraction
resulted from a moderate-intensity aerobic capacity/endur-
ance training program.157 Higher levels of physical function
are associated with resistance training in older adults,227,228
which Slade and associates228 have postulated may be the
result of the higher levels of anaerobic power achieved with
strength training.
Jozsi and associates noted that men in their sixth decade
may realize greater absolute strength gains than women
with progressive resistance training.229 However, research
indicates that older women (60+) may engage in safe,
enjoyable heavy-resistance weight training with resul-
tant gains in muscular strength and body composition.230
Research also indicates that individuals in their 10th
decade may participate in simple progressive exercise
training that results in increased muscle power.166
High-intensity resistance exercise (at an intensity of
85% to 90% 1 RM of three sets to failure, a frequency of
two times per week, a duration of 16 weeks, and a mode
of leg press and half squat, leg extension) in untrained
older men resulted in significant strength gains and
increases in fiber size and capillary density.185
Older adults (78 to 84 years of age) who performed
dynamometer strength training using voluntary maximal
isometric, concentric, and eccentric exercises had increased
342 SECTION II • Principles of Practice
neural activation with their increase in muscle strength at
least during eccentric contractions.231 In addition, older
athletes (70 to 81 years) who trained for strength, speed,
and endurance had greater muscle function than non-
athletes of the same age. While the strength and speed
athletes showed the greatest gains in muscle strength, the
endurance athletes also had excellent strength.232 Tai chi
has also been found to increase muscle strength and force
control in older adults.233
Muscle Strength in Frail Elderly. Singh and asso-
ciates observed that frail elders responded robustly to
resistance exercise training, which resulted in significant
increases in muscle area and in musculoskeletal remodel-
ing.234 The significant muscle hypertrophy that occurs in
frail elderly with resistance training programs indicates
that age does not decrease the capacity to adapt to such a
training program.226 Progressive resistance exercise train-
ing in frail individuals resulted in adaptation of the muscle
contractile protein synthetic pathways to the increased
contractile activity associated with the training.235
LaStayo and associates also found that eccentric exer-
cise for the lower extremities increases muscle structure
and may be of greater benefit for frail elderly individuals
who are unable to perform traditional resistance exercises
requiring high muscle forces.174 Hortobagyi and DeVita
also found strength gains that were 1.8-fold greater
with a short-term (7 days) eccentric overload program
as compared to a standard load distribution program.186
They also found significantly lower cardiovascular stress
(heart rate, mean arterial pressure, rate pressure product,
and perceived exertion) with eccentric overload, thus
supporting this type of resistance training for elders, the
deconditioned, and those with chronic diseases.186
Progressive resistance exercise training is both a safe
and an effective method of increasing strength in both
debilitated and frail, high-risk patients with a history
of falls resulting in injury.168,236 Fiatarone and associates
found significant increases in muscle strength and size in
frail nursing home residents up to 96 years of age after
they had participated in high-resistance weight train-
ing.237 Aquatic exercises (70 minutes per day and 3 days
per week for 12 weeks) were also found to significantly
increase muscle strength in older frail individuals.187
Flexibility
Flexibility improves, even in healthy, older adults between
the ages of 60 and 71 years of age, as a result of a low-
intensity exercise program.238 Spinal mobility was signifi-
cantly improved in older women through the use of back
flexibility exercises performed three times per week for a
duration of 20 to 30 minutes per session over the course
of 10 weeks.239
Of interest was the finding that range of motion may
be increased in older inactive adults through the use
of resistance exercise training.240 Individuals who par-
ticipated in a long-term regular tai chi exercise program
showed significant increases in flexibility. These increases
were measured using a modified sit-and-reach test and a
total body rotation test.189
Bone Density
Weight-bearing or bone-loading exercises performed
over time coupled with high-intensity resistance/strength
training exercises positively affect three aspects of bone—
bone mass, bone size, and bone microarchitecture—
throughout life.241 Young women who participated in a
program of aerobic conditioning/endurance training and
weight/strength training over a 2-year period of time had
enhanced BMD.242 Not only has exercise been found to
effect bone, but it also prevents or retards bone mineral
density loss that occurs gradually after 40 years of age.
Exercise increases osteoblastic activity, muscle mass and
strength, and serum osteocalcin. In addition, it leads to
endogenous electrical activity, inducing bone formation,
and promotes the release of growth hormone from the
pituitary gland, thus increasing bone formation.243,244
Twenty-one randomized controlled trials were ana-
lyzed and were found to suggest that the physiological
decrease of bone mineral density with age can be delayed
through regular physical exercise, reducing the risk of
osteoporosis245 and preventing osteoporotic fractures.241
In women with osteopenia, exercise was found to increase
the lumbar spine bone density.246
One’s level of previous physical activity, coupled with a
moderate level of current physical activity, appears to have
a protective effect on bones and decreases the risk of hip
fracture in postmenopausal women.247 Epidemiological
evidence suggests that the incidence of hip fractures in
the older population can be cut nearly in half with physi-
cal activity throughout life.248 Vincent and Braith found
that in healthy elderly subjects (60 to 83 years of age),
a high-intensity resistance exercise training program
improved the bone mineral density of the femoral neck
and suggested an increase in bone turnover.249 Wolff
and associates found that the 1% per year femoral neck
and lumbar spine bone loss was reversed with exercise
training programs.250
Long-term exercise prevents osteoporosis because
exercise has an impact on mobility, on bone structure
through muscle strengthening, and on risk of falling
at increasing age.251 Bone health across the life span is
enhanced with exercise that maximizes peak bone mass
attained in youth and maintains bone mass or reduces
age-related bone loss.252
Varied types of exercise programs have been studied
for their effect on bone density. High-impact, versatile
movement exercises that loaded the bones with rapidly
rising force improved skeletal integrity in premeno-
pausal women.253 In postmenopausal women, moder-
ate-intensity physical activity over a prolonged period
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
of time was associated with higher BMD than was low-
intensity physical activity.254 Aerobic exercise combined
with high-impact exercise at a moderate intensity will off-
set the decline in BMD in postmenopausal women with
osteopenia.178,255
Two different exercise protocols—one a general aero-
bics class and the other a general aerobics class in addition
to upper body weight/strength training—significantly
increased both bone mineral content and bone mineral
content/bone width in postmenopausal women (57 to
83 years of age) as compared to nonexercisers.256
A program of five different high-intensity strength-
training exercises performed twice a week was effec-
tive in preserving bone density (as well as increasing
muscle mass and strength) in postmenopausal women.257
A progressive resistive exercise program focusing on large
muscle groups and utilizing three sets of eight repetitions
at 75% of 1 RM over a 1-year period of time resulted in
significant strength changes, which were believed to par-
allel changes in BMD in elderly postmenopausal women
(mean age 68.8 years).258
A long-term therapeutic exercise program performed
regularly may even slow bone loss in sedentary post-
menopausal women.259 In early postmenopausal women,
tai chi has been shown to retard bone loss in weight-
bearing bones.260–262
Data indicate that physical activity levels and back
muscle strength may contribute to the bone mineral den-
sity of the vertebral bodies in postmenopausal women.263
Sinaki and associates found that back extensor strength
was negatively correlated with the number of vertebral
compression fractures264 and with the extent of thoracic
kyphosis.265 Strengthening of the back extensor muscles
in both healthy estrogen-deficient women (49 to 54
years of age) and women with osteoporosis and kyphotic
thoracic spines helped to decrease the thoracic kyphosis
and improve the strength of the back extensors.264,266
Osteoarthritis
Exercise has been shown to be effective and safe for
individuals with osteoarthritis (OA), and many of the
benefits of exercise (aerobic conditioning/endurance
training, strength training, flexibility training) discussed
earlier apply to these individuals. Of note was the find-
ing that no association appeared to exist between moder-
ate long-distance running and the future development
of OA. Data also suggested that heavy mileage and the
number of years running did not contribute to the future
development of OA.267
Both aerobic capacity/endurance training and
strengthening exercises appear to be equally effective in
reducing pain and increasing function in individuals with
OA.268 Aquatic aerobic exercise training over 12 weeks for
persons with OA significantly improved aerobic capacity,
50-foot walking time, and physical activity. Depression
343
and anxiety were reduced.269 Postural sway was signifi-
cantly improved in individuals with OA who had long-
term weight training and participated in aerobic walking
programs. The likelihood of larger postural sway distur-
bances leading to potential falls decreased.270 Hand exer-
cises, coupled with joint protection techniques, increased
the grip strength and hand function in persons with OA
of the hand.271
Performance of the 12 forms of Sun-style tai chi by older
women with OA for 12 weeks decreased arthritic symp-
toms and improved balance and physical functioning.272
A moderate tai chi program was shown to increase func-
tional mobility and enhance arthritis self-efficacy and qual-
ity of life in older adults (mean age 68 years) with OA.273
Many studies have focused on the knee joints of indi-
viduals with OA. The following information summarizes
these findings. High-intensity strength training substan-
tially increased strength and physical function, decreased
pain, and enhanced the quality of life for persons with
knee OA.183,274 Older individuals with knee OA who
participated in aerobic conditioning/endurance train-
ing or resistance exercise training had increased physical
performance, decreased pain, and improved measures of
disability.275,276 Supervised fitness walking and education
were shown to improve the functional status in individu-
als with knee OA without worsening pain or exacerbat-
ing symptoms.277 An exercise and walking program had a
positive effect on the quality of life of elderly individuals
with knee OA.278
Low- and high-intensity cycling were equally effective
in improving gait and function, increasing aerobic capac-
ity, and decreasing pain in older adults with knee OA.
Cycling may therefore be considered as an alternative
exercise modality for these individuals.279
Exercises combined with weight loss were shown to
increase physical performance and decrease pain and
disability in older adults with knee OA.280 The biome-
chanical trend data suggest that exercise combined with
weight loss may additionally improve gait when com-
pared to exercise alone.
Rheumatoid Arthritis
Individuals with early rheumatoid arthritis (RA) who
underwent a regular dynamic strength training program
(50% to 70% 1RM for all major muscle groups of the upper
and lower extremities and trunk) combined with aerobic
conditioning/endurance training recreational activities had
improved muscle strength and physical function. There
were no adverse effects on disease activity.281 Persons with
early RA also underwent a 2-year strength training pro-
gram at home. Results indicated that strength and function
were improved and were sustained for 3 years.282
High-intensity strength exercise training led to sig-
nificant increases in strength and decreases in pain and
fatigue in individuals with well-controlled RA. Thus, this
344 SECTION II • Principles of Practice
form of exercise was shown to be feasible and safe and
did not exacerbate disease activity or joint pain.283 In
persons with well-controlled RA, an exercise regimen for
the quadriceps muscle increased the muscle’s sensorimo-
tor function decreased lower limb disability, and did not
exacerbate disease activity or pain.284
Individuals with active RA participated in a short-
term intensive exercise program (consisting of knee
and shoulder dynamic and isometric resistance muscle
strengthening exercises five times per week and an aero-
bic conditioning/endurance training bicycle program
three times per week) that was provided in addition to a
conservative physical therapy exercise program of range
of motion and isometric exercises. The intensive exercise
program was shown to be more effective in improving
muscle strength without any adverse effects on disease
activity than the conservative program.285 Even individu-
als with functional class II and III RA who participated
in low load resistive exercise training had increased func-
tional capacity.286
People with RA who participated in 4 hours of com-
munity-based physical therapy over a 6-week period of
time had significant improvement in morning stiffness,
disease management knowledge, and self-efficacy.287
Twelve-week aquatic and walking exercise programs for
persons with RA led to significant improvement in aero-
bic capacity, walking time, and physical activity. In addi-
tion, depression and anxiety decreased.269
Of particular interest is the finding that in spite of
existing data of the effectiveness and safety of high-inten-
sity exercise programs for persons with RA, physical ther-
apists believe that conventional exercise programs offer
more than do high-intensity exercise programs.288
Effects on Body Fat
Aerobic exercise and resistance exercise appear to be
beneficial in reducing body fat, while resistance exercise
also appears to increase fat-free mass.289 A well-rounded
12-week aquatic exercise program 3 days per week (20
minutes of warmup and stretching, 10 minutes of resis-
tance exercises, 30 minutes of aerobic conditioning/
endurance training exercises of walking and dancing,
and 10 minutes of cooldown exercise) led to signifi-
cant improvements in body fat in older adult women.187
Strength training in the elderly led to decreased total and
intra-abdominal fat.183
Effects on the Neuromuscular System
Colcombe and associates studied older adults and found
a strong biological basis for the benefits of aerobic exer-
cise on brain health.290 Motor performance appears to be
more highly related to the amount of physical activity over
the life span than to age.291 The role of physical activity
and fitness in the elderly population for enhancement of
neuromuscular performance is totally supported by the
research data. Exercise improved neurobehavioral function
(as measured by the Up & Go Test and the Functional
Reach Test) in individuals over 75 years of age.292
A regular walking program may enhance stability in
old age. Healthy older subjects who walked regularly
showed improved postural control, especially static bal-
ance, as compared to nonregular walkers. Older subjects
who walked regularly did not suffer from falls.293
Functional and structural neuromuscular adaptations
have been shown with both unilateral and bilateral pro-
gressive heavy resistance strength training exercises.221
Negative work in the form of lower extremity eccentric
resistance exercise improved balance and stair descent.174
A 12-month exercise program for older persons (60
to 85 years) resulted in long-term sensorimotor func-
tion improvements. They had increased strength and
improved reaction time, neuromuscular control, and
body sway (on a firm surface with the eyes open, and
body sway on a compliant surface with the eyes open and
closed).294 Older women who participated in a regular
aerobic exercise program enhanced their premotor time,
reaction time to both simple and discriminatory stimuli,
contractile time, and speed of movement following the
reaction responses.295
Regular participation in exercise and physical activity
appears to be correlated with the preservation of visual
attention skills in individuals across the life span.296
Elder individuals who participated in a long-term
regular tai chi program showed increased rhythmic weight
shifting forward and backward, significantly better right
and left leg standing with eyes closed, and increased pos-
tural stability in positions of challenge (eyes closed with
sway surface, sway vision with sway surface) as compared
with those who did not practice tai chi.189,297
Balance
A community-based exercise program for 65-to-75-year-
old women with osteoporosis improved their strength
and dynamic balance. Both of these factors are determi-
nants of risk for falls in this population.298 Balance train-
ing increases muscular strength and equalizes muscular
imbalances.299
Exercise programs for older women result in improved
single-stance postural sway.300 Elder persons with non-
peripheral vertigo and unsteadiness who participated in
balance training appeared to have improved objective,
as well as perceived, balance.301 Elder persons who par-
ticipated in balance strategy training using varied exercise
work stations significantly reduced falls when compared
with those who participated in traditional exercise classes
for improving balance.302 Frail, demented elderly patients
with a history of falls who participated in a physical
activity exercise training program for two sessions per
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
week for 16 weeks showed improved walking ability and
static balance.303
Elderly men who participated in tai chi and golf showed
improved joint proprioceptive acuity and dynamic stand-
ing balance control.304 Elder individuals who regularly
practiced tai chi not only showed better proprioception at
the ankle and knee joints when compared to their seden-
tary controls, but they also showed better ankle kinesthesis
when compared to swimmers and runners. The enhanced
proprioception observed in these individuals may allow
them to maintain balance control.305 Elder individuals
who regularly practiced tai chi were also observed to have
better postural stability than those who did not.262
Gait
Gait velocity was significantly improved in older per-
sons (mean age, 82.1 years) who performed postural
control exercises and resistance training to fatigue for
knee extension, hip abduction, ankle dorsiflexion, hip
extension, and knee flexion three times per week.306 Gait
velocity and related parameters of gait were increased in
older women who participated in lower extremity muscle
strength training.148,307
Combined programs of strength and endurance training
also resulted in increased gait velocity in elderly women.308
Walking endurance improved with a 3-month resistance
strength-training program in healthy elderly persons.309
Low-intensity strength training resulted in increased gait
stability and especially in mediolateral steadiness in elders
who were disabled. Gait performance improved even when
the elders achieved only moderate strength gains.310
Risk of Falls
The risk for falls is a major problem in our aging popula-
tions. Falls account for 87% of all fractures among elderly
individuals, and they contribute to many nursing home
admissions.311 Many risk factors for falling exist in the elderly
population. These include impairments in upper and lower
extremity strength and in gait, locomotion, and balance.
Functional limitations, particularly in the areas of transfers
from bed to chair or to the toilet or bathtub, also increase
the risk for falling. In addition, the use of at least four pre-
scription medications, the use of sedatives, and postural
hypotension all compound any physical limitations plac-
ing the elderly at risk for falls.312 Tinetti and associates also
found that in addition to impairments in gait, locomotion,
balance, and cognition, the presence of at least two chronic
conditions and low body mass index were also associated
with the potential for serious injury resulting from a fall.313
Since the risk for falls is related directly to impaired
balance and gait, the benefits of exercise and physical
activity become even more important in maintaining
mobility and independence in our increasingly elderly
population and in reducing the costs to society of the
sequelae of falls in the elderly.314
345
Balance and mobility improve with regular exercise
and have been shown to reduce the likelihood of falls
in community-dwelling older adults with a history of
falling.315 Participation by at-risk, community-dwelling
elder individuals in group exercise activities (including
resistance training exercises, agility training exercises, and
balance training) coupled with additional home exercises
improved balance and reduced the risk for falls.316,317
Ryushi and associates postulated that an older person’s
perception of his or her ability to avoid falls may be the
result of increased strength in the quadriceps femoris,318
which facilitates accurate movement of the body’s center
of gravity farther from the center toward the rear.
Exercise sessions that led to increased strength, endur-
ance, gait, and function and reduced the risk for falls in
older individuals have consisted of varied modes of exer-
cise. These have included progressive resistance exer-
cises, lower extremity eccentric exercises, ambulatory
strength training, endurance training, mobility training,
agility training, balance training, and progressive func-
tional training. Aerobic dance exercises and tai chi have
also been used to reduce the risk of falls by improving
selected components of balance and locomotion/agility.
The exercise programs have been composed of 45 to 90
minutes of varied-intensity activity with a warmup and
cooldown, usually three times per week.174,297,311,319-321
Even walking on a regular basis was shown to have its
benefits in older individuals. Those who walked regularly
did not suffer from falls and exhibited better postural
control, especially static balance, than nonwalkers.293
Weight-bearing exercises for frail older individuals (62 to
95 years) were shown to prevent falls while maintaining
physical function.322
Individually tailored home exercise programs consisting
of muscle strengthening exercises and balance retraining
for elderly women and men (65 to 97 years) were shown
to reduce falls and injuries (especially in those 80+ years),
and the benefit of the program was sustained for longer
than 2 years. For those with a history of falls, there was a
higher absolute reduction in falls leading to injury.323-325
Strength training also decreased the risk for falls in elderly
individuals with osteoarthritis of the knee.183
Parkinson’s Disease
While physical activity, exercise, and fitness have been
shown to have effects on many individuals with neuro-
muscular disorders, this section reviews the data available
for those persons with Parkinson’s disease and multiple
sclerosis.
Despite the neurological deficit that results from the
disease, individuals with mild to moderate Parkinson’s
disease have the potential to maintain normal exercise
capacity with regular aerobic exercise.326 Exercise pro-
grams for individuals with Parkinson’s disease increase
perceived functional independence and quality of life.327
346 SECTION II • Principles of Practice
Resistance exercise training in individuals with mild-
to-moderate Parkinson’s disease results in increases
in strength similar to normal adults.328 High-intensity
resistance training has also been shown to improve mus-
cle strength and balance in individuals with idiopathic
Parkinson’s disease.329 A 10-week exercise program
produced improvements in spinal mobility and physi-
cal performance for people in the early and midstages
of Parkinson’s disease.330 An intensive exercise program
(two times a week over 14 weeks) for individuals with
early to medium stage Parkinson’s disease not only
increased motor function but also improved mood and
subjective well-being.331
Multiple Sclerosis
Research now suggests that appropriately modified exer-
cise programs can provide all of the benefits to individuals
with multiple sclerosis that are gained by healthy individ-
uals. As with any other individual, clinicians must design
exercise programs individually based on the person’s
impairments, functional limitations, disability, or activity
restriction. Despite limitations, individuals with multiple
sclerosis and mild to moderate disability who participated
in an aerobic exercise program (at a frequency of three
times per week and a duration 40 minutes for 15 weeks)
showed increased VO2 max and physical work capacity
and decreased triglyceride levels, very low density lipo-
proteins, and skinfold measurements.332 Muscle disuse
findings in individuals with multiple sclerosis highlight
the need for muscle training to enhance decreased oxida-
tive capacity, increased fatigue, and impaired metabolic
response to exercise.333
Petajan and White created a “physical activity
pyramid” model (Figure 16-1) to achieve an optimum
level of physical activity for individuals with multiple
Figure 16-1
Physical activity pyramid. (From Petajan JH, White AT:
Recommendations for physical activity in patients with MS, Sports Med
27(3):186, 1999.)
sclerosis. At the base of the pyramid were the activities
of daily living and instrumental activities of daily living
(dressing, toileting, shopping), upon which were the
“built-in inefficiencies” (parking further away from the
office and walking), followed by “active recreation” (30
minutes of moderate-intensity walking, cycling, garden-
ing, table tennis, bowling); on top was the “structured
aerobic program” (which could range from wheelchair
pushups to walking or using a treadmill, arm or leg
ergometer, and aquatic exercise). Those 30-to-40-year-
old individuals who had multiple sclerosis with mini-
mum impairment were able to engage in aerobic activity
at an exercise intensity of 60% to 85% of their peak heart
rate or 50% to 70% of their peak VO2, three or more
times per week, for 20 to 30 minutes. The 5-minute
warmup and cooldown were lengthened if needed to
reduce overheating and spasticity.334-337
Petajan and White also developed a “muscular fit-
ness pyramid” (Figure 16-2), which consisted of “pas-
sive range of motion” at the base, followed up by “active
flexibility and resistance exercise” (including those exer-
cises and also tai chi, yoga, or Swiss ball exercises), then
“specific muscle strengthening” (bands, weights, water
resistance exercises that were modified to the disabil-
ity), and “intensive strength training program” on top
(weight training three times per week, three sets of 10 to
12 repetitions though the full range of motion).334
Exercise programs for individuals with multiple scle-
rosis must consider several factors. When and if exacerba-
tions occur and depending on the severity, activity may
be modified/suspended or the person may still perform
stretching, walking, and water exercises.338,339
Muscle spasticity or weakness should be evaluated for
its impact on the exercise program and adjustments made
as necessary. Exercises may be adapted, and intensity and
Figure 16-2
Muscular fitness pyramid. (From Petajan JH, White AT:
Recommendations for physical activity in patients with MS, Sports
Med 27(3):185, 1999.)
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
duration may be modified. Supportive or assistive devices
and equipment may facilitate continued participation.336
Individuals with multiple sclerosis may experience car-
diovascular dysautonomia, which may lead to cardioac-
celeration and hypotension. Continuous monitoring of
heart rate, blood pressure, and rate of perceived exertion
during exercise is essential, and adjustments to intensity
should be made accordingly.336,340
To meet the problems of overheating, exercises should
be performed in cool environments. Aquatic exercises and
swimming (at a water temperature at or below 82°F) are
excellent modes of exercise. In addition, the Schwinn Air-
Dyne bicycle provides cooling while cycling. Adequate
hydration must be maintained.336
The individual who experiences fatigue may take rest
periods and can schedule strenuous activities for early in
the morning when the body temperature is lower. Also,
the individual may use adaptive or supportive equipment,
and the type of fatigue (normal muscle, cardiovascular,
substitution) should be differentiated.341
Problems with balance and coordination may be best
handled with aquatic exercises. Swiss ball and tai chi
activities may also be used.336
Effects on Mental Health
Exercise has been shown to have many positive benefits on
mental health, particularly in elderly individuals. Lack of
regular physical exercise in older persons (64 to 84 years)
has been significantly associated with a higher prevalence
of depression as these individuals have reported that they
find less meaning in life and have lower subjective views
of their health.342 Exercise training produced a tranquil-
izing effect on elderly subjects58,343 and was found to be
significantly related to less anxiety and fewer depressive
symptoms.343 Increased self-respect may develop with
exercise, especially as effort tolerance increases.58
Aerobic exercises significantly reduced depressive
symptoms in older individuals (60+ years).344 Individuals
who participated in aerobic exercise training perceived
improvement in a number of psychological and behav-
ioral dimensions.178 Progressive resistance training has
been shown to be an effective antidepressant in depressed
elders.147,162
Yaffe and associates found that older community-
dwelling women who participated in higher levels of
physical activity were less likely to develop declines in
cognition.345 Thus, their finding supported the role of
physical activity in preventing cognitive decline. Exercise
classes (at a frequency of three times per week for a dura-
tion of 3 years at an intensity meeting ACSM guidelines)
reversed or slowed certain age-related declines in speed
of cognitive processing.96 Fitness training programs
enhanced cognition, especially in executive-control pro-
cesses.346 Group exercise may also have beneficial effects
347
on cognitive functioning in older individuals.347 On the
other hand, Hill and associates found little, if any, effect
of long-term exercise training on cognitive function in
their older adult sample.348
An aerobic exercise program that lasted longer than 10
weeks had a positive effect on attentional processes, par-
ticularly alternation speed and time-sharing efficiency in
elder individuals.349 Submaximal aerobic exercise (up to 60
minutes) enhanced aspects of information processing.350
Effects on the Endocrine System
Diabetes
Aerobic training performed at a moderate-intensity by
elder individuals had a positive effect on glucose toler-
ance.351 Regular aerobic conditioning/endurance training
and resistance strength training exercises have been shown
to significantly reduce diabetes risk and insulin resistance in
elderly individuals, while enabling them to maintain their
independence through increased levels of physical activity
and the ability to perform activities of daily living.126,183
Evans found a reduced risk of developing type II dia-
betes with aerobic exercise and an increased insulin action
with high-intensity resistance (above 60% of the 1 RM)
strength training exercise in the elderly.226 Increasing
physical activity moderately along with a decrease in
body weight and a change in diet can prevent or delay
the onset of type II diabetes.352
Significant differences in metabolic responses (acid-
base balance, potassium, triglycerols, glucose, cholesterol,
FFA, free glycerol, lactate, and uric acid) were found in
individuals with type I and type II diabetes after an aerobic
conditioning/aerobic capacity bicycle ergometer program.
Rybka noted that exercise must be a basic component of
the management of individuals with diabetes.353
Common carotid and femoral arterial stiffness signifi-
cantly decreased, which was associated with improved
insulin resistance in patients with type II diabetes who
underwent a short-term aerobic conditioning/endur-
ance training exercise program.354
Balance was improved in patients with diabetic neu-
ropathy with a 3-week exercise program aimed at rap-
idly increasing balance and distal extremity strength.355
Mobility and strength in patients with diabetes increased
when they participated in a resistance strength-training
program of moderate intensity.356
Hormones
Men and women (60-to-75-year-olds) who participated in
heavy resistance strength training using squats for 2 weeks
over a 24-week period of time had increased levels of
serum growth hormone; in men, the testosterone/corti-
sol ratios increased as well.151 Such training was also shown
to produce a significant increase in total testosterone and a
significant decrease in resting cortisol in older men.357
348 SECTION II • Principles of Practice
Effects on Cancer
The risk of breast and colon cancer for adults may be
reduced through participation in moderate-intensity
physical activity for a duration of 30 minutes or more
per session with a frequency of 5 or more days per week.
Further reduction of the risk may be achieved through
participation in moderate- to vigorous-intensity physical
activity for a duration of 45 minutes or more per session
with a frequency of 5 or more days per week. For chil-
dren and adolescents, the recommendation is participa-
tion in moderate- to vigorous-intensity physical activity
for a duration of at least 60 minutes or more per session
with a frequency of 5 or more days per week.358
Health Promotion for Those with
Disabilities
While clinicians, especially physical therapists, have a key
role in promoting health, wellness, and fitness for the
increasing aging population, they also have a prominent
role in maintaining health and wellness in the millions of
Americans who live with disabilities. Promoting a long-
term healthy lifestyle for individuals with disabilities is of
paramount importance in reducing the long-term impacts
of their impairments on functioning in daily life.359,360
Adults with disabilities are referred at lower rates for
preventive and maintenance of health and well-being than
nondisabled counterparts. Krahn and associates proposed
several avenues of needed activity to increase clinician
participation in health and wellness programs for those
with disabilities including assessing both incentives and
barriers to clinician practices that promote prevention,
maintenance of health, wellness, and fitness; exploring
insurance reimbursement to support health, wellness,
and fitness programs by clinicians; supporting inclusion
of knowledge and skill in promoting healthy behaviors
by health care providers into clinician educational pro-
grams; and making information available to persons with
disabilities to assist in planning, along with their clinician,
the interventions for achieving and maintaining health,
wellness, and fitness.361
Clinicians must understand that for persons with
disabilities, being healthy and well depends not only on
the individuals themselves and their own motivation but
also on their social, cultural, and architectural environ-
ments. Health and wellness in this population is facilitated
through participation in exercise and sports activities
and continued physical activity over time. Clinicians are
responsible for educating their patients/clients with dis-
abilities on ways to promote healthy lifestyles, to prevent
secondary conditions, to use wellness resources, and to
maintain a lifetime commitment to physical fitness. The
clinician will need to have a thorough knowledge of ways
to enable easy and continued participation in a lifelong
exercise program, know local exercise resources, and
facilitate accessibility to them.33,362-366
Health Promotion in the Workplace
Clinicians have had roles in health promotion, wellness,
and fitness in the workplace, particularly in the areas of
prevention of onsite injuries. Now the role must include
health promotion, wellness, and fitness as more corpora-
tions realize the importance of these programs. Worksite
health promotion is an approach that a corporation takes
to enhance the health of the company and its employ-
ees. As Thomsson and Menckel have noted, it “includes
all efforts made in all contexts where individuals work”
that “are designed to increase well-being and health.
Workplace health promotion is concerned with causes
of ill-health, but focuses on opportunities for good
health.”367
Others have made this observation:
A healthy workplace provides mutual benefits for employ-
ers and employees within a common belief that good
health practices by both will lead to individual and orga-
nizational self-fulfillment and productivity. Health pro-
motion is the process of enabling employees to increase
control over and to improve their physical, emotional and
social health.3648
These health promotion efforts may include awareness
education, changes in behavior and lifestyle, and creating
supportive environments.
It has been reported that over 80% of worksites with
50 or more employees and almost all worksites with
more than 750 employees have health improvement pro-
grams.369 Complete wellness centers are found in most
large corporations, and many small- to midsize corpora-
tions have some type of wellness program.370
Workplace programs to enhance wellness, health pro-
motion, and physical fitness may include screening pro-
grams, healthy lifestyle programs (e.g., weight loss and
smoking cessation), and programs that provide access to
health clubs or exercise facilities either onsite or at a dis-
counted rate at a local facility.28 The U.S. Department of
Labor found that 18% of all employees (including part-
time) were eligible for wellness programs, and 9% were
eligible for fitness center programs.371
Corporations accrue many benefits by offering well-
ness programs at work. Johnson & Johnson estimated
that by providing wellness programs in its corporation’s
environments, the company realized savings of at least
$1.9 million through decreased medical costs, reduced
sick leave, and increased productivity.372 Johnson &
Johnson’s health and wellness program focuses on pre-
vention, self-care, risk factor reduction, and disease man-
agement. Many of the program’s benefits were found to
occur later on in life.373
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
More than 8000 Procter & Gamble employees who
participated in the company’s health promotion program
over a 3-year period had significantly lower health care
costs as compared to nonparticipants.374 Other companies
with major cost-saving health promotion and prevention
programs include Motorola’s Wellness Initiatives, which
found that for employees who regularly used onsite
Motorola Wellness Centers or used the reimbursement
benefit for membership in external fitness centers there
was a $3.93 saving for every $1 invested or a total savings
for the company of more than $6.4 million; Northeast
Utilities WellAware Program, which in its first 24 months
reduced lifestyle and behavioral claims by $1.4 million;
Caterpillar’s Healthy Balance program, which is pro-
jected to result in long-term savings of $700 million by
2015; and Union Pacific Railroad, which classified health
and welfare as a “big financial deal” and now has more
than 450 company-sponsored, free-of-charge exercise
facilities.375
Barriers/Lack of Adherence to Exercise
The ability to continue to provide programs of health
promotion, wellness, and fitness will depend on the clini-
cian’s recognition of the barriers to exercise. Clinicians must
recognize that motivation to change behaviors and adopt
a healthy lifestyle is frequently associated with knowledge,
attitudes, and beliefs. Therefore, clinicians must know how
and why people think and the barriers they encounter that
discourage change in physical activity.376
In a sample of almost 3000 women (40+ years of age),
several personal and environmental factors were noted to
be significantly associated with inactivity. These included
older age, decreased level of education, American Indian
ethnicity, lack of energy, absence of enjoyable scenery,
no hills in the neighborhood, and infrequent observation
of others exercising in one’s neighborhood. Two of the
top four barriers that were reported most frequently for
all participants were caregiving responsibilities and a lack
energy to exercise.377
In another study of more than 8000 participants,
activity participation was associated with being younger,
being male, having good long distance vision, being non-
diabetic, and not having a fear of falling, as well as living
in a rural environment and eating more nutritious foods
(more fruits and vegetables). The primary barriers iden-
tified to regular physical activity were health problems
(72%), lack of time (7%), and pain (4%).378
Barriers to Exercise
● Personal
● Environmental
349
In older women, decreased participation in physical
activity was also associated with greater adiposity.379 Nied
and Franklin put forth 12 factors that they determined
were common barriers to exercise in older adults.128
These included decreased self-efficacy, negative attitude,
discomfort from exercise, level of disability, presence of
poor balance, fear of injury, inability to make exercise
a habit, a fixed income, lack of environmental factors
(e.g., malls in which to walk, senior centers), decline in
cognition, and presence of illness/fatigue.128
Barriers to Exercise in Older Adults128
● Decreased self-efficiency
● Negative attitude to exercise
● Discomfort from exercise
● Level of disability
● Poor balance
● Fear of injury
● Inability to make exercise a habit
● Fixed income
● Lack of environmental factors
● Cognitive decline
● Presence of illness
● Presence of fatigue
Other environmental barriers to exercise and physical
activity include water and air pollution, weather conditions,
crime, and dangerous automobile traffic. The CDC began a
program called Active Community Environment Initiatives
(ACES) to promote the development of community places
for safe, easily accessible activity participation.380
Other personal barriers include finding it inconvenient to
exercise, not finding exercise enjoyable or finding it boring,
lacking skill, business-related traveling schedule, family
obligations, urinary incontinence, and lacking encourage-
ment from family, friends, or significant others.381
Certainly, clinicians armed with an awareness of these
multiple barriers must design increasing, multifaceted
physical activity programs that will encourage patients and
clients to adopt a healthy lifestyle that promotes physical
fitness. Overcoming barriers may best be handled by pre-
scribing exercise in a manner similar to a pharmacological
prescription along with requiring the individual to keep
a record of the new behavior, incorporating exercise into
activities of daily living, and offering exercise education
to health care staff.382
Other techniques that clinicians may use to overcome
barriers include beginning exercises slowly, progressing
slowly, and giving encouragement frequently. If cognition
is a problem, the clinician should keep exercises simple.
Clinicians should also find enjoyable activities and describe
the personal benefits to be achieved with increased physi-
cal activity. It is important for clients to vary the intensity
350 SECTION II • Principles of Practice
and use cross training, avoid overdose, use assistive devices
if needed, work on balance and strength to overcome the
fear of falling, make exercise and physical activity a part
of one’s daily routine, use activities that do not require a
financial commitment, and use community facilities, espe-
cially when the weather is inclement.128
Adherence to exercise is related to several factors.
Self-reported improvement in strength, actual muscle
strength, and reasoning ability were all associated with
adherence to an exercise program, while decreased mus-
cle strength, slow reaction time, and the use of psychoac-
tive drugs were associated with nonadherence.383
Exercise Prescription
Exercise and physical activity should be prescribed on
as scientific a basis as possible. Governmental agencies
and health-related organizations have made recommen-
dations. The CDC and the ACSM originally recom-
mended that all adults engage in at least 30 minutes of
moderate-intensity physical activity 7 days per week.41
Currently the recommendation is participation 5 or
more days of the week. The physical activity program
for older adults should include aerobic conditioning/
endurance training, strength training, balance training,
and flexibility exercises. Their recommendations strongly
support the fact that no one single type of activity will
produce all the benefits of physical activity. Therefore,
it is essential to include all of the aspects of fitness in
the exercise prescription, especially for older adults. The
recommendations for each type of activity include the
following: moderate-intensity aerobic conditioning/
endurance training at a frequency of 3 to 5 days per week
with each session having a duration of at least 30 min-
utes; strength training/resistance exercises done 2 to 3
days per week; and flexibility/stretching exercises done
daily.384 Recommendations for children and adolescents
are participation in moderate-intensity physical activity
with a duration of at least 60 minutes and a frequency of
most days of the week, preferably daily.385
The CDC has also provided guidelines of how to prog-
ress activity based on current participation or lack thereof.
If one does not participate in regular physical activity, a
few minutes of activity should be incorporated into one’s
daily life, and the duration should be gradually increased to
30 minutes or more of moderate-intensity activity. If one
participates in some physical activity but not at the levels
recommended by the CDC/ACSM, the individual should
attempt to participate in moderate-intensity physical activ-
ity (for a duration of 30 minutes or more and a frequency
of 5 or more days per week) or vigorous-intensity physical
activity (for a duration of 20 minutes or more and a fre-
quency of 3 or more days per week). If one participates in
moderate-intensity activities (for a duration of at least 30
minutes and a frequency of 5 or more days per week), the
intensity or the duration should be increased. Finally, if
one participates in vigorous-intensity activities (for a dura-
tion of 20 minutes and a frequency of 3 or more days per
week), continuing that routine is important.386
Ainsworth and associates defined moderate-intensity
physical activity as activity that burns 3.5 to 7 calories per
minute and vigorous-intensity physical activity as activity
that burns more than 7 calories per minute. Table 16-3
details many physical activities according to their level
of intensity.387,388 Table 16-4 provides a comprehensive
list of physical activities and their level of intensity.389 To
burn 1000 calories per week, one has to burn a mini-
mum of 150 calories per day for 7 days per week through
regular participation in one or more moderate- or vigor-
ous-intensity physical activities. If one engages in moder-
ate-intensity activity, it will require 30 minutes per day to
burn 150 calories, while vigorous-intensity activity may
only require 22 minutes or less per day.386
Research has shown that the body composition (total
weight, percentage of body fat, waist circumference)
of middle-aged women who took at least 10,000 steps
per day was more likely to be within the recommended
ranges. Whereas women who took fewer than 6000 steps
per day were more apt to be classified as overweight or
obese with higher waist circumferences, which are pre-
dictors of increased cardiovascular disease risk.390
Controversy exists as to whether step-counting pedom-
eters should be used to guide individuals in meeting their
daily physical activity goals. The ACSM recommends that
step-counting pedometers should be used to enable the indi-
vidual to reach the daily physical activity guidelines (30 min-
utes of moderate-intensity physical activity most, if not all,
days per week) and not just to reach target steps per day.391
Le Masurier noted that step counting is best for beginners,
but again the emphasis should be on reaching the recom-
mended daily dose of moderate physical activity.392
Exercise prescription for elderly populations should be
preceded by a thorough examination of the individual’s
cardiovascular and musculoskeletal systems and an assess-
ment of the person’s heat tolerance and motivation. Then
the exercise prescription should be individualized and of
appropriate intensity and duration to physically challenge
the individual in accordance with the examination results.58
The exercise prescription for the elderly should incorpo-
rate straightforward and fun aerobic conditioning/endur-
ance training, balance training, flexibility exercises, and
strength training. The exercise prescription should also be
aimed at the individual’s health needs, goals, and beliefs.128
It has been recommended that the exercise prescription
for the elderly emphasize gradually progressive activities
that are of low to moderate intensity and low impact and
that avoid heavy static-dynamic lifting. The prescribed
training heart rate is 40% to 80% of maximal heart rate
reserve (compared with 50% to 85% recommended for
young and middle-aged individuals).393
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness
Table 16-3
Physical Activity Requirements to Burn 150 Kcalories
Number of Minutes of Activity Required to Burn 150 kcalories (More vigorous physical activities require less of a time duration. Less vigorous physical activities
require more time.)

0-15 Min 0-20 Min 0-30 Min 0-35 Min 30-40 Min 30-45 Min 0-45 Min 45-60 Min

Stair walking Basketball Water aerobics Walking Wheeling self in Gardening Playing Washing windows
Shoveling snow Wheelchair Walking 2 miles 1-3/4 miles wheelchair (standing) volleyball or floors
Running 11/2 miles basketball (15 min/mile) (20 min/mile) Playing touch Washing and waxing
(10 minute miles) Swimming laps Raking leaves football a car or boat
Jumping rope Dancing fast
Bicycling 4 miles (social)
Bicycling 5 miles
Shooting
basketballl

From Centers for Disease Control and Prevention, US Department of Health and Human Services: Physical activity for everyone: recommendations: how active do adults need to be to gain
some benefit? www.cdc.gov/nccdphp/dnpa/physical/recommendations/calories_text.htm.

351
352 SECTION II • Principles of Practice

Table 16-4
Level of Intensity of Physical Activities
General Physical Activities Defined by Level of Intensity in Accordance with CDC and ACSM guidelines

Moderate Activity* 3.0 to 6.0 METs† Vigorous Activity* Greater than 6.0 METs†
(3.5 to 7 kcal/min) (more than 7 kcal/min)

Walking at a moderate or brisk pace of 3 to 4.5 mph on Racewalking and aerobic walking—5 mph or faster
a level surface inside or outside, such as Jogging or running
• walking to class, work, or the store, Wheeling your wheelchair
• walking for pleasure, Walking and climbing briskly up a hill
• walking the dog, or Backpacking
• walking as a break from work. Mountain climbing, rock climbing, rapelling
Walking downstairs or down a hill Roller skating or inline skating at a brisk pace
Racewalking—less than 5 mph
Using crutches
Hiking
Roller skating or inline skating at a leisurely pace
Bicycling 5 to 9 mph, level terrain, or with few hills Bicycling more than 10 mph or bicycling on steep uphill
Stationary bicycling—using moderate effort terrain
Stationary bicycling—using vigorous effort
Aerobic dancing—high impact Aerobic dancing—high impact
Water aerobics Step aerobics
Water jogging
Teaching an aerobic dance class
Calisthenics—light Calisthenics—pushups, pullups, vigorous effort
Yoga Karate, judo, tae kwon do, jujitsu
Gymnastics Jumping rope
General home exercises, light or moderate effort, getting up Performing jumping jacks
and down from the floor Using a stair climber machine at a fast pace
Jumping on a trampoline Using a rowing machine—with vigorous effort
Using a stair climber machine at a light-to-moderate pace Using an arm cycling machine—with vigorous effort
Using a rowing machine—with moderate effort
Weight training and bodybuilding using free weights, Circuit weight training
Nautilus- or Universal-type weights
Boxing—punching bag Boxing—in the ring, sparring
Ballroom dancing Wrestling—competitive
Line dancing Professional ballroom dancing—energetically
Square dancing Square dancing—energetically
Folk dancing Folk dancing—energetically
Modern dancing, disco Clogging
Ballet
Table tennis—competitive Tennis—singles
Tennis—doubles Wheelchair tennis
Golf, wheeling or carrying clubs —
Softball—fast pitch or slow pitch Most competitive sports
Basketball—shooting baskets Football game
Coaching children’s or adults’ sports Basketball game
Wheelchair basketball
Soccer
Rugby
Kickball
Field or rollerblade hockey
Lacrosse
Volleyball—competitive Beach volleyball—on sand court

(Continued)
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness 353

Table 16-4—Cont’d
Level of Intensity of Physical Activities
General Physical Activities Defined by Level of Intensity in Accordance with CDC and ACSM guidelines

Moderate Activity* 3.0 to 6.0 METs† Vigorous Activity* Greater than 6.0 METs†
(3.5 to 7 kcal/min) (more than 7 kcal/min)

Playing Frisbee Handball—general or team

Juggling Racquetball
Curling Squash
Cricket—batting and bowling
Badminton
Archery (nonhunting)
Fencing
Downhill skiing—with light effort Downhill skiing—racing or with vigorous effort
Ice skating at a leisurely pace (9 mph or less) Ice-skating—fast pace or speed skating
Snowmobiling Cross-country skiing
Ice sailing Sledding
Tobogganing
Playing ice hockey
Swimming—recreational Swimming—steady paced laps
Treading water—slowly, moderate effort Synchronized swimming
Diving—springboard or platform Treading water—fast, vigorous effort
Aquatic aerobics Water jogging
Waterskiing Water polo
Snorkeling Water basketball
Surfing, board or body Scuba diving
Canoeing or rowing a boat at less than 4 mph Canoeing or rowing—4 or more mph
Rafting—whitewater Kayaking in whitewater rapids
Sailing—recreational or competition
Paddle boating
Kayaking—on a lake, calm water
Washing or waxing a powerboat or the hull of a sailboat
Fishing while walking along a riverbank or while wading —
in a stream—wearing waders
Hunting deer, large or small game —
Pheasant and grouse hunting
Hunting with a bow and arrow or crossbow—walking
Horseback riding—general Horseback riding—trotting, galloping, jumping, or in
Saddling or grooming a horse competition
Playing polo
Playing on school playground equipment, moving about, Running
swinging, or climbing Skipping
Playing hopscotch, 4-square, dodgeball, T-ball, or tetherball Jumping rope
Skateboarding Performing jumping jacks
Roller-skating or inline skating—leisurely pace Roller-skating or inline skating—fast pace
Playing instruments while actively moving; playing in Playing a heavy musical instrument while actively running in
a marching band; playing guitar or drums in a rock band a marching band
Twirling a baton in a marching band
Singing while actively moving about—as on stage or in church
Gardening and yard work: raking the lawn, bagging grass Gardening and yard work: heavy or rapid shoveling (more
or leaves, digging, hoeing, light shoveling (less than than 10 lbs per minute), digging ditches, or carrying
10 lbs per minute), or weeding while standing or bending heavy loads
Planting trees, trimming shrubs and trees, hauling Felling trees, carrying large logs, swinging an ax,
branches, stacking wood hand-splitting logs, or climbing and trimming trees
Pushing a power lawn mower or tiller Pushing a nonmotorized lawn mower

(Continued)
354 SECTION II • Principles of Practice
Table 16-4—Cont’d
Level of Intensity of Physical Activities
General Physical Activities Defined by Level of Intensity in Accordance with CDC and ACSM guidelines
Moderate Activity* 3.0 to 6.0 METs†
(3.5 to 7 kcal/min)
Shoveling light snow
Moderate housework: scrubbing the floor or bathtub
while on hands and knees, hanging laundry on a clothesline,
sweeping an outdoor area, cleaning out the garage, washing
windows, moving light furniture, packing or unpacking
boxes, walking and putting household items away, carrying
out heavy bags of trash or recyclables (e.g., glass, newspapers,
and plastics), or carrying water or firewood
General household tasks requiring considerable effort
Putting groceries away—walking and carrying especially
large or heavy items less than 50 lbs.
Actively playing with children—walking, running, or
climbing while playing with children
Walking while carrying a child weighing less than 50 lbs
Walking while pushing or pulling a child in a stroller
or an adult in a wheelchair
Carrying a child weighing less than 25 lbs up a flight of stairs
Child care: handling uncooperative young children
(e.g., chasing, dressing, lifting into car seat), or handling
several young children at one time
Bathing and dressing an adult
Animal care: shoveling grain, feeding farm animals, or
grooming animals
Playing with or training animals
Manually milking cows or hooking cows up to
milking machines
Home repair: cleaning gutters, caulking, refinishing furniture,
sanding floors with a power sander, or laying or removing
carpet or tiles
General home construction work: roofing, painting inside
or outside of the house, wallpapering, scraping, plastering,
or remodeling
Outdoor carpentry, sawing wood with a power saw
Automobile bodywork
Hand washing and waxing a car
Occupations that require extended periods of walking,
pushing, or pulling objects weighing less than 75 lbs,
standing while lifting objects weighing less than 50 lbs, or
carrying objects of less than 25 lbs up a flight of stairs
Tasks frequently requiring moderate effort and considerable
use of arms, legs, or occasional total body movements,
for example:
• Briskly walking on a level surface while carrying a suitcase
or load weighing up to 50 lbs
• Maid service or cleaning services
Vigorous Activity* Greater than 6.0 METs†
(more than 7 kcal/min)
Shoveling heavy snow
Heavy housework: moving or pushing heavy furniture
(75 lbs or more), carrying household items weighing
25 lbs or more up a flight or stairs, or shoveling coal
into a stove
Standing, walking, or walking down a flight of stairs while
carrying objects weighing 50 lbs or more
Carrying several heavy bags (25 lbs or more) of groceries
at one time up a flight of stairs
Grocery shopping while carrying young children and
pushing a full grocery cart or pushing two full grocery
carts at once
Vigorously playing with children—running longer distances
or playing strenuous games with children
Race walking or jogging while pushing a stroller designed
for sport use
Carrying an adult or a child weighing 25 lbs or more up
a flight of stairs
Standing or walking while carrying an adult or a child
weighing 50 lbs or more
Animal care: forking bales of hay or straw, cleaning a barn
or stables, or carrying animals weighing over 50 lbs
Handling or carrying heavy animal-related equipment or tack
Home repair or construction: very hard physical labor,
standing or walking while carrying heavy loads of 50 lbs or
more, taking loads of 25 lbs or more up a flight of stairs or
ladder (e.g., carrying roofing materials onto the roof), or
concrete or masonry work
Hand-sawing hardwoods
Pushing a disabled car
~Occupations that require extensive periods of running,
rapid movement, pushing or pulling objects weighing
75 lbs or more, standing while lifting heavy objects of
50 lbs or more, walking while carrying heavy objects of
25 lbs or more
Tasks frequently requiring strenuous effort and extensive
total body movements, for example:
• Running up a flight of stairs while carrying a suitcase or
load weighing 25 lbs or more
(Continued)
 CHAPTER 16 • Clinicians’ Roles in Health Promotion, Wellness, and Physical Fitness 355

Table 16-4—Cont’d
Level of Intensity of Physical Activities
General Physical Activities Defined by Level of Intensity in Accordance with CDC and ACSM guidelines

Moderate Activity* 3.0 to 6.0 METs† Vigorous Activity* Greater than 6.0 METs†
(3.5 to 7 kcal/min) (more than 7 kcal/min)

• Waiting tables or institutional dishwashing • Teaching a class or skill requiring active and strenuous
• Driving or maneuvering heavy vehicles (e.g., semitruck, participation, such as aerobics or physical education
school bus, tractor, or harvester)—not fully automated instructor
and requiring extensive use of arms and legs • Firefighting
• Operating heavy power tools (e.g., drills and jackhammers) • Masonry and heavy construction work
• Many homebuilding tasks (e.g., electrical work, plumbing, • Coal mining
carpentry, drywall, and painting) • Manually shoveling or digging ditches
• Farming—feeding and grooming animals, milking cows, • Using heavy nonpowered tools
shoveling grain, picking fruit from trees, or picking vegetables • Most forestry work
• Packing boxes for shipping or moving • Farming—forking straw, baling hay, cleaning barn,
• Assembly-line work—tasks requiring movement of the or poultry work
entire body, arms or legs with moderate effort • Moving items professionally
• Mail carriers—walking while carrying a mailbag • Loading and unloading a truck
• Patient care—bathing, dressing, and moving
patients or physical therapy

From U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for
Chronic Disease Prevention and Health Promotion, Division of Nutrition and Physical Activity: Promoting physical activity: a guide for community
action. Champaign, Ill, 1999, Human Kinetics. (Table adapted from Ainsworth BE, Haskell WL, Leon AS, et al: Compendium of physical
activities: classification of energy costs of human physical activities. Medicine and Science in Sports and Exercise 1993;25(1):71-80. Adapted with
technical assistance from Dr. Barbara Ainsworth.) Accessed from Centers for Disease Control and Prevention, US Department of Health and
Human Services: Physical activity for everyone: recommendations, www.cdc.gov/nccdphp/dnpa/physical/pdf/PA_Intensity_table_2_1.pdf.
*For an average person, defined here as 70 kilograms or 154 pounds. The activity intensity levels portrayed in this chart are most applicable
to men aged 30 to 50 years and women aged 20 to 40 years. For older individuals, the classification of activity intensity might be higher. For
example, what is moderate intensity to a 40-year-old man might be vigorous for a man in his 70s. Intensity is a subjective classification.
†
The ratio of exercise metabolic rate. One MET is defined as the energy expenditure for sitting quietly, which, for the average adult, approximates
3.5 ml of oxygen uptake per kilogram of body weight per minute (1.2 kcal/min for a 70-kg individual). For example, a 2-MET activity requires
two times the metabolic energy expenditure of sitting quietly.
Data for this chart were available only for adults. Therefore, when children’s games are listed, the estimated intensity level is for adults
participating in children’s activities.
To compute the amount of time needed to accumulate 150 kcal, do the following calculation: 150 kcal divided by the MET level of the activity
equals the minutes needed to expend 150 kcal. For example, 150/3 METS = 50 minutes of participation. Generally, activities in the moderate-
intensity range require 25 to 50 minutes to expend a moderate amount of activity, and activities in the vigorous-intensity range would require less
than 25 minutes to achieve a moderate amount of activity. Each activity listed is categorized as light, moderate, or vigorous on the basis of current
knowledge of the overall level of intensity required for the average person to engage in it, taking into account brief periods when the level of
intensity required for the activity might increase or decrease considerably.
Persons with disabilities, including motor function limitations (e.g., quadriplegia), may wish to consult with an exercise physiologist or physical
therapist to properly classify the types of physical activities in which they might participate, including assisted exercise. Certain activities classified
in this listing as moderate might be vigorous for persons who must overcome physical challenges or disabilities.
Note: Almost every occupation requires some mix of light, moderate, or vigorous activities, depending on the task at hand. To categorize the
activity level of your own position, ask yourself: How many minutes each working day do I spend doing the types of activities described as light,
moderate, or vigorous? To arrive at a total workday caloric expenditure, multiply the minutes spent doing activities within each intensity level
by the kilocalories corresponding to each level of intensity. Then, add together the total kilocalories spent doing light, moderate, and vigorous
activities to arrive at your total energy expenditure in a typical day.

Exercise programs may be prescribed in a variety of
formats from individually performed programs at home
to programs in a fitness facility or community center.
Community-based programs tend to improve functional
and well-being outcomes.394 A videotaped strength train-
ing program (titled “Strong-for-Life”) for use at home
resulted in increased strength, social functioning, and
perceived vigor, as well as control of perceived anger and
tension.395
Researchers have also investigated the frequency of the
exercise prescription. One hour of exercise was prescribed
for 12 weeks to three different groups of elderly women
356 SECTION II • Principles of Practice
(60 to 75 years of age) who performed the exercises once,
twice, or three times per week. A fourth group served as
the control. All three groups had significant increases in
balance, muscular endurance and coordination, and sit
and reach flexibility. The improvement found in each of
the three experimental groups was proportional to the
frequency of the program.396
Motivation
Clinicians must develop strategies that stress the intrinsi-
cally motivating benefits of physical activity and exercise
and must build into their interventions those aspects of
exercise that patients and clients value. Nied and Franklin
found that in order to motivate individuals to begin exer-
cising, one must focus on each individual’s goals, bar-
riers to exercise, and concerns.128 They suggest using
individualized behavioral therapy, active lifestyle, and
the “stages of change” model as strategies for adopting
exercise and physical activity as a lifelong commitment.128
The “stages of change” model shows a gradual change in
behavior whereby one goes from the precontemplation
stage (being unwilling, unaware, or uninterested in mak-
ing a change), to the contemplation stage (considering a
change), to the preparation stage (deciding and prepar-
ing to make a change), and finally to the action stage
(making a change). Maintenance and relapse prevention
are part of the process as the individual attempts to main-
tain the new behavior over time.397
Motivators for Exercise128
To motivate individuals to exercise, one must focus on:
● Individual’s goals
● Determining barriers to exercise
● Individual’s concerns
Stages of Change397
● Precontemplation
● Contemplation
● Preparation
● Action
● Maintenance and relapse prevention
Long-term compliance with a program of health pro-
motion, wellness, and fitness is best achieved when the
exercise prescription is fun, straightforward, and based
on the individual’s health needs, beliefs, and goals.128
Goal targeting, the use of exercise tests to chart prog-
ress, appropriate supervision, and an optimal exercise
prescription are all factors that need to be considered if a
program is to be implemented successfully.398
Conclusion
Clinicians’ Role
● The expertise of clinicians, especially physical therapists, as
movement scientists, strategically positions them to make a
major contribution toward altering the staggering costs of health
care and reversing the decreases in function all too often seen in
today’s sedentary society.
● Embracing the wellness model for all patients and clients requires
a shift away from the sickness model and requires clinicians
to devise programs of physical activity and exercise that will
overcome all the potential barriers to activity and exercise and will
meet the individual’s needs and goals.
The benefits of promoting a healthy lifestyle, increasing
physical activity, encouraging progressive exercise pre-
scriptions, and achieving the set of attributes included in
physical fitness are vigorously supported by a multitude
of research. The effects of physical activity and exercise on
various physiological and psychological parameters across
the life span support their roles in preventing disease and
improving function and health. The effects of physical
activity and exercise on the mobility and independence of
the elderly, the older old, and the frail elderly must be of
paramount importance for all clinicians as our populations
continue to age. Ample evidence points to the necessity
of challenging preconceived notions of low expectations
of physical activity and exercise levels for the elderly and
for those with impairments, functional limitations, and
disabilities. Ever increasing data support the need to con-
tinuously and scientifically overload the system regardless
of how low the starting point, and maintaining fitness is
the foundation of functional ability regardless of age.
To paraphrase Evans and Campbell, no pharmacolog-
ical intervention holds a greater promise of improving
health and promoting independence in the elderly than
does increasing physical activity and increasing exercise,
both of which will lead to increasing physical fitness.144
With their knowledge and skills, clinicians, especially
physical therapists, must embrace, publicly declare, and
provide programs of health promotion, wellness, and fit-
ness across the life span as part of their inherent responsi-
bility of enhancing the lives of our citizenry.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 398 references for this chapter.
 17
C H A P T E R

P HYSIOLOGICAL P RINCIPLES OF
C ONDITIONING FOR THE I NJURED
AND D ISABLED
Howard A. Wenger, Paula F. McFadyen, Laura Middleton, and Ross A. McFadyen

Introduction Principles of Conditioning

This chapter addresses the principles that form the foun- ● Performance principle
dation for designing conditioning programs. These prin- ● Fitness principle
ciples provide guidelines for prescribing exercises that will ● Optimization principle
enhance both physiological function and performance in ● Homeostasis principle
different activities, occupations, and sports. The application
● Individualization principle
● Overload principle
of these principles varies with the activity, individual, stage ● Underload principle
of development, and time of year. These principles should ● Progression principle
be integrated into a training program to achieve both ● Variety principle
optimal physiological function and peak performance. ● Skill principle
● Specificity principle
Performance Principle ●

●
Stimulus principle
Rest principle
Many factors contribute to or detract from human perfor- ● Maintenance principle
mance (Figure 17-1). The extent of this contribution var- ● Interference principle
ies in different individuals, in different sports or activities, ● Loading/unloading principle
and at different stages of development. The importance
● Overtraining principle
● Recovery principle
of these factors must be identified, prioritized, assessed, ● Preparation principle
and modified to elicit optimal performance. At times some ● Taper principle
factors must be de-emphasized to devote time to others ● Evaluation/monitoring principle
that may be hindering performance. It is also important to ● Periodization principle
be aware of the interactions of multiple factors and their
impact on performance. Some factors can complement,
supplement, or magnify the effects of other factors such
that the entire effect is greater than the sum of the parts. sary to de-emphasize one gear in order to redevelop or
Figure 17-1A portrays each performance factor as a strengthen a weaker one.
gear in the machine (human body). For the performance Different individuals bring different strengths to any
gear to function at optimal rates, each of the other gears physical endeavor. Often exceptional development in one
must also be operating optimally. Often it is neces- area has contributed to successful performances, but at

357
358 SECTION II • Principles of Practice
Figure 17-1
The performance factors. (From Wenger HA, McFadyen PF,
McFadyen RA: Physiological principles of conditioning. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 191, Philadelphia, 1996, WB Saunders.)
the expense of development in other areas. Therefore,
it is necessary for clinicians to evaluate the status of each
of these factors and determine optimal combinations to
achieve an individual’s performance or fitness goals. This
is even important at different stages of growth, develop-
ment, and maturation. For example, in young persons, it
may be more important to focus on skill development and
to use fun activities to build sufficient fitness to perform
the skills. As they mature, more and more emphasis can
be placed on mental skills, tactics, and physiological
development.
Figure 17-1A suggests an interaction between factors
such that well-developed mental skills enhance one’s ability
to train and develop physical fitness and vice versa. Figure
17-1B illustrates some of the variables that affect physiology
and demonstrates that for each of the major factors described
in Figure 17-1A there are many variables that influence its
effectiveness in enhancing fitness and performance. The
physiological gear is enhanced by good health, proper bal-
ance of training, rest, and nutrition but can be impaired by
injury, fatigue, or travel. Other factors such as skill, tactics,
psychology, equipment, and environment each have their
own set of variables that enhance or detract from the effec-
tiveness of that factor in producing optimal performance.
In many sports or recreational activities, highly devel-
oped skills can allow high levels of performance in spite
of low levels of development in other areas. For example,
high skill levels but a poorly developed aerobic energy
system can limit a client’s performance by causing fatigue.
Similarly, strength imbalances can result in injury, and
inappropriate equipment selection, such as the type of
wax for skis or a type of footwear, can lead to poorer
performance. Because many factors influence perfor-
mance, it is important that we are able to prioritize and
match the factors that most affect our performance goals
and determine which variables must be altered to offset
weaknesses or enhance strengths.
Fitness Principle
Physical fitness has many connotations in society. Although
it is often associated with the state of the cardiorespiratory
system (aerobic fitness), it must embrace a wider, all-inclu-
sive number of physical attributes (Figure 17-2). The
extent to which each of these attributes affects the specific
level of fitness necessary to achieve our performance goals
depends on the activity, the strengths and weaknesses of the
individual, his or her training background, and the level of
desired performance.
Figure 17-2 implies that physical fitness is a composite
of many different components: energy systems, the car-
diorespiratory system, the neuromuscular system, body
composition, and flexibility. The level of development in
each of these components varies based on the physical
demands of the activity and the extent to which fitness
affects performance, as shown in Figure 17-1.
Energy Systems
The power and capacity of the three energy systems must
be matched to the demands placed on the individual by
daily activity, the rigors of training, and the requirements
of daily activity. Different sports or daily activities rely on
different energy systems to different degrees.1 Also, the
interrelationship between systems is highlighted by the
importance of aerobic development for recovery from
high-intensity anaerobic exercise.2 Sports such as ice
hockey, soccer, basketball, and field hockey all demand
short bursts of high-intensity effort followed by peri-
ods of lower intensity work during which fuel stores are
replenished and metabolites removed. Performance in
these activities has a high reliance on anaerobic energy
systems. However, recovery during training, games, and
rehabilitation, as well as between games and throughout
a workday, demands a well-developed aerobic energy sys-
tem, as this system is responsible for restoration of alactic
stores and is instrumental in facilitating the removal of
lactic acid.
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled
Figure 17-2
Components of physical fitness. (From Wenger HA, McFadyen PF, McFadyen RA: Physiological principles of conditioning. In Zachazewski JE,
Magee DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 192, Philadelphia, 1996, WB Saunders.)
Cardiorespiratory System
The need to develop the cardiorespiratory system, either
centrally or peripherally, depends on its importance for
recovery, oxygen and fuel supply, removal of waste prod-
ucts, and heat dissipation or retention during both the activ-
ity and training. Cardiorespiratory fitness is important for
recreational activities, physically demanding occupations,
and sports, which tax the aerobic energy supply system
for extended periods of time. Highly developed levels of
aerobic fitness facilitate the removal of waste products, the
maintenance of thermal balance, and the need to recover
quickly. The single best measure of this fitness component
is maximal oxygen consumption (VO2max).3 Cross-coun-
try skiing, middle- and long- distance running, and row-
ing are excellent examples of sports in which performance
depends on a highly trained cardiorespiratory system (>70
mL/kg/min) for the uptake, delivery, and utilization of
oxygen and fuels. High volumes of training are required to
develop VO2max or the ability to work at a high percentage
of VO2max. Recreational pursuits and daily activities usually
require the cardiorespiratory system primarily for recovery,
and demand only an optimal level in this system rather than
maximal levels. When health is the primary objective, exer-
cise that enhances the cardiorespiratory system will improve
the blood lipid profile, decrease blood pressure, elevate
metabolic rate, and enhance the immune system.1
Neuromuscular System
Adaptations in the neuromuscular system for enhanced
strength, power, and endurance are mandatory in many
359
sports, recreational activities, and physically demanding
occupations. The neuromuscular system is important for
overcoming external forces as well as accelerating loads
relative to body mass. This system involves not only force
and power production by the muscles, but also the precise
application of force and power to simple and complex
movements. Therefore, in some sports and occupations,
the neuromuscular system is developed to attain high
levels of absolute strength, power, and endurance, whereas
in others, strength, power, and endurance relative to body
mass are the critical determinants of neuromuscular effec-
tiveness. For weight lifters, interior linemen in football,
participants in combative sports, and downhill skiers,
high amounts of absolute strength and power are critical
for peak performance. However, gymnastics, sprinting,
jumping, and team sports that demand high accelerations
(e.g., soccer, tennis, and lacrosse) are more dependent on
high levels of strength and power relative to body mass.
Similarly, in sports such as weight lifting, shot putting, and
javelin throwing, the movements are fixed and relatively
simple, whereas other sports involve “read-and-react”
situations that create unpredictable applications of power
and require coordinated multijoint movements. Thus, the
acquisition of neuromuscular strength and power must be
accomplished in settings similar to those in which the ner-
vous system is utilized specifically in the movement pattern
necessary for performance (the specificity principle).4
Body Composition
The degree to which body composition—fat and fat-free
mass—contributes to performance varies with different
360 SECTION II • Principles of Practice
sports, activities, and occupations. Some sports require
a high body mass for stability or inertia (such as that
required of offensive linemen in football and sumo wres-
tlers). In these instances, the nature of the mass is not as
critical as the amount. Similarly, in activities in which body
mass does not have to be moved or in which it is sup-
ported, as in cycling and rowing, the nature of the mass
is also not as critical as other variables. However, when
body mass must be accelerated quickly or rotated using
strength and power, excess fat is detrimental (as in sports
such as tennis, squash, gymnastics). Because fat requires
blood flow, the ability to effectively perfuse muscle dur-
ing both exercise and recovery can be jeopardized when
optimal levels of body fat are exceeded. The insulative
properties of fat can also impair thermoregulation, and
increased levels are highly associated with elevated blood
pressure and type II diabetes. Thus, with excess levels of
body fat, performance, training, and daily functioning can
be compromised as a result of reduced muscle blood flow,
ineffective recovery, overheating, or dehydration.
Flexibility
Flexibility involves the range of motion about a joint or
series of joints and reflects the ability of the muscle-tendon
units to elongate within the physical restrictions of the
joint.5 A causal relationship between flexibility and per-
formance has not been clearly established, but individuals
must move through the required range of motion to
excel aesthetically or functionally. However, hypermobil-
ity or instability may make the joint more susceptible to
injury in contact sports or when high speeds and forces
are generated around the joint and there is some evi-
dence that static stretching may impede force produc-
tion in movements requiring high amounts of strength.6
The relationship between flexibility, performance, and
injury may be joint specific and sport/activity specific.7
Therefore, an optimal amount of flexibility is desired
(the optimization principle). A fitness profile must be
developed for each individual that matches the demands
of his or her sport, occupation, activity level, and personal
goals. The relative importance of each of the preceding
fitness components must be determined and then devel-
oped according to the guidelines described in all of the
principles that follow.
Optimization Principle
In many sports, activities, and occupations, the factors
that have the greatest influence on performance are skill
level, tactics, equipment, environment, physiological
function, and mental skills (the performance principle).
In some occupations and sports, it is not always necessary
to develop maximum capabilities in each fitness compo-
nent; instead, it is only necessary to attain optimal or suf-
ficient levels to meet the demands of the activity, permit
sufficient recovery to train and travel, and minimize the
chance of injury. As reflected in Figure 17-3, the opti-
mal levels of a fitness component are often less than the
maximum that the individual can achieve. Because it may
take less frequency, intensity, and time to achieve these
optimal levels, time can then be allotted for developing
other factors that can influence performance.
Different occupations and sports have different energy
requirements.1 For example, midfielders in soccer require
80% of their energy from the anaerobic energy systems
and 20% from the aerobic energy supply, whereas cross-
country skiers derive 85% of their energy from the aero-
bic system and only 15% from anaerobic sources. In a
physically demanding occupation like urban fire fighting,
participants often work at 65% to 70% of their aerobic
power for repeated 10-minute intervals and use up to
80% of their maximum strength at repeated intervals.
If the energy supply has high loading as a performance
factor, then near maximal levels of those energy systems
are necessary. However, if other factors such as skill or
tactics are the predominant influence for success, then
only optimal levels of the appropriate energy production
systems are required. Even though the energy system pri-
marily used during intermittent sports and occupations
such as soccer, basketball, ice hockey, and fire fighting is
predominantly anaerobic, a highly developed aerobic and
cardiorespiratory system is mandatory for recovery from
high-intensity work during breaks in play, between games,
and throughout a day; during high volumes of training;
and to deal with the added demands of travel and shift
work. Although there is not a great deal of evidence that
delineates a specific level of aerobic development sufficient
to permit recovery in activities requiring intermittent levels
of activity or to provide the recovery to handle high vol-
Figure 17-3
Physiological adaptations to progressive increases in the training
stimulus. (From Wenger HA, McFadyen PF, McFadyen RA:
Physiological principles of conditioning. In Zachazewski JE, Magee
DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 193,
Philadelphia, 1996, WB Saunders.)
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled
umes of anaerobic training, a VO2max of 60 mL/kg/min
for males and 56 mL/kg/min for females is often used.
Because this fitness component is the baseline that per-
mits sufficient time to develop other fitness components
and both skill and tactics, it should be emphasized early
during the training year (the periodization principle).
Once this optimal level is achieved, VO2max can then be
maintained (the maintenance principle) and other fitness
components or performance factors emphasized.
Baseline Aerobic Levels
● 60 ml/kg/min (males)
● 56 ml/kg/min (females)
In addition to these requirements for optimal aerobic
development, maximal strength may not be necessary.
For example, upper body strength may not be essential
in some sports to attain peak performance, but optimal
levels of strength around the shoulder girdle and the
abdominal and lower back areas can reduce the risk of
injury during impact or during high training loads and
allow training and performance to be uninterrupted.
Homeostasis Principle
Homeostasis refers to the need of the body to maintain an
optimal internal environment in which cells can function
best. The equilibrium of the body gets disrupted during
exercise, travel, and sickness, as well in heat, in cold, and
at altitude. For optimal performance, it is essential for the
body to cope with such stressors and return the internal
environment to optimal conditions.
In optimal conditions, the body is at equilibrium.
There is a balance between physiological function and
the demands imposed by daily physical loads (see Figure
17-1A). Any strain will create an imbalance in the short
term (see Figure 17-1B) and stimulate our physiology
to return our internal milieu to normal. Repeated expo-
sures to a particular overload will initiate an adaptation
in the anatomical structures and physiological functions
involved. This training effect now allows us to deal more
effectively with the stimulus (see Figure 17-3).
As fitness improves, the body is better able to cope with
environmental strain, adapt more quickly, and withstand
greater loads. For example, a highly trained person sweats
sooner8 and sweats more9 at high temperatures. Highly
trained and acclimatized athletes can also withstand heat for
longer periods despite similar rises in core temperature.10
Individualization Principle
According to the individualization principle, each indi-
vidual responds uniquely to the same training stimulus.
361
An individual’s response depends on the following vari-
ables:11 genetic endowment, biological age, training
state, health status, and fatigue state. To maximize the
adaptation for each individual, training programs must
factor in all of these variables.
Fitness and Individual Variables
● Genetic endowment
● Biological age
● Training state
● Health status
● Fatigue state
Genetic Endowment
Genetic factors account for about 40% of variation in
aerobic fitness.12 Each individual has a given genetic
potential for each element of fitness that will limit the
extent to which each component can be developed
through physical training. The farther an individual is
from the genetic limit, the larger will be the improve-
ments to a given load (stimulus). As the individual gets
closer to the limit, less improvement will be elicited, even
with increases in the stimulus (see Figure 17-3).11 If an
individual’s genetic limit for VO2max is 5 L/min and his
or her present level is 3 L/min, large increases will occur
during the initial 6 to 8 weeks of training. However,
when VO2max reaches 4.5 L/min, less improvement
will be elicited, even with greater magnitudes of train-
ing. Although higher intensities and volume of train-
ing are required as an individual approaches the genetic
ceiling, individuals must be made aware of the risk of
overuse injuries or overtraining (the overtraining prin-
ciple). Thus, periods of high-volume, high-quality load-
ing must be interspersed with periods of unloading (the
loading/unloading principle).
Another implication of the genetic impact on
physiological adaptations to training is that some
individuals respond very early to a training stimulus,
whereas others are late responders.13 Therefore, for
some individuals, the training load should be increased
frequently; for others the steps should be more pro-
longed. Evaluation of progress (the evaluation/moni-
toring principle) must be planned throughout each
training cycle to either determine or account for the
differences in adaptation time.
Also encompassed in genetic endowment is gender.
Postpuberty, women tend to have less muscle mass and
more body fat at a given training level. In similar sized
men and women, aerobic power is usually at least 30% to
40% less in women.14 However, response to both aerobic
training14 and strength training15 is similar in men and
women.
362 SECTION II • Principles of Practice

Biological Age
An individual’s biological age can restrict the degree to
which he or she can adapt to certain training stimuli;
furthermore, certain stimuli may even be detrimental or
dangerous. For example, in prepubertal boys, the lack of
testosterone restricts the amount of muscle mass that can
be developed with resistance training, and high loads may
even damage the skeleton or impede growth. Strength can
be increased with either increased muscle mass or enhanced
neuromuscular adaptations (synchrony or recruitment).
Thus, when strength gains are desired in this population
to permit skill development or provide protection, resis-
tance protocols should focus on proper technique and low
resistances to avoid the risks and facilitate neuromuscular
adaptations. Young adults and older adults also have dif-
ferent training responses. Younger adults have a greater
response to training than do older adults.15

Training State
The state of training can determine the rate of improvement
in most fitness variables. Individuals at low levels of fitness
will respond with a higher rate and magnitude of adapta-
tion than when they possess higher levels of fitness.16 This
tendency is reflected in Figure 17-3 and outlined in the sec-
tions that explore the optimization and overload principles.

Health Status
An individual’s health status can affect the quality of
both training and performance. During either sickness or
injury, the amount of adaptive energy is reduced, along
with the inability to perform at optimal intensities and
volumes of work. Therefore, during illness or injury, the
prescription of exercise and recovery must be reduced
to allow the individual to regain optimal health before
reestablishing the training regimen.
Fatigue State
Short-term fatigue brought about by the depletion of fuels,
substrates, the accumulation of metabolites, heat stress, or
dehydration will limit one’s ability to work at optimal inten-
sities or durations. Therefore, to maximize the training stim-
ulus and thus maximize the training adaptation, recovery
from fatigue should be accomplished with proper dietary,
rehydration, and active and passive recovery strategies.
Overload Principle
When cells, tissues, and organs are loaded beyond what
they normally are required to do, they will adapt to permit
them to deal with these new loads more effectively (Figure
17-4). External stimuli such as the environment or exer-
cise will cause a disturbance in the internal environment
Figure 17-4
The effect of overload on stimulating adaptation to elicit an increased
training effect. (From Wenger HA, McFadyen PF, McFadyen RA:
Physiological principles of conditioning. In Zachazewski JE, Magee
DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 194,
Philadelphia, 1996, WB Saunders.)
of the body. With repeated exposures, adaptations occur
that reduce the degree of disturbance and enhance the
rate of return to optimal conditions. The adaptations
enable the body to cope with the new conditions and may
take many forms, from an increase in specific proteins, to
cell division, to fuel storage, and to fluid shifts.
Physical loads stimulate an increase in physiologi-
cal capabilities. When loads are applied, they should be
specific to the desired effect (the specificity principle),
be appropriate to the individual (the individualization
principle), consider the time in the seasonal calendar
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled
(the periodization principle), and be appropriate in
terms of the type of stimuli (frequency, intensity, and
duration) (the stimulus principle). For example, when
the size of muscle is being increased through strength
resistance training, the prescription may consist of 8 to
12 repetitions for two to three sets, performed approxi-
mately three times per week. If bench press is a prescribed
exercise and 150 pounds permits the proper number of
repetitions in the first set, then when 10 to 12 repetitions
can be completed in the third set, the load should be
increased by up to 5% to bring the number of repetitions
back within the desired range to ensure overload (the
progression principle). When aerobic power is being
developed, the prescription should involve aerobic inter-
vals of 1 to 3 minutes in duration with a 1:1 work-to-rest
ratio at 90% to 100% of VO2max performed with 6 to 10
repetitions.17 The load can be progressed by increasing
the length of the work interval, decreasing the length of
the rest interval, or increasing the number of repetitions.
It must be remembered that chronic overloading with-
out sufficient rest (see Rest Principle) and unloading (see
Loading/Unloading Principle) can result in overtraining
(see Overtraining Principle) or injury and therefore may
be counterproductive to training or performance.
Underload Principle
When a body is overloaded, it adapts such that the physi-
ological capacity is increased. If the load is reduced below
what is normally performed (underloaded), the body will
adapt by decreasing its ability in the underloaded compo-
nent (detraining). Similar to overloading, detraining will
be specific to the stimulus.
Underloading may occur because of sickness, travel,
work, holidays, or other interfering factors. Fitness can
be maintained with less duration than it takes to build
it (the maintenance principle). If aerobic training
is only reduced by one third to two thirds in train-
ing frequency and duration, VO2max and performance
can be maintained. However, if intensity is reduced
by one third to two thirds, VO2max and performance
decrease.18
Detraining occurs quickly after the cessation of
training. A reduction in VO2max can be detected within
4 weeks of detraining. This initial decrease appears to be
due to a reduction in stroke volume of the heart. Further
reduction after 4 weeks corresponds with reductions in
the oxygen absorbed by the muscle from the blood.
Within muscle, detraining also occurs when train-
ing ceases. However, there is little decrease in the initial
4 weeks of underloading. Even after 8 weeks of detrain-
ing, muscle is still stronger than if never trained. Despite
detraining effects, people who have trained will main-
tain higher fitness levels than will untrained individuals
despite years passing since the last training period.19
363
Progression Principle
A load will only stimulate adaptation when the existing
functional capabilities of the body are strained. Once an
adaptation has taken place to a specific load or stimu-
lus, this load is no longer an “overload.” To get further
improvements, the load must be progressively increased
(see Figure 17-3).20,21
The increase in load may be in frequency, intensity, or
duration. Progression may vary by increasing the number
of training sessions per week, increasing the rate or load
in each session, or increasing the training time or num-
ber of repetitions or sets in a training session. For endur-
ance runners, improvement in overall performance could
result from overloading on duration to increase average
running speed or to shift to higher intensity interval
training to improve maximal aerobic power.22
Variety Principle
To elicit the widest range of benefit from training loads,
different activities and movements can be included in the
training sessions. Since each load demands a specific adap-
tation (the specificity principle), a variety of loads will
stimulate a variety of adaptations. The more similar the
variations, the more overlap will occur in adaptations.
Cross training can add variety to an aerobic training
program. Sports such as running, cycling, swimming,
and rowing are effective cross-training methods for aero-
bic improvements; however, the adaptation may not be
activity specific. Changes in the central components of
the oxygen transport system such as cardiac output and
blood volume can be similarly achieved with different
modes of training.
Variety can be included in strength training by chang-
ing grip, joint actions, body position, or type of con-
traction, which will place a stress on different muscles,
change recruitment patterns, and alter the center of grav-
ity. For example, in bicep curls, a supinated grip stresses
the biceps brachii while a pronated grip places more
stress on the brachioradialis (the specificity principle).
In addition to achieving a more extensive adaptation,
variety also provides interest and enthusiasm to the train-
ing regimen.
Skill Principle
Skill is associated with enhanced mechanical efficiency
and reduced risk of injury. Skill in exercise-specific actions
should be established before the training load is increased
to reduce the possibility of injury.
Optimizing skill can improve performance without
any change in physiological capacity. Skilled performers
are often able to outperform their competitors despite
similar or inferior physiological capabilities. For example,
364 SECTION II • Principles of Practice
Kenyan runners have had superior performance relative
to their European counterparts in recent decades despite
similar physiological variables.23 This superior perfor-
mance is due to enhanced mechanical efficiency. Elite
athletes are able to cover similar distances with less energy
cost24,25 and less fatigue. A skillful application of forces
can also result in more effective and powerful move-
ments without an improvement in the force-generation
capabilities of skeletal muscles. Independent from effi-
ciency, technique may also reduce strain on joints and
ligaments.
Specificity Principle
The adaptations that the body makes to exercise loads
(training effect) are to a large degree specific to the
structures and functions that are loaded. Training
effects are specific to the energy supply systems that have
been utilized, the locale of the stimulus (i.e., whether
the central circulation or peripheral muscle has been
loaded), the specific muscle groups, the joint action(s),
the type of contraction (i.e., concentric, eccentric, or
isometric), and the speed of contraction. This principle
implies that overload results in adaptations specific to
those cells, tissues, organs, or systems that have been
overloaded. The adaptation that results depends on the
type and amount of overload. As Figure 17-5 shows,
the energy systems follow a continuum from the high-
power, low-capacity (alactic) systems, to the moder-
Figure 17-5
The maximal power and capacity of the three energy systems. (From
Wenger HA, McFadyen PF, McFadyen RA: Physiological principles
of conditioning. In Zachazewski JE, Magee DJ, Quillen WS, editors:
Athletic injuries and rehabilitation, p 195, Philadelphia, 1996,
WB Saunders.)
ate-power and moderate-capacity (lactic) systems, and
then to the low-power, high-capacity (aerobic) systems.
The characteristics of these energy systems have been
described in detail elsewhere.1,2 In terms of development
through specific conditioning programs, the power or
capacity of each system must be challenged by a stimu-
lus that overloads the specific energy component. For
event-specific adaptations, the intensity of the training
should mimic the intensity of the event.22
Applications for Specificity
● Energy systems
● Locale of stimulus (central/peripheral)
● Muscle group
● Joint action(s)
● Type of contraction
● Speed of contraction
● Intensity of activity
For example, because the maximum power of the alac-
tic system occurs within the first 5 seconds (see Figure
17-5), loads requiring maximal power in up to 5-second
bursts stimulate adaptations in the rate of energy supply
from this system. Similarly, because the capacity of the
lactic system extends from 45 to 180 seconds, exercise
that challenges muscle maximally over this time frame
provides the optimal stimulus for adaptation. It should
be noted that the power of the aerobic system is also
challenged during the same time frame as lactic capacity.
Thus, interval exercise designed to challenge the aerobic
power can also stimulate significant adaptations in lactic
capacity. This is consistent with the specificity principle:
since both energy supply systems are overloaded, both
will adapt.
Prolonged stimulation of the cardiorespiratory (cen-
tral) system results in changes in heart, vascular, and
blood function. Changes to the central circulation
enhance delivery of oxygen, fuels, hormones, and water;
removal of metabolic wastes such as lactate, ammonia,
and carbon dioxide; and maintenance of thermal balance.
All of these adaptations improve prolonged performance
in such activities as cross-country skiing, rowing, or mill-
work and recovery from high-intensity intervals during
intermittent activities such as basketball, ice hockey, soc-
cer, fire fighting or during high-intensity resistance or
interval training. The prolonged stimulus can be either
continuous at moderate intensities or repeated intervals
at intensities corresponding to VO2max.
In skeletal muscle, different motor unit types (slow
oxidative [type I], fast oxidative-glycolytic [type IIa],
and fast glycolytic [type IIb]) are recruited with differ-
ent intensities and duration of load and stimulus. The
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled
characteristics of these motor units and the nature of
their recruitment patterns have been described in detail
elsewhere.26,27 During moderate-intensity prolonged exer-
cise, slow-twitch motor units are primarily recruited. As
they begin to fatigue after approximately an hour of activ-
ity, fast-twitch oxidative-glycolytic motor unit (type IIa)
recruitment is increased, followed by the fast glycolytic
pool (type IIb). However, high-intensity aerobic interval
programs of 1 to 3 minutes duration require a significant
contribution from the fast-twitch motor units, thus stimu-
lating aerobic changes in these muscles much sooner than
would happen with continuous, prolonged low-intensity
training. To enhance aerobic power, these programs must
either be of long duration (in excess of 1 + hours) or consist
of high-intensity intervals to elicit maximal adaptations at
the cellular level in all three fiber types.
The adaptation to skeletal muscle is also specific to
both the muscle groups used and the joint action(s). For
example, force overload achieved through biceps curls
challenges biceps brachii maximally when the forearm is
supinated. When in the pronated position, less recruit-
ment from the biceps is invoked, but greater demand is
placed on the brachioradialis muscle. Similarly, in many
actions, stabilizers for the surrounding or support-based
muscles and synergists are also critical for both proper
technique and optimal performance. Therefore, isolating
single muscle groups during resistance training can be less
effective for transferring strength to multijoint or com-
plex movements than performing such movements under
loaded conditions. However, in multijoint movements,
each individual muscle group is not loaded maximally.
Therefore, if one muscle group is weaker because of
injury or disuse, it is wise to load it independently to
build strength, then combine actions into multijoint
sport-specific movements.
Similarly, the type of contraction (isometric,
concentric, or eccentric) and the speed of contraction
also affect the type of adaptation and, therefore, the
ability to perform different types and speeds of move-
ment. Therefore, when performance requires concen-
tric movements in single or multijoint actions, then
the training load should be applied concentrically for
maximum return for the time invested. Likewise, when
eccentric contractions contribute to muscular perfor-
mance, then eccentric loads should be incorporated into
the training prescription.28 However, caution should
be used in the prescription of eccentric exercise, since
delayed-onset muscle soreness (DOMS), which occurs
24 to 72 hours later, can severely limit training time and
enthusiasm.29,30 Therefore, to minimize the effects of
DOMS, eccentric loads should be applied gradually and
used in combination with concentric contractions and
proper preparation (the preparation principle), and
recovery strategies should be employed (the recovery
principle).
365
Even though significant tension can be imposed on
muscle in isometric modes, the adaptations are specific to
the joint angle trained, and less improvement is evident
at joint angles further removed from the training angle.
However, during rehabilitation, this type of training can
elicit significant changes at points in the range of motion
that are limiting performance because of injury.
The velocity of contraction also elicits changes that are
specific to the speed, such that resistance training at low
velocity produces the greatest changes in low-velocity
strength, whereas high-velocity training elicits maximum
benefit at high-velocity contractions. The transfer of
training from one speed to another is less clear, but
high-velocity training has been shown to provide more
improvement at low velocity than vice versa. The neural
mechanism behind this has yet to be determined. For
maximum benefit in performance that involves speed-
or velocity-specific requirements, the training stimulus
should be applied at or above the required velocity.31
Stimulus Principle
Many characteristics of the exercise load act as stimuli
for both the type and magnitude of training effects.
The characteristics are intensity (i.e., speed, resistance),
duration of the exercise session, frequency (number of
sessions per week), length (number of weeks or months),
pattern (continuous versus interval), and mode (e.g.,
running, cycling).
Exercise Characteristics to Consider in Designing
Programs
● Intensity
● Duration
● Frequency
● Length of total program
● Pattern of activity
● Mode
Several prescriptive programs have addressed the com-
bination of these different stimuli. The fitness industry
has adopted the FITT principle, which incorporates
frequency (F), intensity (I), time (T), and type (T) of
exercise to achieve optimal levels of health and fitness for
the general public. These same stimuli are also the critical
ingredients of the adaptive process for the patient or ath-
lete. The overload that achieves a training effect is a func-
tion of the combination of these stimuli. Progressions
in the total load (volume) can be achieved by increas-
ing intensity, time, or frequency, or a combination of the
three. However, the nature of the adaptation will differ
if the volume has been increased because of changes in
366 SECTION II • Principles of Practice
intensity versus changes in time and frequency (the speci-
ficity principle). The type of exercise will depend on the
availability of equipment, the training location, and the
specificity of the adaptation required for performance.
For changes in the aerobic energy system, intensities
approaching VO2max act as a stimulus for adaptations in
aerobic power when the maximum rate of energy pro-
duction from this system is critical. However, at these
intensities, duration is limited to 5 to 10 minutes of
continuous effort. Therefore, to increase the volume
of this type of training, intermittent periods of recov-
ery must be interspersed with work intervals of 1 to
3 minutes. The intensity of these VO2max intervals can
be monitored by measuring heart rate and ensuring that
it is maintained within five beats of maximum during
the training interval. The heart rate during the recovery
interval must be allowed to decrease to 30 beats per min-
ute below maximum heart rate.1 In the early stages of this
type of training, four to five intervals may be completed.
The number of repetitions can be progressed to 8 to 10
over the training year. For training aerobic capacity, in
which changes in the total volume of energy from the
aerobic system, improvements in cardiovascular function,
and high levels of caloric expenditure are desired, then
lower intensity (70% to 85% maximum heart rate) and
longer duration work (35+ min) are recommended, with
a frequency of three to six times per week.16
Way for Patients to Improve Aerobic Capacity
● Work at 70% to 85% of maximum heart rate
● Do activity for 35 minutes or longer
● Do activity three to six times/week
The intensity component for challenging the anaero-
bic energy systems is altered by increasing either the speed
of movement or the resistance. Therefore, short-term
explosive actions at either high speed or high resistance
challenge the power of either the alactic or lactic energy
supply, depending on the time interval during which
these energy supply systems are designed to be operative
(see Figure 17-5). At present, it is best to monitor these
intensities by the loads (speed or resistance) that permit
maximal effort over the appropriate time. For example,
20-meter sprints accomplished over 2.5 to 3 seconds at
maximum velocity will challenge anaerobic alactic power.
This same power can also be challenged by a maximal
effort at a relatively slow pace against high resistance
using a leg press. If repeated intervals result in a decrease
in the speed or load moved, then maximal alactic energy
supply is no longer being challenged. Thus, sufficient
recovery must be incorporated between intervals to per-
mit maximum effort, usually in a 1:6 work-to-rest ratio
(i.e., 5 seconds work to 30 seconds recovery). Recovery
should consist of either rest or very-low-intensity exer-
cise to permit replenishment of phosphagen stores.1 This
type of training should be done early in a training ses-
sion when the individual is well rested. Similarly, chal-
lenges to the lactic power should force maximal rates
of energy supply from this system, which usually occurs
at 15 to 25 seconds of all-out effort (see Figure 17-5).
Work-to-rest ratios of 1:3 or 1:4 are often prescribed to
ensure sufficient training volume.
The intensity of the load required for optimal changes
in muscular strength depends on the magnitude of the
resistance offered to the muscle. Greater resistances
require higher tension development in the muscle,
which acts as the stimulus for changes in strength.
Some evidence suggests that loads that permit 4 to 8
repetitions before failure invoke maximum strength
changes without hypertrophy, whereas loads that permit
9 to 12 repetitions stimulate changes in both strength
and muscle size.28,29 When repetitions exceed these lim-
its, the intensity (load) must be increased to provide the
optimal stimulus.
The inverse relationship between intensity and dura-
tion was outlined previously (such that with high-inten-
sity training, duration is reduced, and vice versa). The
capacity (or volume) of energy that can be produced in
any one of the systems is reflected in the amount of time
that the system can produce its energy. Therefore, the
stimulus for increasing the capacity of the alactic, lactic,
and aerobic systems is an increased duration over which
the specific system is required to provide its energy. To
extend the capacity of the alactic energy supply, intervals
of all-out effort from 20 to 30 seconds in duration must
be invoked. Similarly, the capacity of the lactic energy
supply is challenged with work intervals that exceed 45
seconds. The limits of aerobic capacity are extended
when intensity is reduced to a level sufficient to permit
1 to 2 hours of continuous activity involving large muscle
groups.
Many activities require muscle groups to perform
submaximal contractions for extended periods of time.
This capability is often referred to as strength endurance.
The stimulus is imposed by increasing the number of
repetitions to meet the performance demands. The
adaptation consists of increases in either force production
(strength) or endurance (energy supply).
The frequency of training sessions is inversely related
to both the intensity and the duration of the training
loads. When particular cells, tissues, organs, or systems
are overloaded with high-intensity training or long
durations of training, they require extended times for
adaptation, recovery, and regeneration. Therefore, the
application of repeated training sessions is an art as well
as science that requires a sense of how effectively the
individual is adapting to the training loads. In general,
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled
training sessions of high intensity or long duration
require 48 hours between sessions, but when the vol-
ume or intensity of training is reduced, the frequency
can be increased to daily or twice-daily sessions. During
periods in which the intensity, duration, and frequency
are high, periods of unloading are mandatory (the load-
ing/unloading principle) to avoid overtraining (the
overtraining principle).
The length of time (number of weeks) devoted to
developing any one fitness component depends on the
importance of that component for either performing
or training for (the performance principle) a particu-
lar occupation, activity, or sport. It also depends on how
readily the individual responds to the training stimulus
(the individualization principle) and, for competitive
sports, on the competition schedule and the level of
competition (the periodization principle).
The mode of training (type of activity) also dictates
the extent to which adaptations will affect performance.
For example, changes in the cardiorespiratory system can
be achieved through proper stimuli in a variety of activi-
ties that involve large muscle masses (running, cycling,
swimming, rowing, and skiing). These activities can be
undertaken individually or combined in the same train-
ing session (cross-training). However, if changes are
required in specific muscle groups and in specific modes
(e.g., rowing) or if maximum adaptation in that mode
(rowing) is desired, then the stimulus should be specific
to allow changes to both the central circulation and the
specific peripheral muscles.
Rest Principle
In response to a training stimulus, the components that
were overloaded will undergo some breakdown at the
subcellular, cellular, or tissue level, which will temporar-
ily lower the functional ability of the cell, tissue, organ,
or system. A rest period following exercise will allow the
body to adapt by resynthesizing the protein associated
with these components to a higher level than before
the overload.32 This building or synthesis process takes
between 12 and 48 hours depending on the intensity
(quality) of exercise and the volume (total amount) of
load. Lower intensity and lower volume training sessions
take as little as 12 hours of rest, while high-intensity
training sessions can require more than 48 hours to build
the training effect.
Recovery Period Following Exercise
● 12 to 48 hours depending on intensity of exercise and load
volume
367
If the rest phase between two training sessions is too
long, the adaptation will plateau, and performance may
level off. If the rest phase is too short, complete regen-
eration will not occur, and the athlete will train while
fatigued. It is critical to establish a balance between work
and rest to develop an effective training program.
Maintenance Principle
The training effect is fragile. If the training stimulus
is stopped, reduced, or altered, the training effect will
decline. However, the training effect can be maintained,
at least for a few months, if the frequency is reduced to
one third and the intensity and duration are maintained.33
For periods of 2 or 3 weeks, the effect can be maintained
if the duration is reduced to two thirds but the intensity
and frequency are maintained at the level that produced
the training effect.34 The training intensity is critical for
maintaining performance.35
Maintenance
● To maintain a fitness level, intensity and frequency must be
maintained. Duration can be reduced by one third.
It is often necessary during training and a competi-
tive year to change the focus of training either to some
other fitness component or to optimizing performance
for competition or for a return to the patient’s previ-
ous occupation. During these periods of time, ignoring
the previous development of a particular fitness compo-
nent will lead to decrements that can be detrimental to
performance in the long term. Therefore, the ability to
maintain established fitness levels through reduced fre-
quency or duration allows opportunities to emphasize
the development of different fitness components. For
example, when aerobic power has been developed to an
optimal level of 60 mL/kg/min through a training fre-
quency of five times per week in an elite soccer player,
VO2max can then be maintained by reducing the fre-
quency to two times per week or reducing the number
of aerobic intervals per training session to two thirds.
This will then permit the individual to focus on strength
development while maintaining this critical level of
aerobic power. Concomitantly, if strength changes are
developed through a progressive resistance program
three times per week, then the acquired levels can be
maintained with one session per week or a reduction in
the number of sets per session to one third. An example
of the reduced frequency required for maintenance of
either aerobic power or strength is illustrated in days
15 through 28 in Figure 17-6.
368 SECTION II • Principles of Practice

Figure 17-6
An example of the reduction in training frequency to maintain the training effect. Note that intensity and duration are maintained during the
period of reduced frequency; only the number of sessions changes. (From Wenger HA, McFadyen PF, McFadyen RA: Physiological principles of
conditioning. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 199, Philadelphia, 1996, WB Saunders.)

However, over periods of time longer than 8 weeks,

Interference Principle
When training for two different types of adaptations
(e.g., aerobic power and strength), the training stimuli
can interfere with one another and result in less improve-
ment in one or both of the effects. When attempting to
train two different fitness components during a meso-
cycle, there is a risk of reducing the amount of adaptation
when different stimuli are imposed during the same day
or even on subsequent days.36 It seems that the adapta-
tion to low-intensity aerobic stimuli takes less time than
the adaptation to higher intensity strength or power
training, and different motor unit types are recruited.
When strength loads are combined with aerobic training,
the aerobic adaptation is not detrimentally affected, but
there is a negative impact on strength development by
the concurrent aerobic training.36,37 When the strength
and aerobic training occur on alternate days, the adapta-
tions in strength are not impaired by the aerobic train-
ing on the previous or subsequent days over 8 weeks.
even interspersed days of aerobic and strength training
can be detrimental to strength development.38 When
strength and aerobic training are blocked into separate
training periods, there is no apparent interference effect.
However, previously achieved aerobic effects are readily
lost during subsequent strength training, but previously
acquired strength gains are not as fragile when followed
by a period of aerobic training.38
The interference effect becomes an issue when one
must train different fitness components in the same
microcycles within a training phase (research shows that
the effect is most pronounced when training strength and
aerobic fitness concurrently).36 The strength benefits are
reduced if the aerobic training precedes strength work by
up to 8 hours and occurs in the same muscle groups. It
is also likely that interference would affect high-intensity
anaerobic benefits when that type of training is preceded
by aerobic or strength work. Regardless of whether
the mechanism for the interference effect is a strain on
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled
the adaptive processes in muscle or fatigue that reduces
training volume and quality, the solution is to perform
the high-intensity work in as rested a state as possible.
Training should be scheduled so that high-intensity work
in similar muscle groups should occur 24 to 48 hours
apart, and intervening training sessions should use differ-
ent muscle groups or be low in volume. If aerobic train-
ing precedes strength training, it should be scheduled at
least 8 hours earlier or use completely different muscle
groups. If aerobic training follows strength training, then
it should involve different muscle groups and be low in
both volume (<45 min) and intensity (<70 % VO2max).39
Loading/Unloading Principle
For the body to adapt effectively to periods of progressive
overloading, it is necessary to allow the body a period of
reduced load to ensure proper recovery, effective adapta-
tions, and a reduction in the risk of overtraining. There
are a number of different ways to package the loading and
unloading periods (cycles). A common format is three
short periods (microcycles) of 1 week each in which the
loads are progressively increased, followed by a 1-week
microcycle of reduced volume and intensity (Figure 17-7).
This 4-week period has been termed a mesocycle and has
specific objectives for development of a particular fitness
component (the periodization principle).21 Additional
mesocycles for further development of the same fitness
component or a mesocycle for a transition into the
development of another component will have their own
microcycles of loading and unloading.
Although the principle of overload dictates that
progression is necessary to achieve optimal adaptations
(the optimization principle), these progressions must be
interspersed with short periods of unloading to facilitate
the adaptive process through combining physiological,
psychological, and emotional regeneration. Periods of
Figure 17-7
The sequencing of loading and unloading microcycles. (From
Wenger HA, McFadyen PF, McFadyen RA: Physiological principles
of conditioning. In Zachazewski JE, Magee DJ, Quillen WS, editors:
Athletic injuries and rehabilitation, p 198, Philadelphia, 1996,
WB Saunders.)
369
overloading interspersed with periods of recovery allow
for regeneration and improvement of physical capacity.40
Overtraining Principle
Overtraining, also referred to as overstress or staleness,
reflects an inability to recover from exercise, lowered
resistance to injury, and chronic fatigue or exhaustion.
Overtraining is caused by a loss in the body’s adaptive
capability after chronic high-volume loading or in response
to a too-large increase in either duration or intensity of
training. It is a poorly understood phenomenon that
includes such symptoms as loss of appetite, inability to
sleep, lethargy, muscle soreness, chronic fatigue, declin-
ing performance,38 and altered metabolism.41 It is not the
acute fatigue associated with a single or a few training
sessions that can be overcome by short rest, proper diet,
and adequate nutrition. This syndrome can take from
3 weeks to several months to dissipate42 and requires
dramatically reduced training loads or no training at all.
As stated in the discussion of the overload principle,
individuals must overload their cells, tissues, organs,
and systems to stimulate an adaptation. As a result of
overload, fatigue occurs owing to factors such as fuel or
substrate depletion, buildup of metabolites, pH changes,
or dehydration. This fatigue is short term, from a few
hours to a few days. At the same time, the adaptation
to the training stimulus (supercompensation) must also
occur; during adaptation, protein is synthesized to build
new structural or enzymatic protein so that the training
effect can be expressed. The recovery and adaptive peri-
ods can take from a few hours to 2 days. To elicit maximal
adaptations, a number of sports use an “overreaching”
strategy to overload, which could be applied when con-
sidering returning a patient to his or her previous level
of activity. This process involves applying training loads
before recovery and adaptation to the previous load are
completed. Because this overreaching process stresses the
adaptive capability of the organism, a breakdown result-
ing in a mild staleness will ensue and, if continued, will
result in the overtraining syndrome. The solution is to
initiate the appropriate amount of rest (the rest prin-
ciple), recovery (the recovery principle), unloading
(the loading/unloading principle), and progression
(the optimization principle) in a periodized annual plan
(the periodization principle). The use of periodization
to prevent overtraining has been reviewed by Fry et al.40
There have been a number of physiological predictors
suggested for anticipating the overtrained state; these
include increased resting morning heart rate, decreased
body weight in the hydrated state, increased recovery
heart rates after a maximal load, increased blood pressure,
increased cortisol-to-testosterone ratios, and disturbed
sleep patterns.42–44 The two most related variables are
morning resting heart rate, either in the supine position
370 SECTION II • Principles of Practice
or expressed as the difference between lying and stand-
ing heart rates,42 and the recovery heart rate following
maximal exercise. It has also been suggested that these
measures should be obtained following a recovery period
over which acute fatigue should have dissipated.40
Signs of Overtraining
● ↑ Resting morning heart rate
● ↓ Body weight
● ↑ Recovery heart rate
● ↑ Blood pressure
● ↑ Cortisol-to-testosterone ratios
● Disturbed sleeping pattern
Although Figure 17-8 depicts only an inappropriate
training stimulus contributing to the overtraining, other
stressors (e.g., psychological, sociological, and economic
factors) seem to add to the physical stress of training,
which reduces the adaptive capability of the body.45 There
are similar signs and symptoms, neurological occurrences,
endocrine pathways, and immune responses in overtrain-
ing syndrome and clinical depression.44 Therefore, it is
very important to try to keep nonphysical stressors to a
minimum during periods of high loading or to be extra
cautious of extended periods of high-volume loading
when other stressors are present.
Recovery Principle
The purpose of a recovery phase is to restore the mus-
cles and the body to preexercise levels. After training or
Figure 17-8
A model to describe the effects of excessive or optimal training
stimuli. (From Wenger HA, McFadyen PF, McFadyen RA:
Physiological principles of conditioning. In Zachazewski JE, Magee
DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 200,
Philadelphia, 1996, WB Saunders.)
competition, an active recovery promotes venous return
and removal of metabolites from muscle, reestablishment
of fluid balance, replacement of depleted fuel or energy
reserves, and relaxation in muscles that were active.
Following exercise, a short (5 to 10 minutes) low-inten-
sity cooldown (30% to 65% VO2max) will assist in main-
taining venous return and removal of metabolites above
levels in passive rest.46–48 The ingestion of fluids (water,
electrolytes, and up to 20% carbohydrate) will begin to
reestablish fluid balance,49 and carbohydrate-rich foods
will assist in rapid replenishment of glycogen stores.50
A rest period is also necessary to replenish muscle
glycogen following prolonged exercise of a continuous or
interval nature. The rate of replenishment differs depend-
ing on the extent of depletion, the type of exercise, and
the amount of carbohydrate available, as well as the time
of carbohydrate intake after exercise.
Following prolonged continuous or intermittent work,
supplementation of antioxidants such as ascorbic acid
(vitamin C), α-tocopherol (vitamin E), and β-carotene
(vitamin A) has been shown to be effective in removing
waste products of oxidative stress (free radicals).50,51
Various modalities such as massage, hydrotherapy, and
electrostimulation have been used to enhance recovery,
with anecdotal but little scientific support. Athletes feel
better recovered after massage even though blood lactate
levels are the same or higher after massage than after passive
rest.47,52 However, cold baths, massage, and active recov-
ery have been shown to be equally effective in hastening
recovery from high-intensity intermittent activity.53
Stretching techniques have been used to alter the
range of motion (ROM) around a joint, either acutely or
chronically. In addition, they have been used after exer-
cise to decrease muscle tension and facilitate recovery via
increased blood flow. The three most common stretching
techniques are ballistic stretching (rapid changes in length
to the end of the ROM), static stretching (SS) (passive
stretching to the end of the ROM), or proprioceptive
neuromuscular facilitation (PNF). There are two primary
types of PNF stretching: contract-relax (CR), in which
the targeted muscle is contracted isometrically and then
relaxed while it is stretched passively to the end of the
ROM, and contract-relax–agonist contract (CRAC), in
which CR stretching is performed as previously described,
followed by contraction of the agonist muscles to assist in
the stretching of the targeted muscles to the end of the
ROM. In both PNF techniques, clinicians often increase
the stretch torque. Ballistic stretching has been shown to
be ineffective if not counterproductive for ROM,54,55 but
it may have some use as the patient returns to functional
levels for his or her occupation. The SS technique has been
shown to decrease muscle contraction on the electromyo-
gram (EMG) to a greater extent than CR and CRAC.56
Thus, for postexercise recovery, the SS is the technique
that should be employed. It should be noted, however,
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled
that for acute increases in ROM, both SS and CRAC are
equally effective, while the CRAC is most effective for
long-term chronic increases in the ROM.55 This is prob-
ably due to a reduction in other components of muscle
stiffness other than the contraction as reflected by EMG.
Therefore, for one-time increases in ROM before exer-
cise, either SS or CRAC is preferred, whereas CRAC is
the method of choice for chronic increases in flexibility.
Recovery is a multidimensional process that requires
the athlete to get plenty of rest, eat a balanced diet, and
do a proper cool-down and stretching after an activity to
facilitate faster restoration.
Preparation Principle
It is important to be properly warmed up and stretched
before training and competition. The purpose of the
warmup is to elevate the temperature of muscle, blood,
and connective tissue to both enhance performance and
protect against soft tissue injury. Stretching also assists in
relaxing the muscle to permit improved blood flow and
neural activation, although peak force may be reduced.
A warmup involves low-intensity exercise (<60%
VO2max or 70% maximum heart rate) of relatively short
duration (<15 minutes). The primary purpose of a warmup
is to increase core temperature (1° to 2° F) and muscle tem-
perature (up to 5° F), which should do the following:57–59
1. Enhance the rate of both muscular relaxation and
contraction.
2. Lower the viscous resistance in the muscle and
therefore increase mechanical efficiency.
3. Allow hemoglobin and myoglobin to dissociate
more oxygen at the working tissue.
4. Decrease the resistance in the vascular bed through
vasodilation.
5. Increase nerve conduction velocity.
6. Decrease the risk of electrocardiogram (ECG)
abnormalities.
7. Increase the rate of the metabolic processes.
All of these physiological changes have the potential to
enhance performance. However, if the exercise intensity is
too high, the duration is too long, or the recovery period too
short, performance may be negatively affected by fatigue.59
Warmup should be sufficient to enhance VO2 at the onset
of performance but light enough to prevent fatigue.
There are three main types of warmup: passive, gen-
eral, and specific. A passive warmup involves increasing
core temperature by external means such as a hot tub,
shower, or massage. This type of warmup does not pro-
duce a significant change in blood flow or blood redistri-
bution to the working muscles, but swimmers have used
this technique before a swimming event when a warmup
is not available.58 A general (unrelated) warmup involves
performing movements that are not directly associated
with the muscle movements and neural recruitment per-
371
formed during the activity.60 A specific or related warmup
is the most common type. This procedure involves per-
forming movements similar to the activity the individual
performs. The type of warmup chosen depends on the
individual, occupation, type of activity, and facilities.
Types of Warmup
● Passive
● General
● Specific
A 5- to 10-minute warmup at 40% to 60% of VO2max
appears to be ideal for short-term performance. A rest
period of 5 minutes should be allowed for sufficient
recovery before performance. For intermediate or long-
term performance, a 5- to 10-minute warmup at 60% to
70% of VO2max is appropriate and should end less than
5 minutes before the start of performance.59
Ballistic or dynamic stretching is often referred to a spe-
cific warmup and is performed during the preparation phase
before work, training, or competition. Dynamic stretching
prepares the muscle for the range of motion demanded dur-
ing the activity, temporarily elongates the muscles, increases
the range of motion about a joint, and stimulates neural
activation. In addition to being warmed up and stretched,
it is necessary for the muscle to be properly hydrated, and
fuel stores must be replenished before competition or train-
ing. Adequate hydration facilitates transportation of fuels,
removal of wastes, and regulation of body temperature.
In sports, 24 hours before competition, 2 to 3 L of water
should be ingested, with up to 2 L of water ingested 2 hours
before the event.50 Similarly, a well-balanced diet high in car-
bohydrates should be eaten 24 hours before competition to
replenish energy stores, and a pregame meal should be eaten
4 hours before competition to supply additional energy dur-
ing endurance events or prolonged intermittent work.50
Taper Principle
Training sessions result in subcellular, cellular, and tissue
breakdown as well as acute fatigue. Even though a train-
ing effect is being established in response to the train-
ing session, its expression in improved performance can
be masked by short-term fatigue caused by a depletion
of energy stores, dehydration, metabolite accumulation,
or acidity changes resulting from lactic acid and ammo-
nia production. Therefore, it is difficult to produce high-
quality performances during heavy training. However, if
the individual stops training to reduce fatigue, the training
effect will also begin to decrease. Therefore, to elicit peak
performance, the fatigue must be alleviated but the train-
ing effect maintained (Figure 17-9). Fortunately, fatigue
372 SECTION II • Principles of Practice
has a much faster decay time than the training effect.42,61
Thus, to remove the fatigue, the volume of training (dura-
tion and frequency) should be reduced while maintaining
the training effect by holding the intensity of the training
load constant.62 The reduction in volume should be done
progressively 7 to 14 days before competition (Figure
17-10).62,63 Volume should be decreased 50% over the
taper,64 and the program should include high amounts of
carbohydrate and fluid in the diet along with good sleep
and rest.64,65 Because this protocol reduces fatigue while
attempting to hold the training effect at its present level, it
does not build improvement. The taper is achieved at the
expense of training; therefore, priorities for tapering should
be set for those competitions that are most important to
permit both optimal training and peak performance.
This principle has also been adapted in practice in
sports that have an extended competitive season (6 to
8 months) in which games or competition occur two to
three times per week. The highest volumes of training
are imposed as soon as possible after the previous per-
formance. In the days approaching the next competition,
the volume of work is then reduced while intensity is
established at competition levels.
Evaluation/Monitoring Principle
Training programs are designed with specific objectives. It
is therefore necessary to regularly assess whether the pro-
grams have been effective so that they can be progressed
or altered. This evaluation can consist of sophisticated
laboratory testing with a high degree of precision or,
at times, less rigorous but still effective field tests.66 In
either case, it is necessary to take as much care as possible
to make the conditions (e.g., time of day, testing location
and environment, equipment, calibration, and personnel)
Figure 17-9
The growth and decay of fitness and fatigue in response to impulses
of training on separate occasions. (From Wenger HA, McFadyen
PF, McFadyen RA: Physiological principles of conditioning. In
Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 201, Philadelphia, 1996, WB Saunders.)
Figure 17-10
A figure that represents the reduction in training volume with the
intensity varying (hard day/easy day) during a taper before the
competition. (From Wenger HA, McFadyen PF, McFadyen RA:
Physiological principles of conditioning. In Zachazewski JE, Magee
DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 201,
Philadelphia, 1996, WB Saunders.)
as similar as possible at all testing sessions to ensure reli-
ability. For a list of fitness tests, protocols, and normative
values, refer to MacDougall et al.67 and Heyward.68
An effective testing program provides an evaluation
of the person’s strengths and weaknesses as they pertain
to work, sport, or activity; baseline data before train-
ing; a measure of effectiveness of the training program
prescription; an index of the health status; and a unique
means for educating an individual about his or her physi-
ological makeup and individual response to training.66
Although a single test that provides a profile of the fitness
level in selected components is often of interest, repeated
tests that bracket specific training (or competition) periods
throughout the year or across many years will provide a
more in-depth picture of the effectiveness of programs and
the uniqueness of each individual’s response to the train-
ing environment. To provide an objective means of quan-
tifying training changes, testing and evaluations should be
occupation, sport, or activity specific; valid and reliable;
and administered by qualified personnel. Laboratory tests
that isolate specific fitness components do not often per-
mit evaluation in performance-specific modes of exercise.
However, they do offer precision and an assessment of a
specific physiological characteristic. When they are com-
bined with performance- or activity-specific field tests, the
two types of tests will provide a more complete picture of
both the isolated components and their application in an
activity-specific environment. However, where possible,
the laboratory tests should utilize exercise modes that
challenge the person’s physiology as closely as possible to
 CHAPTER 17 • Physiological Principles of Conditioning for the Injured and Disabled 373

the sport-specific demands that he or she will encounter.
Specific examples of testing procedures for the different
components of fitness have been documented.67
When choosing a testing battery, the location, facili-
ties, cost, personnel, and information desired must be
considered. Regardless of what types of tests are chosen,
it is important to standardize the testing conditions at all
testing sessions to ensure reliable results.
Periodization Principle
The training and competitive periods within a year must
be organized and sequenced with specific goals and
objectives to permit effective development of the appro-
priate fitness components (the fitness principle) as well
as the other factors that determine performance (the
performance principle). This chapter focuses on the
physiological factors, but the clinician must sometimes
consider the integration of all factors.
A yearly training program is divided into different
phases characterized by changes in the goals, objectives,
tasks, and contents, as well as training volume and inten-
sity (Figure 17-11). The classic model of periodization
was developed by Mateveyev and incorporates the fol-
lowing training phases: preparation, competition (func-
tional), and transition. Each of these phases has been
termed a macrocycle. Macrocycles outline the opti-
mal training sequence for a 1-year program.21,40,69 Each
macrocycle has specific goals: the preparatory phase
focuses on developing both general fitness and occupa-
tion-specific or sport-specific training; the competition
or functional phase focuses on improving the individual’s
performance and prepares him or her to peak for minor
and major activities or competitions; and the transi-
tion phase, which usually lasts between 2 and 6 weeks,
allows both psychological and physiological regeneration
through rest and active recovery. When planning each of
these cycles, the following factors should be considered:
1. Goals of the individual and clinician, or athlete,
team, and coach
2. The length of the competition schedule and num-
ber of competitions or what the individual will be
doing functionally
3. The individual’s stage of development

Figure 17-11
Yearly training model. (From Wenger HA, McFadyen PF, McFadyen RA: Physiological principles of conditioning. In Zachazewski JE, Magee DJ,
Quillen WS, editors: Athletic injuries and rehabilitation, p 203, Philadelphia, 1996, WB Saunders.)
374 SECTION II • Principles of Practice
By allotting the appropriate amount of time for each mac-
rocycle, there will be adequate time to train all physiologi-
cal components of the activity and peak for performance,
although this may not be possible in a single training year.
Macrocycles are divided into smaller segments called
mesocycles. These cycles along with microcycles (dis-
cussed next) are of more interest to the clinician when
treating individual patients. Mesocycles allow the indi-
vidual/clinician to structure periods of progressive over-
load by increasing training volume and incorporating
periods of reduced training to facilitate regeneration. An
average mesocycle lasts 2 to 5 weeks, during which spe-
cific training objectives are achieved. For example, for
a track runner, one mesocycle may focus on improving
aerobic power at the beginning of a season, and another
mesocycle may focus on improving starts from the
blocks. Mesocycles incorporate the loading/unloading
principle, with the first few weeks focusing on develop-
ment, the next one on super loading, and the last week
on recovery (see Figure 17-7). Complete regeneration
does not necessarily occur at the end of each mesocy-
cle. The accumulation of fatigue over time can facilitate
training adaptations but must not violate the overtrain-
ing principle. It is important to plan each cycle for each
individual as well as for the team to allow time for the
individual to adapt to the training stimulus and to make
a smooth transition from one cycle to the next.
Mesocycles are subdivided further into microcy-
cles.21,40 Microcycles are training periods of up to 7 days
in duration. Microcycles allow the clinician to coordinate
training in conjunction with all other factors that may
influence the injury, training, and performance (the per-
formance principle), as well as unforeseen occurrences
in the everyday life of the individual. The sequence of
loading can change daily throughout the cycle, and the
same microcycle may be repeated two to four times
throughout a mesocycle. Incorporated into the micro-
cycles are rest and recovery days (the rest principle) to
permit optimal adaptations to the training stimulus.
Some training personnel have modified this termi-
nology for the hierarchy of training cycles (i.e., macro-,
meso-, and micro-), but the principles are consistent
and should be considered by the clinician when treating
patients. Presently, the traditional macrocycles are often
termed phases; the term mesocycle is used to depict the 2- to
5-week specialized training periods; and the term micro-
cycle is still used to describe up to 1-week training blocks.
Conditioning Guidelines
The following list summarizes the steps the clinician
should take to integrate the principles of conditioning:
1. Decide which factors (see Figure 17-1) affect
the optimal functional level and performance
of the individual (the performance principle).
Prioritize these factors.
2. Based on the unique physical demands of the indi-
vidual’s occupation, activity, or sport, determine
the specific fitness components (see Figure 17-2)
that must be developed (the fitness principle).
Prioritize each component.
3. Decide on the optimal level of fitness required in
each fitness component for the individual to func-
tion optimally in his or her occupation and daily
activities (the overload principle, the underload
principle).
4. Periodize the training calendar for work and com-
petitions, including general and specific prepara-
tion (the periodization principle).
5. For each microcycle, decide on the type of overload
(the optimization principle). Decide on individual
requirements (the individualization principle);
select the appropriate stimulus (the progression
principle, the variety principle, the skill principle,
the specificity principle, and the stimulus princi-
ple); and allow appropriate rest (the rest principle),
preparation (the preparation principle), and recov-
ery (the recovery principle).
6. Decide on the progression to the next micro-
cycle and the appropriate unloading within the
mesocycle (the loading/unloading principle).
Be aware of the interference effect when training
more than one fitness component (the interfer-
ence principle), and remember that unloading
and varying training is critical to optimize perfor-
mance, reduce overuse injuries, and avoid over-
training (the variety principle, the unloading
principle, and the overtraining principle).
7. Following each mesocycle, evaluate or monitor
the components that were emphasized (the eval-
uation/monitoring principle).
8. When training emphasis shifts to another com-
ponent, maintain previously acquired effects (the
maintenance principle).
9. Evaluate the status of the patient/client for each
of the fitness components (the evaluation/mon-
itoring principle).
10. As return to functional activity approaches, reduce
the training volume (the taper principle).
11. Apply both skills and art in rehabilitation accord-
ing to these scientific principles to help patients/
clients return to optimal functional levels.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the references source and access it on line whenever
possible. There are a total of 69 references for this chapter.

P RINCIPLES OF N EUROMUSCULAR
C ONTROL FOR I NJURY P REVENTION
AND R EHABILITATION
Terese L. Chmielewski, Timothy E. Hewett, Wendy J. Hurd, and Lynn Snyder-Mackler
Introduction
The neuromuscular system is responsible for the coordi-
nated muscular activity that provides dynamic joint stability,
assists in postural control, and produces optimal movement
patterns. It relies on complex interactions between sensory
organs, the central and peripheral nervous systems, and
skeletal muscle to produce this coordinated muscle activ-
ity. Most of the time, the complex interactions result in
our ability to effectively complete our chosen tasks.
Sometimes, however, there is dysfunction in a com-
ponent of the neuromuscular system. Dysfunction in
the neuromuscular system is also referred to as altered
or decreased neuromuscular control. Neuromuscular
control impairments can change movement patterns and
increase the risk for musculoskeletal injury. Conversely,
musculoskeletal injury, by disrupting the interactions
within the neuromuscular system, can be a cause of
altered neuromuscular control.
The purposes of this chapter are to (1) review the
function of the sensorimotor system and how it contrib-
utes to neuromuscular control; (2) explain the theories,
classification, and stages of motor skill development; and
(3) describe the components, development, and imple-
mentation of a neuromuscular training program.
The Sensorimotor System
Sensory receptors in the neuromuscular system are
referred to as mechanoreceptors and are responsive to
18
C H A P T E R
various forms of mechanical deformation, including ten-
sion, compression, and movement. Sensory (or afferent)
information gathered by mechanoreceptors is sent to
the spinal cord by afferent pathways for processing and
ultimately results in a regulation of reflexes and muscle
activity (Figure 18-1). There are four mechanorecep-
tors located in the soft tissues in and surrounding a joint
(joint receptors)1–5 and two mechanoreceptors located
within the musculotendinous unit6 (muscle receptors;
Table 18-1). In addition, there are cutaneous (skin)
receptors that contribute to the ensemble of informa-
tion the central nervous system processes. There is, how-
ever, no evidence that cutaneous receptors contribute
to dynamic joint stability.7 In this section, we focus on
the role of mechanoreceptors in neuromuscular control
at the knee joint, although the concepts apply to other
joints in the body. The distribution and concentration of
joint receptors, however, vary from joint to joint.
Proprioception and postural control are two
components of neuromuscular control that depend
on afferent input. Proprioception is a product of sen-
sory information gathered by mechanoreceptors.8 This
definition views proprioception primarily as a sensory
activity. More recently, authors have expanded the defini-
tion of the proprioceptive system to include the complex
interaction between the sensory pathways and the motor
pathway9 (efferent system; see Figure 18-1). Joint move-
ment sense (kinesthesia) and joint position sense are
physiological processes in the sensorimotor system and
375
376 SECTION II • Principles of Practice

are often described by the term proprioception.10 Postural

Efferent nerve
Spinal cord (to muscle fibers) control (or balance) results from an integration of visual,
vestibular, and proprioceptive inputs.11,12 Therefore,
any disruption in mechanoreceptor input, which affects
proprioception, negatively affects posture.
Joint and muscle receptors play a significant role in the
modulation of extrinsic muscle stiffness13,14 and consequently
may contribute to dynamic joint stability. Muscle receptors
Afferent nerve
directly contribute to muscle stiffness modulation through
two mechanisms: (1) force feedback, which is modulated
Stretch receptor by the Golgi tendon organs;15–17 and (2) length feedback,
which is mediated by the muscle spindle pathway and facili-
Muscle spindle tates motor activity.6,18,19 Two possible mechanisms have also
been proposed for joint receptors in the contribution to joint
stability. The first mechanism is a direct “ligamento-muscu-
Golgi tendon
organ (GTO)
lar protective reflex.” This mechanism has been questioned
because the resulting muscular output is inadequate to pro-
tect against joint injury.20–22 The second mechanism is that
joint receptors indirectly contribute to dynamic joint stabil-
ity. Johansson and Sjölander23 found evidence of a direct link
Figure 18-1 between the afferent nerves of the cruciate ligaments and the
Schematic of sensory receptors gathering information, pathway of muscle spindles in a series of cat experiments. Johansson14
information along afferent pathways (from muscle spindle – activated proposed that because primary muscle spindles participate in
by muscle stretch and Golgi tendon organ – activated by tendon
the regulation of muscle stiffness, the joint receptors prob-
compression due to muscle contraction) to spinal cord, and returning
commands along efferent pathways. ably contribute to preparatory adjustments (also referred to

Table 18-1
Mechanoreceptors in the Sensorimotor System
Response to
Receptor Activation Persistent
Type Location Sensitive to Activated Threshold Stimuli

Joint Receptors
Ruffini endings Capsule and ligaments Joint position Static or dynamic Low Slowly adapting
Intra-articular pressure
Amplitude of movement
Velocity of movement
Pacinian corpuscles Capsule and ligaments Acceleration or Dynamic only Low Rapidly
deceleration adapting
Golgi-Mazzoni Joint capsule Compression Compression Low Slowly adapting
corpuscles applied
perpendicular to
inner surface
Golgi tendon Ligaments Tension in ligaments Dynamic only High Slowly adapting
organ–like (especially end range
of motion)
Free nerve endings Capsule and ligaments Pain from mechanical or Presence of noxious High Slowly adapting
chemical origin stimuli (static
or dynamic)
Muscle Receptors
Golgi tendon organ In series with Muscle force Muscle Low Slowly adapting
musculotendinous contraction
junction
Muscle spindle Parallel to muscle Joint position and Muscle stretch Low Slowly adapting
fibers velocity throughout and acceleration
range of motion
 CHAPTER 18 • Principles of Neuromuscular Control for Injury Prevention and Rehabilitation 377

as presetting) of muscle stiffness and dynamic joint stability.

Practice and past experiences influence the timing and type
of preparatory adjustment made.

Muscle Stiffness Is Modulated by

● Force feedback (Golgi tendon organs)
● Length feedback (muscle spindle)

Motor responses depend on the level of processing of

afferent inputs in the central nervous system. The pro-
cessing can occur at three different levels: the spinal cord,
the brain stem and cerebellum, and the cerebral cortex24
(Table 18-2). The level of processing affects the speed
of motor responses. Spinal reflexes represent the short-
est neuronal pathways, and consequently the most rapid
responses to afferent stimuli. The speed of spinal reflexes
is faster than ligamentous failure, yet such reflexes are not
considered modifiable through training to aid in dynamic
joint stability.25,26 In contrast, sensory information medi- Figure 18-2
ated at the brain stem, cerebellum, and cortical levels Interaction between injury, neuromuscular control system, and
includes longer pathways and slightly slower responses. resultant movement dysfunction.
Studies have shown sensory input processed at central
nervous system levels above the spinal cord level can be Methods of Motor Control
modified with training.25–27 Because of the speed and
Motor control can be classified based on the contribution
adaptability of the responses mediated at the brain stem
of the sensory system to movement. A movement that is
and cerebellum, these pathways are thought to be impor-
brief, predictable, and produced in an unchanging environ-
tant in the maintenance of dynamic knee stability.28
ment does not require sensory information for modifica-
After injury, the complex interactions in the neuro-
tion. These movements are said to be under open-loop
muscular system are disrupted and many different prob-
control (a type of control that involves the use of centrally
lems can occur, including diminished kinesthesia and
determined, prestructured commands sent to the efferent
abnormal patterns of muscle activity. Because the neuro-
system and executed without feedback; Figure 18-3).26
muscular system is highly dependent on normal afferent
Writing one’s name on a piece of paper is a movement that
input from muscle and joint receptors, a change in or
is performed under open-loop control. On the other hand,
loss of this input affects motor responses and propriocep-
movements that rely on feedback from the sensory system
tion, and consequently postural control, dynamic joint
are considered to be under closed-loop control because of
stability, and movement will be changed (Figure 18-2).
the feedback loop formed between sensory information, the
Rehabilitation efforts must therefore be directed toward
intended action, and the final movement (see Figure 18-3).
creating an environment that promotes the restoration
Simple, reactive movements, such as when one reflexively
and development of motor responses and proprioception
withdraws the hand after touching a hot stove, are consid-
in the presence of altered sensory input.
ered to be under closed-loop control. In this example, the
intended action is to put one’s hand on the stove; however,
the heat of the stove activates thermoreceptors that provide
Table 18-2 feedback to change the movement from reaching toward
Motor Response Intervals the stove to withdrawing the hand away from the stove.
Motor Level of Able To Other movements, like using a computer mouse, are more
Response Type Mediation Be Modified complex, but still rely on feedback from the sensory system
to shape the movement as it is being performed.
Spinal reflexes Segmental level of No
spinal cord
Long-loop reflexes Brainstem and No Motor Control Methods
cerebellum
Triggered reactions Cortical centers Yes
● Open loop
Voluntary reactions Cortical centers Yes
● Closed loop
378 SECTION II • Principles of Practice
Figure 18-3
Diagram illustrating feedforward and feedback contributions to the
control of movement. (Modified from Williams GN, Chmielewski T et al.:
Dynamic knee stability, current therapy and implications for clinicians and
scientists, J Orthop Sports Phys Ther 31(10): 546-566, 2001.)
Theories of Motor Control
The motor skills we perform daily pose a complicated
problem for the neuromuscular system because many
muscles crossing multiple joints must be coordinated
to produce a given outcome. Bernstein29 called this the
“degrees of freedom problem.” That is, there is almost
an infinite number of strategies available to execute the
simplest of tasks. The problem the neuromuscular sys-
tem must overcome is choosing the most appropriate
strategy, based on both movement efficiency and suc-
cessful task completion. It would be a problem from a
clinical standpoint if it were necessary to teach individ-
uals how to control every single muscle and joint when
performing a movement or task. Fortunately, this is
not necessary, and two predominant theories have
been proposed to explain how the degrees of freedom
problem is managed by the neuromuscular system.
Motor Control Theories
● Motor program
● Dynamic pattern
The first theory is based on the concept of motor
programs. The most recent update to this theory, put
forth by Schmidt and Lee,26 contends that features that
do not vary between different skills—the relative tim-
ing, force, or sequence of components—are stored in
memory as motor programs, whereas the parameters that
do vary (e.g., speed or duration) are specified according
to the task at hand. Using walking as an example, the
motor program would include the sequencing of muscle
firing and joint motion, but a parameter like cadence
would depend on the environmental demands. The rules
that form the basis for choosing specific parameters, like
cadence, are called schemas.26 Once a schema has been
developed, a person can correctly choose variations of
a parameter for successful completion of a task, even if
the task has not previously been attempted using that
variation—for example, selecting the force required to
throw a ball a new distance using that parameter varia-
tion. Practice is essential to the formation of both motor
programs and schemas.
Dynamic pattern (or dynamical systems) theory is
also used to explain how the degrees of freedom problem
is reduced.29,30 The crux of this theory is that movement
spontaneously results from the interaction between the
environment and the dynamic properties of the body,
controlled by a specific parameter. For instance, a
parameter such as a strength or range-of-motion deficit
will manifest in specific gait compensation. The inter-
action between the body and the environment assists
in forming functional synergies between muscles and
joints. Practice can, however, induce formation of new
functional synergies. In addition, if something in the
environment perturbs the body, the body will sponta-
neously return to a preferred, stable state. Because of
the self-regulating nature inherent in dynamic pattern
theory, storage of motor programs is not necessary;
however, it is important to expose the neuromuscular
system to the conditions for which a movement solution
is needed.
Research and debate will continue to fine-tune the
aforementioned theories of motor control. Quite pos-
sibly, motor control results from a combination of
aspects from both theories. Regardless, the supporting
research for these theories provides evidence that there is
simplification in the neuromuscular system for producing
movement and learning motor skills.
Motor Skill Classification
Every day we perform a variety of motor skills that
place different demands on the neuromuscular system.
To describe the demands on the neuromuscular system,
Schmidt and Lee26 developed the following classification
schemes based on specific characteristics of the motor
skills. Although it is beyond the scope of this chapter to
discuss the classification schemes in depth, it is important
to highlight those aspects that are important in creating
a neuromuscular training program.
First, motor skills can be classified by their orga-
nization. Some of the skills we perform are brief and
comprise one movement with a defined beginning and
end. These skills are called discrete skills. Reaching
to get something out of a cupboard is an example. In
contrast, other skills have a more arbitrary beginning
and end and involve a series of many movements; these
are called continuous skills. Continuous skills, such as
walking, are more complicated and longer in duration.
A continuous skill is more difficult to learn because
several different movements are required to produce
the skill.
 CHAPTER 18 • Principles of Neuromuscular Control for Injury Prevention and Rehabilitation
Motor Skill Classification
● Discrete skills
● Continuous skills
● Closed skills
● Open skills
Movement can also be categorized with respect to
the predictability of the environment. Some motor skills,
such as climbing stairs, are performed in a relatively stable
environment. These are called closed skills. Other motor
skills, called open skills, take place in an environment
that changes and is unpredictable. An example is step-
ping onto an escalator. Closed skills allow an individual
to evaluate the environment and perform the movement
without much modification. In contrast, open skills
require more cognitive processing and decision making
in choosing and adjusting the movement. Quite often,
a specific motor skill may be variably classified as either
an open or closed skill, depending on the environmental
features at that time.
Stages of Motor Skill Development
Individuals progress through three stages as they learn a
new motor skill. Initially, a new task requires great con-
centration, and performance is variable and filled with
errors; this has been termed the cognitive stage.31 During
this stage, movements appear to be stiff or rigid while
the individual is acquiring new motor skills.29 The second
stage is called the associative stage. In the associative
stage, less time is spent thinking about every detail; how-
ever, the movements are not yet automatic. Movements
begin to look smoother and are more consistent. The
associative stage begins when the learner has determined
the most effective way of doing a task. After practice,
when movement becomes more automatic and efficient,
the learner has reached the autonomous stage.31 The
autonomous stage is reached when learning is almost
complete, although an individual can continue to refine
the skill through practice. This stage is called autonomous
because the learner no longer needs to depend on feed-
back from an instructor.
Motor Skill Development Stages
● Cognitive stage
● Associative stage
● Autonomous stage
In rehabilitation, patients are often in the associative
stage because they are familiar with the skills they need
to perform, but movement for a particular skill may
379
be altered and need to be relearned because of neuro-
muscular dysfunction. For example, a patient with gle-
nohumeral instability often demonstrates the ability to
perform activities of daily living (ADLs), but with altered
glenohumeral and scapular stabilization strategies. This
patient would be in the associative stage of learning until
he or she can demonstrate normalized stabilization strat-
egies during all ADLs. Sometimes, however, skills may
be novel, such as providing dynamic stability to a joint
after a ligament rupture or performing a lateral step-
down exercise. In contrast, healthy individuals training
to prevent injury are often in the autonomous stage of
learning for a particular task, but may need to refine
their movement to minimize injury risk. By identifying
the correct stage of learning, clinicians can manipulate
certain variables such as the type of exercise performed
or the type of feedback provided to enhance motor skill
development.
Factors that Influence and Enhance
Motor Skill Development
Practice Conditions
According to the “specificity of practice principle,” motor
performance is superior when practice conditions match
the conditions in which the motor skill will be used.26
In particular, visual and environmental context condi-
tions, as well as characteristics of the person, should be
mimicked. Vision should be allowed during practice only
if it is available during the performance environment.
Similarly, individuals should ideally practice in their per-
formance environment and with the same physical (e.g.,
fatigued), mental, and emotional demands encountered
during performance. It is particularly important to imi-
tate the changing environment (which can be unpredict-
able and challenging, yet most closely resemble daily and
sporting environments) present in open skills. Because
creating practice conditions that exactly match the
performance environment is often difficult in rehabilita-
tion, it is sometimes necessary to involve family members
or other professionals (e.g., athletic trainers, coaches, or
personal trainers) to assist with practice in the perfor-
mance environment.
The design of practice sessions can greatly affect how
well a new skill or movement is learned. Practice sessions
may be blocked, such that a particular skill or specific
component of a skill is practiced repeatedly before going
on to the next skill, or they may be set up in a random
fashion so that different motor skills are practiced inter-
changeably throughout a practice session.26 As an exam-
ple, dribbling and shooting are motor skills needed by
a basketball player. In blocked practice, dribbling and
shooting would be practiced separately and sequentially,
allowing the player to concentrate on one skill at a time.
380 SECTION II • Principles of Practice
Enhancement of Motor Skills
Practice
● Blocked
● Random
● Constant
● Varied
External (Augmented) Feedback
● Knowledge of results
● Knowledge of performance
● Verbal
● Visual
● Auditory
● Timing
In random practice, the athlete may rotate between drib-
bling and shooting several times within a single practice
session. In each case, the same skills would be practiced,
but the order of presentation would differ. Blocked
practice has been shown to promote better initial per-
formance when subjects are in the first stage of learning
a new skill. However, random practice has been found
to promote enhanced long-term learning, meaning that
there is better skill retention when subjects perform the
skill again at a later date.32
A particular skill may also be practiced in differ-
ent ways. Constant practice is when a skill is practiced
repeatedly without changing anything, and varied prac-
tice is when a parameter is changed throughout the prac-
tice session.26 Using the skill of shooting in basketball
and the parameter of distance, shooting only from the
foul line would be an example of constant practice, and
varied practice would involve shooting from the foul
line, the perimeter, and under the basket. Varied practice
helps individuals learn how to select parameters for tasks
(i.e., develop schemas), promoting competence in differ-
ent contexts.26
A combination of random and varied practice, with
characteristics similar to the target context, is thus opti-
mal for motor learning. Random practice allows a mem-
ory of a particular skill to be formed, and varied practice
promotes the development of movement variations that
may carry over to tasks not previously attempted. Finally,
emulating the characteristics inherent to the target con-
text improves the transfer of performance from practice
to the target context.
External Feedback
Feedback from sources outside the body, such as instruc-
tion from a clinician, is external or augmented feedback.
Different aspects of external feedback can influence how
quickly or how well a motor skill is learned. A great deal
of research has been conducted in this area, so only a
synopsis of the salient points is presented.
External feedback can be given either about the
success of an individual in performing a motor skill
(knowledge of results) or about the quality of move-
ment (knowledge of performance).26 Receiving the
result of hop or isokinetic testing is an example of
knowledge of results, whereas being told the knee was
in a valgus position while performing a lateral step-
down is an example of knowledge of performance. Both
types of feedback can enhance motor skill development,
but knowledge of performance better facilitates motor
skill learning.33,34 Knowledge of results should primarily
be reserved for instances when individuals are unable
to generate this type of information themselves or
the when the information may serve as a motivational
tool.26
External feedback may be given using different formats
or sensory pathways: verbal, visual, or auditory. Verbal
feedback may include information about the errors dur-
ing performance and possibly instructions for correcting
the error. Instructions for error correction are helpful in
the beginning stage of learning, but statements that only
point out the errors may be sufficient in later stages of
learning.33 Providing visual feedback using videotape can
be beneficial if the critical components of performance
are easily observable. Beginners will benefit most if an
instructor is present to point out critical components
while the videotape is viewed. Auditory feedback is less
common and requires that a sound be linked to perfor-
mance. All three forms of feedback have been used effec-
tively to decrease peak vertical ground reaction force in
landing from a jump.35
The timing of feedback can also be manipulated.
Feedback about performance may be given while an indi-
vidual performs the task or after the task is completed.
Both can be beneficial, but it is important to note that
if feedback is given during performance, it must draw
individuals to critical information they can gain from the
task itself; otherwise, the learner becomes dependent on
the external feedback.26 Dependency on feedback also
occurs if feedback is given after every single practice trial.
Either giving a summary after multiple trials or giving
feedback only if performance falls outside of an accepted
window reduces feedback frequency and enhances skill
learning.26
In conclusion, external feedback should be tailored
to the complexity of the task and the experience of the
learner. If the learner is experienced, external feedback
may not be necessary because the individual has an
awareness of what constitutes successful skill execution.
However, if the learner is new to the skill, external feed-
back should be provided, but it must be monitored so
that a dependency is not fostered.
 CHAPTER 18 • Principles of Neuromuscular Control for Injury Prevention and Rehabilitation 381

Development and Implementation of a Most movement impairments are identified clinically

through observational analysis. Observational analysis,
Neuromuscular Training Program although readily available, requires that the clinician be
Factors That May Limit Training Effectiveness knowledgeable about what constitutes proper movement.
Considering the vast number of skills we perform during
Maximum benefits from participating in a neuromus-
daily and athletic activities, rehabilitation specialists may
cular training program may be realized if participants
find it useful to consult current literature for guidance
initiate training with minimal or no physical limita-
during skill evaluation.
tions. Before initiating a neuromuscular training pro-
In addition to observation analysis, other techniques
gram, individuals must have adequate muscle strength
may be used to evaluate neuromuscular control deficits,
to perform training exercises correctly. Muscle weak-
including electromyography, balance assessment devices,
ness is common postinjury and directly influences
strength testing equipment, and movement analysis.
movement patterns, which may impede correction of
These techniques are not always readily available to
the movement impairment until strength deficits or
clinicians, but they provide a more objective means of
imbalances are addressed.36 A solid strength base is
quantifying components of the neuromuscular system.
preferred for uninjured individuals participating in an
injury prevention program. However, if weakness is
present, training activities may begin at a more baseline
level to ensure that correct technique is being used. Factors Affecting Motor Learning
Examples of baseline-level training activities include ● Proper assessment
weight training, technique instruction, and perform- ● Training method
ing single-plane versus multi-plane movements. Poor
endurance can also interfere with the development of
successful neuromuscular control strategies. Studies
have demonstrated that muscular fatigue, in general, Training Methods
can adversely alter sensory input, resulting in altera-
A variety of training methods are available to clinicians
tions of proprioception and movement.37–43 What has
for use in neuromuscular training programs. The training
not been determined from studies evaluating proprio-
methods can be used in isolation, but typically they are
ception and movement after fatigue protocols is how
used in combination in a neuromuscular training program.
the role of small changes (a matter of a few degrees)
All training methods provide a stimulus to improve neuro-
in proprioception may affect outcomes in clinical and
muscular control; however, the stimulus may be initiated
sports settings.
by the patient or by an external force. The many training
For those individuals who have been injured and are
techniques differ in the demands they place on the neu-
participating in a neuromuscular training program as a
romuscular and musculoskeletal systems; therefore, the
component of their rehabilitation, there are additional
stage of motor learning and the phase of rehabilitation
barriers that must be resolved to benefit maximally from
(e.g., acute, controlled motion, return to function, return
training. Joint effusion, limited range of motion, and
to high-demand activities49) dictate the appropriateness
pain are common after injury and surgery.44–48 Presence
of a neuromuscular training technique. The literature can
of any of these impairments can also result in detection
also be used to assess the effectiveness of a training tech-
of inappropriate sensory information by joint and muscle
nique or program in improving the functional outcome
mechanoreceptors. Consequently, the patient is at risk
for a specific neuromuscular control deficit.
for developing faulty motor control strategies.
A brief overview of the more common techniques
used for neuromuscular training in injury prevention and
rehabilitation is provided here. Factors to consider when
Evaluation
choosing the techniques also are given.
Before developing a neuromuscular training program,
the faulty movement pattern or absent motor skill must
be identified. Although it is possible to use a neuromus- Neuromuscular Training Techniques
cular training program to develop a motor skill, this is
not common in injury prevention and rehabilitation. ● Balance training
Most injury prevention and rehabilitation programs are ● Perturbation training
focused on changing movement patterns for motor skills ● Plyometric exercise
that have already been learned. Techniques for improv-
● Technique training
ing or changing movement patterns are addressed later
● Multifaceted training
in this chapter.
382 SECTION II • Principles of Practice
Balance Training
Balance exercises are used to facilitate the propriocep-
tive component of postural control and thus reduce
postural sway. Balance exercises may be performed
on the floor or on some type of equipment, such as
a wobble board, BAPS board, or rocker board. Using
a piece of equipment, the individual may simply try
to maintain a balanced position on the equipment, or
may try to maintain balance while moving the piece of
equipment.
Variations in the surface and base of support are used
to alter the difficulty of balance activities. Stable surfaces
provide less challenge to postural control compared with
unstable surfaces like compliant mats or wobble boards.
Similarly, a bilateral stance is less challenging than a tan-
dem or unilateral stance (Figure 18-4).
Perturbation Training
Perturbation training,50 like balance training, empha-
sizes the proprioceptive component of postural con-
trol. However, perturbation training involves the
addition of an applied force, directed either at the
person or at the surface on which the person stands,
for the purpose of improving the reactive motor
response, which is particularly helpful in improving
dynamic joint stability.
The level of difficulty experienced during perturba-
tion training relates to differences in the applied per-
turbation, the presence of simultaneous activities, and
alterations in base of support. Perturbations that are
predictable, low in force, or applied slowly are less chal-
lenging to postural control than unpredictable, strong,
or fast perturbations. Support surface disturbances in
single cardinal planes are less challenging than pertur-
bations in multiple planes of movement. Perturbations
applied without the addition of sport-specific activity
(e.g., kicking or throwing a ball) are also less chal-
lenging compared with when sport-specific activity or
another distraction is added. Changing the stance con-
figuration produces an effect comparable to balance
training.
Plyometric Exercise
Plyometric exercise is also known as jump training or reac-
tive neuromuscular training exercise,51 and may be used
to train both the upper and lower extremities. Plyometric
exercise is commonly used in injury prevention programs
or in the advanced phases of rehabilitation for individuals
returning to athletic activities. Plyometrics are not used
in the early phases of rehabilitation because of their bal-
listic nature. The plyometric component of a training
program trains the neuromuscular system to carry out
the stretch–shortening cycle effectively.52 Furthermore,
plyometric training that focuses on proper technique and
body mechanics can reduce serious ligamentous injuries
and may induce adaptations to correct for neuromuscular
imbalances.53 Such adaptations better prepare an individ-
ual for multidirectional sport activities and may reduce
positioning that puts high loads on the joint.54
The difficulty of plyometric exercise for the extremi-
ties primarily results from changes in the forces, although
the addition of simultaneous activities may also be used
(e.g., catching a ball while performing the jumping activ-
ity). The demand on the neuromuscular and musculo-
skeletal systems is less with double- versus single-limb
activity, when exercises are performed without external
devices such as sports cords or medicine balls, and when
the range of motion is reduced.
Technique Training
Technique training involves the performance of specific
movements with an emphasis on proper technique. The
chosen movement may be one that results in a large
percentage of injuries, such as landing from a jump or
performing a cutting maneuver, or it may be a movement
that is impaired after injury, such as the stance phase of
gait.
Clinicians can offer verbal and visual feedback to a
patient both during and after training. Hewett and col-
leagues54 used phrases such as “land light as a feather,”
“be a shock absorber,” and “recoil like a spring” for
visualization cues during each phase of the jump. In tech-
nique training, athletes are encouraged to perform the
movements until fatigued or until they cannot execute
the movement with correct biomechanics. Myklebust
and associates55 used partner training to provide feedback
to the training athlete. Partners encouraged each other
to focus on the quality of their movements, specifically
on the knee-over-the-toe position. Both Hewett and col-
leagues54 and Myklebust and coworkers55 cited critical
analysis of the clinician and both immediate and delayed
feedback as contributors to improved biomechanics and
to anterior cruciate ligament (ACL) injury reduction
in their respective studies. These studies emphasize the
importance of analysis of the biomechanics of movement
activities and effective timed feedback to the patient
regarding proper technique.
Multifaceted Training
Although neuromuscular training programs may con-
sist of a single training method, recent approaches to
the design of neuromuscular training to prevent lower
extremity injury tend to be more comprehensive, using
many different types of training components. Likewise,
rehabilitation programs often incorporate multiple
training methods. Neuromuscular training may incorpo-
rate strength training, plyometrics, balance training, core
stability training, and flexibility exercises. A review of the
reported protocols demonstrates that protocols incorpo-
rating multiple components are more effective at injury
 CHAPTER 18 • Principles of Neuromuscular Control for Injury Prevention and Rehabilitation 383

A B

C
Figure 18-4
Bilateral (A), tandem (B), and unilateral (C) stance on an unstable wobble board.
384 SECTION II • Principles of Practice
reduction.53,55–59 For ACL injury reduction interventions
in female athletes, three of four studies that incorporated
multiple components into the neuromuscular training
protocols reported reductions in ACL injury risk,53,55,56,60
whereas two of two studies that incorporated a single
component did not report injury reduction.57,61
Implementation of Training
Techniques
Neuromuscular Training for Lower Extremity Injury
Prevention
Neuromuscular training interventions, using the appro-
priate motor control principles, may be designed to
address and correct specific neuromuscular control defi-
cits and imbalances for the purpose of preventing lower
extremity injury in patients. For example, female athletes
may present with specific neuromuscular imbalances that
can be corrected,54 and the correction of these imbal-
ances can lead to lower extremity injury reduction.53
The enhancement of neuromuscular control and neuro-
muscular balance is important in every plane: coronal,
sagittal, and transverse.
Execution of jump-and-land maneuvers requires the
coordination of both limbs to maintain body align-
ment and control. Unbalanced limb contribution to any
step of the jump sequence makes the jump difficult to
execute. Proper technique training with feedback assists
the patient in learning bilateral limb control. The patient
will be rewarded with a more easily accomplished and
more optimally performed task.
Plyometrics should be taught and performed with
near-perfect body position and technique. The clinician
and patient should focus on landing without excessive
coronal plane motion. If patients are allowed to perform
the jumps improperly, they may create motor programs
for improper technique. It is important for clinicians to
be skilled in recognizing the desired technique for each
plyometric jump used. The clinician should encourage
the patient to maintain excellent technique for the entire
jump–landing sequence. Landing skills that force a patient
to stabilize the lower extremity over a period of time,
although not necessarily plyometric in nature, force the
patient to recognize and maintain proper limb position
and control and enhance proprioceptive and kinesthetic
abilities. If technique begins to degrade because of
fatigue, the exercise should be discontinued. The goal
of the next training session should be to continue to
improve technique and to increase duration.
Proper technique may be achieved using closed-loop
control principles, especially early in the training pro-
gram. Feedback from the clinician to the patient is critical
in programming the neuromuscular system. Proper
instruction requires the clinician to give both immediate
and delayed feedback to the patient both during and
after each exercise bout. The clinician should begin the
process of giving active feedback to the patient during
even low- to moderate-intensity exercises like wall jumps
and hops that incorporate held landings. This assists the
patient in making immediate closed-loop corrections
to technique. This feedback is easier for the patient to
process during an exercise that does not require maxi-
mal effort. Delayed feedback may also be used after the
patient has completed the exercise because this feedback
allows the patient to analyze more cognitively the proper
knee motion required to perform the exercise. Delayed
feedback is more useful for maximal-effort, multiplanar
plyometrics. Cognitive recognition of proper position
and technique assists in reprogramming motor programs
and allows the patient to reach the autonomous stage of
motor learning.
The exercises must be progressed from easier to more
difficult to maintain patient safety and obtain optimal
results. Many lower extremity injuries, such as non-
contact ACL injuries, occur during landing or during
deceleration on a single limb. Plyometric exercises can
be designed that sequentially approach mechanisms of
lower extremity injury during competitive play. With
adequate preparation, patients can be taught to perform
high-risk maneuvers safely in a simulated risk environ-
ment, thereby assisting in the development of schemas
that may help to prevent future injury. By training the
neuromuscular system to maintain control during rela-
tively high-risk maneuvers, the patient may “expand
the neuromuscular control envelope” and be more pre-
pared for similar positions and forces experienced during
sports.
Patients should be taught to coordinate multiple joint
actions and multiplanar movements (Table 18-3). The
incorporation of multiplanar movements improves both
task performance and neuromuscular control. Complex
movement patterns require greater synchronization and
coordination between legs, which leads to greater bal-
ance in side-to-side muscle recruitment and strength,
coordination, and power. Progression from double- to
single-leg jumps helps to correct side-to-side imbal-
ances in both neuromuscular control and movement
technique. Patients should be taught to recognize and
control rotational forces using plyometrics that incor-
porate turning movements, such as 180° jumps or mul-
tiplanar barrier jumps. The body awareness gained is
similar to that used during competitive play or everyday
activity. The patient cannot completely focus on tech-
nique because cognitive effort is required to control and
maintain body position during more difficult plyomet-
ric maneuvers. In addition, teaching a patient to control
landing forces on unstable surfaces will better prepare
the patient to gauge the proper amount of joint flexion
required on impact and to decrease peak impulse while
 CHAPTER 18 • Principles of Neuromuscular Control for Injury Prevention and Rehabilitation 385

Table 18-3 dynamically stabilizing the joints of the lower extremity

Plyometric Training Progression during competitive play.
Plyometric exercises should also be incorporated that
Plyometric Training Example
Progression Exercises
require the patient to transfer horizontal momentum
into vertical movement, similar to skills used during
1 Double leg (low intensity) Wall jumps competitive play. Examples include the basketball player
Line jumps who is performing a lay-up, the soccer player running
2 Double leg (rotatory) 180° jumps then heading the ball on goal, or the volleyball player
Multidirectional who uses her horizontal approach to gain momentum for
barrier jumps maximum height for a spike.
3 Double leg (power) Squat jumps Neuromuscular training sessions should last approxi-
Tuck jumps
mately one-half hour, 2 to 3 days a week, on alternating
4 Double to single leg Scissors jumps
(transitional) Line hops
days. This recommended training dosage is intended to
5 Single leg (hops) Hops for maximize training benefits without overloading (psycho-
distance logically and physically) the patient. Each training session
Crossover hops begins with a warm-up. After warm-up, plyometric train-
6 Single leg (power) Bounding ing is implemented (Table 18-4).
Single-box
power steps
7 Depth jumps Box drop max Rehabilitation
(sport specific) vertical
Box drop Perturbation-enhanced rehabilitation, one example of
reaction how to implement motor control principles to enhance
dynamic joint stability, is a multifaceted neuromuscular

Table 18-4
Dynamic Neuromuscular Training: Plyometrics
Exercise Repetitions or Time

Initial Phase Weeks 1–2 Weeks 2–3

1. Wall jumps 10–20 sec 15–25 sec
2. Tuck jumps 20 sec 25 sec
3. Broad jumps stick land 5 reps 10 reps
4. Squat jumps 10 sec 15 sec
5. Double-leg cone jumps 20–30 sec 20–30 sec
6. 180° jumps 20 sec 25 sec
7. Bounding in place 20 sec 25 sec
Progression Phase Weeks 3–4 Weeks 4–5
1. Warm-up 30 sec 30 sec
2. Tuck jumps 30 sec 30 sec
3. Jump into vertical 5 reps 8 reps
4. Squat jumps 20 sec 20 sec
5. Bounding for distance 1 run 2 runs
6. Double-leg cone jumps 20–30 sec 20–30 sec
7. Scissors jump 30 sec 30 sec
8. Hop, hop, stick 5 reps/leg 5 reps/leg
Final Phase Weeks 5–6 Weeks 6–8
1. Wall jumps 25 sec 20 sec
2. Step, jump up, down, vertical 5 reps 10 reps
3. Mattress jumps 20–25 sec 20–25 sec
4. Single-leg jumps distance 5 reps/leg 5 reps/leg
5. Squat jumps 25 sec 25 sec
6. Jump into bounding 3 runs 4 runs
7. Single-leg hop, hop stick 14 reps/leg 14 reps/leg
386 SECTION II • Principles of Practice

training program that has been used in the rehabilita-
tion of patients with ACL deficiency62 (see Table 18-4).
Along with diminished ligamentous knee stability after
ACL injury, there is also diminished mechanorecep-
tor input to the central nervous system associated with
ligament injury. Consequently, many patients with ACL
deficiency exhibit an altered motor strategy, including
a pattern of rigid, nonresponsive muscle co-contraction
that results in truncated knee motion and poor dynamic
joint stability.63–65 The goal of rehabilitation is to cre-
ate an environment that enhances dynamic joint stabil-
ity and restores functional knee motion through selective
muscle activation. Perturbation-enhanced rehabilitation
has been proven to be effective in doing just this among
a cohort of ACL-deficient patients.66
Perturbation-enhanced rehabilitation is a 10-session
program (Table 18-5) that incorporates strength train-
ing, agility drills, and three perturbation tasks (e.g.,
maintaining balance on an unstable support surface
while the rehabilitation specialist maneuvers the sup-
port surface). A variety of progressive resistance exer-
cises are implemented and systematically advanced to
address lower extremity muscle weakness. Agility and
perturbation drills are also included and progressed
based on successful completion of each task. Verbal
cues such as “keep your knees soft,” “keep your trunk
still,” and “relax between perturbations” are provided
during perturbation training early in the program to
provide patients with a framework for successful task
completion. The focus of training is not on develop-
ing specific muscle activation patterns; rather, patients
are allowed to develop individualized patterns as long
as the task is successfully completed (i.e., maintain bal-
ance and dynamic joint stability without rigid muscle
co-contraction). During the first five sessions, pertur-
bations are initiated in a block manner in anteroposte-
rior, mediolateral, or rotational planes, and verbal cues
are gradually decreased as the patient becomes more

Table 18-5
Perturbation Training Protocol
Technique Sets/Duration Direction of Board Movement Application

Rocker board Two to three sets, AP, ML Begin in bilateral stance for first session.
1 min each Perform in single-leg stance for
remaining sessions.
Roller board/platform Two to three sets, Initial: AP, ML Subject force is counter-resistance opposite
1 min each, Progression: Diagonal, rotation of rollerboard, matching intensity and
perform bilaterally speed of application so rollerboard
movement is minimal. Leg muscles should
not be contracted in anticipation of
perturbation, nor should response be
rigid co-contraction.
Roller board Two to three sets, Initial: AP, ML Begin in bilateral stance for first session.
30 sec to 1 min Progression: diagonal, rotation Perform in single-leg stance for remaining
each sessions. Perturbation distances are
1–2 inches.

Early Phase (Sessions 1–4)

Treatment goals:
• Expose athlete to perturbations in all directions
• Elicit an appropriate muscular response to applied perturbations (no rigid co-contraction)
• Minimize verbal cues
Middle Phase (Sessions 5–7)
Treatment goals:
• Add light sport-specific activity during perturbation techniques
• Improve athlete accuracy in matching muscle responses to perturbation intensity, direction, and speed
Late Phase (Sessions 8–10)
Treatment goals:
• Increase difficulty of perturbations by using sport-specific stances
• Obtain accurate, selective muscular responses to perturbations in any direction and of any intensity, magnitude, or speed

AP, anteroposterior; ML, mediolateral.

 CHAPTER 18 • Principles of Neuromuscular Control for Injury Prevention and Rehabilitation
proficient with the task. During the last five treatments,
the perturbation directions are applied randomly while
the patient performs a sport-specific task (e.g., kicking
a ball). Intensity, speed, and force of perturbations are
advanced throughout the program.
Summary
Deficits in neuromuscular control alter the coordinated
muscle activity responsible for dynamic joint stability,
postural control, and movement patterns. These deficits
can lead to musculoskeletal injury or can be the result
387
of injury. An understanding of the sensorimotor system
and motor skill development provides the foundation on
which neuromuscular training programs for injury pre-
vention and rehabilitation are based. Implementation of
these concepts into a neuromuscular training program
assists in achieving the best possible outcomes.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the references source and access it on line whenever
possible. There are a total of 66 references for this chapter.

P RINCIPLES OF S TABILIZATION
T RAINING
David J. Magee and James E. Zachazewski
Introduction
Rehabilitation clinicians often talk about “instability,”
but the terminology can mean different things to differ-
ent people. For example, saying the shoulder is “unsta-
ble” may mean that this instability is related to tearing of
ligaments, the capsule, and labrum with an anterior dis-
location of the shoulder. Similarly, the shoulder may be
said to be “unstable” because of weakness of the muscles
controlling the scapula, leading to secondary impinge-
ment. The focus and purpose of stabilization training of
any joint (e.g., the shoulder) or group of joints (e.g., the
lumbar spine) are to allow supporting tissues such as liga-
ments to heal, to strengthen surrounding musculature,
and to reestablish motor control and appropriate move-
ment patterns of that joint.
The purpose of this chapter is to provide the reader
with an understanding of what instability is, what it is
not, the types of instability commonly seen by clinicians
involved in the rehabilitation of the patient, the princi-
ples of stabilization training and a stabilization training
sequence, and where stabilization training “fits” in the
continuum of clinical care.
Hypomobility and Hypermobility
Hypomobility and hypermobility are two terms commonly
used by clinicians in the treatment of patients and cli-
ents. Hypomobility implies decreased movement.
Mobilization and manipulation techniques applied either
directly to the joint or to surrounding structures are
directed toward restoring the characteristics of normal
joint mobility, namely, range of motion (ROM) and joint
388
191
C H CA H
P TA EP RT E R
play. Dysfunction due to hypomobility may most often
be detected by watching for altered patterns of move-
ment, decreased ROM, tissue or joint swelling, decrease
in joint play, abnormal end feel, hypertonic muscles, or
inhibition of the antagonist muscles. The concepts and
methods of treating joint hypomobility are addressed in
Chapter 24.
Hypermobility, on the other hand, implies exces-
sive joint ROM. This excessive joint ROM may be nor-
mal (laxity) or pathologic (instability). Laxity implies
the person has excessive joint ROM, but has the abil-
ity to control the movement of the joint in that extra
range. It is not a pathologic state. Factors that can lead
to increased laxity may be genetic or familial factors, or
occupational or activity factors often related to sports.
Instability implies that the person has increased joint
ROM but does not have the ability to stabilize and con-
trol movement of the joint. Thus, instability may be
associated with a potential or real pathologic state. The
potential for a pathologic state exists when many of the
signs of instability are present (e.g., poorly coordinated
movement, inability to stabilize structures, or abnormal
force-couple action). However, the joint has not been
stressed to such an extent that symptoms are manifested
(e.g., movement is not fast enough, nor is the load of
sufficient magnitude to exceed the tolerance of the joint
or its associated structures/tissues). An example would
be the patient who has an unstable glenohumeral joint
on examination but no pain or apprehension on move-
ment. In a real pathologic state, which is more commonly
seen by the clinician, both signs and symptoms are pres-
ent. Dysfunction due to hypermobility may be detected
by watching for asynchronous or abnormal movement,
 CHAPTER 19 • Principles of Stabilization Training 389

increased ROM, joint swelling for no apparent reason,
protective muscle spasm towards the end of ROM (“joint
does not feel right”), apprehension, “giving way,” or the
presence of an abnormal end feel.
In some cases, hypomobility and hypermobility may
be found in close proximity or even in the same joint. For
example, the joint may be hypomobile in one direction
and hypermobile in the opposite direction, as is com-
monly seen in the glenohumeral joint with secondary
impingement of the shoulder (excessive anterior transla-
tion but restricted posterior translation). When this situ-
ation presents itself, it is often a dilemma for the clinician
to decide what is causing the problem: the hypomobil-
ity or hypermobility. Regardless of which type of mobil-
ity is causing the problem, the clinician must treat the
hypomobility first, to restore normal “play” in the joint
to allow normal joint arthrokinematics. Only then can
hypermobility be properly addressed.
Normal Zones and Barriers
to Movement
When one considers mobilization and stabilization, a
number of concepts must be examined. The first is an
understanding of the zones of normal movement in an
ROM as well as the normal barriers that can be felt dur-
ing this movement. During the range of normal move-
ment, in any osteokinematic or physiological motion
(e.g., flexion, rotation), three zones of movement may
be conceptualized. These are the neutral zone, the elastic
zone, and the plastic zone (Figure 19-1). The neutral
zone is the zone in which there is little or no internal
resistance offered by the tissues to movement. In this
zone, the crimp of the tissue is being taken up.1,2 Thus,
this zone occurs at the beginning of the ROM relative
to a joint’s resting position. As one reaches the end of
the neutral zone, resistance may be felt. This initial resis-
tance to movement is the result of the tissue crimp having
been taken up. Tension (primarily elastic) starts to build
within the tissues. This tension is very subtle, occurring
very early in the range, and is virtually equivalent to the
“taking up of the slack” in joint play motion. This resis-
tance indicates the first barrier or feeling of restriction
to movement, and may be called the crimp barrier.
Increases in the size of the neutral zone (i.e., resulting
in the feeling or perception that the crimp is “taken up”
later in the ROM) can occur because of injury, joint
instability, joint degeneration, or muscle dysfunction

80
Injury
Yield
point
region Total failure
60
STRESS or LOAD (N)

Little or no Physiological 2o
stress on loading 1o 3o
tissue
micro
40 failure

Stress of
clinical test
20

0 2 4 6 8 10 12
STRAIN
Toe Linear stretch Partial failure Total failure
Fiber
reaction

Movement Neutral zone Elastic zone Plastic zone

zone
Paraphysiological zone

Movement Beginning Crimp Physiological Anatomical

barriers of ROM barrier barrier barrier
(end of active (end of passive movement)
movement) Figure 19-1
Integration of fiber reaction, movement
Properties Uncrimping Elasticity Viscoelasticity Tissue failure
zones, movement barriers, and movement
affected Elasticity Viscoelasticity Plasticity (tissue Plastic deformation
Taking up slack Plasticity deformation) properties as they relate to a stress–strain
at end of joint play Stress relaxation Stress relaxation curve. (Not drawn to scale.)
390 SECTION II • Principles of Practice
(leading to loss of muscular control of a movement).2,3
On the other hand, the size of the neutral zone may
be decreased by osteophyte formation, surgical fusion,
muscle spasm, muscle strengthening (hypertrophy), or
tissue shortening as a result of immobilization or loss of
tissue flexibility.
The elastic zone is the zone in which tissue tension
begins to increase as the joint moves through the ROM.1
It extends from the crimp barrier through the physio-
logical barrier (end of active movement) and toward the
anatomic barrier (end of passive movement). The elastic
zone is the zone in which the elasticity of the tissue is taken
up. Within the elastic zone, elastic deformation occurs so
that if the deforming force is removed, elastic recoil occurs
in the tissues. When this occurs, the tissue returns to its
normal unloaded state in the neutral zone, with no tissue
damage.4,5 The elastic zone can be increased by injury to
the joint structures (i.e., the limit of the zone is reached
with less effort or farther into the range because of the
loss of some of the resistance provided by the magnitude
of elasticity found in uninjured tissue; an analogy would
be an elastic band that has become stretched out), col-
lagen abnormalities, mobilization techniques, and muscle
lengthening. The elastic zone may be decreased (i.e.,
the limit of the zone is reached with greater effort or is
reached sooner) by tissue adaptation and shortening due
to osteophyte formation, surgical fusion or repair, muscle
hypertrophy, or immobilization.
The third zone is the plastic zone. In the plastic zone,
deformation of the tissues is extended beyond the tissue’s
elastic recoil and the tissue begins to deform. Plastic
deformation does not allow the tissue to return readily
to its original shape when the stress is removed. In reality,
the plastic zone can extend beyond the anatomic barrier.
Depending on the magnitude of the load or force, the
length of time of application, and the speed of applica-
tion, two things may occur in the plastic zone. First, creep
or plastic flow may occur. Second, within the plastic
zone, some of the tissue fibers experience some degree of
microfailure. If there is sufficient microfailure, injury may
result, leading to the tissue failure called plastic deforma-
tion. In reality, from a clinical perspective, plastic flow and
plastic deformation are the same thing. They are given
different names only for the sake of easier understand-
ing. The plastic zone may be increased by tissue injury
or collagen tissue abnormalities, or through mobilization
techniques. It may be decreased by osteophyte formation,
surgical fusion or repair, or immobilization.
As previously mentioned, three normal barriers are
seen during osteokinematic movement. These are the
crimp barrier, the physiological barrier, and the anatomic
barrier. With pathology, any or all of these barriers may
be decreased (hypomobility) or increased (hypermobil-
ity). Figure 19-2 illustrates these barriers and why they
may increase, resulting in instability.5
Physiological barrier Anatomical barrier
Anatomical (passive) movement
Physiological (active) movement
Neutral Zone
N N N
lengthened hypermobility
instability
muscle
pathological
laxity
mechanical stretch
pathological weakness
clinical/gross
translational
instability
N = normal position
Figure 19-2
Hypermobility and instability. Note how the normal crimp,
physiological, and anatomic barriers move to the right (i.e., increase).
(Not drawn to scale. Normally, physiological and anatomical barriers
are very close together. The neutral zone is normally very small.)
Pathologic Barriers to Movement
Pathologic barriers are restrictions to movement that
occur as a result of a pathologic process. These barri-
ers may be hypomobility barriers, restrictive in nature,
that cause a decrease in the ROM, or they may be
hypermobility barriers occurring as the result of exces-
sive movement. Pathologic barriers may occur any-
where in the ROM, before the crimp barrier or beyond
where the anatomic barrier would normally exist; they
may even occur between the two. Commonly, they are
found within what would be considered the normal
ROM, especially in the case of restrictive (hypomobil-
ity) barriers. Pathologic barriers may be the result of
macrotrauma or microtrauma, muscle spasm, swelling
or edema, pain, or adaptive shortening or lengthening
of the tissue. The three types of pathologic barriers are
motion barriers, collagen barriers, and neurodynamic
barriers.
The motion barrier results from a pathologic con-
dition of contractile tissue (muscle) related to muscle
hypertonus, common muscle spasm, adaptive muscle
shortening/loss of muscle flexibility, or muscle pain.
The term motion barrier was originally used by Mitchell
and colleagues6 to denote a restrictive barrier, such that
when passive movement is performed, it is described by
the patient as a “feeling of altered resistance” or “chang-
ing tension in the muscle”; it also may appear as pro-
tective muscle spasm, or be the result of a “tight” or
shortened muscle.6 Active movement and ROM may
also be decreased.
The second pathologic barrier, the collagen barrier,
results from a pathologic process affecting collagenous
tissues (e.g., ligament, tendon, capsule). This patho-
logic process usually results in adaptive shortening or
 CHAPTER 19 • Principles of Stabilization Training
pain. In this case, the barrier moves to the left, or ear-
lier into the ROM, and the ROM decreases. The col-
lagen barrier end feel is similar to that of normal tissue
stretch, but is found earlier in the ROM and, if the
capsule is affected, typically results in a capsular pattern
of motion restriction. On physical examination, colla-
gen barriers may be described by the clinician as “hard”
(i.e., the capsule is affected or soft because of synovitis
or soft tissue edema). If the collagen barrier increases
beyond the normal anatomic barrier, as in the case of
a dislocation with capsular tearing, then the end feel is
more like muscle spasm (protective) or “empty” (no
end feel) because of patient apprehension or excessive
pain.
The restrictive neurodynamic barrier is the result
of a pathologic process of neural tissues that must
undergo lengthening and shortening in the course of
ROM. This barrier is manifested by the presence of
neurological signs (e.g., nerve pain, paresthesia) that
commonly restrict movement.
Pathologic instability barriers commonly cause each
barrier to be encountered later in the movement (see
Figure 19-2) so the barriers are shifted to the right, or
farther into the ROM. For example, with instability,
the crimp barrier can increase because the patient has
lost control of arthrokinematic movement at the joint
(translational instability). Likewise, the physiological
barrier could increase because of a lengthened muscle,
resulting in what is known as overstretch weakness of the
muscle. The anatomic barrier may increase because of
trauma to the joint, such as a subluxation or dislocation
(clinical or gross instability).7
Clinical Instability
In a clinical context, instability is a condition in which
there is a loss of neuromuscular control, muscle stiff-
ness, resistance to joint stiffness, or some combination
of these, so that the applied external loads cause exces-
sive arthrokinematic movement (e.g., spin, slide, roll)
at a joint. The movement of the opposing joint surfaces
cannot be “controlled” by the patient, resulting in pain,
transitory deformity (instability jog, giving way sublux-
ation, or catch) and weakness, placing the tissues at risk
of being overstressed.8–11 The joint’s static stabilizers
(e.g., ligaments, capsules, labrum) and dynamic stabiliz-
ers (muscles) and their accompanying nerve supply are
unable to limit excessive or abnormal macroscopic or
microscopic movement of the joint.7,8
Instability is most obvious if the movement is executed
too quickly or if the load placed on the joint is too great
for the patient to control. In many cases, the patient may
not be aware of the particular movement (i.e., the patient
is not paying attention to or is not concentrating on the
movement), the patient may assume certain positions that
391
place the joint in a provocative position, or the muscles
that control or resist provocative positions or movements
are fatigued. For example, during a normal examination, a
clinician may find that a patient demonstrates no signs or
symptoms associated with functional complaints. However,
if a swimmer is asked to demonstrate her stroke at functional
speeds, symptoms may appear. Similarly, if a patient is asked
to functionally move a specific weight in a particular way
(mechanism of instability) or assume a certain position (dead
arm syndrome), then symptoms may appear. Instability due
to loss of dynamic stabilizer (muscular) control results from
an inability of the muscles to carry out a neural command,
or an inability of the neurological system to provide accurate
proprioceptive or kinesthetic feedback regarding the joint’s
position in space.9,10 For normal coordinated movement,
muscles must produce and coordinate adequate tension to
perform the desired movement, while the passive restraints
guide, limit, or stop the movement. An instability dysfunc-
tion also may occur because of recruitment problems. In
this case, the muscles that control a specific motion or series
of motions are not recruited in the correct order or with
sufficient force.12,13 This is a motor control problem; the
patient is unable to produce the proper type, rate, or speed
of contraction in individual muscles to perform the move-
ment correctly. (See Chapter 18 for more information on
motor control.)
Commonly, dynamic instability is due to muscular
imbalance, or the inability of stabilizer muscles to stabi-
lize “base” structures (i.e., pelvis, scapula) so that func-
tional movements of the upper or lower extremities can
be performed properly. Base or core structures are the
structures that anchor the origins of muscles controlling
a movement in a limb segment. Similarly, injury to static
restraints may compound the motor control problem.
Stability Systems
Stability normally involves the interaction of three
systems—the neurological or central control system,
the passive or inert tissue (e.g., ligaments, capsule) sys-
tem,14–16 and the contractile (muscular) or active system15,16
(Figure 19-3). These three elements or subsystems of the
stability system are intimately involved in stabilization.
Neural Component
The neural component of the stability system consists of
the central and peripheral nervous systems. These systems
provide control through neural feedforward and feedback
mechanisms.17,18 The central nervous system includes the
brain and spinal cord, which provide control and central
control pathways for movement, whereas the peripheral
nervous system involves nerve roots, peripheral nerves, and
the tissue mechanoreceptors found in skin, joints, muscles,
and surrounding joint tissue, and provides the peripheral
control pathways for movement. The neural subsystem
392 SECTION II • Principles of Practice
Figure 19-3
Elements (subsystems) of stabilization.
provides feedback from the active (muscle spindles, Golgi
tendon organs) and passive systems (joint afferents), helping
determine position, load, and joint demands. It also directs
and controls the contractile system to initiate conscious and
unconscious movement.17–20 Dysfunction of the neural sub-
system may be a result of peripheral nerve injury, peripheral
neuropathy due to a disease such as diabetes, nerve root
injury, spinal cord injury, brain injury, neurological disease,
aging, or prolonged immobilization or disuse.14
Role of Neural Subsystem14,17–19
● Activate conscious and unconscious movement
● Provide motor control (central—neural control centers)
● Provide neural sensory feedback and control (peripheral—reflexes)
● Provide proprioceptive control through
● Muscle, ligaments, capsule, and skin
● Mechanoreceptors
● Provide pain modulation
● Coordinate position, loading and joint demands
Causes of Neural Subsystem Dysfunction14,17–19
● Peripheral nerve injury
● Peripheral neuropathy (disease, e.g., diabetes)
● Nerve root injury
● Spinal cord injury
● Brain injury
● Neurological disease
● Aging
● Prolonged immobilization/disuse
Neurological factors affecting stabilization include
spatial summation and autogenic and heterogenic
stretch reflexes.20,21 The neurological system also
affects muscle–joint and muscle–tendon interaction
through reflexes. Spatial summation is demonstrated
through the progressive recruitment of muscle fibers
as the force needed to stabilize a joint increases. The
autogenic or monosynaptic stretch reflex involves
interfusal feedback from the muscle spindle when a
muscle is stretched, which can modulate the number
of muscle fibers activated in the muscle at a given
time.21 The stretch reflex can increase muscle stiffness
by a factor of one to three. The heterogenic stretch
reflex is influenced by the autogenic reflex of one
muscle modulating the gain of the stretch reflex in
the antagonist muscle.21 Muscle–joint interaction is
demonstrated by the muscle force generated, and the
resulting interaction depends on the joint angle and
the angular velocity at a given time.21 Muscle–tendon
interaction involves the tendons acting as shock and
length absorbers, mediated by the proprioceptive role
played by the Golgi tendon organs.21
Passive Component
The passive subsystem consists of the ligaments, cap-
sules, skin, joints, bones, and other collagenous tissue.
This subsystem’s role is to provide static stability at end
ROM (i.e., at the anatomic barrier) while providing
some stability at the physiological barrier. The passive
subsystem provides minimal stabilization in the neutral
zone. Along with the articular surfaces, passive struc-
tures direct the movement of articular surfaces through
the joint ROM. The passive subsystem, through mech-
anoreceptor input to the nervous systems, provides
static and dynamic proprioceptive and kinesthetic feed-
back. These receptors, which may be modulated by the
speed and velocity of motion changes, provide neural
feedback on the joint’s position and direction of move-
ment, and some pain modulation. Dysfunction of the
passive subsystem is due most commonly to mechanical
injury, overuse or repetitive stress, degeneration (e.g.,
osteoarthritis), or a disease process (e.g., rheumatoid
arthritis).14
Role of Passive Subsystem14,17,18,20
● Provides stability at end range (anatomic barrier)
● Provides some stability at the physiologic barrier
● Provides minimal stability in the neutral zone
● Along with articular surface, directs joint into close-packed and
loose-packed positions
● Statically and dynamically active in proprioceptive role (neural
feedback)
● Provides pain modulation
 CHAPTER 19 • Principles of Stabilization Training
Causes of Passive Subsystem Dysfunction 20,22–24
● Mechanical injury (most common)
● Overuse (repetitive stress)
● Degeneration (e.g., osteoarthritis)
● Disease (e.g., rheumatoid arthritis)
Active Component
The active subsystem consists of the muscles, their
tendons, and their insertions. The active subsystem
provides dynamic isotonic action and static isometric
action stability to a joint throughout the ROM. The
muscles act as dynamic force transducers, concentri-
cally contracting to provide power for movement and
eccentrically contracting to provide braking action to
stop or slow down movement, or act as dynamic shock
absorbers, with stabilization provided through joint
compression. They interact with the neural subsystem
in a proprioceptive role by providing neural feedback
about positioning and movement. This significant
proprioceptive role is mediated through the muscle
spindles and Golgi tendon organs, which help define
position, rate, and the ROM.14,17,18,20
Intrinsic muscle factors affecting stabilization
include temporal summation, length–tension rela-
tionships, force–velocity relationships, and muscle
architecture.21 Temporal summation is a summation
of individual contractile units. This summation can
increase the muscular force by increasing the muscle
activation frequency. The length–tension relationship
shows that at optimum sarcomere lengths, muscles
generate maximum tension. Muscle tension provides
static stabilization (isometric contraction) and dynamic
stabilization (agonist concentric and antagonist eccen-
tric contractions).21 The force–velocity relationship
influences the active subsystem because as velocity
increases, muscle force decreases. During dynamic
stabilization, if the speed of movement increases, the
ability of the muscles to stabilize and provide suffi-
cient regulation of stiffness decreases or becomes more
difficult, so that muscle control may be lost at faster
speeds.21 Muscle architecture relates to the different
shapes of muscles. Many muscles have a longitudinal
Role of Active Subsystem14,17,18,20
● Provides dynamic and static stability throughout range
● Dynamic force transducer providing power for movement, braking,
and stabilization
● Provides dynamic shock absorption and braking
●
Dynamically active (stretch, contraction in proprioceptive
role—neural feedback)
● Provides pain modulation
● Provides increased joint compression
393
architecture, with the muscle fibers oriented along the
axis of force, whereas other muscles have a pennate
architecture, with fibers oriented at an angle to the
axis of the force. These architectural differences influ-
ence the stabilization and control actions of the differ-
ent muscles.21
As with the passive system, the mechanoreceptors
of the muscles assist in providing pain modulation.
Dysfunction of the active subsystem may be due to
an inability to carry out a neural command (injury
to the muscle or its tendon or attachment, or to the
neuromuscular junction), an inability to provide accu-
rate feedback through proprioception or kinesthesia,
an inability to produce adequate muscle tension, or a
failure to produce a coordinated contraction (muscle
balance).14,17,18,20 The active subsystem is commonly
injured by mechanical injury, overuse or fatigue, dis-
ease, aging, loss of neurological input, or prolonged
immobilization or disuse.
Active Subsystem Dysfunction14,17,18,20
● Causes
● Mechanical injury
● Overuse or fatigue
● Disease
● Aging
● Loss of neurological input
● Prolonged immobilization/disuse
● Inability to
● Carry out neural command
● Provide accurate feedback (proprioception)
● Produce adequate muscle tension
● Produce coordinated contraction
Stabilizer and Mobilizer Muscles. For stabiliza-
tion purposes, the active subsystem can functionally be
divided into stabilizer muscles and mobilizer mus-
cles.17,18 Normally, the stabilizer muscles contract first to
provide a stable base from which the mobilizer muscles
can function and position an extremity for functional use
(e.g., overhead motion). They may contract individually
or synchronously, functioning as part of a force couple
to control movement. If there is insufficient contraction
of the stabilizer muscles to act as a counterbalance to the
movement of a distal extremity component or joint, or
if the counterbalancing activity of the stabilizers is late,
incorrect movement patterns will result.
In the peripheral joints, there is one group of stabilizer
muscles, but in the spine, the stabilizer muscles are divided
into two groups: local stabilizers and global stabilizers.22
Generally, peripheral stabilizer muscles and local spinal sta-
bilizer muscles work over one joint (monoarticular) or one
segment (unisegmental), have wide insertions with small
tendons, and are mainly tonic or postural. They are made
394 SECTION II • Principles of Practice
up primarily of slow-twitch (type I) muscles fibers, provid-
ing a low force over a longer period. They tend to control
the neutral zone and play a major proprioceptive role in
providing feedback to the neurological subsystem.20
Stabilizer Muscles—Characteristics22,24,25
● Work over one joint
● Close to joint (deep; short levers and small movement arms)
● Stabilize individual segments (segmental stabilization)
● Control neutral zone
● Isometric/concentric/eccentric action depending on type of con-
traction needed to stabilize; action is independent of direction of
movement
● Tonic (continuous) movement (biased to low load)
● Large proprioceptive role (position, rate, and ROM)
● Cause joint compression
● Tend to weakness
● Dysfunctional if
● There is inadequate tonic/low-threshold recruitment
● They are functionally long
Peripheral stabilizer muscles tend to work eccentrically,
providing deceleration or a braking action, or allowing
controlled movements or stabilization of “base” struc-
tures (i.e., pelvis, scapula) from which other muscles act to
allow function. The stabilization they provide is the result
of muscle stiffness due to joint compression caused by
contraction of these muscles. The joint compressive forces
that result from these muscle contractions have been
demonstrated to increase joint stiffness with as little as 25%
maximum voluntary contraction (MVC) of a muscle.21
Local spinal stabilizer muscles (e.g., multifidus, rota-
tors, transversaria) are close to the joint and have short
levers and small movement arms.17,21 These muscles are
small, running between individual segments or no more
than two or three segments. They are the “nuts and
bolts” that hold the spinal column upright. They stabi-
lize individual segments and control the neutral zone.17,21
They act primarily isometrically, or eccentrically, depend-
ing on the type of contraction that must be stabilized.
Their action is often independent of the direction of
movement.
Peripheral stabilizer and local spinal stabilizer mus-
cle dysfunction is demonstrated by several means22
(Table 19-1). There may be two types of motor control
deficit—delayed muscle “firing” (a timing deficiency, i.e.,
delayed contraction), and a recruitment deficiency, in
which the muscle does not “turn on” or contract (the
threshold for muscle recruitment is too high).17,18,20
Pathologic processes and pain can cause dysfunction
through reflex inhibition, leading to muscle atrophy and
weakness. Decreased muscle stiffness, in turn, can lead
to loss of movement control in the neutral zone, which
leads to poor segment control. With dysfunction, these
muscles become functionally elongated, especially if the
threshold for muscle recruitment is too high.17,18,22
Stabilizer Muscle Dysfunction22–25
● Motor control deficit
● Delayed timing (late or absent contraction)
● Recruitment deficiency (muscle does not “turn on” or inefficient
low-threshold recruitment [duration, force])
● Pathologic process and pain cause inhibition (reflex inhibition
and muscle atrophy)
● Loss of neutral zone control (decreased muscle stiffness of local
stabilizers)
● Poor segmental control (instability jog or catch)
Spinal global stabilizer muscles are long muscles
spanning several segments and may be thought of as
“guy wires” rather than “nuts and bolts” because they
steady the whole spinal column rather than individual
segments. These muscles are the primary “movers” of
the spine (e.g., abdominals, erector spinae).
Mobilizer muscles tend to work over two joints
(biarticular) or several segments (multisegmental),
are superficial, and have narrow insertions with long
tendons.23–26
They are primarily motion accelerators, acting con-
centrically. When they contract, they tend to cause joint
distraction. Because they have long lever arms, mobilizer
muscles generate torque to produce active movement. They
may also provide some shock absorption through eccen-
tric action. These muscles can contribute to stabilization
when the joint is under higher loads or moving at higher
speeds. These phasic muscles tend to be functionally short
and are prone to tightness.7 Mobilizer dysfunction is seen
with muscle shortening (adaptive shortening) or collagen
shortening (hypomobility) of passive structures, which
limits accessory (joint play) and physiological movements,
leading to tight muscles in crossed syndromes.7,27,28 This
adaptive shortening in the tissues is often accompanied by
compensation, resulting in hypermobility in an adjacent
joint or on the opposite side of the same joint.
Mobilizer Muscles—Characteristics23,24,26
● Work over one joint
● Narrow insertions with long tendons
● Primarily accelerators
● Cause joint compression
● Tend to tightness
● Dysfunctional if
● There is inadequate tonic/low-threshold recruitment
● They are functionally too short or long
 CHAPTER 19 • Principles of Stabilization Training
Table 19-1
Examples of Stabilizers and Mobilizers Controlling the Pelvis and Scapula
Pelvis/Spine
Local stabilizers (spine) Multifidus
Rotatores
Intertransversarii
Transversalis
Global stabilizers (spine) Erector spinae*
Transversus abdominis*
Quadratus lumborum
Stabilizers (scapula)
Mobilizers (spine) Rectus abdominis
Internal/external obliques
Psoas
Latissimus dorsi
Mobilizers (shoulder)
*Depending on the movement, may be a global stabilizer or mobilizer.
Before considering retraining of the mobilizer muscles,
the clinician must ensure that a stable “base” or “core” is
present from which the mobilizers can act. This is done
by ensuring that the stabilizers function properly. Once
the clinician has ensured that the stabilizer muscles are
functioning properly, mobilizer muscle training can begin.
Mobilizer muscle training should progress through several
phases, from isometric to concentric, eccentric, and econ-
centric (pseudo-isometric) contractions, to functional
movement. Whether working the stabilizers or mobilizers,
work is always done in the pain-free range but progresses
to full ROM when the patient can control and stabilize the
“base” (the pelvis for lower limb and trunk movement, the
scapula for upper limb movement). By ensuring that the
stabilizer muscles are able to perform their function and
then by teaching the patient to control the “base” (pelvis
and scapula) both statically and dynamically, the patient is
provided time to unlearn incorrect movement patterns and
learn correct movement patterns in a controlled fashion.
Of clinical interest is the observation that often patients
have more difficulty unlearning the incorrect movement
pattern, which has become a habitual pattern, than in
learning the correct pattern. This is often demonstrated by
the patient going back to the incorrect pattern as specific
muscles that control the correct pattern fatigue.
The mobilizer muscles are trained primarily using the
overload principle to ensure strengthening (high load, low
395
Scapula
Serratus anterior
Trapezius (three parts)
Rhomboids (major and minor)
Levator scapulae
Pectoralis minor
Rotator cuff (supraspinatus,
infraspinatus, subscapularis,
teres minor)
Biceps
Triceps
repetitions) and to increase endurance (low load, high rep-
etitions). The clinician must try to achieve balance of the
different muscle groups and force couples, and as strength
and endurance improve, the clinician can take the patient
from stable to unstable positions, eventually using higher-
level functional training exercises such as plyometrics, which
involve preferential type II muscle fiber recruitment.
Retraining Mobilizer Muscles
● Ensure stable base
● Progress from isometric to concentric to eccentric to econcentric
to functional movement
● Work in pain-free ROM but progress to full ROM
● Strengthening (overload—high load, low repetitions)
● Endurance training (low load, high repetitions)
● Muscle balance
● Go from stable to unstable positions
● Plyometrics (preferential type II fiber recruitment)
● Correct movement patterns (must unlearn incorrect pattern)
● Kinesthetic (proprioceptive) training
Muscle Contraction Sequence. During peripheral
joint movement, the monoarticular peripheral stabilizer
muscles normally contract first to stabilize the base (i.e.,
pelvis, scapula) from which the mobilizers work.24–26
396 SECTION II • Principles of Practice
The mobilizers then contract, resulting in a controlled
movement pattern. An example would be the scapular
stabilizers (e.g., trapezii, serratus anterior) contracting
first to stabilize the scapula, with the rotator cuff mus-
cles then contracting along with other shoulder muscles
(e.g., biceps, deltoid) to move the upper extremity into a
functional position. In the spine, the monoarticular local
stabilizers contract first (e.g., multifidus), stabilizing the
individual spinal segments. The multiarticular global
stabilizers (e.g., erector spinae) then contract, acting as
synergists to reinforce the stabilization of the base of sup-
port (i.e., pelvis). In this way, the global stabilizers act as
“guy wires” to stabilize the whole spine or control the
speed of movement of the whole spine initiated by the
global mobilizers (e.g., abdominals in flexion).
With injury, a pathologic process, or other abnormal-
ity, an abnormal stabilizer recruitment pattern can
develop.24–26 In this case, multiarticular mobilizers (in a
peripheral joint) or global stabilizers (in a spinal joint)
contract along with global mobilizers, so the mobilizer
muscles dominate the movement. The result is an incor-
rect movement pattern due to an incorrect sequence of
muscle contraction that, over time, will lead to weakness
of the local stabilizers. Local stabilizer weakness is often
accompanied by lack of extensibility in these muscles
and hypomobility in the associated joints. At the same
time, these monoarticular stabilizers demonstrate a late
Tight
upper trapezius
and
levator scapulae
Weak
rhomboids,
serratus anterior
and
lower trapezius
A B
Figure 19-4
Examples of crossed syndromes. A, Upper crossed syndrome. B, Pelvic crossed syndrome. (From Magee DJ: Orthopedic physical assessment, ed 5,
pp 132, 482, Philadelphia, 2002, WB Saunders.)
or delayed firing pattern or “position weakness,” being
weaker when tested in the new range.7 A delay in mono-
articular stabilizer contraction and weakness results in an
increase in the neutral zone range.
Crossed Syndromes. Muscle weakness, muscle
imbalance, and hypomobility are commonly seen in
the presence of a pathologic process and are sometimes
called crossed syndromes.27,28 The two most common
crossed syndromes are the pelvic crossed syndrome and
the upper crossed syndrome, as elucidated by Janda27
and Janda and Jull28 (Figure 19-4). In reality, a crossed
syndrome can develop at any joint in which movement
dysfunction is present. The key factor of the crossed
syndrome concept is the patterns of lengthened and
weak muscles versus tight and strong muscles. Knowing
such patterns exist makes it easier for the clinician to
identify the tight, hypomobile structures that need to
be stretched and the weak, hypermobile structures that
need to be strengthened.
Pathologic processes and pain cause overactive, low-
threshold, early low-load recruitment, and early muscle
spasm with overactive type I muscle fibers.24–26 This leads
to the muscular imbalance of “weak muscles” seen in
crossed syndromes.27,28 To gain control of the neutral
zone, the clinician must train the local stabilizers to con-
tract first and build their strength and endurance while
ensuring that there is no activation of the global muscles.
Abdominals Erector spinae
(lengthened (tight)
and weak)
Weak PSIS high
deep neck
flexors ASIS low
Gluteals
(lengthened
and weak)
Iliopsoas
(tight)
Hamstring tension (tight)
Tight
pectoralis
(major & minor)
 CHAPTER 19 • Principles of Stabilization Training 397

This is an exceedingly important concept to remember
when doing stabilization training. Unless the stabilizers
are rehabilitated properly and early in the rehabilitation
process, successful stabilization training will be harder to
achieve. This initial process is a slow one that requires
physiological effort and psychological concentration on
the part of the patient and careful observation and cor-
rection by the clinician. Unless the local stabilizers are
functioning properly, the clinician should not progress
to mobilizer training. In some cases, especially with the
spine, muscles may act as both global stabilizers and mobi-
lizers. In this case, their role as global stabilizers must be
emphasized first, and only when their proper function as
global stabilizers has been ensured should the clinician
consider moving on to mobilizer training. This step is
commonly missed by clinicians in their haste to engage
in “more interesting” exercises such as foam roll or ball
proprioceptive therapy, which in fact should be used only
in later phases of stabilization training. The patient must
first learn to activate the stabilizers and control the base
or core structures in a stable, controllable environment
before progressing to less stable, more challenging envi-
ronments.
testing is done at functional speeds or loads, or in specific
joint positions. Atraumatic instability occurs because of
failure of the contractile (muscle) stabilizers to fully sup-
port base structures (scapula, pelvis), or loss of control of
movement due to muscle or nerve dysfunction. Initially,
the inert tissue is normal, but over time it too becomes
pathologic (Figure 19-5). Usually, macrotrauma to the
structure has not occurred, and the instability commonly
is bilateral even if the patient complains of symptoms
only on one side.
Atraumatic instability may occur anywhere in the
ROM. Most commonly, the instability occurs in one
direction, with hypomobility occurring in the opposite
direction. An example is a shoulder that demonstrates
anterior instability but has a tight posterior capsule. As
mentioned, atraumatic instability is most obvious at high
speeds or loads, during particular functional movements,
or in certain positions. The clinician must remember to
take these factors into account when testing for insta-
bility. The usual cause of this type of instability is loss
of muscle or joint stiffness combined with abnormal

Types of Instability
Pathologic instability can take several forms, ranging from
a frank dislocation at the end of the ROM to a subtle
sense that the joint does not “feel right” during certain
movements because of the patient’s inability to control
the movement. A normal or lax joint, in the presence
of microtrauma or macrotrauma, may become unstable.
This instability may be translational, in which there is a
loss of arthrokinematic control of joint movement owing
to poor motor control, or it may be gross (anatomic), in
which there is actually damage to the capsular, ligamen-
tous, or other soft tissues (e.g., labrum in the shoulder)
of the joint.

Translational (Atraumatic) Instability

Translational (atraumatic) instability can be defined as
an inability of the patient to control arthrokinematic and
part of the osteokinematic movements of the joint (loss of
motion segment stiffness) through coordinated muscular
activation, as the joint moves through its ROM.7,29 In
this case, the end of the ROM is usually normal, and the
inert and muscular tissues have normal lengths. However,
in part of the range, the patient “feels” that the joint is
not moving right. An example would be the swimmer
who complains of the shoulder “not feeling right” dur-
ing the catch phase of overarm swimming. To compound
the problem, a regular musculoskeletal assessment may
be negative, with the only indication of problems being Figure 19-5
that the joint does not “feel right” in part of the ROM, Atraumatic instability of scapula (note winging of inferior angle),
and the signs and symptoms become obvious only when demonstrating lack of control of the scapular stabilizers.
398 SECTION II • Principles of Practice
coupling action (force-couple muscles working together)
of the stabilizers and mobilizer muscles. This type of
instability responds best to a stepwise rehabilitation
program (discussed later). Atraumatic instability is pri-
marily a contractile tissue problem. There are some cases
in which surgery may be necessary; however, surgery
should be considered only as a last resort. With this type
of instability, there is loss of functional control in part of
the ROM, often resulting in a very subtle instability jog
that is often described by the patient as a “catching” or
“giving way” somewhere in the ROM. Pain is not a com-
mon sign, although tissues may be tender on palpation.
If present, pain occurs on movement and disappears with
rest or when the muscles are not contracting.
With atraumatic instability, there is commonly an
increase in the neutral zone, whereas the physiologi-
cal and anatomic barriers remain normal. This type
of instability is most obviously associated with activ-
ity. Commonly, the person may take longer to warm
up if he or she does sporting activities. The patient
also will fatigue more quickly, which manifests as loss
of control.30 The muscles around the joint are not as
strong as normal, nor do they have the same endur-
ance. Abnormal movement patterns are seen as other
muscles begin to contract early to compensate for those
that are not firing correctly. An example of this would
be excessive early contraction of the upper trapezius
to prevent early or excessive scapular protraction on
elevation due to weakness of the lower trapezius and
serratus anterior.
Interestingly, most people show some inability to
stabilize the base structures (i.e., pelvis and scapula)
and demonstrate abnormal movement patterns. The
vast majority of these people do not complain of
symptoms (potential pathologic instability). The rea-
son for this is that most people do not stress these
structures functionally and perform only those activi-
ties that do not lead to overload of the muscular,
inert, or neurological tissues. They perform activities
at a level at which maximum motor control, strength,
and endurance are not an issue. If these people were
required to perform at maximum functional level in
vulnerable positions, the instability would begin to
manifest itself.
Signs of Loss of Control/Fatigue
● Erratic movement
● Incorrect movement patterns
● Jerky (phasic) movement
● Trick movements
●
Loss of control of base (pelvis or scapula)
● Instability jog or “catch”
● Breath holding
Traumatic Instability
Traumatic instability involves a subluxation or disloca-
tion of a joint due to a traumatic event. Traumatic insta-
bility (also called gross or anatomic instability) implies
that the patient loses control of movement at the end of
the ROM. An example would be an acutely or chroni-
cally dislocated joint. In this case, the patient can “con-
trol” the joint movement through most of the ROM,
but because the structures at the end of the range are
injured (most commonly inert capsular structures, but
muscles may be stretched or nerves compressed), the
joint is unstable at the end of that particular movement.
The instability occurs at the end range, and on assess-
ment, apprehension is the main clinical sign as the joint
approaches end range. Although pain may be present,
it is not the main symptom except when the joint is
dislocated.
Commonly, this type of instability occurs in one
direction, with damage primarily to the passive stabiliz-
ers to the joint—the capsule, ligaments, labrum, and
bone. A common example is a shoulder dislocation with
displacement of the humerus from the glenoid fossa.
Such injuries are commonly accompanied by a torn
labrum (Bankart or superior labral anterior-posterior
[SLAP] lesion), possible nerve injury (axillary nerve or
brachial plexus), and bone injury (Hill-Sachs lesion).
The cause of such a dislocation is most commonly mac-
rotrauma, but acquired muscle weakness, congenital
weakness of contractile and inert tissue, nerve paralysis
or deformity, or congenital joint laxity may contribute
to the problem or lead to a chronic state. With this type
of instability, the neutral zone usually is normal, but
the pathologic and anatomic barriers are increased (see
Figure 19-2), at least in the initial stages. If the joint is
immobilized for a sufficient time, the physiological and
anatomic barriers commonly decrease (or move to the
left, as in Figure 19-6) because of adaptive shortening,
provided the inert tissues have only been stretched and
not torn.
If the inert tissues are torn, instability and hypermo-
bility signs predominate. If the tissue—especially inert
tissue—is torn, surgery may be required, especially if the
person is active. With traumatic instability, a deformity
is present only while the joint is dislocated. Once the
dislocation is reduced, the deformity and acute pain dis-
appear, although the joint will remain sore or tender.
Muscle spasm, if present, is most common toward the
end of the ROM, and its occurrence is often determined
by how quickly the end range is approached.
This type of injury commonly is associated with the
circle concept of instability. The circle concept of insta-
bility means that although the injury may be obvious pri-
marily in one direction, in fact, all parts of the joint may
be affected, so that with an anterior shoulder dislocation,
posterior shoulder structures may also be injured.31
 CHAPTER 19 • Principles of Stabilization Training 399

Normal physiological barrier Normal anatomical barrier

Normal crimp barrier

Neutral Zone

N N N

restriction of shortened joint hypomobility

arthrokinematics muscle

short tightness

Figure 19-6
Normal movement and hypomobility. Note how the normal barriers move to the left (i.e., decrease). (Not drawn to scale. Normally, the neutral
zone is very short, and physiological and anatomical barriers are very close to each other.)

As with atraumatic instability, rehabilitating the stabi-
lizer muscles first plays a primary role in protecting the
joint as much as possible. Commonly, these instabili-
ties require surgical correction followed by a rehabilita-
tion program that is similar to that used for atraumatic
instability (discussed later).
Voluntary Instability
Voluntary instability, a third type of instability, occurs
in the patient who has a lax joint and is able to sub-
lux the joint voluntarily. An example of this would be
the patient who presents to the clinician saying “What
does it mean when I can do this” and proceeds to sub-
lux the shoulder voluntarily (Figure 19-7). There is
little the clinician can do with these cases, although the
patient should be discouraged from subluxing the joint
to amuse (or horrify) his or her friends. Such action
accelerates the degenerative joint changes that accom-
pany any subluxation. For the most part, these people
live normal lives with few problems. If problems do
exist, they should be treated as in cases of atraumatic
instability.
Involuntary Instability
Involuntary instability, a fourth type of instability, occurs
because the muscles and other soft tissues no longer
function to support a joint owing to disease or another
pathologic process. A patient with a stroke who has a
shoulder subluxation because of the pull of gravity is an
example of involuntary instability (Figure 19-8). In this
case, treatment revolves around protecting the stressed
structures and preventing them from being stretched.
Hypermobility Syndrome
Joint hypermobility syndrome or benign joint hypermo-
bility syndrome is one of a number of related connec-
tive tissue disorders, including Marfan’s syndrome and
Ehlers-Danlos syndrome—hypermobile type (type III),
that have a strong genetic (familial) component with a
wide variety of clinical features and varying degrees of
severity.32–36 Some34 have reported joint hypermobility
syndrome and Ehlers-Danlos syndrome type III as the
same condition. The condition is sometimes associated
with rheumatic disease and fibromyalgia.34,35
Hypermobility is common, but the syndrome is evi-
dent or classified as such only if the hypermobility is
associated with chronic multijoint pain, hyperextensible
skin, impaired scar formation, and striae atrophicae.34
Unlike the other instabilities noted previously, joint
hypermobility syndrome has no known successful treat-
ment, although some attempts have been made to apply
the instability treatment methods outlined in this chap-
ter.34 For more detailed information, the reader is referred
to Keer and Grahame.34
Instability Factors
Several predisposing factors can contribute to any type of
instability. These include injury (both macrotrauma and
400 SECTION II • Principles of Practice

Figure 19-7
Voluntary shoulder subluxation.

microtrauma), loss of muscle strength or muscle endur-
ance, a growth spurt, aging, an abrupt increase in activity
leading to repetitive stress injury, inflexibility, poor tech-
nique when doing an activity, poor fitness level, incor-
rect posture, inability to control base or core structures
(pelvis or scapula), and loss of motor control.
Instability—Predisposing Factors
● Injury
● Loss of muscle strength/endurance
● Growth spurt
● Aging
● Abrupt increase in activity
● Inflexibility
● Poor technique
● Poor fitness
● Posture
● Loss of control (too fast, too much load)
Signs and symptoms of instability may vary. In most cases,
except when the joint dislocates, there is no obvious defor-
mity, although there is abnormal movement in part of the
ROM that shows up as an instability jog, a twitch or catch, or
a giving way.14 This instability jog is often very subtle but can
be dramatic, and the clinician must watch closely for it during
movement. The deformity becomes incapacitating only when
the patient performs a movement that he or she cannot con-
trol. Thus, the loss of control may be evident in one position
and not others, or it may be present when a specific muscle
contracts and disappear with relaxation of that muscle. The
examiner will note protective muscle spasm when the joint is
stressed or unstable. Significant pain is not a predominant fac-
tor except with an unreduced dislocation. Pain is more likely
to manifest as an ache in the joint or surrounding tissues.
Apprehension with protective muscle spasm is a more com-
mon finding, especially with a traumatic dislocation at end
range, as is the complaint that the joint does not “feel right”
or “gives way” with activity. On assessment, the clinician may
find that the joint appears normal or that ligamentous testing
 CHAPTER 19 • Principles of Stabilization Training
Figure 19-8
Involuntary subluxation.
is negative for instability, although pain may be provoked. In
normal-appearing joints, the clinician may find that the joint
has to be stressed in different positions. If a motor control
problem exists, the clinician must watch for incorrect move-
ment patterns (incorrect order of muscles contracting) or for
abnormal movements during functional activities (e.g., high
speed, high load, particular position).
Instability—Signs and Symptoms
● No incapacitating deformity
● Deformity may be present in one position and not in others
● Deformity may be present with muscle contraction and disappear
on relaxation
● Muscle spasm when joint stressed or unstable
● Muscle twitching (instability jog) may be evident during movement
● May be evident only when functional activity is beyond patient’s
control (too fast, too much load, lack of concentration)
● Excessive joint play increase in the neutral zone (may be in only
one direction)
401
Instability Symptoms Depend On:
● Load
● Speed of movement
● Strength of muscles
● Endurance of muscles
● Type of muscle contraction required
● ROM available
Instability may be evident only when functional activ-
ity is beyond the patient’s conscious control and moves
without thinking. The symptoms of a patient with an
unstable joint depend on the joint load being applied, the
speed of movement, the strength and endurance of the
muscles, the type of muscle contraction required (e.g.,
isometric, isotonic, eccentric, concentric), and the ROM
available, as well as the position of the joint. In addition,
excessive joint play may be found only in one direction.
Such hypermobility in one direction increases the neu-
tral zone in that direction, leading to the potential for
arthrokinematic instability.
Stabilization Principles
Stabilization results from the ability of the individual
to control, consciously or unconsciously, macroscopic
and microscopic movements of the joint throughout
its ROM. This means that the patient must demon-
strate a controlled activation of individual muscles
that maintain the joint surfaces in a correct functional
relationship; can perform activities that do not cause
tissue overload; and has established correct motor pat-
terns (engrams). The key to active joint stabilization
is a stable base or core (i.e., pelvis or scapula) from
which mobilizer muscles can function. This stable
base is provided by the stabilizer muscles, allowing
the mobilizer muscles to position the extremity for
function. Although these bases are considered to be
“stable,” they are still moveable, with the muscles pro-
viding stabilization in different positions. Thus, the
muscles work dynamically, functioning as “active” guy
wires that work concentrically to shorten, eccentrically
to lengthen, or isometrically to stabilize the joints
statically.
In the body, there are two primary dynamic bases
or core structures—the pelvis and the scapula—both
of which need to be statically and dynamically stabi-
lized to enable the mobilizer muscles originating from
them or near them to function properly. The pelvis
acts as a base for the whole body, but especially for the
spine and lower limbs, whereas each scapula acts as a
base for its respective upper limb. If the patient can-
not maintain or control this “base,” then a pathologic
process will eventually manifest itself. The patient may
402 SECTION II • Principles of Practice

be unable to maintain a stable base if there is local sta-

bilizer muscle dysfunction, tissue restrictions (hypo- Movement Dysfunction Factors
mobility), or pain, if the ROM and load are too great ● Central nervous system inability to recruit and drive motor units
for the patient to function properly, if the speed of the (incorrect movement patterns)
activity is too great, or if the activity is too advanced ● Coactivation of antagonistic muscles (abnormal firing patterns)
for the patient to perform. Hence, the clinician must ● Decreased contractile capacity (atrophy)
be able to evaluate and provide appropriate interven- ● Decreased muscle stiffness (muscle lengthening)
tions (exercise and awareness education) to correct ● Loss of ROM (hypomobility)
an unstable base during instability training. Failure ● Insufficient and inappropriate timing of muscle activity (force-
to do so leads to frustration on the part of both the couple and mobilizer/stabilizer dysfunction)
patient and clinician, and ultimately to a failed treat-
● Muscle imbalance
● Sensory disorganization (proprioception/kinesthesia)
ment plan. ● Altered metabolic demands
● Anaerobic/aerobic conditioning
If Patient Cannot Maintain Stable Base:
● There is local stabilizer dysfunction
● There are tissue restrictions (hypomobility)
● There is pain Instability Can Lead To:
● Activity ROM is too great
● Load is too great
● Clinical adaptation
● Speed of activity is too great
● Subclinical adaptation
● Activity is too advanced
● Functional/biomechanical adaptation
● Neurological adaptation

The body has several natural stabilization methods.
These include muscle contraction, muscle spasm, osteo-
phyte formation, scar tissue formation, and adaptive
shortening of inert tissue or muscle. The most com-
mon form of natural stabilization is a muscle spasm in
the presence of injury. However, over time, osteophyte
formation, scarring, inert tissue tightening, or muscle
shortening may contribute to stabilization.
Movement dysfunction or motor control factors play a
major role in instability.20,24,26 These factors may involve the
neurological system, the contractile system, the inert sys-
tem, or any combination of the three.
Over time, the presence of instability can lead to sev-
eral types of adaptation, including clinical adaptation, sub-
clinical adaptation, functional or biomechanical adaptation,
and neurological adaptation.15,24,26 Clinical adaptation or
clinically obvious change may result in pain, apprehen-
sion, decreased or increased joint ROM, loss of muscle
power and function, or swelling in the joints combined
with abnormal functioning of the tissue at fault (Table
19-2). Subclinical adaptation is change that often is not
clinically obvious. Subclinical adaptation can lead to altered
movement patterns (i.e., the person can still do the move-
ment, but “cheats” by doing the movement incorrectly),

Table 19-2
Clinical Adaptations to Instability
Clinical Subclinical Functional/Biomechanical Neurological

Pain Altered movement Inflexibility Nonsequential

Decreased range (e.g., gait) Strength imbalance movement
of motion Decreased speed Loss of endurance Noncoordinated
Loss of power Decreased accuracy Instability movement
Loss of function Tissue adaptation Structural (anatomic) Abnormal movement
Swelling (remodeling) Nonstructural patterns (force
Pathologic change Altered fitness level (biomechanical) defects dependent)
in tissue at fault Complications Lack of specificity Abnormal receptor input
(length dependent)
Abnormal firing patterns
Altered proprioception

Adapted from references 15, 24, 26, and 59.

 CHAPTER 19 • Principles of Stabilization Training 403

decreased speed of movement, decreased accuracy, tissue

adaptation or remodeling, and alteration in fitness level. In
functional or biomechanical adaptation, changes result-
ing from a pathologic process or alterations in the healing
process may lead to inflexibility, muscle strength or endur-
ance imbalance, loss of motor control, and nonstructural
deficits that may progress to structural deficits over time.
Neurological or motor adaptation includes movements
that have become nonsequential or noncoordinated,
abnormal movement patterns that may be force or speed
dependent, movements that have an abnormal receptor
input that is time dependent, or movements that demon-
strate abnormal firing patterns, leading to altered proprio-
ception as well as incorrect movement patterns.
Correct movements depend on four factors, any of
which may cause a problem.24,26 First, the joint must have
the freedom to move in its normal arthrokinematic fashion.
Second, there must be proper sequential recruitment of
muscles. This may involve a particular muscle performing
a particular action, or ensuring that the movement is done
correctly with the stabilizers contracting first, followed by
the mobilizers. Third, the muscles must eventually demon-
Figure 19-9
strate an ability to achieve the required velocity and have the
Instability pathway.
appropriate strength and endurance to perform activities
functionally. Fourth, there must be suitable neuromuscu-
lar coordination and control to allow synchronized, skilled an active role in his or her treatment to achieve a successful
movement sequences through balancing and integration of outcome. Success will be determined by the patient and his
the force couples acting over the joint. or her desire to get better, much more than by what the cli-
Injury or abnormality in a joint or several joints can lead nician does. A stabilization program is never a “quick fix.”
to an instability pathway5,7 (Figure 19-9). The abnormality It takes time (often 4 to 6 months), as well as dedication
or injury may be due to overuse, degeneration, a particular on the part of the patient.37 To learn correct movements,
sustained posture, or trauma. These injuries, in turn, lead patients progress through three phases of practice—a cog-
to an impairment involving contractile, inert, or neuro- nitive phase, in which they learn how to do the movements
logical tissue. If one or more of these tissue components is correctly; an associative phase, in which they perfect the
affected, this leads to a movement or motor control impair- movement patterns; and, finally, an autonomous phase,
ment, as evidenced by dysfunction or alteration in normal in which they do the movement automatically, paying little
force couples, muscle imbalance, stabilizer or mobilizer or no conscious attention to what they are doing.37 Proper
dysfunction, or joint hypomobility/hypermobility. These rehabilitation for instability involves carefully “pushing the
movement changes in turn lead to functional limitations envelope” and an understanding on the part of the patient
resulting from incorrect movement patterns and arthro- and clinician of the difference between expectations and
kinematics. Finally, the functional limitation leads to the reality. The clinician needs to make an accurate assessment
disability about which the patient complains. of what tissues are at fault and which movements are incor-
rectly performed to ensure a suitable treatment program.
Stabilization Treatment Principles
Stabilization training is a multifaceted program that cor-
Stabilization Training
rects a disability by improving movement through neu- ● A multifaceted program
romuscular control and coordination of specific muscles ● Corrects impairment by improving neuromuscular control and
and correction of restrictions to restore normal movement coordination of specific muscles and movements
to any unstable joint, whether the spine, shoulder, knee, ● Corrects mechanical factors that predispose or contribute to
or ankle.24,26 Thus, it corrects the mechanical factors that abnormal movement patterns
predispose or contribute to the abnormal movement pat- ● Requires active patient cooperation and participation
terns. To do this, active patient cooperation and participa-
● Needs accurate diagnosis of which muscles are at fault and which
tion are essential components. The patient must be an integral movements are incorrect
part of the training continuum and must be prepared to take
404 SECTION II • Principles of Practice
The goal of stabilization treatment is to obtain adequate
control of movement, particularly through muscle action,
to prevent injury to bone and soft tissue structures. The
clinician should specify work within a ROM that allows
the patient to move without pain or apprehension and
with little or no muscle guarding, while at the same time
ensuring that the patient performs the correct movement
pattern. The aim of the stabilization program is to enable
the patient to attain, first, static, isometric control of the
base structures, and then to maintain that control dur-
ing dynamic movements, ensuring that incorrect move-
ment patterns are eliminated while the patient progresses
to functional movements. With dynamic movements,
the patient begins with concentric contractions and pro-
gresses to eccentric contractions. Ultimately, the eccentric
component is the most important, but it is commonly the
most difficult for the patient to master.
Instability or motor control training involves the coor-
dinated use of the three basic subsystems, the contractile
tissue subsystem, the neurological tissue subsystem, and
the inert tissue subsystem, to ensure proper function.14,15
Instability training involves establishing a stable base or
core before working on a mobile distal segment, regard-
less of which joint is at fault.7,24,26 Thus, the training
involves developing a stable base or core around which
a mobile kinetic chain can function. Once a stable base
is established, a sequential movement of segments from
proximal to distal requiring successive activation of each
kinetic chain segment can be initiated. Sequential activa-
tion of the kinetic chain is desired because specific motor
control patterns stabilize each segment, generate con-
trolled forces for correct movement patterns or braking/
stopping the movements, and position each joint to allow
efficient energy transfer to the terminal mobile segments.
Proper movement pattern development depends on feed-
back from the joint, muscles, skin, and limb position and
motion, so proprioceptive training plays a dominant role
in the program.37
Motor Control Training Involves:
● Maximum psychological concentration
● Minimal resistance
● Specificity (proper patterning)
● Control of stable base
● Minimal speed
● ROM control (work only in ROM that patient can control)
To teach movement control, the patient must first
“unlearn” the incorrect or aberrant movement patterns,
followed by a sequenced learning of the correct movement
patterns.24 Although this seems simple, it is the unlearn-
ing component that is most difficult because the patient
is easily fatigued by motor control training and quickly
reverts to the original, incorrect (habitual) movement
pattern unless he or she is very carefully supervised and
cued, often because of frustration or boredom at spend-
ing so much time learning new patterns. To relearn a cor-
rect movement pattern requires an understanding of what
is to be accomplished and a very conscious effort on the
part of the patient to know what muscles are contracting
and when they are to contract. The patient must work
only in the range in which he or she has control of the
movement. As an example, short arc exercises are com-
monly used early, with many repetitions. Their purpose
is to develop the proper movement engrams and move-
ment while building strength and endurance. Imbalance
patterns must be corrected early to ensure that muscles
function in a coordinated fashion.7,24,26
Once imbalance patterns have been corrected,
the next step is early activation of the local stabilizer
muscles and a decrease in unwanted overactivity of
the mobilizer muscles. The patient must develop an
improved perception of the movement pattern, and the
precision required to perform the movement pattern.
To do this, the movement must be continually repeated
and continually corrected by the clinician. Commonly,
this requires a great deal of patient concentration that,
especially in the early stages, is psychologically as well
as physiologically fatiguing. When performing stabili-
zation exercises, the clinician should never recommend
a specific number of exercise repetitions because the
important issue is to make sure the patient performs
the movements correctly. The clinician must continu-
ally watch for fatigue and teach the patient the signs
of fatigue and to stop when any of them are evident.
For the clinician, watching for incorrect movement pat-
terns and fatigue takes precedence in early treatment.
Thus, early neuromuscular education or control train-
ing involves maximum psychological concentration on
the part of both the patient and clinician.
At the beginning, minimal resistance is provided to
a particular movement. The emphasis is on correcting
imbalance patterns and facilitating the stabilizers to con-
tract first (specificity of activity/contraction). Once the cli-
nician is sure the imbalance patterns are corrected and the
stabilizer muscles can contract isometrically in isolation,
the patient can move toward combining contractions of
the stabilizer and mobilizer muscles in dynamic patterned
movement, using only the range and speed at which he
or she can maintain control. As soon as the patient loses
control, the activity is stopped because the patient will
revert to the old, incorrect pattern with loss of control
or onset of fatigue. In this case, the clinician would then
move on to other exercises for other muscles.
Correct movement depends on freedom of joint
movement, neural control, correct muscle recruitment,
appropriate movement velocity, appropriate strength for
 CHAPTER 19 • Principles of Stabilization Training 405

the velocity of the activity, endurance, coordination of Table 19-3

movement, and synchronization of movement sequences Stabilization Training Sequence
so there is a correct movement pattern and the integra-
Stages Steps Purpose
tion of balance and forces necessary for correct functional
movement.7,24,26 Motor control implies the conscious Stage 1 1.1 Decrease pain
activation of individual muscles or conscious initiation of 1.2 Allow freedom of
a preprogrammed engram. The clinician must be careful movement
to have the patient recruit only those muscles that are Stage 2 2.1 Ensure proper
being trained in order to correct force-couple imbalance. muscle function
Because stabilizers tend toward weakness and atrophy, 2.2 Ensure proper muscle
recruitment
the clinician first teaches discrete control exercises to get
2.3 Correct muscle imbalance
these muscles to contract individually. This is often done
Stage 3 3.1 Correct endurance
in the “muscle test” position or in the inner range with discrepancies
less than a maximal contraction, to isolate the muscles 3.2 Correct strength
as much as possible. Therefore, the training is very spe- discrepancies
cific to the muscles that the clinician wants the patient to Stage 4 4.1 Retrain proprioception
recruit. Specificity is a key issue. No substitution (incor- Stage 5 5.1 Reeducate stabilizing
rect movement patterns) or signs of fatigue should be muscle statically
allowed. Recruitment of the individual muscle takes pri- 5.2 Teach advanced static
ority. As the individual muscles learn to contract and sta- stabilization exercises
bilize, the mobilizers can be included as long as there is 5.3 Teach dynamic
stabilization exercises
no loss of control of the stabilizers because of fatigue.
5.4 Teach advanced dynamic
Second, to develop control of the neutral zone, the clini-
stabilization exercises
cian must remember to train local stabilizers to contract 5.5 Teach functional stabilization
isometrically first. This is done by low-level activation of Stage 6 6.1 Maintain or restore fitness
the stabilizer muscles using a 10% to 30% MVC.24,26 This throughout
type of contraction favors type I muscle fibers, which are
the predominant fibers in the stabilizers, and also helps
isolate the contracting muscle.
Stage 1: Pain Control and the Restoration of
Stabilization Training Sequence Normal Joint Movement by Restoring Normal
Joint Arthrokinematics
The stabilization training sequence involves approximately
6 stages with 12 steps19,22,24,26,38–40 (Table 19-3). Each step First, pain must be controlled and normal arthrokinemat-
plays a significant role in stabilization training, and the cli- ics restored (Step 1.1). To do so, the clinician can consider
nician must ensure that each stage and step is considered treatments such as muscle relaxation techniques, teaching
and dealt with often before proceeding to the next one. joint resting positions, patient education, the use of elec-
If one stage or step is missed, stabilization becomes much trophysical agents, instruction in proper body mechanics,
more difficult to obtain and the patient will have difficulty working in the pain-free range, and the use of medication.41
returning to normal function. With stabilization training, It is important to remember that with instability, pain is
the clinician is trying to teach the patient voluntary control not the primary symptom, but if it is present, it will have
of the different movement patterns. The clinician should an effect on the patient’s performance. Thus, all move-
start with slow, precise movements and stop exercise when ments should be performed in the pain-free ROM.41
the patient becomes fatigued. Movement patterns should To allow freedom of movement and proper arthrokine-
continually be corrected and exercise should be progressed matic movement of the joint (Step 1.2), the clinician may
only when the movement pattern is correct. The patient consider techniques such as joint play mobilization (joint
must be able to perform individual muscle exercises inde- capsule), prolonged passive stretch (inert tissue and mus-
pendently before proceeding to more advanced motions. cle), muscle energy techniques (muscle), active relief tech-
The clinician must try to link the simple tasks done initially niques (muscle), manipulation (joint), and neurodynamic
to the more complex actions that the patient will eventu- techniques (nerve), depending on the tissue causing the
ally use functionally. To increase the patient’s awareness restriction. The purpose is to restore normal joint arthro-
of correct movement patterns, the clinician should divide kinematics and osteokinematics, so that the joint will be
complex movement sequences into simple components able to move properly when stabilization training is initi-
and work at the component level until control of the ated. Thus, when doing stabilization training, it is impor-
movement is assured. tant that hypomobility be treated before the hypermobility.
406 SECTION II • Principles of Practice
Stage 2: Individual Muscle Function
Stage 2 is an essential stage that is often missed or
skipped over by the clinician because it is the most dif-
ficult stage for both the clinician and the patient. This
stage involves three steps. First, the clinician must ensure
that the individual muscles will contract when and how
they should, starting with an isometric contraction of
the isolated muscle (stabilizers first) to ensure proper
muscle function (Step 2.1).20,26,39
Once the muscle is contracting the way it should,
proper muscle recruitment and reeducation are instituted
so the muscles contract in the correct order (e.g., first
stabilizers, then mobilizers; Step 2.2). The clinician and
patient work together to ensure muscle balance between
the various muscle groups and force couples (Step 2.3).
The three steps may be done concurrently, but each
requires special emphasis to ensure good isometric sta-
bilizer function before moving on to dynamic stabilizer
function and then to combined stabilizer and mobilizer
function.
For individual muscle function (Step 2.1), emphasis
is directed primarily at the weak stabilizer muscles to
ensure a strong, stable but mobile base from which other
muscles can act. Specificity is the key to ensure proper
muscle function. The clinician and patient must concen-
trate on individual muscle weakness first, with the patient
learning to do isolated muscle contractions (specificity)
in a pain-free range.26 This is most commonly done in
the inner range or a “muscle test” position. It involves
focused, conscious effort on the part of the patient, so
the clinician must always be alert to psychological (loss
of concentration) and physiological (incorrect move-
ment pattern) fatigue on the part of the patient. To
perform the exercises correctly, the patient soon learns
that a high level of concentration is necessary, and the
clinician must ensure that the patient performs the con-
traction or movement as specifically required so that the
individual muscles contract without synergistic support.
Commonly, the movement is broken into components to
accomplish this. Initially, an isometric minimal (10% to
30%) MVC is used to initiate the type I muscle fibers of
the stabilizers and to isolate these muscles.26,41
Retraining Stabilizer Muscles
● Start by working in “muscle test” position
● Use low isometric contraction (10%–30% MVC)
● Watch for fatigue—stop as soon as evident
● Work in inner range
● Ensure correct pattern of movement
● Move to low-load isotonic contraction (preferential type I fiber
recruitment)
● Progress to eccentric loading (shock absorbing and braking)
● Proprioceptive training throughout
Once the patient can contract the muscle isometri-
cally, concentric movement using the mobilizers can be
initiated, but only if the stabilizer muscles function prop-
erly. Again, movement is often broken down into con-
trollable components. ROM is limited to that in which
the patient has control, and closed kinetic chain exer-
cises are more commonly done initially (Step 2.2). As
the patient gains control, ROM, load (resistance), and
speed can be increased. It is essential that, whatever the
range in which the clinician asks the patient to work, a
correct movement pattern is emphasized, with the clini-
cian always watching for fatigue or incorrect movement
patterns, and stopping the patient as soon as either is evi-
dent. As control is gained, the types of contraction will
move from isometric to concentric to eccentric action
and, where appropriate, econcentric action. Eccentric
training is important for the stabilizers because it allows
them to maintain control at the base while lengthening
during functional movements. It also trains the muscles
to act as eccentric brakes to slow down or stop move-
ment, or to act as a dynamic shock absorber. Econcentric
action allows two joint muscles (mobilizers) to function
(shortening at one end, lengthening at the other—e.g.,
hamstrings) as they do in everyday functional activity.
The clinician should remember that if a muscle acts
concentrically in one direction to accelerate a motion, it
acts eccentrically in the opposite direction to decelerate
the motion, acting as a brake and shock absorber; thus,
both concentric and eccentric training become important
as the stabilization training progresses. Concentric mus-
cle action initiates the movement, providing speed to the
movement and the necessary force for the movement to
occur. Eccentric movement, on the other hand, helps to
control the speed of movement by providing controlled
release in the particular pattern, as well as acting as a brake
to slow down the motion and as a shock absorber to lessen
the stress applied to joints and adjacent structures.
Once the stabilizer muscles functioning properly,
mobilizer muscle training can begin. Muscle balance
(Step 2.3) primarily involves training the various force
couples to ensure that they work together correctly
and function properly to enable proper movement con-
trol and decrease or eliminate incoordination. It may
involve force-couple training between agonists and
antagonists, agonists and stabilizers, antagonists and
stabilizers, stabilizers and mobilizers, or agonists
and synergists. Table 19-4 gives examples of muscle
imbalances commonly seen with crossed syndromes.
In general, to correct muscle length, one should exer-
cise lengthened muscles in the inner range to shorten
them, and stretch short muscles to lengthen them.
Equalization of strength and endurance between left
and right limbs must also be considered. Mobilizer
muscle training moves from isometric to concentric to
eccentric to econcentric to functional movement. As
 CHAPTER 19 • Principles of Stabilization Training 407

Table 19-4
Muscle Imbalance Patterns
Muscle Action Short, Tight Muscle Long, Weak Muscle

Scapular elevators and retractors Levator scapulae Upper trapezius

Scapular retractors Rhomboids Lower trapezius
Glenohumeral medial rotators Pectoralis major Subscapularis
Trunk flexors/pelvic posterior rotators Rectus abdominis External oblique
Hip flexors Tensor fascia lata Iliopsoas
Hip abductors Tensor fascia lata Gluteus medius (especially
posterior part)
Hip extensors and knee flexors Medial hamstrings Lateral hamstrings
Ankle dorsiflexors Extensor digitorum longus Tibialis anterior

From Sahrmann SA: Diagnosis and treatment of movement impairment syndromes, St. Louis, 2002, Mosby.

movement function improves, the clinician can prog- aspects of proprioceptive and kinesthetic training that
ress the patient from stable to unstable positions, work should be included in any stabilization program.
at higher speeds and loads, work on reaction time, and To retrain proprioception (awareness of the static
institute plyometric exercises. position) and kinesthesia (conscious awareness of
movement), the clinician must consider what actions
stimulate the different mechanoreceptors, as well as
Stage 3: Strength and Endurance Training
the pertinent feedback and feedforward systems, bal-
In this stage, the clinician works with the patient to cor- ance mechanisms, reaction times, movement patterns,
rect any endurance (Step 3.1) and strength (Step 3.2) dis- and speed of movement.43–46 Initially, exercises should
crepancies, always keeping in mind the ultimate functional revolve around using a stable base and co-contraction
goal.42 This stage should be initiated only when the patient in a closed kinetic chain,46,47 but can progress to an
has learned to statically control the base structures. Both
stabilizer and mobilizer muscles are included, but the cli-
nician must ensure that the patient can maintain correct Table 19-5
posture and the stabilizer muscles can hold the base sta- Proprioceptive Training in Motor Control Training
ble but still allow it to be mobile. Exercises for stabilizer Increase Awareness of
muscles may involve high-load, low-repetition training for Correct Movement Gain Voluntary Control of
strengthening, but the main emphasis for these muscles Pattern Movement Pattern
is endurance training (low loads, high repetitions). When
correcting endurance discrepancies, the clinician must con- Split complex movement Use multisensory stimulation
sider functional movement repetition, appropriate energy sequence into simple during demonstration and
system training, and decreasing fatigue and improving components performance of exercise
Increase awareness by Start with slow, precise
recovery. For strength discrepancies, the clinician should
passive movement using movements
consider speed of movement, load, and repetitions when multisensory input Stop exercising when patient
doing functional activities. Although both strength and becomes fatigued
endurance are important at this stage, endurance takes Continually correct movement
precedence to build up resistance to fatigue. pattern passively
Progress exercise only when
movement pattern is
Stage 4: Proprioception and Kinesthesia correct
In this stage, the clinician must consider stimulating the Patient must perform
different mechanoreceptors in the skin, joints, ligaments, independently before
proceeding to more
and muscles to improve reaction time and develop more
advanced actions
efficient engrams. This stage could be initiated at the Link simple tasks to form
same time as Stage 3, provided the patient has success- more complex actions
fully completed Stages 1 and 2 and can demonstrate con-
trol of the base (pelvis or scapula). Norris20 has developed From Norris CM: Spinal stabilization. 1: Active lumbar stabilization—
a table (Table 19-5) that clearly illustrates the different concepts, Physiotherapy 81:61–64, 1995.
408 SECTION II • Principles of Practice
unstable base performing different types of concen-
tric exercises. The patient then progresses to eccen-
tric deceleration and plyometric activities involving
the whole kinetic chain. Proprioception is implicated
in increased awareness of correct movement patterns
and maintaining voluntary control of those movement
patterns. Retraining proprioception may involve work-
ing on timing, reaction timing, eccentric deceleration,
and performing patterned movements at controlled
speeds.
The muscle mechanoreceptors (muscle spindles and
Golgi tendon organs) play the most significant role in
proprioception and kinesthesia.18,19,48,49 Muscle spindles
are stimulated by muscle stretch, whereas Golgi tendon
organs are stimulated by muscle contraction, and there-
fore both are always active with movement and play an
important role in stabilization. The muscle spindle is
unique to muscle and is responsive to stretch, being
sensitive to both the static length of the muscle and the
rate of length change.36 They are found predominantly
in the muscle belly between the muscle fibers and lying
parallel to them. The more precise the movement, the
greater the number of muscle spindles. The Golgi ten-
don organs are encapsulated receptors found in the mus-
culotendinous junction. These slow-adapting receptors
detect active tension in the muscle when it contracts.
Golgi tendon organs and muscle spindles work together
to control tension and length in a muscle. With an iso-
metric contraction, the Golgi tendon organs fire in
response to being stretched, but the muscle spindles do
not fire because muscle length has not changed. If a
relaxed muscle is stretched, the muscle spindle fires but
the Golgi tendon organ does not.
Proprioceptive Training in Motor Control Training
● Muscle spindles—muscle stretch
● Golgi tendon organ—muscle contraction
● Golgi ligament endings—end range stretch
● Ruffini corpuscle equivalents—end range tension; active joint
movement direction, amplitude, and velocity
● Golgi-Mazzoni corpuscles—active and passive joint movement
direction, amplitude, and velocity
Several other joint receptors play a significant role
in proprioception19,36,50–56 (Table 19-6). The Golgi
ligament endings are found primarily in ligaments and
are thick, encapsulated endings that are sensitive to
ligament stretch or tension (Figure 19-10). They are
high-threshold, very slow-adapting dynamic mecha-
noreceptors that are inactive in immobile joints. They
respond to tension and are active toward the end of
the ROM, with some being active in each joint posi-
tion, even when it is immobile, or when the stress is
placed on ligaments. These mechanoreceptors signal
static joint position, intra-articular pressure changes,
and changes in the direction, amplitude, and velocity of
active and passive joint movements.
Ruffini corpuscle equivalents are found in the joint
capsule. They are slow adapting and are sensitive to ten-
sion and changes in intra-articular pressure as well as
changes in joint direction, velocity, and amplitude of
movement. They are activated by mechanical deforma-
tion and are good receptors for constant pressure. They
are also stimulated by sudden joint movement, being able
to sense joint position and changes in joint angle.
The pacinian corpuscle equivalents are similar to the
pacinian corpuscles in the skin. They are found in joint
capsules and are sensitive to rapid changes in mechani-
cal stimulation. These encapsulated end organs are rate-
of-motion detectors that signal joint acceleration and
deceleration. They are more densely distributed in dis-
tal joints than in proximal joints. These receptors are
low-threshold, rapidly adapting, dynamic mechanore-
ceptors that are inactive in immobile joints. They are
active only at the beginning of the movement or when
there are sudden movements or changes, and during
deceleration. These mechanoreceptors act as “boosters”
in that they help overcome the inertia in an immobile
joint by firing at the beginning of movement. They are
also activated by pressure in the form of compression
or distortion of the capsule, and by rapid joint angle
changes. These mechanoreceptors tend to fire for very
short periods of time.
The Golgi-Mazzoni corpuscles are found on the inner
surface of the joint capsule. These encapsulated receptors
are low-threshold, slow-adapting static and dynamic
mechanoreceptors that respond to changes in mechanical
stress in the part of the capsule in which they are found.
They are more densely distributed in proximal joints than
in distal joints.
To stimulate the various mechanoreceptors, the clini-
cian must consider their different functions, when they
fire, and what stimulates them to ensure that propriocep-
tive training covers the whole area of proprioceptive and
kinesthetic input. Table 19-6 outlines the activity of the
various mechanoreceptors.56
Stage 5: True Stabilization Training Stage
In this stage, the five different stabilization steps are
integrated into the program.20 The initial step is used to
reeducate the stabilizer muscles to act statically (Step 5.1),
after which the patient progresses to advanced static sta-
bilization exercises (Step 5.2), followed by basic dynamic
stabilization exercises (Step 5.3), then by advanced
dynamic stabilization exercises (Step 5.4), and, finally,
functional stabilization (Step 5.5).
 CHAPTER 19 • Principles of Stabilization Training 409

Table 19-6
Joint Receptors
Parent
Axon (Fiber
Distribution Diameter,
(of Receptor Functional Conduction
Receptor Location Description Sensitivity Type) Classification Velocity)
Pacinian Fibrous layer Single terminal Sensitive to Found in Very rapidly Group II
corpuscle of capsule, within high-frequency all joints adapting; (8–12 µm,
equivalents on capsule– lamellated vibration examined; very low 49 ms);
synovium encapsulation; (>60 Hz), sole mechanical terminal
border, close appears in acceleration, corpuscular threshold branch at
to small clusters of and high- receptor in 3–5 µm
blood vessels 5 or less velocity laryngeal and diameter)
(20–40 × changes in middle ear
150–250 µm joint position; joints; greater
cylindrical) possible density in
sensitivity to distal than
hemohydraulic, in proximal
transient events joints
and rapid
contractile
events or
adjacent
muscles
Golgi-Mazzoni Inner surface Multiple Sensitive to Knee joint and Slowly Group II–III
corpuscles of joint terminating compression many others adapting; (5–8 µm;
capsule endings of joint capsule likely; may response estimated
between within thin in plane have specific is linear 30 ms)
fibrous encapsulation perpendicular distribution function of
layer and (30 × 200 µm to its inner within the compressive
subcapsular cylindrical) surface; joint capsule stress on
fibroadipose insensitive capsule; low
tissue to stretching mechanical
capsule threshold
Ruffini endings Fibrous layer Spray-type Sensitive Few present Slowly Group I–II
(pilo-Ruffini of capsule; terminal to capsule in distal adapting; (13–17 or
complexes) few present endings stretching joints; greater low to high 8–12 µm;
in extrinsic within thin along either of density in mechanical 51 ms)
ligaments encapsulation, its long axes proximal threshold;
with within capsular joints; response
investment plane, direction concentrated is linear
of collagen and speed of in capsular function
fibers (300 × capsule stretch, regions of of axial
300–800 µm, intracapsular most stress components
2–6 endings fluid pressure of capsular
per axon) change, plane stress
amplitude and
velocity of joint
position change
Golgi ligament Extrinsic and Thick Sensitive to Present in Slowly Group I
endings intrinsic encapsulation, tension or most joints adapting; (13–17 µm;
(Golgi tendon ligaments; profuse stretch on except cervical low to high estimate
organ–like) adjacent branching ligaments vertebral, mechanical +51 ms)
to bony (100 × 600 µm laryngeal, threshold
attachments total terminal and ossicular
of ligaments spread) ligaments

(Continued)
410 SECTION II • Principles of Practice

Table 19-6 — Cont’d

Joint Receptors
Parent
Axon (Fiber
Distribution Diameter,
(of Receptor Functional Conduction
Receptor Location Description Sensitivity Type) Classification Velocity)
Free nerve Fibrous Thin, bare One type Present in Slowly Group III–IV
endings capsule, nerve endings sensitive to all joints adapting; (2–5 µm,
(nociceptive ligaments, of small non-noxious examined but low to high <2 µm;
and non- subsynovial myelinated or mechanical density varies mechanical 2.5–20 ms)
nociceptive) capsule, unmyelinated stress; other with joint threshold
synovium, fat axons; profuse type sensitive component;
pads branching to noxious most joints
mechanical or have relatively
biochemical higher density
stimuli in ligaments

From Rowinski MF: Afferent neurobiology of the joint. In Gould JA, editor: Orthopedic and sports physical therapy, St. Louis, 1990, Mosby.

Bone Muscle tendon

Golgi-Mazzoni II III

Articular Capsule
cartilage

Tendinous insertion
to capsule

Menisci Synovial membrane

II
Pacinian
IV
Synovial free nerve III
I II
Figure 19-10
Ruffini III IV
Joint proprioceptive innervation.
(From Rowinski MF: Afferent Ligamentous
neurobiology of the joint. In free nerve I II
Bone
Gould JA, editor: Orthopedic and
sports physical therapy, St. Louis, Golgi ligament
1990, Mosby.)

To reeducate the stabilizing muscles statically
(Step 5.1), the clinician wants to ensure proximal sta-
bilization while allowing distal movement. The clini-
cian must be concerned with the ability of the patient
to maintain a stable static base, while at the same time
moving the distal joints dynamically. Thus, the patient
may be allowed to do only short arc movement exer-
cises in which the base (pelvis or scapula) is controlled
and does not initially move. While the patient performs
these exercises, the clinician watches for the expected
proper sequence of muscle contractions (stabilizers then
mobilizers), correct force-couple action (having ensured
good muscle force-couple balance earlier), and good
muscle co-contraction (static stabilization). To accom-
plish this, the clinician initially uses closed kinetic chain
activities for better static stabilization.46,47 To ensure cor-
rect muscle force-couple action, the clinician must con-
sider proper muscle recruitment and synchronization of
the muscles responsible for that action during loaded
and unloaded activities.
 CHAPTER 19 • Principles of Stabilization Training
Muscle balance is also critical when designing a
patient-specific program, keeping in mind the func-
tional activities to which the patient will eventually
return. In this early stage, force-couple action involves
coordinated co-activation of the muscle groups so mus-
cle torque at the joint is kept low to ensure increased
joint control. The local stabilizers close to the joint are the
primary muscles of concern, and isometric contractions
should be used to ensure minimal change in the length
of the stabilizer muscles. This is accomplished by hav-
ing the patient perform co-contraction or co-activation
activities, which consist of the simultaneous contrac-
tion of agonist, antagonist, and synergist muscles. This
increases static stiffness of the joint, leading to joint
compression, and passive tissue stabilization, which
helps the patient learn to regulate stress distribution in
the joint.47
Reeducating Stabilizing Muscles Statically
● Position statically
● Work proximal to distal (need stable base)
● Watch for correct force-couple action
● Do co-contraction activity
● Use closed kinetic chain activities initially
The next step in Stage 5 is to teach advanced static
stabilization exercises (Step 5.2).26 These exercises
involve taking the patient into the mechanism-of-injury
position and asking him or her to hold the position
statically against resistance. They may also involve the
use of closed kinetic chain activities in different posi-
tions, or exercises in the loose-packed position (less
stable) of the joint while the patient holds the posi-
tion statically. Eccentric “breaks” in which the patient
attempts to hold a position isometrically while the
clinician eccentrically moves it are effective advanced
static stabilization exercises.
Teaching Advanced Static Stabilization Exercises
● Go to mechanism-of-injury position
● Use open kinetic chain activity
● Teach control in different positions
● Use loose-packed positions
● Do submaximal contractions
Basic dynamic stabilization exercises (Step 5.3) involve
the use of controlled movement patterns to ensure the
development of proper movement patterns (engrams)
and voluntary control. These exercises involve movement
of the base, with the control muscles acting eccentrically
411
while distal joints are moved concentrically. In this
case, full range of movement exercises are used so that
stabilizers “learn” to work eccentrically while the distal
muscles function concentrically. Performing an exercise
or activity in this manner enables the stabilizer muscles to
develop the ability to control and handle greater torque
produced by the eccentric movement and teaches the
patient to control the interaction of their stabilizers and
mobilizer muscles. Controlling the interaction of these
muscles enables the patient to control the base with both
agonist and antagonist activity as well as to increase joint
torque. This stage requires greater coordinated sequenc-
ing on the part of the patient to control the movement
and depends on force and speed control. Ensuring correct
movement patterns now becomes the main concern.
Teaching Dynamic Stabilization Exercises
● Use specific movement patterns (to establish most efficient
engrams)
● Ensure voluntary control
● Use agonist–antagonist activities (both concentric and eccentric
control)
● Do activities with proximal stable base and mobile distal segment
Advanced dynamic exercises (Step 5.4) include multi-
directional stability training requiring control at functional
speeds, progressive eccentric exercises at functional speeds,
and stressing of functional diagonal patterns used in the
activities to which the person would be returning in his or
her everyday life.26 It is at this stage that various exercise
apparatus such as foam rolls (two-dimensional activities) and
balls (three-dimensional activities) come to the fore. Other
activities may include open and closed kinetic chain func-
tional activities, medicine ball activities, and plyometrics.57
The last step of Stage 5 consists of teaching func-
tional stabilization (Step 5.5).58 Functional activities
should be broken down into their component parts
early in the stabilization training program (similar to
the process done in Step 4) so that their component
motor skills are developed. The clinician should help
the patient to develop synchronized skilled movement
sequences that are activity specific. During functional
programs, the clinician should watch for appropriate
carriage of the body, which involves weight shift, weight
acceptance, movement symmetry, and control, so that
smooth, unrestricted, and automatic movement occurs
and the whole-body kinetic chain is used to modify for
stressors to the injured joints58 (Table 19-7). In addi-
tion, proper form and skill execution, demonstrated by
patient confidence, are important components of func-
tional stabilization. The clinician must ensure proper
movement patterns by monitoring the speed and
412 SECTION II • Principles of Practice

Table 19-7 restore the aerobic base to enable better recovery from
Observations During Functional Programs activity. As the patient progresses, individual energy
systems can be stressed depending on the patient’s
Carriage Control Confidence
functional activity needs.
Weight shift Smooth Fatigue/appre-
Weight accep- movement hension
tance Unrestricted Speed of activity
Return to Activity
Movement movement Deliberateness For the patient to return to activity, there are several cri-
symmetry Automatic of activity teria the clinician should consider. There should be com-
movement Good carriage plete resolution of acute signs and symptoms related to
Acceleration/ Good control the injury so that there is no pain or swelling with activity.
deceleration
There should be sufficient dynamic, functional ROM of all
Multiplane
movement
joints to enable the patient to do what he or she wants to
Proper form do, with the adequate strength, endurance, and proprio-
and skill ceptive/kinesthetic sense to perform the expected skills
Execution successfully. There should be no alteration of the patient’s
normal mechanics that could predispose him or her to
reinjury. The patient must be able to successfully perform
activity-specific tasks at or above the preinjury level.
degree of deliberation with which the patient performs
the activity. During functional stabilization training,
the clinician must also consider a home program for the Criteria for Full Return to Activity
patient and activity modification if necessary. Skills train-
ing progresses from bilateral to unilateral support and ● Complete resolution of acute signs and symptoms related to injury
from bilateral to unilateral nonsupport. Acceleration
● Full, dynamic ROM of all joints, with adequate strength and pro-
prioception to perform expected skills successfully
and deceleration activities and activity-specific function ● Should be no alteration of patient’s normal mechanics, which may
are all of concern.
predispose to reinjury
● Able to successfully perform activity-specific tasks at or above
preinjury level
Teaching Functional Stabilization
● Break down (motor skills) into component parts
● Use synchronized skilled movement sequences
● Make activity specific to activity to which patient is returning Conclusion
Stabilization training can be difficult and time-consum-
ing for the clinician as well as the patient. It requires a
very concentrated effort on behalf of both individuals.
Stage 6: Maintaining or Establishing a Suitable
There are several possible pitfalls that can occur during
Fitness Level
stabilization training if the clinician is not diligent. These
A patient whose heart rate takes longer than 5 minutes pitfalls are mainly related to failure to follow a stepwise
to return to resting levels after 2 minutes of exercise has progression in the rehabilitation program, so they may
poor cardiovascular function.59 In this case, the clini- include failure to address the pain or hypomobility ini-
cian should consider the energy system (alactic system, tially, and failure to follow the progressive steps, espe-
anaerobic glycolytic system, or aerobic system), speci- cially in ensuring individual muscle function. Another
ficity of the functional activity to which the patient will pitfall is failure to ensure the correct movement patterns
return, and establishment of an aerobic base for good and proper muscle firing or contracting sequences, which
fatigue recovery. For the latter, the patient should be can lead to incorrect movement patterns and hence to
able to exercise at 70% to 85% of maximum heart rate an unsuccessful treatment regimen. Other pitfalls may
for at least 20 minutes.59 This stage may be instituted include a failure to consider and involve the whole
early in the patient’s program, almost from the begin- kinetic chain when restoring function, as well as fail-
ning. If the patient has a trunk or upper limb injury, ure to understand the mechanics of the selected move-
lower limb fitness activities (e.g., biking or walking) ment patterns the patient will be required to perform
may be instituted. If a lower limb injury exists, then functionally when he or she returns to everyday activity.
upper limb activities (e.g., arm ergometer) may be There may also be failure on the part of the clinician
instituted. In the early stages, the aim is to establish or to understand the demands of the activity, or to
 CHAPTER 19 • Principles of Stabilization Training 413

rehabilitate the acceleration and deceleration components

Pitfalls to Stabilization Rehabilitation of the different movements.
● Failure to address pain and hypomobility
● Failure to follow progression steps References
● Failure to ensure proper patterns of movement To enhance this text and add value for the reader, all references have
● Failure to ensure proper muscle firing sequences been incorporated into a CD-ROM that is provided with this text. The
● Allowing incorrect movement patterns reader can view the reference source and access it on line whenever pos-
● Failure to understand the mechanics of selected movements sible.There are a total of 87 references for this chapter.
● Failure to understand demands of patient’s functional activities
● Failure to involve the whole kinetic chain
● Failure to rehabilitate deceleration and acceleration components
of movement

I NTEGRATION OF THE C ARDIOVASCULAR
S YSTEM IN A SSESSMENT AND
I NTERVENTIONS IN M USCULOSKELETAL
R EHABILITATION
Mark J. Haykowsky and Ellen A. Hillegass
Introduction
With the knowledge that the leading cause of death for
both men and women is cardiovascular disease (38% of
all deaths),1 health care practitioners must realize the
importance of assessment of the cardiovascular system
before providing any interventions that would affect this
system. Assessment of the cardiovascular system pro-
vides the practitioner with the justification for monitor-
ing or not monitoring activities during the individual’s
rehabilitation or providing modifications in the exercise
prescription. In addition, interventions provided should
include components to maintain or improve the physi-
ological condition of the client or, in some cases, prevent
physiological deconditioning. Therefore, the aim of this
chapter is to provide an overview of the assessment of the
cardiovascular system, as well as tools to provide safe and
effective cardiovascular conditioning in musculoskeletal
rehabilitation.
Health care professionals working in the rehabilita-
tion of musculoskeletal injuries need to assess the indi-
vidual for safety of exercise in addition to providing a
safe and effective exercise program. This chapter dis-
cusses the clinical assessment of risk for cardiovascu-
lar disease, the normal responses to both aerobic and
414
201
C H A PC TH EA RP T E R
Cardiovascular Assessment
● Helps determine whether activities that may affect the cardiovas-
cular system need to be monitored during rehabilitation
● Allows exercise modification if there are cardiovascular concerns
● Helps maintain or improve patient’s physiological condition
● Prevents physiological deconditioning
strengthening exercises, the role physiological moni-
toring plays in musculoskeletal rehabilitation, and the
components of an exercise prescription. Clinicians must
be knowledgeable about the acute effect that aerobic or
resistance exercise has on altering cardiovascular func-
tion. Clinicians also need to be aware of the effect of
certain conditions on the individual’s current cardiore-
spiratory fitness, such as the effect of aging, the effect
of deconditioning, and the effect of underlying heart
disease, as well as the role that therapeutic exercise
plays in affecting these conditions. Finally, guidelines
that can be used by rehabilitation clinicians to design
an exercise program to improve their clients’ overall
physical fitness are provided.
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation
Cardiovascular Concerns
● Acute effect of aerobic exercise on cardiovascular system
● Acute effect of resistance exercise on cardiovascular system
● Effect of aging
● Effect of deconditioning
● Effect of heart disease
The initial assessment of all clients with a musculo-
skeletal injury should include a systematic assessment of
safety for exercise using a set of questions to direct the
clinician. These questions should be incorporated in all
assessments, and are demonstrated with the use of case
studies throughout this chapter to exemplify the ease
with which this assessment can be integrated into the
rehabilitation of clients with musculoskeletal injuries.
Questions Clinicians Should Ask Themselves
When Assessing Clients
● Is this person safe for exercise? What is his or her risk for
cardiovascular disease?
● If the patient is safe for exercise, what should I monitor during the
assessment?
Are the responses that were assessed normal or abnormal?
●
● Based on the findings, how should the patient be monitored
during the interventions?
● What modifications/precautions should be provided in the exercise
prescription?
Is This Person Safe for Exercise?
What Is Their Risk for Cardiovascular
Disease?
Before beginning any exercise program, the health care
professional should perform a health screening check
or risk factor assessment as part of the initial assess-
ment. One health screening tool is the Physical Activity
Readiness Questionnaire (PAR-Q; Table 20-1). The
reason for the health screening check is to identify indi-
viduals who should consult their physician before initi-
ating an exercise program because of an increased risk
for cardiovascular disease. Because cardiovascular dis-
ease is the number one cause of mortality and morbidity
in men and women, all individuals who are prescribed
exercise should be screened for their risk of cardiovas-
cular disease. Specifically, if a client answers “yes” to any
of the questions, then the client should consult his or
her physician before initiating an exercise program.
The American Heart Association (AHA) has pub-
lished a number of scientific statements that provide
415
important guidelines for exercise testing and training,2
cardiovascular screening, staffing, and emergency poli-
cies at health/fitness facilities;3 the rehabilitation clinician
should be familiar with these. An alternative assessment
to the PAR-Q is the AHA Risk Assessment (Table 20-2).
The Risk Assessment quantifies an individual’s risk for
developing cardiovascular disease.
The risk factors for cardiovascular disease as defined by
the classic Framingham Study are found in Table 20-3.3,4
In the absence of the availability of the PAR-Q or the
AHA Risk Assessment, or any other formal risk factor pro-
file, the clinician can determine whether the client has risk
factors when taking a history by asking the simple ques-
tions provided in Table 20-4. Although the answers are
not quantified as to level of risk for disease, the clinician
can determine if there are significant risk factors present
in the patient’s history and determine if further medical
screening may be indicated. If an individual has the top
three risk factors for heart disease (elevated blood pres-
sure, cholesterol, and currently smoking) or experiences
symptoms during activities, his or her physician should be
contacted before providing an exercise program.4,5
Current evidence points to additional risk factors that
may define or elevate risk for cardiovascular disease.6,7
Emerging Risk Factors for Heart Disease6,7
● Elevated levels of :
● Homocysteine
● C-reactive protein
● Lipoprotein(a)
● Thrombolytic factors (increased clotting or stickiness)
● Endothelial dysfunction (increased reactivity)
● Obesity
● Metabolic syndrome
If Patient Is Determined Safe for
Exercise, Should This Patient Be
Monitored?
All patients should be monitored (i.e., heart rate, blood
pressure, and symptoms) during the initial assessment if
they have been determined safe to exercise based on any
risk factor or healthy lifestyle assessment. This should
be standard practice in all clinics and settings, and is
discussed in the Guide to Physical Therapist Practice.8
Once the individual has demonstrated normal vital
signs and lack of symptoms with the activities, it may
not be necessary to monitor further activities. However,
these responses to the initial assessment should be
documented to justify any needs for monitoring in the
future.
416 SECTION II • Principles of Practice

Table 20-1
Physical Activity Readiness Questionnaire (PAR-Q)

©2002 (Reprinted with permission from the Canadian Society for Exercise Physiology, http://www.csep.ca/forms.asp).
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation 417

Table 20-1—Cont’d
Physical Activity Readiness Questionnaire (PAR-Q)
418 SECTION II • Principles of Practice

Table 20-2

Table 20-3
Risk Factors for Heart Disease
High blood pressure: >140 mm Hg systolic or >90 mm Hg diastolic increases the pressure and trauma on the intima of the artery wall
Smoking: carbon monoxide is an irritant to the intima of the artery wall; increases the release of endothelial releasing factor
Elevated serum cholesterol: especially a total serum level >200, LDL >160 (individuals without heart disease, >100 in individuals
with heart disease), or HDL <40 in men or <50 in women. Also, a total serum level:HDL ratio >4:1
Lack of regular exercise (three or more times per week of regular exercise or moderate physical activity)
Family history (mother or father with heart disease or stroke before age 60 y)
Stress (particularly personality factors of anger and hostility)
Diabetes
Obesity
Sex: men are at greater risk than women until women reach menopause, then equal risk
Age: increasing age increases risk

HDL, high-density lipoprotein; LDL, low-density lipoprotein.

From Hurst W: The heart, arteries and veins, ed 10, New York, 2002, McGraw-Hill.

Table 20-4
Simple Questions to Assess Risk for Cardiovascular Disease
Have you been diagnosed with high blood pressure/are you taking medications for your blood pressure? Do you know what your
blood pressure is?
Have you ever smoked? If so, how many packs/day and how many years? When did you quit?
Do you know your blood cholesterol? Are you taking medications for your cholesterol? Do you eat a lot of foods like cheese, red
meat, fried foods, fast food, etc.?
Does anyone in your family (mother/father/siblings) have any history of heart disease/heart attack/stroke (and at what age)?
Have you been diagnosed with elevated blood sugar/diabetes?
Do you exercise regularly?
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation
Are the Responses to Exercise or to
the Assessment Normal or Abnormal?
Acute Cardiovascular Responses during Aerobic
Exercise
Progressively increasing aerobic exercise (i.e., cycling,
running) is associated with an increase in oxygen con-
sumption (a linear relationship exists) resulting from
an increase in cardiac output as well as an increase in
the arteriovenous oxygen difference (a-vO2diff).9,10 The
increase in cardiac output occurs because of an increase
in heart rate10–12 and stroke volume.11–13 The increase in
the a-vO2diff (or difference between the oxygen content
in the arteries versus the oxygen content in the veins)
occurs because of a decrease in systemic vascular resis-
tance9 and an increase in skeletal blood flow9 and oxygen
extraction by the exercising muscles9,10 (Figure 20-1,
Table 20-5).
The normal clinical responses to progressively increas-
ing aerobic exercise are a linear increase in heart rate
related to the work of the exercise, as well as a linear
increase in systolic blood pressure (related to the work of
40
30
Cardiac Output
(L min−1)
20
10
0 0.00
200
180
160
Stroke Volume
140
(ml)
120
100
80
60
419
the exercise), with little or no change in diastolic blood
pressure (Figure 20-2, Table 20-6; see Table 20-5)
Normal Clinical Response to Exercise
● Linear increase in heart rate
● Linear increase in systolic blood pressure
● Little or no change in diastolic blood pressure
The magnitude of the change in cardiovascular
responses during aerobic exercise is related to the physi-
cal activity status of the patient. Specifically, the two-
fold increase in aerobic capacity found in athletes versus
untrained individuals14 is due to an elevated maximal
exercise stroke volume and cardiac output as heart rate
is not different between athletes and sedentary individu-
als.15 The mechanism responsible for the elevated stroke
volume is due, in part, to the ability of the “athletic heart”
to fill with blood with greater ease (i.e., increased preload
reserve) and to the enhanced ability of the ventricles to
0.20
Arterial - Venous 02 Difference
0.15
0.10
0.05
200
180
160
140
(beats min−1)
Heart Rate
120
100
80 Figure 20-1
Normal effect of aerobic exercise in a trained
60 athlete. Black lines show cardiac output
and stroke volume. Gray lines show A-VO2
40 difference and heart rate.
420 SECTION II • Principles of Practice

Table 20-5 Table 20-6

Acute Cardiovascular Responses during Peak Aerobic
Exercise in Healthy Individuals
Variable
Heart rate
End-diastolic volume
End-systolic volume
Stroke volume
Cardiac output
Arteriovenous oxygen difference
Systemic vascular resistance
Mean arterial blood pressure
↑, increase from rest; ↓, decrease from rest.
eject a greater amount of blood out of the heart (i.e.,
increased left ventricular contractile reserve).
Health care clinicians prescribing therapeutic exer-
cise to maintain their clients’ cardiorespiratory fitness
should be aware of the time course of the change in car-
diac performance associated with aerobic training. The
few investigations performed to date provide evidence
to suggest that favorable improvements in cardiorespira-
tory fitness can occur within 5 to 10 days after beginning
an exercise program. For example, Mier and colleagues16
found that 10 days of cycle exercise (i.e., 60 min/day at
Signs/Symptoms of Exercise Intolerance:
Signs of Clinical Instability
Change from Rest Systolic BP >200 to 210 mm Hg
Diastolic BP >110 mm Hg
↑ Increase in heart rate >50 beats/min with low-level activity
↑ Drop in systolic BP >20 mm Hg
↓ Significant arrhythmias (complex premature ventricular
↑ contractions, ventricular tachycardia, second- or third-degree
↑ heart block, any arrhythmia accompanied by decreased BP)
↑ Moderate dizziness or near-syncope
↓ Syncope
↑ New-onset angina or level 2+/4+ angina
Nausea, vomiting
Unusual or severe fatigue
Marked dyspnea (level 2+/4+)
Ataxia, persistent unsteadiness, mental confusion
Severe claudication (grade III/IV)
Facial expression of severe distress
Cyanosis or severe pallor
Cold sweat
Loss of sustained vigor of palpable pulse
Development of pulmonary crackles/rales
BP, blood pressure.
65% to 95% of maximal oxygen consumption) resulted in
a significant increase in peak exercise stroke volume, car-
diac output, and aerobic capacity in previously sedentary,
younger (mean age, 26 years), healthy individuals.

200

180
Systolic blood pressure
Blood pressure, mm Hg

160

140

120

100

80
Diastolic blood pressure

Figure 20-2
Rest 2 4 6 8 10 12 14
Normal blood pressure responses to
activity. Treadmill elevation, % grade
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation
Case Study 1: Aerobic Exercise for an Athlete
Scenario
A 20-year-old long-distance runner is scheduled for
elective surgery in 2 weeks for an open reduction
and internal fixation of a tibial plateau fracture. As
a result of his injury he is unable to perform any
weight-bearing aerobic exercise; however, the client
is worried that his fitness will decline as a result of
not being able to perform any aerobic training. The
client’s maximal heart rate is 190 beats/min.
Discovery Questions
1. Is this person safe for exercise? What is his risk for
cardiovascular disease?
2. If the patient is safe for exercise, what should
I monitor during the assessment?
3. Are the responses that were assessed normal or
abnormal?
4. Based on the findings, how should the patient be
monitored during the interventions?
5. What modifications/precautions should be pro-
vided in the exercise prescription?
Goal
The important goal from a cardiovascular perspective
is to maintain the client’s aerobic capacity at an
Summary and Implications for the Health Care
Professional
The increase in oxygen consumption during aerobic
exercise is mediated by changes in heart, blood vessel,
and skeletal muscle function that result in increased
oxygen supply and utilization by the muscles. Therefore,
assessment of physiological responses to exercise should
be performed on all individuals and documented as nor-
mal or abnormal. Normal responses to exercise should be
documented to justify the decision not to monitor with
exercise in the future. Abnormal responses should be
assessed for appropriateness to continue with exercising,
or to justify the need to monitor future sessions. When
abnormal responses are detected, but the patient is deter-
mined to be safe to perform exercise, those responses
that were identified as abnormal should be monitored
with all activity.
The clinician should also be aware if the client is tak-
ing any medications, especially ones that may affect heart
rate or blood pressure responses to activity. Clinicians
should particularly be made aware of use of beta-adrener-
gic blocking medications (beta blockers), which are often
used in the treatment of hypertension, arrhythmias, or
coronary artery disease.15 These medications affect heart
421
optimal level before (and after) surgery. To attain
this goal, the clinician can prescribe the following
exercise program.
Mode of Exercise
Arm-ergometer exercise.
Frequency of Exercise
Exercise is performed 3 to 5 days per week.
Intensity of Exercise
Exercise at 70% to 90% of maximal heart rate (equal
to “hard” exercise intensity), which would be a heart
rate of 133 to 171 beats/min for this athlete.
Duration of Exercise
60 minutes per session.
Comment
This training program will attenuate the decline
in aerobic capacity that would occur if this athlete
adhered to a sedentary lifestyle after sustaining his
injury.
rate and blood pressure responses at rest and during exer-
cise and would make responses to activity appear abnor-
mal if the clinician did not know the client was taking
these medications17 (Table 20-7). Patients on beta block-
ers should be monitored for intensity of exercise using
the ratings of perceived exertion (RPE) scale rather than
by monitoring the heart rate response18 (Table 20-8).
The heightened exercise capacity found in elite athletes
is due, in part, to structural and functional changes in the
heart that result in an increased preload and left ventricu-
lar contractile reserve (or stroke volume). Therefore, ath-
letes often demonstrate a lower resting heart rate as well
as a more blunted (lower rate of rise) heart rate response
to increased workload.
Acute Cardiovascular Responses during
Resistance Exercise
Currently, only a few studies have examined the acute
effect of resistance exercise on cardiovascular function.19,20
This is due in part to the difficulty in accurately quantify-
ing left ventricular volumes or function during resistance
exercise. The magnitude and directional change in cardiac
volume and function during resistance exercise are, for
422 SECTION II • Principles of Practice

Table 20-7 the most part, opposite to those that occur during aerobic
Beta-Adrenergic Antagonists: Beta Blockers exercise (Table 20-9). Submaximal or maximal resistance
exercise is associated with a transient and marked rise in
Response
mean arterial pressure and systemic vascular resistance,
Compared
Physiological with
with an associated decline in stroke volume.19 Also, the
Category Medication Variable Normal increase in cardiac output during lifting is due to an
increase in heart rate because stroke volume decreases
Nonselective Propranolol HR during resistance exercise.20 Thus, the increased vascular
(Inderal) Resting Lower resistance occurring with very high skeletal muscle force
Timolol Exercise Lower associated with lifting a weight results in a reduced ejec-
(Blocadren) HRs tion of blood from the heart compared with that which
Nadolol Maximal Lower occurs during aerobic exercise.
(Corgard) HR
The physiological responses to strength training the cli-
Pindolol
(Visken)
nician observes are an elevated heart rate response (in the
Labetalol absence of increased stroke volume) and elevated blood pres-
(Normodyne) sure responses (especially the diastolic blood pressure).21–23
Sotalol The effect of long-term resistance training on altering
(Betapace) the cardiovascular responses during an acute bout of resis-
Carteolol tance or aerobic exercise has received minimal attention.
(Cartrol) Fleck and Dean23 found that experienced bodybuilders
Beta1 Metoprolol BP had a significantly lower peak systolic and diastolic blood
selective (Lopressor) Resting Lower pressure and heart rate compared with novice weight train-
Atenolol Exercise Lower ers or sedentary control subjects during upper or lower
(Tenormin) BPs
extremity resistance exercise. The favorable improvement
Acebutolol
(Sectral)
in cardiovascular function associated with resistance train-
Esmolol ing may carry over when performing aerobic exercise. For
(Brevibloc) example, Fisman and colleagues24 have shown that acute
Alprenolol cardiac responses (i.e., heart rate, stroke volume, cardiac
Alpha and Carvedilol output, and ejection fraction) during peak cycle exercise
beta (Coreg) were not different between elite weightlifters and runners.
selective These findings suggest that resistance training may lead to
favorable cardiac adaptations that enhance left ventricular
BP, blood pressure; HR, heart rate. performance during aerobic exercise.25

Summary and Implications for the Health Care

Professional
Resistance training is associated with acute cardiovascu-
Table 20-8 lar and pulmonary responses that differ from those in
Borg Ratings of Perceived Exertion aerobic training. The elevated heart rate and blood pres-
sure responses are not directly associated with the task
6
7 Very, very light
8 Table 20-9
9 Very light
10
Acute Cardiovascular Responses during Submaximal and
11 Fairly light Maximal Resistance Exercise in Healthy Individuals
12 Variable Change from Rest
13 Somewhat hard
14 Heart rate ↑
15 Hard End-diastolic volume ↓
16 End-systolic volume ↓
17 Very hard Stroke volume ↓
18 Cardiac output ↑
19 Very, very hard Systemic vascular resistance ↑
Mean arterial blood pressure ↑
From Borg G: Borg’s perceived exertion and pain scales, p 31,
Champaign, Ill, 1998, Human Kinetics. ↑, increase from rest; ↓, decrease from rest.
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation 423

performed. Favorable changes in arterial pressure may
also occur with long-term resistance training that can
reduce left ventricular wall stress during exercise. Regular
resistance training may induce favorable left ventricular
morphological adaptations that result in an increased
stroke volume and cardiac output during aerobic exercise.
Therefore, health care professionals should incorporate
this mode of training as part of the therapeutic exercise
program for individuals with a musculoskeletal injury to
maintain their overall physical fitness. Caution should be
taken with individuals who have elevated blood pressure
responses at rest or with activity, and monitoring may be
indicated when these individuals perform new activities.
Acute Cardiovascular Responses during Aerobic
Exercise: Effect of Bed Rest or Deconditioning
Because some musculoskeletal injuries may necessitate a
period of little or no exercise or bed rest, it is impor-
tant that the clinician be knowledgeable about the det-
rimental effects that deconditioning and bed rest have
on cardiovascular function (Table 20-10). Detraining is
often seen in patients with significant musculoskeletal
injuries that impair their movement and confine them to
a bed or wheelchair for a prolonged period while they
recover. These are critical factors to consider for clini-
cians involved in inpatient or acute rehabilitation, skilled
nursing, or long-term care.
One of the most extensive investigations to examine the
effect of bed rest on cardiovascular function was performed
by Saltin and associates.26 These investigators examined
the effect of 20 days of strict bed rest on aerobic perfor-
mance (i.e., cardiac output and a-vO2diff) in five young,
healthy men. A main finding of this investigation was that
20 days of bed rest was associated with a 28% decrease
in aerobic capacity.26 Of greater concern, the decline in
aerobic capacity after 20 days of bed rest was greater than
that found after 3 decades of aging in the same subjects.27
The decline in aerobic capacity was due to the reduction
in stroke volume and cardiac output because there was no
change in a-vO2diff during maximal exercise.26
Of greater importance for the clinician is the rapid decline
in cardiorespiratory fitness that occurs during the first few
weeks of deconditioning (as may occur in a previously physi-
cally fit individual who suffers a musculoskeletal injury and
adheres to a sedentary lifestyle during the recovery period).
In particular, Coyle and colleagues28 assessed endurance ath-
letes’ aerobic capacity before and after 3 months of decon-
ditioning. A main finding of this study was that 3 months of
deconditioning resulted in a 16% decline in maximal oxygen
consumption. Moreover, nearly half of the decline in fitness
occurred after 12 days of detraining and was attributed to the
decline in stroke volume and cardiac output. Interestingly,
the previously trained athletes’ maximal oxygen consump-
tion after 3 months of detraining was 17% higher than
that found in healthy control subjects. This key finding has
important implications for clinicians. Specifically, if a client is
scheduled for an orthopedic procedure or operation that will
be followed by a period of inactivity, then he or she should
be encouraged (within the safety limits of the underlying
condition) to perform an exercise regimen to ensure that
the highest level of physical fitness is maintained during the
period of inactivity, or before the surgery.
Rehabilitation and Cardiovascular Training
● Cardiovascular training must be an integral part of any
rehabilitation program to prevent or decrease the rate of
deconditioning in a patient.
Interventions that can prevent the decline in cardiovas-
cular function will play an important role in maintaining
aerobic capacity during bed rest. A number of investigators
compared the effect of 21 to 30 days of bed rest alone,29,30

Table 20-10
Effect of Aging, Cardiovascular Disease, and Bed Rest Deconditioning on Cardiovascular Function
during Peak Aerobic Exercise
Age-Mediated Bed Rest–Mediated Heart Disease–
Variable Change Change Mediated Change*

Heart rate ↓ ↑ ↓
Stroke volume ↔ ↓ ↓
Cardiac output ↓ ↓ ↓
Arteriovenous oxygen difference ↓ ↔ ↓
Systemic vascular resistance ↑ ↑ ↑
Mean arterial blood pressure ↑ ↓ ↓
Aerobic capacity ↓ ↓ ↓

↓, decrease; ↑, increase; ↔, no change.

*Compared with age-matched, healthy individuals.
424 SECTION II • Principles of Practice
bed rest plus cycle exercise,29,30 or bed rest plus isokinetic
leg exercise30 on cardiorespiratory fitness in healthy men
19 to 42 years of age. A major finding of these studies was
that 21 to 30 days of bed rest resulted in a 9% to 18%
decrease in aerobic capacity that remained unaltered in the
bed rest plus cycle exercise group. Greenleaf and cowork-
ers30 also found that the relative decline in aerobic capacity
in the bed rest plus isokinetic leg exercise training group
was 50% less than in the bed rest alone group. Thus, both
aerobic and resistance exercise appear to be effective modes
of training that can attenuate or prevent the loss in aerobic
capacity that occurs with bed rest.
Summary and Implications for the Health Care
Professional
Rehabilitation clinicians need to be aware that there is a
marked decline in aerobic capacity that occurs within the
first few weeks of becoming sedentary because of injury or
illness. Three weeks of bed rest is associated with a greater
decline in aerobic capacity than that which occurs after 3
decades of aging. Thus, exercise training should be incorpo-
rated (within the safety limits of the underlying condition) to
maintain optimal cardiorespiratory fitness. Aerobic and resis-
tance training are effective modes of exercise that can attenu-
ate the decline in aerobic capacity associated with bed rest or
deconditioning. Thus, clinicians should prescribe aerobic or
strengthening exercise to maintain overall physical fitness.
Acute Cardiovascular Responses during Aerobic
Exercise: Effect of Aging
Increased age is associated with structural and functional
changes in the cardiovascular system that lead to a decline
in aerobic capacity. Fitzgerald and colleagues31 and Wilson
and Tanaka32 have shown that aerobic capacity declines
by as much as 55% in healthy sedentary men and women
between the third and ninth decades of life. The reduced
aerobic capacity is related to the decline in peak cardiac
output10,32 secondary to an impairment in heart rate and
left ventricular contractile reserve32 and to an increased
vascular tone10,32 (see Table 20-9). An abnormality in
oxygen utilization by the active muscles may also result
in a reduced a-vO2diff during peak exercise.10
The loss in cardiovascular function associated with
aging may be secondary to an adherence to a sedentary
lifestyle as a person ages.31,32 An example of the effects of
training on an individual as he or she ages is demonstrated
by the heightened aerobic capacity in endurance-trained
master athletes versus age-matched sedentary individuals.
The improved aerobic capacity found in endurance-trained
master athletes is due to a higher peak exercise end-dia-
stolic volume,33 stroke volume,33,34 cardiac output,33,34
and a-vO2diff,34 and a lower systemic vascular resistance.34
Master endurance athletes’ aerobic capacity is approxi-
mately 40% higher than that of age-matched healthy sed-
entary individuals. Therefore, exercise training appears to
be an important intervention that can attenuate the loss in
aerobic capacity associated with aging (see Case Study 2).
The improvement in cardiorespiratory fitness with
short-term training does not appear to be affected by the
aging process because 5 to 10 days of aerobic training
resulted in an increase in maximal oxygen consumption
in healthy men and women in their seventh and eighth
decades of life.35–37 Therefore, older individuals who
require rehabilitation for a musculoskeletal injury may
also benefit from an overall endurance exercise program,
particularly if they were sedentary before the injury.
Summary and Implications for the Health Care
Professional
Increased age is associated with structural and functional
changes in the cardiovascular system that lead to a decline
in aerobic capacity; however, the mechanism responsible for
this decline is, at least in part, an adherence to a sedentary
lifestyle with increasing age. This finding reinforces that
exercise training is an important intervention that can atten-
uate the decline in aerobic capacity that occurs with advanc-
ing age, and that may ameliorate the effects of inactivity in
the older person who suffers a musculoskeletal injury.
Acute Cardiovascular Responses during Aerobic
Exercise: Effect of Heart Disease
Individuals with heart disease have a reduced cardiorespi-
ratory fitness related to abnormalities in cardiac and mus-
culoskeletal function. Individuals with coronary artery
disease have an aerobic capacity that is 38% to 50% lower
than that found in healthy individuals.38,39 The abnormal
aerobic capacity is secondary to a reduction in cardiovas-
cular function. In particular, individuals with coronary
artery disease have a lower peak exercise heart rate,38,39
stroke volume,38 ejection fraction,38,39 and cardiac out-
put38 and a higher end-diastolic volume38 and systemic
vascular resistance38 compared with healthy individuals
(see Table 20-10). Also, abnormalities in skeletal muscle
blood flow and oxidative enzyme activity lead to reduced
oxygen delivery and extraction by exercising muscles.
Finally, the decline in muscle strength found in individ-
uals with coronary artery disease leads to an impaired
ability to perform vocational and recreational activities of
daily living that require a certain level of strength.
Individuals with coronary artery disease may also be
taking medications that affect not only the physiologi-
cal responses to exercise (see Table 20-7) but also the
contractility of the heart muscle. Good history taking on
the initial assessment should include a list of all medica-
tions the patient is taking as well as any history of coro-
nary artery disease. In addition, the clinician should be
knowledgeable about the effects of all medications on
any exercise that has been or will be prescribed.
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation
Case Study 2: Aerobic Training in the Ninth Decade of Life
Scenario
Mr. Lake is a healthy, 89-year old man who slipped
on an ice patch while walking and suffered a Colles
fracture that was treated with a closed reduction and
plaster cast in the emergency department. Mr. Lake is
referred to your physical therapy clinic to improve the
range of motion and muscle strength in his affected
limb. However, when the clinician discusses the treat-
ment plan with Mr. Lake, he asks the clinician if he can
help him walk farther because he becomes fatigued
when he walks one block.
Discovery Questions
1. Is this person safe for exercise? What is his risk for
cardiovascular disease?
2. If the patient is safe for exercise, what should I
monitor during the assessment?
3. Are the responses that were assessed normal or
abnormal?
4. Based on the findings, how should the patient be
monitored during the interventions?
5. What modifications/precautions should be pro-
vided in the exercise prescription?
Goal
Although Mr. Lake’s referral is related to rehabilita-
tion of the Colles fracture, an important goal from
a cardiovascular perspective is to improve Mr. Lake’s
exercise capacity. Because Mr. Lake has an upper
extremity injury and has very low fitness, the initial
Exercise training is a safe and effective intervention
that can partially restore the reduced aerobic capacity40–42
and muscle strength42–45 in individuals with coronary
artery disease. As with all clients who are prescribed exer-
cise, these individuals should be initially monitored to
assess their responses to activity. Accordingly, clinically
stable individuals with coronary artery disease should be
encouraged to perform exercise training to maintain an
optimal level of physical fitness (see Case Study 3).
Summary and Implications for the Health Care
Professional
Individuals with coronary artery disease often demon-
strate a decreased aerobic capacity because of abnormal-
ities in cardiac and muscular structure and function, and
may be taking medications that affect their responses
to exercise. Clinicians should be aware of any medi-
cal history of coronary artery disease and review the
individual’s medications so that the patient may be
monitored accordingly. The Borg Rating of Perceived
Exertion Scale (see Table 20-8) should be used to mon-
425
mode of exercise should consist of low-intensity exer-
cise performed on a cycle ergometer, while the patient
is monitored.
Mode of Exercise
Initially, he can perform cycle exercise; once his cast
is removed, he can resume walking on a treadmill in
the rehabilitation facility.
Frequency of Exercise
Exercise is performed 3 to 5 days per week.
Intensity of Exercise
Mr. Lake has very low fitness and, as a result, a light
exercise intensity (Borg Rating of Perceived Exertion
Scale rating of 10 to 11) should be prescribed.
Duration of Exercise
Initially, 3 to 5 minutes of continuous exercise fol-
lowed by a 2- to 3-minute rest period should be per-
formed. This cycle should be repeated until 20 to 30
minutes of exercise is completed. The goal of this
exercise program is slowly to increase the duration,
rather than the intensity of exercise.
Comment
Improving Mr. Lake’s cardiorespiratory fitness will
allow him to perform functional and recreational
activities of daily living that have an aerobic compo-
nent with greater ease.
itor intensity of exercise in individuals who are on beta
blocking medications.
Special Considerations
Acute Cardiovascular Responses during Aquatic
Aerobic Exercise
Aquatic therapy is an effective intervention that can be
used in the rehabilitation of individuals with orthopedic
injuries.46,47 Use of the aquatic environment allows for
conditioning to occur while minimizing the impact of
weight-bearing and gravity-loaded activities for the patient
with complex musculoskeletal rehabilitation requirements.
However, the acute cardiovascular responses during aero-
bic exercise performed in water are different from those
during aerobic exercise performed on land. For instance,
the increased hydrostatic pressure associated with upright,
head-out-of-water immersion results in a central shift in
blood volume and a concomitant rise in end-diastolic
volume,48,49 stroke volume,48–50 ejection fraction,48,49 and
426 SECTION II • Principles of Practice
Case Study 3: Aerobic Training for an Individual
with Clinically Stable Coronary Artery Disease
Scenario
Mrs. Plasty is a 65-year-old woman who is referred
to your outpatient clinic for rehabilitation of a first-
degree rotator cuff tear. Mrs. Plasty suffered a heart
attack 5 years ago and has not had any difficulties
with her heart condition since then. Mrs. Plasty has
been exercising since being discharged from a car-
diac rehabilitation program 5 years ago. However,
she is concerned that she will “lose her fitness level”
because she is unsure if she can exercise with her
shoulder injury. At her annual exercise stress test
2 weeks ago, Mrs. Plasty’s resting heart rate was
75 beats/min and her maximal heart rate was 130
beats/min. In addition, she had a normal heart rate
and blood pressure response during the exercise
stress test and did not have any chest discomfort.
Discovery Questions
1. Is this person safe for exercise? What is her risk
for cardiovascular disease?
2. If the patient is safe for exercise, what should I
monitor during the assessment?
3. Are the responses that were assessed normal or
abnormal?
4. Based on the findings, how should the patient be
monitored during the interventions?
5. What modifications/precautions should be pro-
vided in the exercise prescription?
Goal
Aerobic exercise training as part of a comprehensive
cardiac rehabilitation program has been shown to
result in an improvement in mortality rates in indi-
viduals with cardiac disease. Accordingly, clinicians
should incorporate aerobic training when rehabilitat-
ing such individuals with a musculoskeletal condition.
Mrs. Plasty is clinically stable and has been exercising
regularly before her shoulder injury. Thus, it is impor-
tant to prescribe aerobic exercise as part of her overall
rehabilitation program.
cardiac output,48–50 with a concomitant reduction in sys-
temic vascular resistance.47–50 Volume load also is increased
during aerobic exercise performed in water. Specifically,
cycle exercise performed in the pool results in a greater
increase in end-diastolic volume,47,50 end-systolic vol-
ume,47,50 and stroke volume47 compared with cycle exer-
cise performed on land. A consequence of the ability of
the heart to eject a greater amount of blood with each
contraction when exercising in the pool is that the heart
Mode of Exercise
Mrs. Plasty can perform her aerobic training pro-
gram on a treadmill; if necessary, she can hold on to
the hand rail with her noninjured limb.
Frequency of Exercise
Exercise is performed 3 to 5 days per week.
Intensity of Exercise
Because the rehabilitation clinician has a recent copy
of Mrs. Plasty’s exercise stress test (i.e., resting and
maximal heart rates), the intensity of exercise can
be prescribed using the heart rate reserve method.
Specifically, the intensity of exercise can be set at 40%
to 60% of heart rate reserve (i.e., a light to mod-
erate exercise intensity). In this case, Mrs. Plasty’s
exercise heart rate would be between 97 and 108
beats/min.
Duration of Exercise
The duration of exercise can be set at 30 minutes
and gradually increased over 1 to 2 months to 60
minutes of continuous aerobic exercise.
Comment
The rehabilitation clinician should monitor Mrs.
Plasty’s heart rate continuously with a heart rate
monitor. In addition, he or she should take Mrs.
Plasty’s blood pressure every 5 minutes. Mrs. Plasty’s
heart rate and blood pressure should remain constant
throughout the exercise training program when she
has reached her target heart rate zone. The key to
performing exercise rehabilitation for clinically stable
individuals with cardiac disease is to start low and
go slow. An important goal is to increase the client’s
exercise capacity by increasing the exercise duration
rather than by increasing the exercise intensity. If the
client becomes more fatigued or short of breath than
normal during the program, he or she should con-
sult with their primary care physician.
does not have to beat as quickly to supply muscle with oxy-
gen during exercise. Thus, the heart rate response during
high-intensity (>75% maximal oxygen consumption) aero-
bic exercise performed in the pool is 10 to 16 beats/min
lower than that seen during aerobic exercise performed on
land. Because of the differences in heart rate between land
and pool exercise, clinicians should use the Borg Rating of
Perceived Exertion Scale (see Table 20-8) when prescrib-
ing aquatic exercise for their clients.
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation
Target Heart Rate in Water
● Heart rate response to high-intensity aerobic exercise performed
in water is 10 to 16 beats/min lower than with the same exercise
performed on land. Thus, training heart rate should be calculated
as 10 to 16 beats/min less than that on land.
The role an aquatic aerobic exercise program may play
in altering cardiovascular performance in healthy indi-
viduals has not been well studied. However, Sheldahl
and associates51 showed that the improvement in aerobic
capacity after 3 months of cycle exercise (3 days/week at
60% to 80% maximal oxygen consumption for 30 min-
utes/session) performed in water was as great as that
found with the same type of training performed on land.
Thus, aerobic training performed in a pool appears to be
a useful mode of training to improve aerobic capacity in
individuals with an orthopedic injury that is aggravated
by weight bearing (see Case Study 4).
Summary and Implications for the Health Care
Professional
Aerobic exercise performed in water is an effective inter-
vention that can improve aerobic capacity. However, water
Case Study 4: Aerobic Training in the Pool
Scenario
Mrs. Jones is a healthy, 70-year-old woman with
bilateral osteoarthritis who is referred to the out-
patient physical therapy department in your hospi-
tal. Her chief complaint is severe pain when weight
bearing, which has caused her to assume a sedentary
lifestyle. As a result, she now becomes excessively
fatigued when walking.
Discovery Questions
1. Is this person safe for exercise? What is her risk for
cardiovascular disease?
2. If the patient is safe for exercise, what should I
monitor during the assessment?
3. Are the responses that were assessed normal or
abnormal?
4. Based on the findings, how should the patient be
monitored during the interventions?
5. What modifications/precautions should be pro-
vided in the exercise prescription?
Goal
The goal of treatment is to improve Mrs. Jones’ exer-
cise tolerance while minimizing her pain on exertion.
Aquatic aerobic exercise training is an effective inter-
427
immersion is associated with a central shift in blood volume
that leads to an increase in end-diastolic volume, stroke vol-
ume, and cardiac output. A consequence of the heightened
stroke volume is that the heart rate during high-intensity
aerobic exercise is lower than that found during similar
exercise performed on land. Thus, the rehabilitation cli-
nician should use the Borg Rating of Perceived Exertion
Scale when prescribing aerobic exercise in the pool.
Based on the Assessment Findings,
How Should Patients Be Monitored
during the Interventions?
Clinicians should monitor heart rate, blood pressure, and
symptoms for all patients during the initial assessment.
Once the clinician has determined that the responses are
normal, there may no longer be any indication to con-
tinue to monitor heart rate and blood pressure; however,
there are some clinical indicators that justify continual
monitoring. These indicators include a high risk for or a
history of coronary artery disease, a history of elevated
blood pressure, or abnormal symptoms demonstrated
during activity. The clinician should use his or her pro-
fessional judgment in these cases to determine the need
for further monitoring with interventions.
vention that will allow Mrs. Jones to perform aerobic
exercise while minimizing the load on her knees.
Mode of Exercise
Exercise consists of walking or running in the pool.
Frequency of Exercise
Exercise is performed 3 to 5 days per week.
Intensity of Exercise
The intensity should be prescribed at a light to
moderate level using the Borg Rating of Perceived
Exertion Scale (i.e., a Borg rate of 10 to 13 is consid-
ered a light to moderate exercise intensity).
Duration of Exercise
The duration is set to 20 to 30 minutes per session.
Comment
Mrs. Jones may not be able to perform 20 minutes of
continuous aerobic exercise during the first few weeks
of the rehabilitation training program. If this is the case,
she should perform 5 minutes of exercise followed by a
few minutes’ break, and then repeat this cycle until 20
to 30 minutes of aerobic exercise is completed.
428 SECTION II • Principles of Practice
Indicators That Patient Should Be Monitored
Closely during Exercise
● History of coronary artery disease
● History of elevated blood pressure
● Abnormal symptoms (e.g., feeling faint) during activity
When the responses to activity during the initial assess-
ment have been identified as abnormal, the first decision
to be made is whether the patient is demonstrating signs
or symptoms of exercise intolerance or clinical instabil-
ity. If the responses are considered clinically unstable
(see Table 20-6), the activity should be stopped and the
physician notified before resuming activity in rehabilita-
tion. However, if the responses are considered abnormal,
but if changing or decreasing the intensity of the activity
improves the response, the patient could continue per-
forming the activity on subsequent visits as long as the
physiological signs and symptoms are monitored. New
activities that are introduced should also be monitored.
The clinician should document all abnormal signs and
symptoms during each session and interpret these signs
and symptoms on the patient’s chart (in the assessment
section) because this provides justification for monitor-
ing the therapy sessions. When the responses to the activ-
ities are considered normal, these responses should also
be documented and interpreted to justify the decision to
conduct unmonitored sessions.
Developing an Exercise Prescription:
Healthy Individuals in Rehabilitation
The therapeutic exercise program should include the fol-
lowing components:52
1. Frequency of exercise: The aerobic component of the
exercise program can be performed 3 to 5 days per
week, whereas resistance training can be performed 2
to 3 days per week.
2. Duration of exercise: The aerobic phase of the train-
ing program should consist of 20 to 60 minutes of
continuous exercise. Also, a 5- to 10-minute warm-up
and a similar cool-down period of stretching and low-
intensity aerobic exercise (i.e., cycling or treadmill
walking) should occur before and after the aerobic
phase of training. The duration of the aerobic phase
of the program depends on the prescribed exercise
intensity and the client’s fitness level. For example,
the duration of exercise will be less when high-inten-
sity (>85% maximal oxygen consumption; anaerobic)
exercise is performed. Conversely, individuals with
very low fitness levels may have to perform a number
of repetitive sets consisting of 3 to 5 minutes of aero-
bic exercise followed by a few minutes of rest.
3. Mode of exercise: The mode of aerobic and resis-
tance training depends on the location of the mus-
culoskeletal injury. For example, if an individual
has suffered a shoulder injury, then lower extrem-
ity aerobic training can be performed using a cycle
ergometer (Figure 20-3), whereas lower extremity
resistance training can be accomplished using leg
extension or leg press exercises. Also, upper extrem-
ity resistance exercise of the noninjured limb can be
performed with biceps curl or shoulder press exer-
cises. If an individual has a lower back injury, aerobic
training may be performed on a semirecumbent cycle
ergometer (Figure 20-4) or a treadmill. Finally, if the
individual has suffered a unilateral lower extremity
injury, he or she can perform upper extremity aero-
bic exercises (arm ergometer; Figure 20-5), bilateral
shoulder presses, latissimus dorsi pulldowns, and
arm curls, as well as leg extension exercises for the
noninjured lower extremity.
Components of a Therapeutic Exercise Program
● Frequency of exercise
● Duration of exercise
● Mode of exercise
● Intensity of exercise
4. Intensity of exercise: The intensity of aerobic training
can be prescribed using a percentage of maximal heart
rate (55% to 90% of maximal heart rate; Table 20-11)
or maximal heart rate reserve (40% to 85% of heart rate
reserve) for a target heart rate. The initial exercise inten-
sity depends on the patient’s physical fitness. For decon-
ditioned or sedentary individuals, the initial exercise
intensity may be prescribed at the lower end of the exer-
cise intensity range (55% to 60% of heart rate reserve
is the normal range; even 40% to 55% is considered
moderate for sedentary individuals), whereas athletic
individuals are able to tolerate higher-intensity exercise
(>80% heart rate reserve) at the outset. As an example,
if a patient’s maximum heart rate is 190 beats/min and
the prescribed exercise intensity is between 55% and 90%
of maximum heart rate, then the patient’s target heart
rate range would be between 105 and 171 beats/min
(see Table 20-11). Unfortunately, in most orthopedic
rehabilitation clinics, it is unlikely that the clinician will
have the expertise or equipment required to perform a
maximal exercise test to obtain his or her patient’s maxi-
mal heart rate. In this instance, the maximal heart rate
can be estimated. Most clinicians are familiar with esti-
mating maximal heart rate using the formula, estimated
maximal heart rate = 220 − age. However, Tanaka
and associates53 recently revealed that this commonly
used formula underestimates the actual maximal heart
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation
Figure 20-3
Aerobic training using a cycle ergometer for a patient with an upper
extremity injury.
Figure 20-4
Aerobic training using a semirecumbent cycle ergometer.
rate by 6 to 15 beats/min for individuals between 60
and 90 years of age. These researchers also reviewed the
findings from 351 studies with 18,712 participants and,
using a special statistical technique, derived a new for-
mula to estimate the age-predicted maximal heart rate.
Specifically, the new formula that clinicians should use is
429
Figure 20-5
Aerobic training using an arm ergometer for a patient with a lower
extremity injury.
Table 20-11
Exercise Prescription Using Percentage of Maximal Heart
Rate or Heart Rate Reserve
Target Heart Rate Using Percentage of Maximal Heart Rate
Maximal heart rate = 190 beats/min.
If the prescribed exercise intensity is 55% to 90% of maximal
heart rate, then the target heart rate is between
105 beats/min and 171 beats/min.
Target Heart Rate Using the Heart Rate Reserve
Resting heart rate = 70 beats/min and maximal heart rate =
190 beats/min.
If the prescribed exercise intensity is 55% to 90% of heart rate
reserve, then the target heart rate is between
0.55 × (190 − 70) + 70 = 136 beats/min
and
0.90 × (190 − 70) + 70 = 178 beats/min
estimated maximal heart rate = 208 − (0.7 × age).54
Once the estimated maximal heart rate is obtained,
the training target heart rate can then be calculated
as described previously, using the estimated maximal
heart rate.
A second method that can be used to prescribe the
exercise intensity is the heart rate reserve method
(see Table 20-11). Using this method, the resting
heart rate is subtracted from the maximal heart rate
to obtain the heart rate reserve. The reserve value is
then multiplied by the prescribed exercise intensity,
which is then added to the resting heart rate ([0.40
to 0.85] × [maximal heart rate − resting heart rate]
+ resting heart rate). Regardless of which formula is
used, the clinician should keep in mind that formulas
are estimations, and therefore it is more important
to be conservative in prescribing exercise intensity
430 SECTION II • Principles of Practice
for any sedentary individual, older individual, or
someone at moderate to high risk for cardiovascu-
lar disease. In addition, if the individual is taking
medications that may affect heart rate and blood
pressure responses (e.g., beta blockers), all heart rate
formulas are inaccurate and should not be used to
prescribe intensity. For patients taking beta blockers,
the only method of prescribing exercise intensity is
based on the Borg Rating of Perceived Exertion (see
Table 20-8). The exercise intensity for the aerobic
phase should be between 12 to 14 on the Borg Scale.
This method can be used in all individuals who have
difficulty taking their pulse, or who are symptomatic
with exercise and cannot be monitored using the tar-
get heart rate method. When determining the target
heart rate, the medium (i.e., air or water) should also
be considered.
To increase muscular strength and endurance,
resistance training should be performed for one set
of upper and lower extremity exercises with a weight
that will allow 10 to 15 repetitions to be performed.
What Modifications or Precautions
Are Necessary to Consider in Exercise
Prescription?
Modifications or precautions in an exercise prescription
may be necessary in individuals who are sedentary, older,
or at increased risk for cardiovascular disease, or who
have some other disease or dysfunction. Modifications
include a decreased initial intensity of exercise, shorter
initial exercise duration, different frequency, or even a
different choice of mode of exercise. The following con-
siderations are provided for clinical professionals to aid in
developing exercise prescriptions for their population.
Exercise Modifications for Older, Sedentary, or
“At-Risk” Cardiac Patients
● Decreased intensity (40%–55%)
● Shorter duration
● Rest periods
● Different frequency
● Different mode of exercise
● Do more endurance-type exercises (lower load, more repetitions)
Special Considerations: Healthy Older Individuals
Because of the increased life span of North Americans,
it is certain that clinicians will treat a substantial number
of older individuals in their orthopedic clinics. The
exercise prescription principles discussed earlier for
healthy younger individuals also apply to healthy older
adults. However, the rehabilitation specialist may have
to make some modifications to the exercise program.
Specifically, the aerobic intensity at the outset should
be prescribed at the lower limit discussed previously
(even including 40% to 55% of heart rate reserve) and
gradually increased as tolerated for deconditioned older
individuals. Also, some older sedentary individuals may
not be able to perform 30 minutes of continuous aero-
bic exercise when beginning a therapeutic exercise pro-
gram (see Case Study 2). As such, they may need to
decrease the duration of the exercise and add brief rest
periods between bouts of exercise, which will allow for
the desired duration of exercise to be obtained. Older
individuals may have other comorbidities that limit
them from performing weight-bearing exercise. In this
situation, non–weight-bearing exercise such as cycling
or aquatic exercise can be performed (see Case Study
4). Finally, healthy older individuals should also be
encouraged to perform light resistance (1 set of 10 to
15 repetitions using large muscle groups) and flexibility
exercises as part of the rehabilitation program.
Summary and Implications for the Health Care
Professional
Aerobic training performed 3 to 5 days a week for 20
to 60 minutes at a moderate to high exercise intensity
can improve cardiorespiratory fitness in healthy individu-
als. In addition, resistance training can increase maximal
muscular strength and mass. Thus, clinicians should
(within the safety limits of the underlying musculoskele-
tal injury) prescribe both modes of exercise to lead to the
most favorable improvement in their client’s physical fit-
ness. Before initiating an exercise training program, the
clinician must perform a health screening check, which,
at a minimum, should include the PAR-Q & YOU or the
AHA risk assessment.
Exercise Training for Low-Risk Individuals with
Stable Coronary Artery Disease
The exercise program provided in this section focuses on
individuals who may have a musculoskeletal injury but,
more important, have some type of preexisting underly-
ing coronary artery disease (i.e., myocardial infarction,
coronary artery bypass surgery, percutaneous translu-
minal angioplasty, angina pectoris). These individuals
may or may not be clinically stable (Table 20-12). If a
previous history of cardiovascular disease exists, these
individuals should consult with their primary care physi-
cian and obtain medical clearance before participating in
an exercise rehabilitation program. The general exercise
prescription principles discussed previously for healthy
individuals are also used to design an exercise program
for clinically stable individuals with coronary artery dis-
ease. However, the following considerations should be
incorporated in the program’s design:
 CHAPTER 20 • Integration of the Cardiovascular System in Musculoskeletal Rehabilitation 431

Table 20-12 until 30 minutes of exercise is completed. It is important

Signs of Clinical Stability in Individuals with History of that the clinician monitor these individuals’ heart rate,
Cardiovascular Disease blood pressure, and rate of perceived exertion during the
exercise session. Also, the Valsalva maneuver should be
No evidence of heart failure2
Aerobic capacity >6 METS (i.e., sitting at rest is equal to avoided during resistance exercise in individuals with coro-
1 MET)2 nary artery disease because of the effect it may have on
Absence of ischemia or angina (i.e., no chest pain) at rest or blood pressure and, ultimately, stress on the heart.
during an exercise test at ≤6 METS1
Appropriate increase in systolic blood pressure during exercise2 Summary and Implications for the Health Care
Absence of sustained/nonsustained ventricular tachycardia2 Professional
Able to self-monitor exercise intensity2 Clinically stable individuals with coronary artery dis-
ease can perform moderate-intensity aerobic training as
MET, metabolic equivalent. well as light resistance training to maintain an optimal
level of physical fitness while attending an orthopedic
rehabilitation program.
1. Frequency of exercise: Aerobic exercise training for
individuals with clinically stable coronary artery dis-
ease can be performed 3 days per week,1 whereas Summary
resistance training can be performed 2 to 3 days per
A primary goal for the clinician, from a cardiovascular
week1 (see Case Study 3).
standpoint, concerning the rehabilitation of an individual
2. Duration of exercise: Continuous aerobic exercise
with a musculoskeletal injury is to prevent the decline
should be performed for 30 minutes per session
in cardiorespiratory fitness that occurs with disuse or
(not including the warm-up or cool-down periods).1
deconditioning. Specifically, the clinician should be
Resistance training can be performed for 1 set of 10
aware that a significant and marked reduction in aerobic
to 15 repetitions with a light resistance.1
capacity occurs within the first few weeks when highly fit
3. Mode of exercise: Aerobic training should be performed
individuals adhere to a sedentary lifestyle. A more alarm-
using large muscle groups (i.e., cycling or treadmill),
ing finding is that the decline in aerobic capacity associ-
whereas resistance training should include upper (chest,
ated with 3 weeks of bed rest is greater than that which
back, and arms) and lower extremity (quadriceps, ham-
occurs with 3 decades of aging. As such, rehabilitation
strings) exercises. However, as discussed previously for
specialists should (where possible and within the limits
healthy individuals, the mode of aerobic and resistance
of the underlying disease process) prescribe aerobic and
exercise depends on the underlying musculoskeletal
resistance training for individuals whom they know will
injury. Specifically, aerobic and resistance training
be subjected to a period of inactivity or bed rest after
should focus on the noninjured extremities.
an intervention (i.e., surgical procedure or casting of a
4. Intensity of exercise: Aerobic exercise can be performed at
limb). Alternatively, they should incorporate aerobic and
a moderate intensity (40% to 60% of heart rate reserve).
resistance training into the rehabilitation program to
However, individuals with coronary artery disease may
improve their clients’ overall physical fitness and recovery
be taking medications (beta-adrenergic blockers) that
potential. Finally, aerobic and resistance exercise train-
lower resting and exercise heart rate and blood pres-
ing can maintain the overall physical fitness of healthy
sure. In this instance, the prescribed exercise intensity
older individuals or of individuals with clinically stable
can range from 11 to 13 (fairly light to somewhat light)
coronary artery disease while they participate in an out-
on the Borg Rating of Perceived Exertion Scale.
patient orthopedic rehabilitation program.
Special Considerations
Deconditioned individuals with clinically stable coronary References
artery disease may not be able to perform 30 minutes
To enhance this text and add value for the reader, all references have
of continuous aerobic exercise. Instead, they should be been incorporated into a CD-ROM that is provided with this text. The
encouraged to exercise for 3 to 5 minutes followed by a few reader can view the reference source and access it on line whenever pos-
minutes of rest, and this exercise–rest cycle can be repeated sible. There are a total of 54 references for this chapter.

P HYSIOLOGICAL P RINCIPLES
OF R ESISTANCE T RAINING
AND F UNCTIONAL I NTEGRATION
FOR THE I NJURED AND D ISABLED
Daniel J. Cipriani and Jeffrey E. Falkel
Introduction
One of the most important aspects of rehabilitation after
any injury is to ensure that the patient has regained any
strength lost due to injury, disease, or illness. Regaining
strength requires the use of some form of resistance
training. Resistance training is included in a rehabilita-
tion program to provide the patient with the overload
necessary to develop the strength for functional or sport-
related activities. It is critical that clinicians understand
the concepts, principles, and physiology of resistance
training to provide the optimal exercise prescription for
each of their patients. This chapter provides the clinician
with an overview of the physiological principles and con-
cepts of resistance training and how they apply to the art
and science of rehabilitation.
Throughout this chapter, the authors use the term
resistance training to describe any form of overload resis-
tance specifically applied to enhance and develop muscu-
lar strength, endurance, and power. Resistance training
uses several different types or modalities for strengthen-
ing, ranging from body weight to elastic rubber products,
to conventional free weights and fixed-motion machines.
Several other terms must be defined to clarify the con-
cepts presented in this chapter. Strength is the maximal
432
211
C H AC PH TA EP RT E R
force a muscle or muscle group can generate at a speci-
fied speed of contraction.1 Endurance is the ability of a
muscle to perform a particular number of contractions
with proper form until muscle fatigue or degradation of
proper technique occurs. Power is the product of the
force exerted on an object and the velocity of the object
in the direction in which the force is exerted.2 With the
exception of a single, maximal contraction, all exercise
really involves the concept of power as it relates to force
and velocity. Therefore, the velocity component of power
should always be taken into consideration in the devel-
opment of a resistance training program for rehabilita-
tion. This is particularly important for the rehabilitation
after a long-term debilitation, such as osteoarthritis, in
that one of the primary functional losses that need to be
redeveloped is the speed of movement. Health care clini-
cians and medical professionals must look carefully at the
speed of movement during the rehabilitation phase and
strive to assist their patients in gaining a more normative
speed of movement with which they can perform their
daily living or recreational activities. From a functional
point of view, most patients who have either orthopedic
or neurological dysfunction are unable to move as quickly
as they once did. However, the world they must live in
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
moves at an ever-increasing speed. For example, crossing
a busy intersection may take longer than the “walk” sign
will allow. Pressing on the accelerator or brake in their car
may not be fast enough to avoid an accident. The patient
may not be able to get out of the way of a shopping cart
in a busy grocery or department store quickly enough to
prevent getting hit by the cart. Although it is critical for
clinicians to work to get their patients back into society,
traditionally, many clinicians fail to train their patients
adequately to move quickly enough to be safe and truly
functional in the real world.
Critical Terms in Resistance Training
● Strength: maximal force a muscle or muscle group can generate
at a specified speed of contraction.
● Endurance: ability of a muscle to perform a particular number of
contractions with proper form until muscle fatigue or degradation
of proper technique.
● Power: the product of the force exerted on an object and the
velocity of the object in the direction in which the force is
exerted.2
● Intensity: the power output (rate of performing work) of the
exercise.3
● Volume of training: the amount of work performed is calculated
by multiplying the resistance (force × distance) by the total
number of repetitions performed in a specified period of time.3
Volume may be calculated by adding the frequency and duration
of rehabilitation or training sessions.
Two other terms—intensity and volume of training—are
used throughout this chapter as they relate to resistance
training. Intensity is the power output (rate of perform-
ing work) of the exercise.3 In practical terms, intensity
refers to the load or resistance under which the patient
exercises. The volume of training is estimated by deter-
mining the amount of work performed. This is calculated
by multiplying the resistance (force × distance) by the total
number of repetitions performed in a specified period of
time.3 Volume may be calculated by adding the frequency
and duration of rehabilitation or training sessions. It is
suggested that the rehabilitation clinician use these terms
to describe and document the resistance training and reha-
bilitation programs that are established for each patient.
Use of these terms will allow the clinician to provide more
objective and quantifiable documentation of progress.
Bioenergetics of Resistance Training
Bioenergetics, or the flow of energy in a biological sys-
tem, is the conversion of food energy or chemical energy
into biologically usable forms of energy, and concerns the
sources of energy for muscular contraction.3,4 The break-
down or conversion of chemical bonds in the molecules
433
of food—carbohydrates, fats, and protein—releases the
energy necessary to perform exercise involving muscular
contractions.4
In an excellent review of bioenergetics, Conley4
provides a model for the breakdown of large molecules into
smaller molecules (catabolism) and the synthesis of larger
molecules from smaller molecules by using the energy
produced from catabolic reactions (anabolism). Figure
21-1 shows this model, demonstrating how exergonic
(energy-releasing) and endergonic (energy-requiring)
reactions form the general scheme of metabolism (the
total of all catabolic/exergonic and anabolic/endergonic
reactions in a biological system).4
The final source of energy for muscular contraction
is the adenosine triphosphate (ATP) molecule. An ade-
quate supply of ATP is necessary for muscular contrac-
tion.3 The catabolic breakdown of the chemical bonds
of the ATP molecule provides the energy necessary to
allow myosin cross bridges to pull the actin filaments
across the myosin filaments, which results in muscle
contraction.3,5,6 To accomplish muscle contraction of
various intensities and durations, a source of ATP must
be readily available to the muscle. The muscle cell has
three sources of ATP available. The first two sources,
ATP-phosphocreatine (ATP-PC) and lactic acid, which
are formed without the need for direct sources of oxy-
gen, are anaerobic energy sources. The third source of
ATP for muscular contraction requires oxygen and is an
aerobic energy source.3 Table 21-1 provides an overview
of the bioenergetics of maximal effort based on the
duration of the exercise event. Although it is beyond
the scope of this chapter to provide a detailed descrip-
tion of biological energy systems and supplies of ATP,
a brief overview is necessary to appreciate the physi-
ological justification for the use of resistance training
in rehabilitation programs for athletes as well as other
patients. Many implications for the energy systems arise
in the design of resistance training and conditioning
Large molecules
Catabolic/exergonic
reactions
Energy ATP Small molecules
Small molecules
Energy
ADP
Anabolic/endergonic
reactions
Large molecules
Figure 21-1
The general scheme of metabolism. (From Stone MH, Conley
MS: Bioenergetics. In Baechle TR: Essentials of strength training
and conditioning, p. 68, Champaign, Ill, 1994, Human Kinetics.
Copyright 1994 by the National Strength and Conditioning
Association. Reprinted by permission.)
434 SECTION II • Principles of Practice
Table 21-1
Bioenergetics and Maximal Effort Duration
Primary System Duration of Event
ATP-CP 0–10 sec
ATP-CP + anaerobic glycolysis 10–30 sec
Anaerobic glycolysis 30 sec-2 min
Anaerobic glycolysis + oxidative system 2–3 min
Oxidative system >3 min and rest
ATP-CP, adenosine triphosphate–phosphocreatine.
From Stone MH, O’Bryant HS: Weight training: a scientific approach,
p 32, Minneapolis, Minn, 1987, Burgess International. An imprint of
Burgess International Group, Edina, Minn.
programs for patients; therefore, it is important for the
clinician and rehabilitation professional to understand
how these systems are trained, and the consequences
of detraining. The reader is referred to several excel-
lent sources for a detailed explanation of bioenergetics
and energy metabolism.4–6
Energy Sources
ATP-Phosphocreatine
A limited amount of energy is available from the ATP-
PC energy system for immediate use by the muscle for
contraction. The ATP molecule is broken down into
adenosine diphosphate (ADP), phosphorus (P), and
energy for contraction. When PC is broken down to
creatine, P, and energy, the energy from this reaction
is used to “rebuild” ADP and P into ATP that can be
used for additional muscular contraction.3 Several stud-
ies have demonstrated that ATP-PC energy sources are
exhausted in 30 seconds or less after an all-out exer-
cise effort.3,7,8 However, despite the limited amount of
ATP-PC available for muscular contraction, there are
two distinct advantages of this source of energy: it is
an immediate source of energy for muscular contrac-
tion, and the ATP-PC energy source has a large power
capacity in that it is capable of providing the muscle
with a large amount of energy per unit of time.3
Lactic Acid
Muscles have a constant need for energy to allow them
to contract. To provide for this need for an immedi-
ate source of energy, muscles store a limited amount
of carbohydrate called glycogen. Glycogen consists of
long strings of glucose sugar molecules. These glucose
molecules are split when immediate energy is needed
into pyruvate, yielding the energy needed to make ATP
for muscular contraction.3 Pyruvate is then transformed
into lactic acid, and this entire process, which does
not require the presence of oxygen, is called anaerobic
glycolysis, as seen in Figure 21-2.3,9
The accumulation of lactic acid in the contracting mus-
cle is probably most recognized in sport and resistance
training by the initial sensation of “pins and needles” in
the hands, fingers, or toes, followed by the sensation of
pain in the local musculature as a result of lactate con-
centrations high enough to affect the nerve endings. As
the exercise continues at the same or higher intensity,
and more lactic acid is produced, there is a change in
the acidity, or pH, of the muscle. Once the muscle pH
drops below a certain level, phosphofructokinase (PFK),
which is one of the rate-limiting enzymes in the process
of glycolysis, shuts down, and local energy production
then quickly ceases until replenished by oxygen stores.
It has also been suggested that excess lactic acid in the
muscle also interferes with calcium binding sites in the
muscle, thus further limiting muscle contraction and use-
ful power production.10 Therefore, the amount of energy
that can be produced by the lactic acid energy system
is limited because of the various side effects due to the
accumulation of lactic acid in the muscle.3
Lactic acid is the major energy source for providing
the muscle with ATP during exercise bouts that last from
1 to 3 minutes (e.g., a long set of repetitions during resis-
tance training, or running 400 to 800 m). This is also the
time it takes for most functional activities of daily living
(e.g., carrying groceries, taking out the trash); therefore,
the design of resistance training and conditioning pro-
grams as part of the total rehabilitation program for most
patient populations should include work bouts of 1 to 3
minutes to develop the lactic acid system for optimum
performance of functional activities. The lactic acid sys-
tem produces a larger amount of energy than the ATP-
PC system, although it cannot supply the muscle with
as much energy per unit of time as does the ATP-PC
system. Consequently, the lactic acid system is not as
powerful as the ATP-PC system.3
Oxygen Energy Source
The oxygen energy system is the major source of ATP
for prolonged muscular contraction (e.g., for periods of
exercise longer than 5 to 10 minutes). This energy sys-
tem directly uses oxygen to produce energy and is thus
considered to be the aerobic energy source.3 The oxygen
energy system has the ability to metabolize both carbo-
hydrates and fats for energy production. The maximal
amount of energy that can be supplied by the aerobic or
oxygen energy system is determined by the ability of the
body to obtain and use oxygen at the level of the local
exercising tissues. Maximal
. aerobic power, or maximal
oxygen consumption (VO2max), is the maximal amount
of oxygen that can be supplied to the body and then used
to allow for the continued aerobic production of energy.
Although it is well understood that aerobic activities
such as long-distance running, swimming, cycling, or row-
ing are the primary type of activities that stress the aerobic
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
Figure 21-2
The glycolytic pathway. (From Stone MH, O’Bryant HS: Weight training: a scientific approach, Minneapolis, Minn, 1987, Burgess International.
An imprint of Burgess International Group, Inc., Edina, Minn.)
energy system, it has been shown that resistance train-
ing can also effectively place demands on aerobic energy
sources. Because of the large energy and caloric expendi-
ture associated with aerobic exercise, most training pro-
grams designed to expend large amounts of calories for
weight loss have focused on aerobic training. However,
several studies have clearly shown that resistance train-
ing, particularly in the recovery period between sets, can
cause the athlete to consume large amounts of oxygen and
consequently can be effective in caloric reduction pro-
grams.11–15 In fact, a study by Dohmeier and colleagues13
demonstrated that heavy resistance training can provide a
sufficient aerobic stimulus to elicit an aerobic adaptation
similar to that seen with treadmill exercise.9,13 The amount
of the aerobic contribution to resistance training depends
on several factors, such as intensity, rest interval, the vol-
ume or number of repetitions, and the duration of the
435
resistance training session. Although the oxygen energy
system is not normally considered a major contributor
to the energy needs of resistance training, it does indeed
contribute in some fashion that is specific to the type,
intensity, and volume of the training. However, during cir-
cuit training for cardiac patients and the rehabilitation of
orthopedic conditions, all of the energy systems are used,
thus making this type of training advantageous for many
patient populations. Circuit training is discussed in detail
later in this chapter.
It is important that clinicians understand the relative
energy sources needed for the types, intensities, and vol-
umes of exercise that they prescribe for the athletes and
patients they treat. With this knowledge, they can more
accurately and specifically design resistance training pro-
grams to meet the demands and requirements of specific
sports and activities.
436 SECTION II • Principles of Practice

Table 21-2
Possible Factors Increasing Excess Postexercise
Contributions of Anaerobic and Aerobic Mechanisms
Oxygen Consumption (EPOC)4,16,17 to Maximal Sustained Effort
● Resynthesis of ATP and creatine phosphate stores Duration of Effort (sec)
● Resynthesis of glycogen from lactate (20% of lactate accumulation)
0–5 30 60 90
● Oxygen resaturation of tissue water
● Oxygen resaturation of venous blood Exercise intensity 100 55 35 31
● Oxygen resaturation of skeletal muscle blood (percentage of
● Oxygen resaturation of myoglobin maximum power
● Redistribution of ions within various body compartments output)
● Repair of damaged tissue Percentage 96 75 50 35
● Additional cardiorespiratory work contribution of
● Residual effects of hormone release and accumulation anaerobic
● Increased body temperature mechanisms
Percentage 4 25 50 65
contribution of
aerobic mechanisms

Recovery or Replenishment
of Energy Sources
Recovery from an intense exercise bout, such as that seen
with resistance training, is critical to the body’s ability to
continue training, both immediately and over the long
term. After an intense exercise session, anaerobic energy
sources must be replenished before they can be called on
again to provide energy for muscular contraction.3 The
anaerobic energy sources of ATP-PC and lactic acid are ulti-
mately replenished by the oxygen-based or aerobic energy
system. The extra oxygen that is taken in to replenish the
anaerobic energy sources after cessation of the exercise
effort has historically been termed the oxygen debt.11 This
oxygen recovery phase is currently more accurately referred
to as excess postexercise oxygen consumption (EPOC),12
which is the oxygen consumption above resting levels that is
needed to restore energy sources.4,12 Numerous factors may
influence EPOC; these factors are listed in Table 21-2 and
diagrammatically displayed in Figure 21-3. Recovery from
exercise takes place over time; the time required is based on
the intensity and duration of the exercise. Low-level aerobic
exercise has a very short EPOC, whereas heavy resistance
training can result in a prolonged EPOC, well above resting
oxygen consumption, for periods of greater than 30 min-
utes after cessation of the exercise.14,15
From a practical standpoint, it is important in the design
of resistance training programs to provide sufficient recov-
ery time to allow for replenishment of anaerobic and aero-
bic sources of energy before the next exercise session. This
takes on additional significance when resistance training is
used as an adjunct to or part of the total conditioning and
training program for an athlete. Elite-level power lifters,
who are training only to develop maximal power in one of
three events, sometimes have 7 to 10 days between train-
ing sessions to allow for adequate recovery of the muscles
from the demands of the previous resistance training ses-
sion.18 When a resistance training session is only one of
From Conley MS: Bioenergetics in exercise and training. In Baechle TR,
Earle RW, editors: Essentials of strength training and conditioning, ed
2, p 87, Champaign, Ill, 2000, Human Kinetics. Copyright 2000 by
the National Strength and Conditioning Association. Reprinted by
permission.
several training sessions in a given day for an athlete, it is
critical that the relative intensity and volume of resistance
training be taken into account in the total program design.
Failure to allow for sufficient recovery from any training
session, particularly resistance training exercise bouts, can
Oxygen deficit
VO2 required
for exercise
VO2max
VO2
EPOC
Rest Exercise (1 min) Recovery
Figure 21-3
High-intensity, non–steady-state exercise metabolism (80% of
maximal power output). The required VO2 is the oxygen uptake that
would be required to sustain the exercise if such an uptake were possible
to attain. Because it is not, the oxygen deficit lasts for the duration of
the exercise. EPOC, excess postexercise oxygen uptake; VO2, maximal
oxygen uptake. (From Stone MH, Conley MS: Bioenergetics. In Baechle
TR, Earle RW, editors: Essentials of strength training and conditioning,
p. 77, Champaign, Ill, 1994, Human Kinetics. Copyright 1994 by
the National Strength and Conditioning Association. Reprinted by
permission.)
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
result not only in system failure, but also in an increased
probability of injury. The clinician must work closely with
the patient and, in the case of a competitive athlete, the spe-
cific sport coach to ensure the proper design of the train-
ing program as well as the recovery program.
It may be even more important for the clinician to take
rest and recovery into account with their patient popula-
tions. For example, it is almost a universal phenomenon
for patients who receive lower extremity total joint arthro-
plasties to exhibit excess fatigue for many weeks after even
minimal exercise.19 The physiological mechanism for this
excessive fatigue is currently under investigation.20 It may
be due to some related neurological dysfunction relating
to the surgical procedure, or a localized depletion of gly-
cogen storage capacities. In any case, it happens in most
patients, and the rehabilitation clinician needs to be aware
that this occurs. Clinicians need to ensure that adequate
rest and recovery periods are included between sets of
exercise as well as between exercise sessions in the design
of their patients’ rehabilitation programs.
Resistance Training for Rehabilitative
Program Design
Clinicians may be involved in the development of resis-
tance training programs from several perspectives. They
should assist coaches in the design of specific resistance
training programs to meet the demands of a given sport.
They also must develop resistance training programs as
part of the total rehabilitation program of an athlete or
any other patient after an injury. This section addresses
some of the basic adaptations that occur with resistance
training, types of resistance training, methodology for
documentation of resistance training, various systems of
resistance training, and the design of individualized resis-
tance and rehabilitation programs.
Basic Adaptations that Occur with Resistance
Training
The design of a resistance training program for any patient,
whether an athlete or not, must facilitate systemic processes
that allow for a physiological adaptation of the system over
time.21 The adaptation that occurs with resistance train-
ing depends on how much potential for adaptation exists
in the patient, as well as the process and design of the
resistance training program.21 Genetic and physiological
factors determine the ultimate adaptation that occurs with
resistance training and conditioning programs. Kraemer21
has found that a genetic ceiling exists for every physiologi-
cal function, and performance gains in most sports and
other functional activities are related to the physiological
adaptations in many systems. Every individual undertakes
a strength and conditioning program, either for sport-
437
specific training or rehabilitation, with his or her own
genetic predisposition; potential for improvement; willing-
ness to train appropriately; and, with the underlying state
of conditioning, deconditioning and injury pathomechan-
ics that all interact to determine the adaptation that will
occur as a result of resistance training and conditioning.21
This section focuses on the adaptation that occurs in the
musculoskeletal system with resistance training.
There have been several excellent and extensive reviews
of the physiological effects of resistance training.22–27 Table
21-3 provides a summary of the contrasting physiologic
adaptations that occur with resistance training and endur-
ance training.21 One of the major adaptations that occurs
with resistance training is the alteration of muscle fibers.
For many years it was thought that the initial adaptation
to resistance training was a modification or adaptation of
the nervous system for the acquisition of a skill and maxi-
mal activation of the muscle.28–30 It was speculated that
the adaptations and changes in strength seen in the first
6 to 8 weeks were the result of these neural adaptations.
However, Staron and colleagues31 have demonstrated that
skeletal adaptations can occur in various skeletal muscle
fiber types in as little as 2 weeks if the training inten-
sity is sufficiently high. Although a detailed description
of human muscle physiology is beyond the scope of this
chapter, the authors review the basics of muscle fiber types
and the alterations and transformations that occur in dif-
ferent muscle fiber types with resistance training.
Skeletal muscle is best described as comprising two
distinctly different fiber types that are classified by their
contractile and metabolic characteristics.32,33 Type I fibers
(also referred to as slow-twitch fibers) are best suited
for the performance of endurance or aerobic activities.
These fibers contain large concentrations of mitochon-
dria, myoglobin, and the enzymes necessary to allow the
fibers to be fatigue resistant. Type II (or fast-twitch)
fibers are more suited for anaerobic or power production
seen in short, intense bouts of exercise. Type II fibers are
larger, can fire with greater velocity, and develop greater
force production. However, research by Staron and col-
leagues31,34–37 has identified various subtypes of both
type I and type II fibers, and it appears that much of
the physiological adaptation that occurs with resistance
training takes place in these subtypes.
There appears to be a continuum in the aerobic-to-
anaerobic capabilities and qualities of skeletal muscle.34
Along this continuum three subtypes are identified: type
A, which possess good aerobic and anaerobic characteris-
tics; type B, which possess fair aerobic and poor anaerobic
characteristics; and type C, which appear to be an inter-
mediate alteration between type A and B fibers and are
somewhat rare in humans.34,35 There is also an AB fiber
type that serves as an intermediate step between type A
and type B. These fiber types, identified from a muscle
biopsy sample, are further characterized by histochemical
438 SECTION II • Principles of Practice

Table 21-3
Comparison of Physiological Adaptations to Resistance Training and Aerobic Training
Variable Result after Resistance Training Result after Endurance Training

Performance
Muscle strength Increases No change
Muscle endurance Increases for high-power output Increases for low-power output
Aerobic power No change or increases slightly Increases
Maximal rate of force production Increases No change or decreases
Vertical jump Ability increases Ability unchanged
Anaerobic power Increases No change
Sprint speed Improves No change or improves slightly
Muscle Fibers
Fiber size Increases No change of increases slightly
Capillary density No change or decreases Increases
Mitochondrial density Decreases Increases
Fast heavy-chain myosin Increases in amount No change or decreases in amount
Enzyme Activity
Creatine phosphokinase Increases Increases
Myokinase Increases Increases
Phosphofructokinase Increases Variable
Lactate dehydrogenase No change or variable Variable
Metabolic Energy Stores
Stored ATP Increases Increases
Stored creatine phosphate Increases Increases
Stored glycogen Increases Increases
Stored triglycerides May increase Increases
Connective Tissue
Ligament strength May increase Increases
Tendon strength May increase Increases
Collagen content May increase Variable
Bone density No change or increase Increases
Body Composition
Percentage body fat Decreases Decreases
Fat-free mass Increases No change

From Kraemer WJ: Physiological adaptations to anaerobic and aerobic endurance training programs. In Baechle TR, Earle RW, editors: Essentials
of strength training and conditioning, ed 2, p 144, Champaign, Ill, 2000, Human Kinetics. Copyright 2000 by the National Strength and
Conditioning Association. Reprinted by permission.

and biochemical analyses of a muscle enzyme, myofibril-
lar adenosine triphosphatase (mATPase), and a total of
six fiber subtypes (I, IC, IIA, IIB, IIAB, and IIC) can be
distinguished based on their staining intensities and the
pH level of the analyses.34
Figure 21-4 provides a schematic illustration of the
staining intensities of the six fiber types at three pH lev-
els.34 It is important to know the pH level at which the
fibers are tested, because type I fibers are stable in the
acid ranges (staining dark) but labile in the alkaline ranges
(staining light). Type II fibers are stable in the alkaline
ranges (staining dark) but labile in the acid ranges (stain-
ing light). The three pH ranges are used to show trans-
formations and fiber type conversions that occur with
resistance training.31
Within this continuum of fiber types, there appears
to be a consistent order of recruitment of fiber sub-
types based on the intensity of the exercise:34,38 type I
fibers first, followed by IC, IIC, IIA, IIAB, and, finally,
IIB fibers. The smaller motor units are recruited first
because they are easiest to stimulate, and the larger
motor units are stimulated based on the total amount
of force necessary to perform the muscular contraction.
Because the IIB fibers are recruited last, it has been spec-
ulated that the IIB fibers are the “strength” fibers and
possess the greatest anaerobic potential.32 However, the
research by Staron and colleagues has shown that the
IIB fiber is not the strength fiber, and its performance
during exercise is inversely related to both aerobic and
anaerobic conditioning.39 However, because muscle is
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
Figure 21-4
Schematic of histochemical fiber typing based on myofibrillar
adenosine triphosphatase (mATPase) staining intensity after
preincubation at various pH values. (From Staron RS, Hikida RS:
Histochemical, biochemical and ultrastructural analysis of single
human muscle fibers with special reference to the C fiber population,
J Histochem Cytochem 40:564, 1992.)
an extremely dynamic structure, fiber types can actu-
ally be transformed along the recruitment continuum.
One of the primary and initial adaptations of strength
training is a transformation of and reduction in the
number of type IIB fibers.
Figure 21-5 presents data from a single subject before
and after a high-intensity resistance training program.31
Over time, there was an adaptation in the size of the muscle
fibers and a transformation of type II fibers. High-intensity
resistance training causes a transformation of IIB fibers into
IIAB and IIA fibers. In fact, in some of the subjects in this
investigation, and in another high-intensity resistance train-
ing study of female subjects,38 no type IIB fibers could be
found at the conclusion of the training program.31,38 This
adaptation of skeletal muscle to resistance training occurs
rapidly with the initiation of high-intensity training, and as
long as the athlete continues to incorporate some compo-
nent of resistance training in his or her total strength and
conditioning program, the adaptations will remain.
The other major adaptation that occurs in skeletal
muscle with resistance training is the change in cross-
sectional area of the muscle, resulting in hypertrophy of
the muscle tissue. It appears that this increase in cross-
sectional area results from an increase in the myofibril-
lar volume of the individual muscle fibers, not from an
increase in the number of fibers per unit area.21,26,32,40,41
There remains some debate over the muscle’s ability
to change the number of myofibrils (hyperplasia), with
some investigators supporting42–44 and some45,46 rejecting
the concept that the hyperplasia occurs in humans.
439
Physiological adaptations also occur in the cellular,
hormonal, connective tissue, and skeletal systems with
resistance training. The magnitude of these adaptations
is the result of several factors: (1) intensity and volume of
training, (2) pretraining physiological status, (3) extent of
pathophysiological limitations, and (4) age of the patient
or client. Kraemer and associates21,22 and Bandy and
colleagues26 provide excellent reviews of these systemic
adaptations, which are summarized in Table 21-3.
Deconditioning, as might be expected, results in a
reversal of many of the adaptations and training effects
that are gained as the result of resistance training. Several
studies have reported a reduction in cross-sectional area,
a reduction in muscular enzymes, histochemical and bio-
chemical alterations, and a regression of muscle fibers
toward pretraining values.47–52 Two investigations exam-
ined the effect of immobilization on the biochemical and
cross-sectional areas of skeletal muscle after a period of
heavy resistance training.53,54 These studies found that
the adaptations in skeletal muscle that occurred with
heavy resistance training were negated and actually
reversed after a period of immobilization-induced dis-
use; changes were particularly marked in type II fibers.
Deconditioning is a significant problem for the clinician,
not only with regard to individuals who must reduce or
discontinue training as the result of an injury, but (and
perhaps more so) with regard to individuals who are just
starting a conditioning program for fitness, functional
activity, or some sporting activity. The latter individu-
als have been deconditioned for a significant amount of
time, and the clinician must use caution and care in the
design of their resistance training program.
Deconditioning may be an even larger concern for
the rehabilitation clinician, whose patients may have
had their disability or dysfunction for so long that their
degree of deconditioning may actually be described as
unconditioned.19 This is particularly true of the patient
with degenerative joint disease, in whom the disease has
progressed for so long that his or her physiological sta-
tus at the time of joint replacement surgery is extremely
poor. These patients have been deconditioned for years,
and it can take a significant time for them to return to a
more normal level of functional ability and performance
of activities of daily living.
Adaptations to Resistance Training
in Selected Populations
The physiological adaptations to resistance training
have been well documented in healthy male subjects,
both nonathletes and athletes. However, a growing
number of pediatric, female, and elderly athletes and
individuals have found a marked benefit of resistance
training as it applies to their sports and activities of
daily living.
440 SECTION II • Principles of Practice

Figure 21-5
Serial cross-sections of muscle samples taken from male control subject at beginning (a-c) and end (d-f) of study and from male strength-trained
subject at beginning (g-i) and after 8 weeks of high-intensity training (j-l). Sections were assayed for myofibrillar adenosine triphosphatase
(mATPase) activity after preincubation at pH values of 10.2 (top row), 4.3 (middle row), and 4.6 (bottom row). Arrows indicate scattered atrophic
fibers. I, type I; IC, type IC; C, type IIAC; A, type IIA; AB, type IIAB; B, type IIB. Bar = 100 µm. (From Staron RS et al.: Skeletal muscle
adaptations during early phase of heavy resistance training in men and women, J Appl Physiol 76:1247–1255, 1994.)

Children
Kraemer and Fleck55 and Faigenbaum and Westcott56 have
extensively researched the area of resistance training for
young children and have found it to be safe and effective if
done properly. Children can improve strength and power,
local muscular endurance, and balance and proprioception;
become more resistant to injury; and develop a more positive
body image and sport performance perspective with the use
of appropriate resistance training. Table 21-4 provides some
basic guidelines for resistance training for children.55,56 It is
important for the clinician to realize that before puberty, the
young child will gain significant strength and power without
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
Table 21-4
Basic Guidelines for Resistance Exercise Progression
in Children
Age (yr) Considerations
≤7 Introduce child to basic exercises with little
or no weight; develop the concept of a
training session; teach exercise techniques;
progress from body weight calisthenics, partner
exercises, and lightly resisted exercises; keep
volume low.
8–10 Gradually increase the number of exercises;
practice exercise technique in all lifts; start
gradual progressive loading of exercises; keep
exercises simple; gradually increase training
volume; carefully monitor toleration to the
exercise stress.
11–13 Teach all basic exercise techniques; continue
progressive loading of each exercise; emphasize
exercise techniques; introduce more advanced
exercises with little or no resistance.
14–15 Progress to more advanced youth programs
in resistance exercise; add sport-specific
components; emphasize exercise techniques;
increase volume.
≥16 Move child to entry-level adult programs after
all background knowledge has been mastered
and a basic level of training experience has been
gained.
Note: If a child of any age begins a program with no previous
experience, start the child at beginning levels and move him or her to
more advanced levels as exercise tolerance, skill, amount of training
time, and understanding permit.
From Kraemer WJ, Fleck SJ: Strength training for young athletes, p 5,
Champaign, Ill, 1993, Human Kinetics. Copyright 1993 by William J.
Kraemer and Steven J. Fleck. Reprinted by permission.
a concomitant increase in muscle hypertrophy. Until the
child reaches puberty, he or she does not have sufficient
hormonal levels to allow for the skeletal muscle hypertrophy
that is seen in older resistance-trained athletes.55–57
To allow a young individual to undertake a resistance train-
ing program, the clinician should ensure that the program is
designed specifically for the child and use body weight and
medicine balls or tubing as resistance. Children should be
progressed at their own rate and work only with resistance
equipment that can be adapted to their size. Proper instruc-
tion is very important, as is adequate supervision.
Faigenbaum and Westcott56 have suggested several equip-
ment and program considerations when designing resistance
programs for children to ensure that resistance training is
provided in a fashion suitable to children. Based on the avail-
able research, Faigenbaum and Westcott56 have established
guidelines for the development of safe and effective strength
training programs for children to ensure proper safety and
progression.
441
Considerations for Resistance Training
for Children
● Do not impose an adult training program on a child
● Use body weight or medicine balls for resistance in the early
phases of strength training for children
● Make sure the resistance apparatus fits the child properly
● Do not let the child progress too quickly. It takes longer for
children to adapt to resistance training loads
● Do not push children to get into resistance training: they are
ready when they are ready
● Proper instruction in resistance training techniques
is paramount
● Adequate supervision to ensure proper lifting technique
is critical
Faigenbaum and Westcott’s Equipment and Program
Design for Resistance Training with Children56
● Equipment should be of an appropriate design to accommodate
the size and degree of maturity of the child or adolescent
● It should be cost effective
● Equipment should be safe, free of defects, and inspected
frequently
● It should be located in an uncrowded area, free of obstructions,
with adequate lighting and ventilation
● The child should have the emotional maturity to accept coaching
and instruction
● There must be adequate supervision by coaches/clinicians who
are knowledgeable about strength and resistance training
● Strength training should be part of a comprehensive program to
increase motor skills and fitness
● There should be an adequate warm-up and cool-down period
after the strength and conditioning session
● The program should emphasize dynamic concentric and
eccentric contractions through a full range of motion
Faigenbaum and Westcott’s Guidelines for Safe
Resistance Training with Children56
● Strength training two to three times per week for 20–30 minutes
per session
● The child should apply no resistance until he or she can
demonstrate proper exercise technique and form for any strength
training exercise
● Six to 15 repetitions equal 1 set of a particular exercise, and the
child should do 1 to 3 sets per exercise
● Increase the weight or resistance in 1- to 3-pound increments
after the child can perform 15 repetitions with proper form
442 SECTION II • Principles of Practice
Women
Women have also significantly increased the amount of
resistance training they do. Whether resistance training is
used as a supplement to training for a particular sport, or
alone to enhance strength and muscle tone or for reha-
bilitation, women are becoming involved in resistance
training in record numbers. Women are also involved in
the competitive resistance training sports of body build-
ing, power lifting, and, most recently, Olympic lifting.
Staron and colleagues31,38 have shown dramatically that
women experience muscular adaptations similar to those
seen in men, provided they are trained with a similar high-
intensity resistance program. The National Strength and
Conditioning Association (NSCA) has published a posi-
tion paper on strength training for female athletes,58 pro-
viding 162 references that address the physiological and
hormonal adaptations of women to resistance training,
as well as considerations for resistance training program
design for female athletes. This position paper is an excel-
lent reference and would be invaluable for any sports
medicine clinician who works with female athletes.
Although men and women tend to respond similarly
to resistance training, women may be at a greater risk of
injury using eccentric muscle training compared with men,
particularly if performing the standard maximum resistance
program with eccentric training.59 In a recent study, how-
ever, Schroeder and coworkers59 demonstrated that young
women can achieve strength gains and muscle/bone adap-
tations with submaximal eccentric training comparable with
those obtained with maximal eccentric training. In fact,
after a 16-week training program, women performing low-
intensity eccentric progressive resistive exercise (i.e., 75% of
the concentric one-repetition maximum [1-RM]) demon-
strated greater improvements in bone mineral content than
women performing high-intensity eccentric exercise (i.e.,
100% of the concentric 1-RM). In addition, both groups
demonstrated comparable strength gains. Thus, the female
athlete might be better advised to perform submaximal
eccentric exercise as a part of a resistance exercise program,
both for the benefits and the safety.
Along with the general benefits of strength training
(i.e., strength development, changes in body compo-
sition, performance enhancement), strength training
provides benefits unique to women. Women are sus-
ceptible to injuries and conditions unique to their sex.
These conditions include a greater incidence of osteo-
porosis and a greater rate of tears to the anterior cruci-
ate ligament (ACL) of the knee compared with males.
For instance, as reported by Paterno and colleagues,60
women sustain a tear to the ACL at a rate four to six
times greater than in men. Cussler and associates61 dem-
onstrated the effects of resistance exercise on bone min-
eral density (BMD) in postmenopausal women. Decline
in BMD is a major issue that primarily affects women,
often resulting in osteoporosis in older age. Cussler and
associates61 demonstrated the positive effects of resis-
tive exercise on BMD in women after a 1-year strength
training program. Their research is supported by a
number of other studies examining the effectiveness of
resistance exercise to reduce the risk of osteoporosis in
women.62,63
As for the incidence of ACL tears in women, resistance
training and neuromuscular training provide avenues for
injury prevention. Ford and colleagues64 and Malinzak
and coworkers65 report on the increased genu valgus
observed in women, which is accentuated with jump-
ing and landing activities. This valgus force places the
female knee at greater risk of ACL tear compared with
men. Paterno and colleagues60 demonstrated the ben-
efits of neuromuscular training at the knee to improve
mediolateral stability in women. This type of exercise and
resistance training may pay dividends as a preventative
measure for women to protect against ACL injuries. In
addition, the added benefit of improved quadriceps and
hamstring strength has been demonstrated to reduce the
risk of ACL tears in athletes.60
Exercise and resistance training are also safe for
pregnant women.66–69 Most women who follow their
physician’s recommendations can safely exercise dur-
ing pregnancy. There are distinct benefits of exercise
during pregnancy, including improved fitness, facili-
tated recovery, reduced recovery times and symptoms,
less weight gain, more energy resources, and enhanced
well-being.
Benefits of Exercise during Pregnancy
● Improved cardiovascular and muscular fitness
● Facilitated recovery from labor
● Faster return to prepregnancy weight, strength, and flexibility
levels
● Reduced postpartum abdominal laxity
● Reduced back pain during pregnancy
● Greater energy reserve
● Fewer obstetric interventions
● Less weight gain
● Enhanced well-being and reduced feelings of stress
There are, however, situations in which exercise and
resistance training are contraindicated during preg-
nancy. These include hypertension and other cardio-
vascular symptoms, pregnancy and birthing problems,
uncontrolled diabetes, excessive obesity, and low body
weight. The American College of Obstetricians and
Gynecologists68,69 has suggested several criteria for exer-
cise safety during pregnancy, including things to do and
things to avoid.
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
Contraindications to Exercise during Pregnancy
● Pregnancy-induced hypertension (preeclampsia)
● Significant cardiovascular or restrictive lung disease
● Severe anemia
● Ruptured membranes
● Premature labor
● Persistent bleeding after 12 weeks
● Premature cervical dilation (incompetent cervix)
● Multiple-birth pregnancy that creates a risk of premature labor
● Poorly controlled diabetes
● Extreme obesity
● Extremely low body weight (BMI < 12)
● History of smoking
● Orthopedic limitations
American College of Obstetricians and
Gynecologists Guidelines for Exercise Safety
during Pregnancy68,69
● Perform 30 minutes or more of moderate exercise on most, if not
all, days of the week
● Avoid exercise in the supine position after the first trimester
● Exercise should not continue past the point of fatigue and should
never reach exhaustion levels
● Non–weight-bearing exercises such as swimming or cycling are
favored over running for aerobic conditioning, particularly after
the first trimester
● Large increases in body temperature should be minimized
through adequate hydration, appropriate clothing, and optimal
environmental surroundings
● Resistance training with light weights can be cautiously
continued throughout pregnancy
● Heavy resistance training should be avoided
● Resistance training using machines that can be properly fit to the
woman are safer than using free weights
● Avoid Valsalva maneuver with proper breathing techniques
The Elderly
Resistance training has also been studied with respect to
the effects and adaptations of resistance training in the
elderly. The decline in strength in elderly individuals is
accompanied by increases in falls, functional decline, and
impaired mobility.70–72 Fiatarone and coworkers73 stud-
ied the effects of resistance training on subjects older than
70 years of age. Their subjects trained for 45 minutes per
day, 3 days per week, for 10 weeks at 80% of the established
1-RM. This investigation found a significant increase in both
muscular strength and muscle cross-sectional area. Grimby
and colleagues74 also used resistance training in a group of
78- to 84-year-old men and found significant increases in
muscular strength and endurance in their subjects. As with
443
any resistance training program, proper instruction, proper
fit of the equipment, and proper supervision allow resistance
training to be an effective tool to increase muscular strength,
endurance, and power, even in the very old.
Research on the elderly supports the notion that
rote exercises contribute to functional abilities.75–77 For
example, Cress and associates76 studied the effects of a
standard rote exercise program for total body strength
and endurance. They evaluated two groups of healthy
elderly individuals. One group performed exercises while
the control group performed no exercise. Exercises for
the training group included traditional free-weight
dumbbell exercises, stair-stepping machines, leg press
machines, and cuff weight exercises. After a 6-month
training program, the exercising group reported signifi-
cant gains in function, as measured by the Continuous
Scale—Physical Performance Functional Performance
test (CP-PFP). In addition, this group demonstrated
significant gains in maximal oxygen consumption (11%)
and muscle strength (33%).
The investigation by Cress and associates76 supports
the results of previous investigations looking at the
impact of lower extremity strengthening on function in
the elderly. Studies by Ades and colleagues77 and by Judge
and colleagues75 demonstrated that strength training of
the lower extremities significantly improved walking
endurance and walking speed in elderly populations.
There have been other investigations that have shown
the benefits of resistance training for the nonathletic
elderly. Decreased resting blood pressure after resistance
training has been reported.78–81 Improved lipid profile
after resistance training has also been shown to occur in
the elderly,82–87 and, most important, resistance training
has been shown to dramatically reduce the effects of
osteoporosis in both men and women.88–95 Westcott and
Faigenbaum66 have provided guidelines for resistance
training in the elderly.
Westcott and Faigenbaum’s Guidelines for
Resistance Training of the Elderly66
● Perform resistance training 2 to 3 nonconsecutive days per week
● Limit the intensity to 60% to 90% of maximum with a
corresponding repetition range of 4 to 16 repetitions
● Use single and multiple joint movements for the following major
muscle groups: quadriceps, hamstrings, gluteals, pectorals,
latissimus dorsi, deltoids, biceps, triceps, erector spinae, and
abdominal muscles
● Control the speed of movement (typically 2–4 sec/repetition)
● Exercise through a full range of motion
● The keys to safe and successful resistance training with the
elderly population are good instruction, proper fit of equipment,
and adequate supervision
444 SECTION II • Principles of Practice

Cardiovascular Patients program, a cardiac patient should have a minimum of 3

Resistance training has also proved to be not only safe,
but also extremely effective as a tool in the rehabilitation
of patients with cardiovascular disease.87,96–102 If the resis-
tance training is performed with a slow progression in
both intensity and volume, and if instruction and super-
vision are given to limit the breath holding or Valsalva
maneuver in these patients, such training has been shown
to dramatically improve muscular fitness and physical
performance, as well as maintain desirable body weight
and a positive self-concept in patients with cardiovascular
disease. Resistance training intensity should stay below the
anginal threshold, and the volume of the exercise should
be high (e.g., 3 to 5 sets of 10 to 15 repetitions per exer-
cise). Table 21-5 gives recommendations or guidelines
for resistance training from the American College of
Sports Medicine (ACSM), the American Association
of Cardiopulmonary Rehabilitation (AACPR), and the
American Heart Association.67
Another form of resistance training exercise that has
proved very successful with cardiovascular disease patients
is circuit training.96–102 With circuit training, the work-
to-rest ratio is controlled based on the cardiovascular
responses of the patient. Before starting a circuit training
months of cardiovascular exercise training, be at least 4
months from any form of cardiac surgery, have a diastolic
blood pressure at rest of less than 100 mm Hg, have a
functional capacity of at least 6 metabolic equivalents,
and not have any uncontrolled arrhythmias.
Types of Resistance Training
Figure 21-6 presents a strength model for the clinician
who designs resistance training programs for both ath-
letes and nonathletes. As discussed earlier, strength is tra-
ditionally defined as the maximal force a muscle or muscle
group can generate at a specified speed of contraction.1
Figure 21-6 divides strength into three components:
maximal strength, explosive strength, and endurance
strength. Athletic endeavors and specific sport skills
require one or more of these types of strength, and a
resistance training program must be designed to address
one or all types of strengthening.

Recommendations for Resistance Circuit Training

for Cardiovascular Patients
● Use 8 to 12 stations
● Progress to three circuits, two to three times per week
● Machines work better than free weights for ease of changing
resistance
● Cardiovascular responses of heart rate and blood pressure should
be monitored several times during the circuit, as well as before
and after exercise
● Intensity should be approximately 30% to 50% of an estimated
one-repetition maximum
● The work-to-rest (w:r) ratio will increase as fitness improves:
● Start out with 15 sec work to 45 sec rest (1:3)
● Progress to 15:30 sec (1:2) Figure 21-6
● Progress to 30:30 sec (1:1) Theoretical model of strength and muscular contraction. (From Falkel
● Progress to 45:30 sec (2:1.5) JE, Cipriani DJ: Physiological principles of resistance training and
rehabilitation. In Zachazewski JE, Magee DJ, Quillen SW, editors:
● Finally, 45:15 sec (3:1)
Athletic injuries and rehabilitation, p 214, Philadelphia, 1996, WB
Saunders.)

Table 21-5
Guidelines for Resistance Training in People with Cardiac Disease
Sets Repetitions Exercises Frequency

American College of Sports Medicine (ACSM) 1 8–15 8–10 2 days/wk

American Association of Cardiopulmonary Rehabilitation (AACPR) 1–2 12–15 8–10 2–3 days/wk
American Heart Association (AHA) 1–2 8–15 8–10 2–3 days/wk
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration 445

Types of Muscle Contraction

Based on the amount of force needed for the strength
application, the muscular contraction type will vary along
a continuum from isometric to dynamic. Dynamic con-
tractions are then further divided into three components:
concentric, eccentric, and econcentric muscular contrac-
tions. Concentric muscular contractions are defined as
the shortening contractions in which tension develops
as the insertion of the muscle moves toward the origin,
enabling the muscle to initiate and carry out a move-
ment103 (Figure 21-7). Eccentric muscular contrac-
tions are those in which the muscle is lengthened under
tension, with the insertion moving away from the ori-
gin, resisting or lowering the resistance against gravity
and enabling the muscle to act as a shock absorber, an
eccentric brake to slow or stop movement, or a dynamic
stabilizer during movement103 (Figure 21-8). Concentric
contractions require significantly more motor units
and thus more strength to move against the same resis-
tance than do eccentric contractions. Eccentric contrac-
tions require less energy expenditure, although they are
thought to be related to some aspects of the postexercise
muscle soreness that develops after a new or unfamiliar
exercise is undertaken.
Gray and colleagues104 have introduced the concept
of a muscular contraction that combines concentric and
eccentric contraction, called an econcentric muscu-
lar contraction. Deusinger105 identified a hypothetical,

Figure 21-7
Concentric muscle contraction model. (From Falkel JE, Cipriani DJ: Physiological principles of resistance training and rehabilitation.
In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and rehabilitation, p 215, Philadelphia, 1996, WB Saunders.)
446 SECTION II • Principles of Practice

pseudo-isometric muscle contraction that involves a con-
trolled concentric contraction of a muscle with a con-
current eccentric contraction of the same muscle as the
movement occurs over two or more joints. This type of
contraction is possible only for multiarticulate muscles.
Because the ongoing concentric muscle contraction
occurs at one joint simultaneously with the eccentric con-
traction over the second joint, Deusinger105 believed this
type of contraction was due to an apparent lack of length
in the multiarticulate muscle during activity. Gray and
colleagues104 redefined this type of contraction as “econ-
centric” because it involves both an eccentric and a con-
centric contraction, but also because it is an economical
type of muscular contraction in multiarticulate muscles.
Functionally, econcentric movement is important because
this is how two joint muscles, which are the most commonly
injured muscles, act in everyday life. Thus, when training
multiarticulate muscles, the clinician must include this
type of exercise if true functional recovery is expected.
Figure 21-9 presents the econcentric contraction model.
The biceps brachii is a biarticulate muscle that crosses both
the elbow and shoulder joints. The biceps is capable of
producing flexion of either joint or controlling extension
of either joint. During an activity such as lifting a dumb-
bell (see Figure 21-9), the biceps works concentrically to
flex the elbow, bringing the resistance close to the body. At
the same time, the shoulder is extending from a forward
flexed position to bring the dumbbell up in the shortest
path. This shoulder extension is controlled eccentrically
by the biceps at the shoulder. Thus, while the biceps is

Figure 21-8
Eccentric model contraction model. (From Falkel JE, Cipriani DJ: Physiological principles of resistance training and rehabilitation.
In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and rehabilitation, p 216, Philadelphia, 1996, WB Saunders.)
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration 447

actively shorting at the elbow during flexion, it is actively
lengthening at the shoulder during eccentric extension.
In appearance, the biceps has not changed actual length,
producing a pseudo-isometric type of contraction.
In the lower extremity, contraction of the soleus during
gait, either walking or running, is a prime example of an
econcentric muscle contraction. The soleus is a two-joint
muscle, crossing both the talocrural and subtalar joints.
During the “transition period” of gait, or mid-stance, the
soleus functions at the talocrural joint to decelerate the
tibia eccentrically as it dorsiflexes over the fixed foot. At
the same time, this muscle tension works concentrically
to create inversion of the calcaneus, assisting with the
transition from pronation of the subtalar joint to supina-
tion. Again, the soleus works eccentrically at the ankle
and concentrically at the subtalar joint, resulting in an
econcentric contraction.
This concept of econcentric contraction becomes
very important in the rehabilitation and training envi-
ronments. Muscles and proprioceptors adapt as they are
trained. Typical muscle rehabilitation and testing have
relied on single-joint motions and on isolated evaluation
and rehabilitation of a muscle at only one of its joints
at a time. The dumbbell curl is a typical example: the
biceps is normally rehabilitated only as it functions at the
elbow. However, the biceps would be best served if it

Figure 21-9
Econcentric model contraction model. (From Falkel JE, Cipriani DJ: Physiological principles of resistance training and rehabilitation.
In Zachazewski JE, Magee DJ, Quillen SW, editors: Athletic injuries and rehabilitation, p 217, Philadelphia, 1996, WB Saunders.)
448 SECTION II • Principles of Practice

were rehabilitated as it functions at both the elbow and

the shoulder. Because most multijoint muscles are capa-
ble of pseudo-isometric function, the rehabilitation and
program design for resistance training should include
econcentric exercises for these muscles. Specificity
of training demands that the muscle be trained and
rehabilitated econcentrically.

Isometric, Isokinetic, and Isotonic Training

Traditionally, three forms of muscular contractions have
been used during resistance training exercises: isometric
contractions, isokinetic contractions, and “isotonic”
contractions.
Some of the early research in resistance training was
done with isometric contractions. Isometric, or static
resistance training, refers to a muscular contraction in
which no apparent change in the length of the muscle
takes place.3 The muscle does not generate sufficient
force against the resistance to result in movement of the
resistance.
Isometrics was introduced in the early 1950s with
the work of Hettinger and Muller,106 and the definitive
text on isometrics was written in 1961 by Hettinger.107
Isometrics can result in gains of 5% to 30% in maximum
voluntary contraction (MVC), depending on the percent-
age of MVC, the duration of the contraction, and the
number of repetitions of the isometric contractions.3,106–108
Strength gains with isometric contractions are limited to
the specific angle of the exercise and, as a result, isometric
training has not been viewed favorably as the method of
choice for dynamic strengthening for sport and activity.
However, one form of isometric training, functional iso-
metrics, has specific implications in the design of resistance
training programs for athletes. Functional isometrics con-
sists of the application of isometric force and contraction
at multiple angles through the functional range of motion.
It has proven to be beneficial in providing strength gains
at specific angles during a functional movement when
the joint mechanics and muscle length relationships are
less than optimal. Functional isometrics at these “sticking
points” results in greater functional strength and can be
used successfully as a component of a functional activity
or sport-specific resistance training program.109 Figure 21-
10 shows the use of functional isometrics at the sticking
point of a bench press to gain strength and improve overall
bench press strength.
Isokinetic resistance training refers to the perfor-
mance of muscular contraction at some constant, pre-
determined speed of movement. Unlike other types of
resistance training, there is no set resistance to meet;
rather, the velocity of movement is set and any force
applied against the equipment results in an equal reac-
tion force.3 The reaction force is similar to the force
applied to the apparatus throughout any given range of
Figure 21-10
The use of functional isometrics at the sticking point in a bench press.
(From Fleck SJ, Kraemer WJ: Designing resistance training programs,
Champaign, Ill, 2004, Human Kinetics. Copyright 2004 by Steven J.
Fleck and William J. Kraemer. Reprinted by permission.)
motion, which would theoretically make it possible for a
muscle to exert a continuous, maximal force throughout
the predetermined range of movement.3 Because of its
accommodating resistance, isokinetics is frequently used
in the rehabilitation of athletic injuries and in the testing
of dynamic strength.
Isotonic resistance training offers the clinician the
greatest flexibility and variability in the design of resistance
training programs. In isotonic resistance training, the
external resistance (e.g., sandbags, dumbbells, barbells,
plates on a weight stack) stays the same. However, because
the resistance is moved through the range of motion, the
relative force needed to move that resistance must vary.
Therefore, the more accurate description of this type of
resistance training is dynamic constant external resistance
training, or DCER.3 The speed and range of motion are
controlled by the athlete, and these variables add to the
variety of program design in DCER resistance training.
In DCER resistance training, a variety of modalities can
be used for the external resistance: free weights (sandbags,
dumbbells, barbells, and medicine balls), body weight,
or any of a plethora of machines for isolated muscle
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
strengthening. Although DCER machines are most popu-
lar in health clubs, they are very limiting in terms of range
of motion, and unless they truly “fit” the individual prop-
erly, they are restricted in their ability to improve func-
tional strength. Free weights are truly free in that they do
not restrict range of motion, speed of movement, or the
use of multiplanar resistance training. Functional move-
ments and sport skills are rarely uniplanar or unidirectional
and are rarely limited to a single joint movement or muscle
function. Free weights therefore allow for the incorpora-
tion of activity- or sport-specific movement patterns and
speeds of movement. With proper instruction and correct
spotting techniques, free-weight exercises can provide the
individual with an optimal resistance training program to
address any form of strengthening that is required for a
specific sport or activity.
As exercises, the squat and bench press are probably
two of the most common lifts performed for any sport
training and are used as a barometer of strength by many
coaches. The squat, when done correctly, is a safe and
excellent exercise to increase overall lower extremity
and trunk strength. It is one of the most functional of
our activities of daily living, and yet many clinicians are
fearful and concerned about using this lift in the resis-
tance training programs of their athletes and patients.
NSCA Safety Issues with the Squat Exercise110
● Squats, when performed correctly and with appropriate supervision,
are not only safe but may be a significant deterrent to knee
injuries
● The squat exercise can be an important component of a training
program to improve the athlete’s ability to forcefully extend the
knees and hips and can considerably enhance performance in
many sports
● Excessive training, overuse injuries, and fatigue-related
problems do occur with squats. The likelihood of such injuries
and problems is substantially diminished by adherence to
established principles of exercise program design
● The squat exercise is not detrimental to knee joint stability when
performed correctly
● Weight training, including the squat exercise, strengthens connective
tissue, including muscles, bones, ligaments, and tendons
● Proper form depends on the style of the squat and the muscles to
be conditioned
● Although squatting results in high forces on the back, injury
potential is low with appropriate technique and supervision
● Conflicting reports exist as to the type, frequency, and severity of
weight training injuries. Some reports of a high injury rate may be
based on biased samples. Other reports have attributed injuries
to weight training, including the squat, that could have been
caused by other factors.
● Injuries attributed to the squat may result not from the exercise
itself, but from improper technique, preexisting structural abnormalities,
other physical activities, fatigue, or excessive training
449
The NSCA has written a position statement and review
of the literature on the squat as an exercise in athletic
conditioning.110
The squat is a safe and valuable exercise and can be
included in the program design for most patients with
lower limb problems. Proper instruction and technique
can be learned from a variety of sources,18,111 and clini-
cians should learn proper techniques and applications of
the squat and share them with their athletes and patients
alike.
The deadlift is another form of power lift, and, like the
squat, when done correctly and with proper form, it is
a valuable resistance training exercise with many applica-
tions, not only to sport, but also to normal activities of
daily living. Hatfield18 and Garhammer111 both provide
excellent instruction in the technique and biomechanics
of the deadlift, and the clinician should encourage the
use of the deadlift as one of the core lifts of most resis-
tance training programs.
A final form of competitive lifting that has some appli-
cation to the general population is Olympic lifting. These
lifts are the clean and jerk and the snatch. Although
detailed descriptions of the Olympic lifts are beyond the
scope of this chapter, there is a role for this type of train-
ing in the rehabilitation of patients who will need to lift
objects over their head when they return to their jobs
and functional activities of daily living. For those rehabil-
itation clinicians unfamiliar with the power and Olympic
lifts, we recommend contacting the NSCA (www.nsca-
lift.org) for educational materials and instruction.
Plyometric Training
The term plyometrics (from the Greek, meaning “mea-
surable increases”) was introduced in 1975 by Wilt,112 who
used it to describe what had been an Eastern European
training technique known simply as jump training.113
Plyometrics are exercises that enable a muscle to reach
its maximal strength in as short a time as possible.113,114
They allow exploitation of the muscles’ cycle of length-
ening and shortening to increase power.115
Plyometric exercises begin with rapid stretching of
the muscle by an eccentric contraction, followed by a
shortening of the same muscle in a concentric contrac-
tion.114 These exercises are based on use of the serial
elastic properties and stretch–reflex properties of the
muscle.114 When a muscle is loaded during the eccentric
contraction, there is an increase in muscle tension, which
allows for a greater concentric muscle contraction. The
proprioceptors of the muscle spindles and ligaments
and tendons surrounding a joint are also used during
plyometric training, in that they play a role in preset-
ting muscle tension and relaying sensory input from the
rapidly stretching muscle for activation of the stretch
reflex.114–116
450 SECTION II • Principles of Practice
Plyometric training is similar to any other form of
resistance training in that it uses the overload principle to
impose gradual adaptations on the muscles and joints.115
Plyometrics can be done with the lower body, trunk,
and upper body, but before a successful plyometric pro-
gram can be implemented, the athlete or patient should
develop a baseline level of strength.113–116 Activities as
basic and simple as walking and running incorporate
plyometric principles, and as such, plyometrics should
be included in all resistance training programs for both
athletes and patients.
Because the demands of plyometric training are great,
most clinicians recommend only one to three plyometric
training sessions per week.113,115 The intensity of
plyometric exercise is almost always high, and therefore
plyometric exercises should progress from low-intensity
exercises, to in-place exercises, to medium-intensity exer-
cises, and then to high-intensity exercises.115,117 Recovery
between sets, between exercises, and between training
sessions is critical. Recovery between sets should be long
enough to allow maximal effort on the next set (from 5
to 10 seconds to 2 to 4 minutes), and recovery between
training sessions should be at least 2 days, and most often
as long as 4 days.115
Plyometric exercises can and should be done in all
three planes of motion, using multiplanar movements as
much as possible. Most functional movements and sports
skills involve at least two planes of movement, and there-
fore plyometric training should be done in at least two
and preferably all three planes of movement.
One of the major goals of plyometric training is to
maximize force in a minimum amount of time.116 The
transition phase between the eccentric landing and the
concentric movement into the desired direction, or the
amortization phase, should be as short as possible so
that more of the force is generated into the concentric
phase to achieve greater distance or power. Realistically,
plyometrics need to be included in the overall rehabili-
tation program for most patients as well as for athletes
and healthy clients. One of the most frightening things
for a patient using an assistive device for ambulation is
having to stop suddenly, change direction quickly, and
get out of the way of another object or person (e.g., in
a store or shopping mall). To do this successfully, these
patients need to be trained with lower-level or less stress-
ful plyometric exercises to allow them to gain the bal-
ance, coordination, and body control needed to perform
these maneuvers during gait without increasing their risk
of falling.19 Simple loading and unloading of the lower
extremity in different planes with partial, full, or added
body weight can give patients the plyometric strength
and speed needed for safe ambulation in any situation.
Plyometric training for patient populations can be easily
and safely accomplished in the water.117 The buoyancy
of the water allows patients with limited weight-bearing
status to simulate plyometric types of movements (e.g.,
quick changes in direction, quick loading and unload-
ing the affected limb), and these types of exercises have
worked extremely well with a variety of patients, even
those with total knee arthroplasties.19 Plyometric training
in the water is an extremely valuable and effective way to
assist patients with a wide variety of conditions and dys-
functions to prepare themselves for the functional needs
of plyometric demands in their everyday lives.
Medicine Ball Training
Medicine ball, or weighted ball training and exercise,
one of the oldest forms of resistance training, has made
a comeback in recent years.114,118 Medicine balls provide
the opportunity to improve strength, balance, and coor-
dination through dynamic movements with minimal
equipment. Unlike resistance or weight machines that
train individual muscles, medicine ball exercises train the
body as a functional unit, increasing and improving total
body speed of movement and enhancing dynamic bal-
ance. These dynamic movements can be the same move-
ments used in functional activities of daily living as well as
many sport movements, offering a very exercise-specific
method of training. Medicine ball training can be done
by people of all ages and abilities, from the youngest
athletes (4 to 6 years of age), to patients with orthope-
dic limitations, to the elite-level competitive athlete.118
Upper and lower body medicine ball exercises can also
work directly on the core and trunk musculature in all
planes of movement, training the core muscles in their
role as dynamic stabilizers.
Another advantage to medicine ball training is its abil-
ity to allow patients, clients, and athletes alike to develop
fast-speed movements in a safe and functional manner.
Moving a barbell quickly during a resistance training
exercise often leads to injury, and is contraindicated.
Medicine ball exercises, however, allow the fast-twitch
fibers to be turned on, thus allowing greater speed,
quickness, and power.118 By using medicine balls of dif-
ferent weights and sizes, a total conditioning program
can be developed that involves all aspects of functional
movement.
In designing a medicine ball program, the intensity
can be controlled by varying the selected training vari-
ables, such as weight of the ball, number of repetitions,
and choice of the exercise. Medicine ball exercise training
principles, like all other forms of resistance training, can
be easily remembered by the acronym PROS—progres-
sion, regularity, overload, and specificity.118 Progression
refers to increasing the challenge to the muscle with
each training session by adding more distance between
partners, increasing the complexity of the exercise, or
changing the number of sets and repetitions. Regularity
means that, like most other resistance training exercises,
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
medicine ball exercises should be done at least twice per
week on nonconsecutive days. Training three to four
times per week is recommended to optimize gains in
performance. Overload means that a greater stress must
be placed on the muscles each training session to achieve
a positive training adaptation. This can be accomplished
most easily by using progressively heavier weighted balls
as the muscle gets stronger. Specificity is the principle that
applies to all forms of resistance training, that is, the body
will respond to how it is trained. For example, if a person
does only upper extremity medicine ball exercises, his or
her lower extremity strength will not improve. Because
sport and functional activities of daily living take place
in all three planes, medicine ball exercises are one of the
best ways to specifically train the body for the demands of
everyday life.118 Table 21-6 shows a comparison between
medicine ball and other methods of resistance training.
Designing a Medicine Ball Training Program
● Order of exercise: Unlike other forms of resistance training, in
which multijoint exercises should be done before single-joint exer-
cises, medicine ball exercises can be done in almost any order.
● Training weight: Using a heavier ball for 3–5 repetitions will
enhance strength, whereas a lighter ball for 15–20 repetitions
will develop muscular endurance. Mediate and Faigenbaum118
recommend a weight that can be done correctly 7–10 times per
set (2–4 pounds for beginners, 4–8 pounds for intermediates, and
8–12 pounds for advanced participants). The weight is increased
as strength improves.
● Rest intervals: The rest between sets influences both energy
recovery and the training adaptations. Longer rest intervals are
needed for strengthening exercises, shorter rest periods are
desirable for improving muscular endurance. In general, a rest
period of 30–45 sec is recommended.
● Exercise speed: Speed of movement with the medicine ball is
controlled by the person, but the natural speed or rate of movement
is used most often.
Table 21-6
Comparison of Different Modes of Strength Training
Medicine Balls Weight Machine
Cost Very low High
Portability Excellent Limited
Ease of use Excellent Excellent
Functionality Excellent Limited
Variety Excellent Limited
Motor learning Excellent Limited
Space needs Low High
Adapted from Mediate P, Faigenbaum AD: Medicine ball for all training handbook, Monterey, Calif, 2004, Healthy Learning. Copyright 2004.
Reprinted with permission.
451
Tubing/Elastic Band Training
Another very common form of resistance training seen in
almost every clinic is the use of tubing or elastic bands.
Tubing or elastic bands are relatively inexpensive, can be
used by most patients without significant assistance or
spotting, and allow patients to exercise a muscle in a very
functional plane of movement, one that often cannot be
accomplished with traditional forms of resistance training.
Tubing has been used for many years with athletes such
as swimmers and golfers to allow them to perform resis-
tance training in planes of motion that closely simulate
the movements during their stroke or golf swing.119,120
Although the resistance increases only during the con-
centric phase of muscle contraction with tubing and elas-
tic bands, there is a progressive overload placed on the
muscle, and improvements in strength with this type of
resistance training have been shown to be effective, par-
ticularly in patient populations.121–124 Tubing and elastic
band exercises can also be effective in helping patients
to start moving their arms or legs while sitting, thus
increasing energy expenditure and preparing the severely
deconditioned patient for more aggressive and strenuous
exercise. Elastic tubing has also been used very effectively
in patients with total knee replacements to assist in gain-
ing speed of movement for functional activities, such as
quickly moving from the accelerator to the brake while
driving.19
Periodization of Resistance Training
Vorobyev125 and Matveyev,126 two Eastern European
physiologists, developed a model for year-round train-
ing of weight lifters called the periodization model.
The theory behind this model was based in part on
Selye’s general adaptation syndrome and proposes that
there are three phases of the body’s adaptation when it
is confronted with the stress stimuli of resistance train-
ing: shock, adaptation, and staleness.3 In the first phase,
new training results in soreness, and performance actu-
Free Weight Body Weight
Moderate None
Variable Excellent
Variable Variable
Limited Excellent
Good Excellent
High Variable
Moderate Low
452 SECTION II • Principles of Practice

ally decreases. The body then adapts to the new stress

and training stimulus, and performance increases. In the
third phase, the body has already adapted to the new
stress, and no more adaptations take place. Periodization
is used to avoid the staleness phase and to keep the exer-
cise stress effective in creating new levels of performance
and adaptation.3,9,127
The periodization model is made up of various cycles.
A microcycle, the smallest period in the model, con-
sists of 1 week of training. Mesocycles contain multiple
microcycles, and the periodization model contains sev-
eral distinct mesocycles. The largest cycle is the mac-
rocycle, which usually refers to an entire training year.
The number of mesocycles in a macrocycle depends on
the goals of training, the number of major competitions, Figure 21-11
and the athlete’s initial level of training and fitness. Stone Matveyev’s model of periodization. (Modified from Stone MH,
and O’Bryant9 have adapted the Matveyev periodization O’Bryant HS: Weight training: a scientific approach, Minneapolis,
model, as shown in Figure 21-11 and Table 21-7.9 The Minn, 1987, Burgess International. An imprint of Burgess
hypertrophy stage is an early preparation stage designed International Group, Inc., Edina, Minn.)
to allow the athlete to make the necessary physiological
adaptations to prepare for the upcoming season. The vol-
ume of exercise is high and the intensity low; the empha- generation of maximum power; thus, volume is decreased
sis on technique and the technical aspects of the sport is to prevent fatigue and overtraining, the intensity is very
also low. high, and technical aspects are of utmost importance.
The second stage is the basic strength stage, a later The fourth phase is the competition or peaking/main-
stage of preparation for the season, in which the emphasis tenance phase, in which the stress is on preparing for the
is on near-maximal strength development, which serves competitive effort, maximizing technique, and keeping
as a foundation for the upcoming stages of power devel- volume low to prevent injury and fatigue. The fifth phase,
opment. Volume starts to decrease, whereas intensity and which was added to the original Matveyev model, is the
technique take on larger and more important roles. active rest phase. In the current competitive environment,
The third stage is the power/strength stage, which there really is no off-season, but the athlete needs some
acts as a transition period between the preparatory time to pursue other athletic interests and to “get away”
and competition phases. The emphasis in this stage is from the rigors of training. Active rest is designed to allow

Table 21-7
Theoretical Model of Strength Training (Associated with Matveyev’s Periodization Model)

Transition 1: Competition:
Phase Preparation
Strength and Peaking or Transition 2:
Hypertrophy Basic Strength Power Maintenance* Active Rest

Sets† 3–10 3–5 3–5 1–3 Athlete does

Repetitions 8–12 4–6 2–3 1–3 other activities
Days/week 3–4 3–5 3–5 1–5 during this
Times/day 1–3 1–3 1–2 1 period
Intensity cycle (weeks)‡ 2–3/1 2–4/1 2–3/1 –
Intensity Low High High Very high to low
Volume High Moderate to high Low Very low

*Peaking for sports with a definite climax or maintenance for sports with a long season such as football.
†
Does not include warm-up sets.
‡
Ratio of number of heavy training weeks to light training weeks.
From Stone MH, O’Bryant HS: Weight training: a scientific approach, p 123, Minneapolis, Minn, 1987, Burgess International. An imprint of
Burgess International Group, Inc., Edina, Minn.
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
the athlete to maintain some level of fitness, strength, and
power by participating in other sports or activities unre-
lated to his or her competitive sport.
The concepts of periodization should be incorporated
in the design of every training program for both athletes
and nonathletes. The clinician must work closely with the
coach or physician in designing the necessary microcycles
and mesocycles to assist the athlete or nonathlete to be
maximally prepared for the competitive season or return
to work and normal activities of daily living at the proper
functional level. The periodization model may have to
be modified to fit the individual needs of the athlete or
nonathlete, but the basics of the model can be adapted to
fit each individual as needed.
Methodology for Documentation of
Resistance Training Exercises
Given the specificity of training and the need for indi-
vidualization of training programs, it becomes imperative
that a method of documentation of resistance training
exercises be established for each athlete. The documenta-
tion system should be one that any sports medicine cli-
nician can interpret, understand, and use to direct the
individual athlete or nonathlete in the proper technique
and execution of his or her resistance training program.
Gray128 has established a documentation system for
resistance training exercises that provides information
about posture, equipment, volume, intensity, body
positions, exercise motions, and planes of movement
(Figure 21-12).
By applying these simple rules to the documentation
of resistance training exercises, any exercise can be docu-
Figure 21-12
Free-weight exercise chart. (From Gray GW: Chain reaction, Fort
Wayne, Ind, Wynn Marketing, 1993.)
453
Gray’s Definitions for Documentation128
● Anatomic position is the reference relative to the plane of
movement and starting position
● The free weight motion can be parallel with gravity, perpendicular
to gravity, or a combination of these two motions
● The posture is prone, supine, side-lying, kneeling, sitting, standing,
stride stance, single-leg stance, wide stance, or narrow stance
● The equipment is any apparatus that facilitates the posture to be
used, such as an incline bench or preacher curl bench
● The amount of weight is the poundage being used for whatever
type of equipment is being used in the exercise
● The type of weight can, for example, be a dumbbell, barbell,
medicine ball, body weight, or any combination
● The fixed positions are positions other than anatomic position and
should be described in increments of 20°, 45°, 70°, 90°, 110°,
and 135°
When describing motion/exercise, movements occur from proxi-
●
mal to distal and from inferior to superior
● Combination movements are documented with a slash (/)
(e.g., shoulder flexion/abduction/external rotation)
● Transitional movements are documented with an arrow (→)
(e.g., elbow flexion → shoulder flexion)
mented and, more important, reproduced or replicated
by another clinician who might supervise the athlete or
nonathlete during a resistance training session. With its
emphasis on reproducible and accurate documentation
of exercise, this system provides a simple, easy, and repro-
ducible documentation system for any clinician.
Systems of Resistance Training
Most health care students have been introduced to the
DeLorme system of resistance training, developed by
DeLorme and Watkins in 1948, in which the patient
determines his or her 10-repetition maximum (10-
RM).129 The first set consists of 10 repetitions at 50%
of the 10-RM resistance, the second set consists of 10
repetitions at 75% of the 10-RM, and the third set con-
sists of 10 repetitions at 100% of the 10-RM. Although
this system of resistance training has proven to be effec-
tive in the development of strength and endurance, there
are a multitude of other systems of resistance training.
This section presents and describes a variety of resistance
training systems to give the clinician more choices in
the design of resistance training programs and allow the
patient to go beyond “3 sets of 10.”
A modification of the DeLorme system, developed by
Knight,130,131 is called the daily adjustable progressive
resistance exercise (DAPRE) system. The DAPRE pro-
gram ensures that the athlete works at or near optimal
capacity for each set, thus gaining gradual adaptation to
the resistance training stimulus.
454 SECTION II • Principles of Practice
The DAPRE system consists of four sets. The first set
of 10 repetitions is with the “working weight,” which is
an estimate based on the stage of conditioning or decon-
ditioning after an injury. The resistance is adjusted in the
second set so that six repetitions are completed against
approximately 75% of the working resistance. The third
and fourth sets are against the full working resistance,
and this is where the daily adjustment of the progressive
resistance takes place. In the third set, a maximal num-
ber of repetitions is attempted and, based on the number
of repetitions completed, the working weight is either
increased or decreased to allow approximately five to
six repetitions in the fourth set. The resistance is thus
adjusted daily based on performance. The DAPRE sys-
tem has been successful in producing significant strength
gains in a patient population.125
Fleck and Kraemer3 have written the definitive text
on designing resistance training programs, describing in
detail a number of systems of resistance training that have
proved successful in both the research and athletic envi-
ronments. The accompanying box describes some of the
more popular systems of resistance training. For more
detail and for scientific references about these systems,
the reader is referred to Fleck and Kraemer’s text.3
These are just a few systems of resistance training. The
key to designing a resistance training system is to provide
an adequate stimulus to elicit training adaptation, based
on the needs and demands of the athlete or nonath-
lete. The clinician must understand the progression and
modification of a resistance training program to prevent
the athlete or nonathlete from getting stale, injured, or
bored with the training program. By modifying the resis-
tance training programs or systems, variety and adapta-
tion can be maintained, and the athlete or nonathlete
will continue to make progress and enjoy the resistance
training program.
Individualization of Resistance
Training Programs
Before the clinician can design a resistance training pro-
gram for an athlete or nonathlete, he or she first must
conduct a “needs analysis” to determine the exercise
movements needed for the specific sport skill, the meta-
bolic system needed for energy supplies, and appropri-
ate exercises for injury prevention or rehabilitation.3 The
needs analysis will be different for each patient. A key role
of the clinician is to assist the sport coach or individual in
designing personalized, specific resistance training pro-
grams. All too often in sports, an entire team performs
the same resistance training workout, with no modifica-
tion of volume or intensity. This is similar to all injured
patients undertaking a given or set protocol as part of
rehabilitation after an injury or surgery. Each patient pro-
Popular Systems of Resistance Training
● Single-set system: Only 1 set per exercise is performed, with 8 to
12 repetitions maximum.
● Multiple-set system: Two to three warm-up sets are performed
with increasing resistance, followed by two to five sets at 5- to
6-repetition maximum (RM). This system seems to yield optimal
results for increases in strength.
● Light-to-heavy system: This is the DeLorme system (see
discussion in text).
● Heavy-to-light system: After a warm-up set, a set of three to six
repetitions is performed with heavy weight, followed by sets with
lighter weight, keeping the number of repetitions the same with
each successive set.
● Triangle or pyramid program: A warm-up set of 10 repetitions is
followed by successive sets in which the resistance is increased
and the number of repetitions is decreased. Once 1-RM is
achieved, this is reversed, with weight decreased and repetitions
increased until the starting resistance and 10 to 12 repetitions
are reached.
● Super sets: Two distinct exercises are performed with the same
body part, one right after the other, with no rest between the two
exercises.
● Circuit program: This is a series of resistance training exercises
performed one right after the other with only minimal rest (10–15
sec) between sets. Ten to 15 repetitions are normally performed
in each set at approximately 40% to 60% of the established
1-RM. The exercises in the circuit can be done per some time
factor (e.g., 30 sec of exercise, 15 sec of rest), and the circuit is
normally repeated two to four times. For patients with
cardiovascular disease, some circuit resistance training programs
will also include several aerobic stations, such as stationary
cycle, treadmill, or rowing machine. The same principles of
work–rest ratios apply when incorporating these aerobic stations
with resistance training stations.
● Peripheral heart action program: This is a variation of the circuit
program in which there are several sets of five to six exercises,
each for a different body part. The training session consists of
four to six sequences, each containing different exercises for
each body part.
● Tri-set system: Three exercises for the same body part are
performed in succession, with little or no rest between the three
exercises.
● Multi-poundage system: This system requires two spotters to
assist with removing a set amount from the bar after each set of
repetitions. The athlete does as many repetitions as possible at
the given resistance, the spotters remove some of the resistance,
and another set is attempted.
● Blitz program: This system exercises only one body part in one
exercise session (e.g., back on Monday, chest on Wednesday,
legs on Saturday).
● Exhaustion set system: The objective of this system is to perform
each set to exhaustion or to degradation of proper form, rather
than to a given number of repetitions.
● Forced repetition system: After completion of a set to
exhaustion, a spotter assists the lifter with just enough help to
allow for several more repetitions.
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
gresses, heals, and responds differently to the stress of the
injury. Forcing a patient to progress too rapidly may risk
further damage or complications; conversely, preventing
a patient from progressing more rapidly will prolong
the rehabilitation process and yield a less-than-optimal
result. Resistance training and rehabilitation programs
should not be set up in protocol formats, but should
have general guidelines such as when to progress, add
exercises, and increase volume and intensity. In this way
the resistance training program is custom designed for
the individual, who will then get the most out of the
resistance training program.
One final consideration in the design of a sport-
specific or activity-specific resistance training program:
in terms of designing strengthening exercises for the
lower extremities, the clinician must assess muscle func-
tion as it pertains to the gait activities of that sport or
activity. Because of the strong influence of specificity of
exercise, lower extremity muscles and movements must
be strengthened and trained based on their functions
during gait.132 The term gait-abilitation was introduced
to encourage clinicians to design exercises for the lower
extremity based on muscle function during the different
stance/swing phases of gait.133 More specifically, gait-
abilitation is designed to train muscles to work in the
ranges in which they will be working during the gait of
the sport or activity.
Rehabilitation strategies for the lower extremities
have undergone a gradual shift in the focus of exercise
for rehabilitation, from a focus on isolated exercises
toward a focus on integrated exercises.134,135 More spe-
cifically, clinicians have developed a greater appreciation
for functionally oriented exercises, compared with joint-
or muscle-oriented exercise approaches. In other words,
lower extremity rehabilitation places a great emphasis on
exercises that incorporate weight-bearing activities and
mimic specific lower extremity tasks (e.g., stair-stepping
exercises, squats, lunges, standing balance drills). These
“functional” exercises are in addition to the traditional
joint and muscle isolation exercises. Thus, lower extrem-
ity rehabilitation, from the clinician’s perspective, can be
viewed as a continuum that progresses from least func-
tional—mostly joint or muscle isolating—toward more
functional—mostly integrated movements.104
The gait function of the gluteus medius provides an
example of the need for specificity in training. During
gait, the gluteus medius functions eccentrically to stabi-
lize the pelvis in the frontal plane.136 This muscle func-
tion occurs during the initial loading of early stance,
as well as during mid-stance. The range of motion in
which the gluteus medius functions is approximately 5°
to 10° of hip adduction. However, in a clinical setting,
the hip is typically strengthened in a position of abduc-
tion through a range of 0° to 20° of abduction. With
455
regard to the actual function of the gluteus medius, it
has a reverse muscle action on the pelvis during gait.
During the stance phase, the gluteus medius controls
the frontal plane drop of the pelvis at the hip by stabi-
lizing the pelvis. The gluteus medius must be trained
to stabilize the pelvis on the femur, not to abduct the
femur at the hip.
Strengthening muscles and joints based on gait sim-
ply follows the concept of specificity of exercise. Lower
extremity muscles must be trained in terms of their func-
tion (e.g., walking, running, jumping) and in the ranges
they will function during these activities. The clinician
is encouraged to examine closely the gait biomechanics
of the athlete’s sport or the patient’s activity of daily
living and to design exercises that closely replicate these
functions. This requires a thorough appreciation and
understanding of joint kinematics and joint positions
during gait. Keeping gait in mind can ensure specificity
of training as an adjunct to resistance training and reha-
bilitation programs.
Traditional lower extremity exercises address the spe-
cific pathomechanics involved in the lower extremity dys-
function. With traditional rehabilitation, sports medicine
and rehabilitation specialists apply exercise approaches
that tend to isolate the area of dysfunction, implement-
ing exercises that address the specific deficiency of the
involved joint or muscle. For example, in the case of
rehabilitation after a hip fracture, clinicians address spe-
cific issues of hip range of motion and muscle strength
around the hip complex, and focus exclusively on these
issues. Exercises such as the prone hip extensions, supine
straight leg raising, isometric setting exercises of the glu-
teus maximus, and side-lying hip abduction exercises are
a few examples of the exercise programs that dominate
traditional lower extremity rehabilitation. Moreover,
because individuals perform these exercises in a non–
weight-bearing position, with the distal segment (i.e.,
the foot) free, clinicians applied the label of open kinetic
chain (OKC) to these exercises.135,137–139
These isolating exercises focus on the measured
deficiency of the lower extremity. As in the preceding
example of the hip fracture rehabilitation plan, exercise
programs attempt to restore strength and mobility of the
involved hip joint. As strength and mobility improve, the
rehabilitation program moves individuals toward weight-
bearing exercises such as gait training, stair climbing, and
transfer training.140 However, individuals first need to
demonstrate adequate performance of the non–weight-
bearing exercises before progressing to the weight-
bearing program.
By the end of the 1980s and into the early 1990s,
clinicians began questioning the role of isolated exer-
cises.104,141 Continuing education courses and research
began to address the issue of exercise efficacy and exercise
456 SECTION II • Principles of Practice
specificity.104,132 Weight-bearing exercises (i.e., func-
tional progression exercises) began to gain in popular-
ity as the primary source of exercise. Research supported
the notion that weight-bearing exercises such as the leg
squat and step-up exercise could be equally as effective
for gaining strength and mobility as the more traditional,
non–weight-bearing version (e.g., knee extensions, hip
extensions).
For example, Augustsson and colleagues142 success-
fully demonstrated that weight-bearing exercises were
actually more effective for strengthening the quadri-
ceps muscles than non–weight-bearing exercises. They
compared the traditional standing squat exercise (closed
kinetic chain exercise group) with the traditional seated
knee extension and hip adduction exercises (OKC exer-
cise group). Although post-test strength results increased
for both groups of subjects, the group performing stand-
ing squat exercises demonstrated greater strength gains
than the seated exercise group (31% gain versus 13%
gain, p < 0.05). They further noted that weight-bearing
exercises more closely reproduced the function of the
quadriceps (i.e., controlling knee flexion in stance) than
non–weight-bearing exercises.
In addition, research supports the notion that weight-
bearing exercises may better prepare an individual for
return to normal activities of daily living compared
with non–weight-bearing exercise.142–144 Worrell and
colleagues144 examined the effects of a 4-week progres-
sive strengthening program of the lower extremity in
healthy individuals. The program consisted of a common
weight-bearing exercise, the lateral step-up/down exer-
cise. Subjects performed multiple repetitions of stepping
up/down on a step while holding a prescribed amount of
weight in each hand for external resistance. The weight
component was increased gradually over the course of
the strengthening program using the DAPRE protocol.
All subjects were pretested and post-tested for non–
weight-bearing strength using an isokinetic dynamom-
eter as well as for functional strength using hop tests and
step tests. At the conclusion of the training program, all
subjects demonstrated significant gains in hopping and
stepping abilities (p ≤ 0.05). The investigators did not
observe significant gains with the isokinetic (non–weight-
bearing) strength testing. Finally, studies by Greenberger
and Paterno145 failed to show any strong relationships
between non–weight-bearing strength testing and functional
performance abilities.
Sports medicine and rehabilitation specialists now
classify functional exercises on a continuous scale. Non–
weight-bearing exercises represent one end of the scale,
typically the lower end of function, whereas weight-
bearing exercises represent the opposite end of the
scale, namely, more functional. Essentially, although the
prone hip extension exercise does not replicate any typical
movement of function, it is on the continuum of func-
tion. This exercise elicits muscle effort from the gluteus
maximus and hamstrings and requires hip movement
through the available range. However, a squatting exer-
cise also elicits effort from the gluteus maximus and ham-
strings and requires hip movement through the available
range. In addition, the squatting exercise requires move-
ment from the ankles, knees, and pelvis, as well as effort
from the posterior calf muscles (i.e., gastrocnemius and
soleus), the quadriceps, and the back extensors. Thus,
the squatting exercise integrates the entire lower extrem-
ity rather than isolating the hip joint. Clinicians now con-
sider this weight-bearing exercise to be more functional
than the hip extension exercise. In addition, the squat
exercise closely resembles the components of motion
involved in the process of sit-to-stand and stand-to-sit.
Thus, the squat exercise is classified as more functional
than the hip extension exercise, which does not resemble
any typical daily activity of the lower extremity. Table 21-
8 lists common weight-bearing exercises and the func-
tional activities they replicate.
Thus, it would seem that the likely solution to lower
extremity rehabilitation would be the combination of
both rote-type exercises and task-oriented exercises. In
addition, it would seem very appropriate to begin the
task-oriented exercises as soon as possible, simultaneous
with the rote exercises. The rote program would focus
Table 21-8
Lower Extremity Exercises Simulating Function
Exercise Functional Stimulation
Squats Replicate movements encountered
during gait, stair climbing/descending,
and sit-to-stand/stand-to-sit
Lunges Replicate movements encountered
during initial loading in gait; can be
performed in sagittal, frontal, and
transverse planes
Automated Replicates forces similar to stair
stair climber climbing
Biomechanical Replicates transverse plane forces of
ankle platform the entire lower extremity
system
(BAPS board)
Cross-country Replicates sagittal plane forces, without
ski machine major ground reaction forces
Versa climber Replicates forces similar to stair climbing
and ladder climbing, including
reciprocal arm motions
Treadmill Allows forward, backward, and sideward
walking for gait training in the clinical
setting
Total gym One- and two-legged squats to
incline replicate forces similar to standing
board squats in a protected position
 CHAPTER 21 • Physiological Principles of Resistance Training and Functional Integration
mainly on the raw muscle strength and range of move-
ment necessary to perform functional tasks, addressing
the isolated deficiencies. The task-oriented component
would focus on neuromuscular education, skill development,
and confidence building.
Summary
The rehabilitation professional has a major responsibil-
ity to the athlete, coach, and patient in the design of
a specific and appropriate resistance training program
to maximize the client’s abilities and potential. With
consideration of the bioenergetics of muscle contraction,
457
the physiology and adaptation of muscle during resis-
tance training, and the implementation of a sport-spe-
cific, individualized resistance training program, the
athlete or nonathlete will get the most out of a resis-
tance training program and have maximal functional
abilities.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 145 references for this chapter.

P SYCHOLOGY OF THE I NJURED P ATIENT
Cal Botterill, Frances A. Flint, and Lydia Ievleva
Introduction
The psychological dynamics in and around human injury
and illness have become increasingly complex and signifi-
cant. It is easy in today’s busy world to take our health
for granted. As a result, when we face health challenges,
we are often ill prepared and dramatically affected. Basic
human needs often trigger powerful psychological and
emotional dynamics.
The study and practice of sports medicine have inter-
esting implications for health care and rehabilitation in
general. Because health is such an essential part of being
an athletic performer, health loss can be a traumatic blow
to patient identity and dreams. On the other hand, mul-
tidisciplinary, proactive approaches to rehabilitation used
in sports would appear to have important implications
for the rehabilitation of all patients.
There appears to be an increasing awareness regarding
the significance and potential of psychological and emo-
tional factors in medical rehabilitation and health care.1–3
To optimize health, performance, and response to reha-
bilitation, all human and environmental factors need to
be considered. Achterberg has clearly articulated how
significant the two-way “psycho-physiology” relationship
can be in health and medicine.1 This chapter attempts to
openly explore psychological factors and strategies that
may be valuable in patient rehabilitation.
Psychological Reactions to Injury
When an injury occurs, and achievement goals and daily
activities such as physical exertion and social interaction
with others are affected, the injured individual may expe-
rience severe psychological upset. What does occur psy-
chologically when a patient suffers from a major injury
(or illness) that leads to an extended hiatus from normal
activities? When Drake Berehowski, a National Hockey
League player, tore his anterior cruciate ligament and
458
221
C H A PCT HE AR P T E R
was out of competition for 9 months, he expressed the
feeling of loss that the injury created. “You can’t be with
the guys anymore. You have to go back and do your
therapy, and that’s probably the hardest thing that I
had to deal with, just being away from everyone, being
away from the action, not being able to play.”4 When
a first-year university level basketball player suffered a
third-degree tear to her anterior cruciate ligament she
stated, “At first, you might just think it’s the end of the
world; I did.”5 A senior in high school basketball who
experienced the same injury agreed and commented,
“I thought I had just twisted it. . . . When I came to
the realization that I was going to be off for months,
that’s when the fear set in and the discouragement.”6
Anecdotal testimony provides depth to the psychologi-
cal experience and the beginning of an empirically based
foundation of knowledge on which to build psychologi-
cal rehabilitation programs.
Quantitative and qualitative research is beginning to
contribute to knowledge relating to the psychophysio-
logical reactions of individuals to injury.7–11 In the search
to understand how people psychologically respond to
injury, two primary approaches have been proposed. The
first is borrowed from the death and dying literature and
has been called the stage model.
Kübler-Ross,12 in On Death and Dying, described the
sequential progression through specific stages in reac-
tions to death; the stages are denial, anger, bargaining,
depression, and, finally, acceptance. It was hypothesized
that injured people (especially athletes) would initially
deny the injury; would then become angry; would try to
bargain about the injury; would progress to depression;
and then, finally, would accept the injury. Timelines were
not clear for these reactions; but it was suggested that it
might be detrimental to injured patients if they did not
progress through the stages in order to finally accept the
injury. These specific emotions and behaviors appear to be
 CHAPTER 22 • Psychology of the Injured Patient 459

relatively common among injured performers. However,
there has been limited empirical support for the premise
that patients enter the death and dying paradigm. Because
injured individuals typically have every intention of return-
ing to sport, or their job, after rehabilitation, their sense of
“loss” is generally temporary. Thus, it seems unreasonable
to extrapolate totally from the death and dying literature to
the realm of injured people, as it may restrict how we view
the psychological reactions to injury. On the other hand,
a strong emotional reaction to serious musculoskeletal
injury and dysfunction is likely. Emotional concerns about
self, family, and career are understandable. Processing and
responding to fears should be a priority.
The second approach to psychological reactions to
injury involves a cognitive appraisal model, which
seems to recognize the athlete’s individuality and poten-
tial interaction with the situation.13–15 The basis for the
model is the work of Lazarus and Folkman,16 which deals
with stress and the response to stress. It suggests that
reactions to stress involve a process by which the individ-
ual interacts with both situational and personal demands.
This cognitive appraisal model (Figure 22-1)17 does not
tell us what psychological reactions and emotions will be
evident after injury, but it does outline how emotions
and psychological reactions can develop and occur.
The cognitive appraisal model shows the stressor the
individual faces (injury) including all factors that may
be influential on the injury (for example, the severity
and timing of the injury). The patient now processes
and appraises the injury as threatening or nonthreaten-
ing based on his or her perception of how bad the injury
is. In addition, the patient evaluates available coping
resources (for example, therapists) that may be available
to help. At this point, negative self-talk (e.g., I blew out
my knee and I’ll never play again. I injured my back, can
I go back to doing physical work? What else can I do,
I’ve never done anything else? How will I support myself
and my family?) may become evident. Additionally, the
individual considers how serious the injury is and how
much of an impact this injury is going to have on goals
and future career decisions. This processing or appraisal
establishes how the individual will respond emotionally,
and this is a direct result of the patient’s perception of
his or her ability to cope and the costs or benefits of the
injury. Finally, we see the consequences of this appraisal
as the patient shows whether or not he or she will cope
with the injury appropriately. Either the individual will
demonstrate positive coping skills by adhering to reha-
bilitation, maintaining a positive outlook, and showing
a determination to recover, or there will be negative

Stressor (injury) Cognitive Appraisal

Injury history Perceived severity
Injury severity Available personal
Sport situation resources
Work situation Ability to cope

Emotional response
Psychological
reactions
Emotional reactions
Reentry into the process Psychological
responses
New medical
information
Injury improvement
or setbacks

Behavioral consequences
or coping responses
Performance, health, or
psychological behavior
Positive or negative
coping response

Figure 22-1
Cognitive appraisal model relating to sport
Lack of recovery
Recovery injury. (Redrawn from Flint FA: Psychology
or
from injury of sport injury, p 4, Champaign, Ill, 1998,
delayed recovery
Human Kinetics.)
460 SECTION II • Principles of Practice

consequences potentially resulting in a failed recovery.
By watching how the patient responds behaviorally, we
can determine what strategies may be necessary to help
the individual succeed in the recovery process.
Evidence of Positive Coping Mechanisms
● Adherence to rehabilitation
● Positive outlook
● Determination to recover
Regardless of what model is used to evaluate the
psychological responses to injury, it is important to
remember that each patient is different, as is each
injury situation. Was the injury a macrotraumatic
event in which a single episode of trauma caused the
physical injury as demonstrated by a fractured leg
from a single major blow? Or was the injury mecha-
nism repeated minor trauma (microtrauma) built up
over time as can be seen in a long-distance runner
with a stress fracture? Each of these mechanisms of
injury, macrotrauma and microtrauma, could result
in very different psychological reactions in patients.
The interaction of the patient and the injury situation
can be influenced by a multitude of factors that can
generally be classified into four main groups: activity/
work/sport influences, injury influences, personal
influences, and social influences (Figure 22-2).
Each of the factors listed in the injured patient sce-
nario interaction presented in Figure 22-2 can play a
part in influencing a patient’s cognitive appraisal and
resultant behavior. External influences such as the
nature of the activity (for example, expressing pain in
soccer), the culture of risk where individuals go beyond
reasonable boundaries,18 and public interest all contrib-
ute to an individual’s injury response. Supervisors (or
coaches) have considerable influence on psychological
and behavioral responses since they determine what
concessions will be made as a result of the injury and
often influence the nature of activity during and after
injury. One varsity rugby coach often showed his play-
ers a bullet and remarked that they should either bite
the bullet and play through injury or use it to end their
misery. The messages sent by coaches, supervisors, par-
ents, friends, and health care professionals are powerful
mediators of behavior.
Evidence of Positive Coping Mechanisms
● How health care professionals act toward a patient can be a
powerful mediator of behavior.

Injured
Patient

Activity Injury Personal Social

Influences Influences Influences Influences

Nature of Cause of Age, sex, Social

particular Injury maturity, support
activity general health (friends)

Onset of
Status of injury (macro Previous Predisposing
individual in vs micro) injury conditions
activity experience and life
experiences
Severity of
Individual vs injury Availability of
group (team) clinical Ethnic
activity practitioners background
Body part
injured
Timing of (upper vs
injury Pain Family
lower)
Figure 22-2 tolerance support
Injured patient scenario interaction. (Redrawn and
from Flint FA: Integrating sport psychology Supervisor Potential to expression
and sports medicine in research: the dilemmas, impact
career
J Appl Sport Psych 10(1):83-102, 1998.)

The key message concerning psychological reactions to
injury is that the individual is the most important factor
to consider. Each individual patient has a unique profile
involving situational and injury factors presenting a multi-
tude of possibilities for behavioral responses. Health care
professionals must address the individual responses and
needs in designing a rehabilitation program.
A review of research and literature by Vallerand can
help the health professional appreciate the spectrum of
human emotions that athletes commonly experience.19
Of the seven categories of emotion identified by Vallerand
and listed here, it is interesting to note that as many as
five might be identified as having “negative” dimensions:
fear, anger, embarrassment, surprise, sadness, happiness,
and interest/excitement. Emotional management and
preparation skills can make a big difference in how we
respond to emotions.20
Even though it is desirable to operate as much as
possible in the positive emotional domains, it clearly is
important to learn to appreciate and respond to the func-
tional dimensions of the other emotions. Injured patients
often experience the full spectrum of negative emotions,
and those around them can often help by empathizing
and helping these patients to identify, accept, and respond
constructively to these feelings.
Emotions, with the possible exception of sadness and
grieving, tend to produce energy that when responded
to or harnessed can have functional payoff. Even sadness
(feeling down, sorry for oneself or others) can eventually
lead to recovery and a feeling of gratitude, but it can be
the least functional and possibly the most dysfunctional
emotion if one allows oneself to dwell in this domain.
The act of accepting and responding to our emotions
is a large part of what life is about. Learning to draw on
and effectively use and respond to the full spectrum of
emotions is part of what can be learned and worked on
as a result of injury. It is often a “teachable moment” and
a “perspective producer.”
Psychological Needs During
Rehabilitation
A review of the basic human psychological needs identified
by Glasser provides a valuable framework for anticipating
and recognizing needs during injury rehabilitation.21 As
human beings, we have basic needs for acceptance, suc-
cess, sensation, and control. For many patients, activity and
feedback on the job provide a large part of their identity
and meet many of their basic needs. Upon injury and dur-
ing rehabilitation, these basic needs in such fundamental
areas are likely to be heightened. These patients are likely
to have a greater than normal need to be accepted, appre-
ciated, and included. They are likely to have a greater
than normal need to be considered worthy, capable, and
important human beings. They may have heightened
CHAPTER 22 • Psychology of the Injured Patient 461
needs for sensation, enjoyment, and stimulation through
new means when mobility and capability are affected.
And most important, the individuals involved are likely to
have heightened needs for control, direction, and assur-
ance. Most elite performers are strong-minded, asser-
tive individuals with a high need for control who have
learned to “take charge” of as much of their life as they
can. It is extremely frustrating for them when, because
of an injury, a huge part of their destiny and prospects
now seems beyond their control. It is critical to point out
the important areas that are within a patient’s control in
responding to an injury and rehabilitation, and the ele-
ments that need to be respected to optimize short-term
and long-term health and welfare.22–24
Evidence of Positive Coping Mechanisms
● It is important that health care professionals help patients clarify
what is beyond their control and what is reasonably within their
control.
Elite performers often have tremendous body aware-
ness and a greater than normal need to know what is
happening to and is possible with their bodies. In the
absence of educational initiatives and strong advice and
evidence, injured athletes may, out of frustration, try to
“take charge” of their rehabilitation prescription and cre-
ate their own diagnosis and prognosis, based on real or
imagined personal needs. Clinicians should recognize
that sharing control in the rehabilitation plan can make a
big difference in the athlete’s response. Efforts to increase
body awareness and the individual’s understanding of the
injury (and rehabilitation process) can help every patient.
Uncertainty is often the biggest source of fear, and educa-
tion can be an important step in reducing fear and actively
involving the patient in facilitating their rehabilitation.
Injury time can be a critical “teachable moment” in
the lives of patients. It can produce an awakening in
terms of placing “the need to excel” in work/school
and one’s own vulnerability in perspective. All too often,
fairly irrational beliefs have crept into the lives of people.
For example, (1) my self-worth is on the line in the next
few moments; (2) I must perform for others; (3) I must
be perfect; or (4) the world must be fair.
Injuries sometimes sensitize patients to the reality that
there is life after work, and that even though their career
is an exciting vehicle for development and accomplish-
ment, it is best kept in perspective. Performers who face
life-threatening or career-threatening injury can end up
being happy to be alive and better able to put perceived
pressures into perspective.
Irrational beliefs and their created pressures can some-
times be corrected and relieved in responding to injury.
462 SECTION II • Principles of Practice
If not, they may contribute to the individual’s being
prone to injury and illness because of the inherent stress,
pressure, distraction, and psycho-emotional “baggage”
associated with an irrational perspective.
What Patients Need to Know about Their Injury
● Injury/illness time can provide the teachable moment to sensitize
individuals to the critical dynamics of their psychophysiology.
Glasser has pointed out that at any given moment,
human beings have four interactive components of total
behavior:21 (1) doing, (2) thinking, (3) feeling, and (4)
physiology. Of the four components, feeling is probably
the hardest to control directly but certainly is dynami-
cally affected by behavior, thoughts, and physiology.
The use of biofeedback equipment is sometimes the best
way to demonstrate what a profound effect thoughts
or behavior can have on feelings or physiology, or vice
versa.
This highly dynamic model that we all influence and
respond to every day is the key to our health and wel-
fare as well as our performance potential. Certainly, if
we dwell on fears and negative thoughts, the tension
produced can interfere with circulation and physiological
healing as well as performance.
Most elite performers also recognize that if they do
not look after their physiology (with proper exercise,
diet, rest, and hydration), their ability to feel good,
think positively, and behave effectively will eventually
be influenced. Health challenges are often a teachable
moment for patients regarding actively managing these
influences. When experiencing the frustration and stress
of an injury, it is important for the clinician to encourage
therapeutic functional exercise with other body parts to
the extent possible and to promote and monitor effec-
tive diet, rest, and hydration habits. The cognitive and
behavioral habits and focusing skills that can help opti-
mize psychophysiology and performance can be taught
and worked on as a result of the injury rehabilitation
challenge.
Many performers who are experiencing their first
major injury have little understanding of what the future
holds. Since previous personal knowledge of injury and
rehabilitation is usually not available, the patient may feel
lost and alone in unfamiliar territory.25 To someone who
strives to control his or her own body and thrives on the
pursuit of excellence, this loss of control can create feel-
ings of helplessness and frustration.
Of prime importance at this stage is a fear of the
unknown. In this case, some of the unknown factors
include a knowledge of the healing process, how much
pain there will be, what surgery and rehabilitation
involves, whether the performer can return to prein-
jury skill levels, fear of disfigurement, and whether the
individual’s status or place in life is assured.
What Patients Need to Know about Their Injury
● Knowledge of the healing process
● How much pain there will be
● What surgery involves
● What rehabilitation involves
● Whether they can return to preinjury activity levels
● Whether there will be disfigurement
● How their life will be affected
The level of fear expressed by an injured patient may
be strongly influenced by the amount of control over
his or her future the injured individual perceives.26 If the
injured individual has a feeling of control over the reha-
bilitation process and the return to action, she or he may
experience less fear and have a strong sense that the phys-
ical effects of the injury can be overcome. The best kind
of information to give an injured patient is a combination
of sensory and procedural details that can foster accu-
rate expectations and help the individual to form correct
cognitive interpretations of the sensations he or she will
experience.27
Through this information, both procedural stress
(immediate aspects such as rehabilitation) and outcome
stress (long-term factors such as a return to career) can
be reduced.28 Regardless of the specificity of the infor-
mation, it is vital that open lines of communication
exist so that the injured individual can express his or
her fears and gain input to help clarify the issues.29,30 In
the absence of accurate, honest, and optimistic informa-
tion, complicating misperceptions and behaviors often
develop.
When an individual is injured and is told to “get”
rehabilitation, the usual order of daily organization and
workout scheduling is no longer in existence. Routines
are disrupted, some functions are impossible, parenting
responsibilities become complicated, roles may have to
change, and relationships may be stressed. This is par-
ticularly significant if the patient has never been injured
before and does not know what rehabilitation means. At
this point, it is vital that the patient regain a sense of
order by being involved in planning the recovery.31 This
planning can give the patient a feeling of being in con-
trol again and can provide the security of a structure in
which the individual can work to overcome the injury.
One method of demonstrating to the injured individual
that he or she can gain control over the physical recov-
ery process is through the example of previously injured
patients.32,33 Berehowski gained valuable information
from formerly injured performers on a return to com-
petition after a major ligament reconstruction.4 “I did a

lot of reading up on people who had been injured, and
I realized that people have come back from this.” Since
Berehowski did not know what to expect from his injury,
he needed to gain a sense of control over the future, and
previously injured performers helped provide a basis for
knowledge and understanding.
Modeling in Injury Rehabilitation
How can clinicians ensure that the injured patient is
receiving appropriate information about the recovery
process? One of the best methods of communicating
attitudes, behaviors, and skills is through observational
learning, or modeling.34 Modeling has long been con-
sidered an influential instructional tool in sports for the
learning of motor skills and social behaviors.35 The pre-
dominant theory of the modeling-behavior relationship
comes from Bandura,34,36,37 social-cognitive modeling
theory being the most popular.
Bandura’s theory proposes that modeling, or obser-
vational learning, facilitates the transmission of socializa-
tion information and cognitive skills through behavioral
and verbal cues provided by the model.34 As an observer
watches the model, symbolic representation, or verbal
coding, takes place, and these cues are stored in mem-
ory. Through this vicariously gained information, deci-
sion-making criteria are formed, and new behavioral
patterns may be learned. Because we tend to compare
our capabilities with those of others, seeing someone
similar to ourselves complete a new task or demonstrate
a particular behavior provides us with the information
that we also have the capacity to re-create the action.34
Examples of modeling effects are evident in sports, and
teachers and coaches often rely on this teaching tool to
enhance the learning of new physical skills.35,38
Observational learning has also had an impact
in a medical context and has been used with cardiac
patients,39 children having surgery,40 and endoscopy
patients.41 Within a sports rehabilitation setting, a vid-
eotaped modeling intervention has been found to aid in
the recovery of women basketball players after anterior
cruciate ligament surgery.25 The extension of this tech-
nique into the realm of injury management provides
injury rehabilitation information, incentive, and behav-
ioral cues for recovering individuals. Thus, patients who
have already recovered from injury and returned to their
careers are ideal models.
What Patients Need to Know about Their Injury
● Seeing someone similar to oneself successfully overcome the
obstacle of an injury can help an injured individual believe that
recovery is possible.
CHAPTER 22 • Psychology of the Injured Patient 463
Within the sports setting, there are numerous examples
of the modeling effect with notable athletes such as Wayne
Gretzky (hockey), Silken Laumann (rowing), Mike
Foligno (hockey), and Kerrin Lee-Gartner (skiing), all of
whom have recovered from major debilitating injury. In
the case of Lee-Gartner, the 1992 Olympic winter games
gold medal winner in women’s downhill skiing, her recov-
ery from five knee surgeries and one broken ankle set the
example for other Canadian skiers. The head coach of the
Canadian ski team noted, “It will make us believe again. It
will make injured skiers like Kate Pace and Lucie LaRoche
say, ‘I can win again.’ ”42 Indeed, Kerrin Lee-Gartner’s
example helped Kate Pace win a gold medal in the 1993
World Cup downhill competition while skiing with a frac-
tured wrist. Pace’s example of recovery from injury now
establishes her as a model for other injured skiers.
In most cases, these sports’ modeling examples
provide motivation and incentive to injured individu-
als, but they convey little information on the details
of overcoming injury. The observer generally sees the
successful end result of months of rehabilitation and
is not exposed to the intricacies of the recovery pro-
cess. Psychological strategies used to overcome obsta-
cles, methods of maintaining motivation through the
rehabilitation plateaus, and goal-setting techniques for
reentry into one’s career are not communicated. In this
sense, then, the modeling experience is informal and
may be of only motivational benefit. To ensure that
pertinent details of the actual process of recovery are
passed on to injured patients, the modeling exposure
should be formalized. “In formal modeling, a situa-
tion is created whereby one or more models presents
specific verbal or visual cues that expose the observer
to vicarious experiences, verbal persuasions, and emo-
tional exhortations.”25 Thus, a model-observer situa-
tion is created so that knowledge, behavior cues, and
psychological strategies can be transmitted.
Kulik and Mahler provided an example of formalized
modeling within a medical setting.39 Coping models were
used to demonstrate the progression from the difficulties
of immediate postsurgical conditions to self-sufficiency
several days after surgery. Newly hospitalized cardiac
patients were paired with postsurgical cardiac roommates
and were thus exposed to postoperative sensations and
events through this coping model. New patients learned
what to expect immediately after the surgery, and their
possible fears about the actual process were reduced by
example in a formal modeling situation.
One way to ensure that the observer is provided
with an optimal amount of information regarding the
recovery from injury process and possible psychologi-
cal strategies for handling problems is through film or
videotape.25,40,43 Flint used a coping model videotape as a psy-
chological intervention with female basketball players.25 The
videotape consisted of interviews with seven basketball
464 SECTION II • Principles of Practice
players, all of whom had recovered from anterior cru-
ciate ligament surgery. One player was followed from a
few weeks postsurgery to 16 months after surgery and
demonstrated the entire recovery process and return to
competition. The other six players were interviewed at
various stages of recovery from surgery extending from
2 weeks to 7 years after surgery. All demonstrated a full
and complete recovery from the injury and the surgery.
Within the interviews, the models discussed the problems
they encountered, how they overcame these obstacles,
and how good it felt to return to action. Each inter-
view culminated with scenes of the model’s full physical
function and capability to play basketball. This video-
tape modeling process would seem to have tremendous
potential for all major medical conditions.
The modeling videotape was shown to female
athletes who had just undergone reconstructive surgery
for a torn anterior cruciate ligament. These recover-
ing athletes viewed the videotape immediately after
surgery, 2 months later, and 4 months postsurgery.
Throughout this process, they were asked to identify
anything or anyone in the videotape that caught their
attention. One athlete noted, “A different part of each
person caught my attention, either their determination
or how quickly they recovered. I think it will [affect]
my rehab progress, positively, of course.”5 In this case,
an affinity between the models and the individual per-
former provided motivation and incentive during the
rehabilitation process. This individual was encouraged
throughout her rehabilitation by the thought that if
they can do it, then so can I.
In another case, one of the models provided specific
information about goal setting, and this was of partic-
ular relevance to an athlete viewing the videotape. Bev
Smith, a former All-American and a member of Canada’s
national basketball team, was a model in the videotape,
and her experiences of overcoming several knee surger-
ies gave her insight into the difficulties of rehabilitation.
The athlete noticed Smith and commented, “She spoke
of setting daily goals during rehab and trying to keep
things in perspective. She also spoke of channeling energy
into other things. This approach has certainly made my
rehab time less frustrating.”5 Here we see that informa-
tion has been provided on a specific psychological strat-
egy for overcoming the frustration of long months of
rehabilitation. While facing obstacles in the recovery
process, this athlete was able to recall the words and
actions of Bev Smith and use them to her advantage.
It was interesting that the observers noted specific
characteristics, actions, or verbalizations of the models.
In general, immediately after surgery, most of the mod-
els’ comments identified by the observers related to the
pain and emotional response to the surgery. There
seemed to be a bond between some of the models and
observers because of the shared experience of pain and
emotional release. Two months later, the observers had
moved from the emotion of the surgery and tended to
notice specific aspects of the rehabilitation process.
They identified with the model who progressed from
one-legged bicycle pedaling to a complete bicycle work-
out. Finally, after 4 months of rehabilitation, the observ-
ers began noticing details such as which models wore
a brace when returning to action and the degree of
dedication of the models throughout the rehabilitation
process. Through the qualitative information gathered
from recovering performers, it was evident that they had
identified with and paid attention to the examples set by
the videotaped models.
The videotape format provides an opportunity to
reconstruct the most desirable scenes and conditions
that may be difficult or unrealistic to capture in a clinical
setting.44 By utilizing coping models, the injured patient
can obtain the information she or he needs to promote
the psychological aspects of recovery. Seeing a similar
individual struggle through rehabilitation, hearing a
recovered performer, such as Bev Smith, speak about set-
ting daily goals for recovery and her commitment to the
small details of rehabilitation, or hearing a similar athlete
talk about the frustration of injury and the recovery pro-
cess and the joy related to returning to action can have a
significant effect on recently injured athletes.
Factors That May Affecting Healing Time
● The knowledge gained vicariously through coping models may
provide the injured individual with a sense of belief and control
over the situation.
For the patient who has never experienced a major
injury and does not know what to expect from rehabilita-
tion, this may be particularly pertinent. In this sense, the
injured patient gains an understanding of the task ahead
and, more important, what strategies can be used to
overcome any obstacles during the rehabilitation process.
What will ensure the strongest possible link between
the injured observer and the model so that the observer
will be encouraged to pay attention to the model?
Bandura37 and McCullagh and colleagues35 have stressed
the importance of model and observer characteristics. It
is hoped that the observer will relate to the model and
form a bond by identifying similarities and hence that the
observer will have an incentive to pay attention to the
actions or verbalizations of the model.35 In sports injury
rehabilitation, the most pertinent model and observer
characteristics appear to be the similarity of the injury or
surgery, shared emotion (e.g., pain), feelings of frustra-
tion, the dedication to recovery, and the achievement of
rehabilitation.5

Individuals who have sustained a major injury for the
first time in their careers may not know if they have the
capability to fully recover and return to action. Since they
do not have injury rehabilitation experience on which to
rely, they may tend to judge their own prognosis on the
basis of the experience of other people who have suffered
from the same injury. Thus, the provision of models who
have successfully recovered from injury (or illness) can
help furnish a strong psychological foundation on which
to build confidence in the recovery process. The use of
modeling, individually and in combination with other
psychological intervention strategies, is a relatively new
realm in rehabilitation. Successful models “in person” are
ideal, but credible videotape footage can help with edu-
cation, preparation, coping, and inspiration. The strat-
egies are simple but multidimensional in effects. They
help with belief and understanding regarding the realities
and possibilities of rehabilitation.
Exceptional Patients
This section discusses the mental attributes and skills
found to be associated with exceptional cases of injury
recovery. Much of the information draws from extensive
consulting experience, anecdotal information, plus the
results of two comprehensive survey studies that exam-
ined a number of psychosocial factors related to injury
rehabilitation of ankle and knee injuries.45,46 Scores
between those identified as either fast- or slow-healing
subjects based on recovery time were compared. In the
original study by Ievleva and Orlick,45 the rate of recov-
ery was found to be significantly related to the amount
of practice of certain mental activities, most notably goal
setting, healing mental imagery, and positive self-talk.
The follow-up study by Loundagin and Fisher revealed
a similar pattern of results and added focus of attention
and stress reduction as a factor that was also significantly
related to recovery time.46
Factors That May Affect Healing Time
● Goal setting (daily and long term)
● Healing mental imagery
● Positive self-talk and attitude
● Focus of attention
● Stress reduction (relaxation)
● Commitment to rehabilitation
● Patience
● Tenacity
Commitment and Belief
Just as commitment and belief are at the core of mental
attributes and activities in pursuit of excellence,47
CHAPTER 22 • Psychology of the Injured Patient 465
so too are they keys to achieving optimal recovery from
injury. Patience and tenacity are necessary requisites
when confronting any challenge, and they apply to the
effort required to achieve full recovery from injury (or
illness) as well. Without faith and belief in one’s own self-
healing capacity and in the clinician’s skill, it is difficult
to mobilize mental powers of healing to their fullest
capacity. This difficulty can be especially pronounced in
severe injury cases, in which great courage is required
to commit the full effort toward an uncertain outcome.
For many patients, it sometimes takes a leap of faith to
attempt to beat the odds, to overcome self-imposed or
external limitations. The root meaning of the word cour-
age draws from Latin cor, meaning heart. Therefore, to
act with courage is to act with heart despite unknown
consequences. Those who transcend the odds are never
totally free from fear and doubt. What distinguishes
exceptional performers and healers is that they do not let
the fears or doubts overshadow their hearts’ desire. They
acknowledge the shadow, and press forward regardless,
mobilizing positive efforts to achieve their goal.
Steve Nicholson, a courageous young man from
Winnipeg, Canada, somehow survived and recovered
from one of the most serious industrial burn accidents
ever.48 For weeks Nicholson’s life hung in the balance,
while doctors and health professionals worked around
the clock and family and friends prayed for his survival.
Nicholson’s belief and commitment seemed life saving.
Even the attending surgeon was tearful in describing
Nicholson’s courage. Amazingly, Nicholson has surfaced
with an even stronger perspective on life and the power
of belief.
Seeing the Opportunities and Potential Payoffs
Seeing the opportunity for personal learning and growth is
conducive to enhancing the process of recovering from an
injury. Although the injury may pose a crisis in an individu-
al’s life, it can be approached in two ways. Just as the word
for crisis in Chinese has two meanings, danger and oppor-
tunity, rather than viewing an injury as a major obstacle
and setback that destroys the chances for future success,
one may instead view the injury as a challenge to overcome, a
learning and growth opportunity, or a strengthener.
Injuries (or illness) often produce unplanned but
sometimes beneficial “time outs” from performance
demands. The break from demands can result in a more
rested, clearer-minded individual with a better focus and
perspective. In addition to the break from performance
demands, the patient might adjust priorities and return
to action refreshed with a better perspective, an increased
sense of mission, and decreased pressures and expecta-
tions. In some cases, built-up stress, fatigue, pressures,
and a questionable perspective may have contributed to
injury or illness “proneness.”
466 SECTION II • Principles of Practice
Just as a broken bone heals stronger following proper
rehabilitation, patients should be reassured that they can
come back mentally tougher and stronger from injury
setbacks. Exceptional patients use the injury rehabilita-
tion challenge as an opportunity to apply and develop
the attitudes, mental skills, and behaviors that can make a
difference in rehabilitation and in the rest of their lives.
When asked in the Ievleva and Orlick study whether
the time out provided by the injury resulted in any valu-
able lessons or perspectives that contributed to later
achievement, subjects in the fast-healing group reported
deriving enhanced insight and enjoyment from their pur-
suit, whereas those in the slow-healing group could find
no benefits whatsoever.45 These patients showed greater
determination to see the positives than the negatives.
These findings are supported by the Loundagin and
Fisher study,46 in which athletes in the fast-healing group
reported feeling more positive about the time out and
recognized greater benefit from the opportunity, whereas
the slow-healing group viewed the experience as com-
pletely negative. This is consistent with observations of
world-class athletes who have made remarkable recover-
ies from serious and potentially career-ending injuries in
which there was always some form of gain in terms of
insight or approach to training that substantially improved
the athlete’s subsequent training, performance, or both.
Factors That May Affecting Healing Time
● Those individuals who accepted the injury as a challenge and
opportunity and drew lessons from the experience demonstrated
much shorter recovery times.
According to Ievleva and Orlick, “To enhance the
recovery process, exceptional athletes accept the injury,
and do everything in their power to initiate a positive
and complete recovery. They also take advantage of what
can be learned from the experience (e.g., about oneself
and the relationship to one’s sport).”30 Caregivers and
others in an injured patient’s support network are in an
excellent position to assist this process of exploration
and growth, which may ultimately take the performer to
a higher level later than he or she might have achieved
without the injury experience.
Another burn victim in Winnipeg (Lars Wennberg)
was severely burned in a motorbike accident when he
was 14 years old. Wennberg was an excellent trap and
skeet shooter, and he quickly discovered the mental skills
he had learned in sport could help him respond to the
challenges of his rehabilitation. He learned that his relax-
ation skills could help with body temperature regulation,
and his imagery, focusing, and preparation skills could
help him with the painful treatments. He soon realized
he was going to come out of the rehabilitation stronger
and with enhanced attributes. After several months of
hospitalization (and still facing extensive rehabilitation),
Wennberg was propped up at a trap and skeet meet and
he shot a personal best. Wennberg clearly had discovered
enhanced perspective and skills.
Mental Skills
Mental skills or activities associated with successful
preparation and performance may likewise be applied to
exceptional recovery from injury. Some of the key skills
include goal setting, positive self-talk, relaxation, and
mental imagery.
Goal Setting
Goal setting and visualization of goals being achieved
constitute the first step toward applying mental training
skills, whether goals are performance or recovery oriented.
The results from several injury studies indicate that fast
healers practice much more goal setting than the slower
healers.45,46,49,50 This was especially the case with daily goal
setting.45,46 Many recommend that specific and objectively
measurable goals related to rehabilitation be set for every
physical therapy session and every day, week, or month.
Having set goals, the practice of mental imagery may
be applied to deepen and promote the conviction of the
desired end. Goal setting is an indirect link to the prac-
tice of end-result or affirmation imagery. Setting a goal is a
statement of expectation, hence a conceptualization of suc-
cess. Inherent in goal setting is the periodic contemplation,
or imagining of, achievement of that goal. The act of goal
setting alone conjures up an image of success, control, or
those activities in which one can engage that are consistent
with achieving that goal. Goals that are most immediately
attainable are also most easily conceived and seen in the
imagination. This is consistent with the findings from the
Ievleva and Orlick study,45 in which both daily goal setting
and healing imagery were more closely related to recovery
time than other categories of goal setting and imagery prac-
ticed. Orlick, however, has identified several kinds of goals
that can be beneficial in developing motivation, focus, and
perspective in the patient or performer.47
Factors That May Affecting Healing Time
● Dream goals can often have tremendous motivational and
focusing value, although individuals need to combine these with
realistic short-term goals.
The challenge of matching or exceeding a best-ever
rehabilitation or post-injury performance can sometimes
produce tremendous energy, conviction, and persistence.

This was exemplified in the case of Jana Pittman, a 2003
world champion in 400-meter hurdles who injured her
knee within weeks of her first heat at the Athens Olympics
in 2004 and was given only a 1% chance of competing.
Pittman was not willing to give up on her Olympic dream
and set out to overcome the odds. She applied the same
determination and commitment she was renowned for,
drawing on her well-honed mental skills of meditation
and visualization as well as the best of medical care. Not
only was she able to run, but she made the finals and
finished a close fifth. A continuum of target possibilities
from exceptional through typical to complicated helps the
patient respect and appreciate the spectrum of possibilities
but often triggers dream goals and high aspirations.
Probably the most important goal is that of the daily
process—making improvement in focus, attitude, rehabili-
tation exercises, and relationships. Some patients even take
advantage of injury opportunities to develop new attributes
(e.g., lower-body flexibility or upper-body strength). In
addition to improved mental skills, individuals can emerge
from rehabilitation with new physical capacities.
Goals in school, outside interests, time, and relation-
ship management can also be important during rehabili-
tation. Orlick also encourages goals of self-acceptance
and self-appreciation in the event that some dreams are
temporarily delayed or not possible.51 This helps people
separate their self-worth from their goals and frees them
to strive unburdened.
In one case, a young tennis player’s rapid rise in the
ranks was cut short by the need for anterior cruciate liga-
ment (ACL) reconstruction, and she found that the long
road to recovery was daunting. During one conversa-
tion with her, it was pointed out that she was in good
company, as the top-ranked player she most looked up to
was also sitting out the Wimbledon championships at the
Table 22-1
Examples of Positive Self-Talk from the Fast-Healing Group and of Negative Self-Talk from the Slow-Healing Group
Positive Self-Talk
How can I make the most out of what I can do now?
I can beat this thing.
I can do anything.
I can do it. I can beat the odds and recover sooner
than normal.
I want to go spring skiing. I'll be totally healed
by then.
I have to work to get my leg as strong as the
other one.
It’s feeling pretty good.
It’s getting better all the time.
From Botterill C, Flint FA, Ievleva L: Psychology of the injured athlete. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic
injuries and rehabilitation, p 798, Philadelphia, 1996, WB Saunders. Adapted from Ievleva L, Orlick T: Mental paths to enhanced
recovery from a sports injury. In Pargman D, editor: Psychological bases of sport injuries, Morgantown, WV, 1993, Fitness Information
Technology.
CHAPTER 22 • Psychology of the Injured Patient 467
time because of a knee injury. This did little to alleviate
her fears of returning to form. When the only goal is the
ultimate recovery and when one’s return to competition
(a big picture goal) is so far down the track, it is natural
to feel discouraged. This player was advised to set more
immediately achievable goals (a little picture goal) on the
road to recovery, as well as to visualize each step along
the way. By doing this, the player was more readily able to
observe and acknowledge her progress, which she found
to be very encouraging; this inspired her to more fully
engage in the recovery process and eventually led to a
successful return to the tennis courts.52
Positive Self-Talk and Attitude
Thinking in positive ways contributes to personal well-
being and enhanced health. A positive outlook indicates
adjustment to the new condition and an orientation
toward improvement. In contrast, a negative outlook
indicates preoccupation with the implication of the injury,
which can reduce one’s effort toward improvement.
Internal dialogue is a reflection of one’s attitude
and outlook. As such, the degree to which this self-
talk is positive may be the degree to which healing is
enhanced. This theory was confirmed in an injury study
demonstrating that those whose self-talk was positive,
self-encouraging, and determined healed more rapidly
than those whose self-talk tended to be totally negative,
self-deprecatory, and unforgiving.45 In addition, the
Loundagin and Fisher study reportedly found that the
greatest incidence of self-talk control occurred during
exercise.46 See Table 22-1 for representative examples.
It is generally accepted that success in any endeavor
depends on the extent to which one has a positive attitude.
This may be particularly challenging in lengthier rehabili-
tations in which the road may seem endless. The quality
Negative Self-Talk
It’s probably going to take forever to get better.
I’ll never make up for the lost time.
What a stupid thing to do—dumb mistake.
It will never be as strong again.
What a useless body.
Stupid fool. Stupid injury. Stupid leg.
I talked to myself about how frustrated I was.
There is nothing good about this, and there is nothing
I can do about it.
Why me?
468 SECTION II • Principles of Practice
of recovery, however, depends on maintaining a positive
perspective to permit the physiological healing processes
to occur unobstructed. Although one cannot control the
fact that one is injured and possibly facing a long rehabili-
tation, one can control and direct one’s thoughts about
it. Rather than focusing on all that has gone wrong and
dwelling on the negative, it is more effective to focus on the
positive possibilities —those within personal control—and
what can be done to enhance the situation and recovery.
In his book Full Catastrophe Living, Kabat-Zinn discussed
his work with severely physically impaired patients who
come to his stress reduction clinic as a final resort after
exhausting the resources of the medical system.53 During
the course of his 8-week class in mindfulness meditation,
he counsels the participants to recognize that there is often
much more right with one’s body than there is ever wrong.
Thus, it is much more conducive to healing to appreciate
what is going well than to focus on what is not.
Positive thinking can influence belief and perspective,
and belief is often translated into action through positive
self-talk. Monitoring internal dialogue can be effective in
taking control, guiding positive thoughts, and reducing
negative thoughts. To do this, the injured person first
plans to think in positive terms and then responds to any
negative thoughts that may still occur, using them as cues
to switch to positive thoughts. Injured patients invariably
have moments when they make disparaging remarks to
their injured body part (e.g., “stupid, useless knee”). The
clinician can ask these individuals to reflect on how they
would feel and respond if spoken to in such terms and
then invite them to consider speaking positively, kindly,
and lovingly to the injured part, much as one might speak
to an injured child (e.g., “It’s okay, knee. I’m going to
take care of you; you’re going to take care of me; you’re
getting stronger all the time. Together we’re going to
make you as good as new.”).30
Staying positive may be challenging for high-profile
individuals who are constantly being asked about their
injury and how they became injured. This kind of atten-
tion may cause the individual to continually revisit and
imagine the original injury, which is counterproductive
to the recovery process. As an example, the captain of
one professional team began to avoid the press and fans
because it was becoming increasingly distressing for him
to continually focus on the injury while he was trying to
recover. But after embarking on a program of mental skill
application to rehabilitation, he began to look forward to
queries about his injury, for he enjoyed turning the focus
to his goals and how well his rehabilitation was going.
Relaxation
Relaxation practice in any of its various forms—for exam-
ple, physical relaxation, meditation, progressive relax-
ation, breath control, or yoga—plays an integral role in
behavioral medicine and stress reduction programs. The
health and wellness benefits accrued from engaging in
relaxation on a regular basis have been well documented.
Numerous studies have established a list of relaxation
effects (Table 22-2) that are the specific means by which
the health benefits take place.
Relaxation helps open the mind-body channels that
regulate the body. Through relaxation practice, awareness
of and connection to the body can be increased, thereby
enabling inner control over the body. Using relaxation in
combination with imagery, it is also possible to initiate
physical and behavioral change.54–56
It is common for one’s tension level to increase, espe-
cially in the injured area, because of the stress of being
injured and body processes to protect the injury.57,58
Regularly practicing a relaxation routine can be effective
in relaxing the area and relieving the tension. Staying
loose and relaxed facilitates recovery. When the body is
more relaxed, blood circulation improves. The greater
the blood flow, the faster injured tissues are repaired.30,59–61
Also, the fact that cortisol levels rise with stress62,63 and
inhibit muscle fiber repair64 further suggests the need for
stress reduction in the form of relaxation, and the benefit
becomes more evident because relaxation has been shown
to reduce cortisol levels.65-71 The fast-healing group in the
Loundagin and Fisher study used relaxation techniques
to manage stress levels to a greater extent than did the
slow-healing group.46
Mental Imagery
It is important to recognize that the body’s healing
powers are continually in progress, whether or not one
chooses to exercise conscious control over healing.
Employing positive images of healing and images of
being fully recovered, however, is useful in enhancing
one’s belief and mobilizing one’s own healing powers to
maximize the healing potential already existing within an
individual. Five basic kinds of imagery may be applied
during injury rehabilitation (Table 22-3).
Table 22-2
Effects of Relaxation
Decreased heart rate
Reduced blood pressure
Reduced respiration and hypertension
Enhanced oxygen consumption
Reduction in lactate
Reduction in cholesterol
Reduced muscle tension
Enhanced reactivity to stress
Decreased galvanic skin response
Reduced cortisol
Redistribution of blood flow
Enhanced immune system
Note: Stress tends to reverse the effects for each of these items.
 CHAPTER 22 • Psychology of the Injured Patient 469

Table 22-3
Types of Imagery That Can Be Part of Rehabilitation
Recovery, end result, or Imagining one’s recovery goals being achieved or imagining
affirmation imagery oneself with the capacity to achieve all goals
Healing imagery Envisioning and feeling healing taking place
Pain-reducing imagery Imagining the pain being soothed away or an ice pack
Treatment imagery Imagining the physical therapy treatment promoting quick and
efficient recovery
Performance imagery Mentally rehearsing performance skills

Both of the injury studies mentioned next found a
significant relationship between the practice of imagery
and recovery time. In the Ievleva and Orlick study,45 heal-
ing imagery was most closely related with fast recovery,
whereas in the Loundagin and Fisher study,46 both healing
and recovery imagery were equally related to fast recov-
ery. In addition, negative imagery, or images in which the
injured person relives the initial injury, tended to cancel
out the benefits of positive healing imagery.30,45
End Result or Affirmation Imagery. For those who
have difficulty seeing or feeling their goals being achieved,
or who get negative images, researchers suggest that they
stop and acknowledge their doubts and fears, and then
make a list of all the positive attributes that will help them
to reach their goal (talent, treatment, tenacity, etc.) (Table
22-4). This affirmative thinking helps them believe or
recognize that they have the tools necessary to meet the
goals and are in control. Ievleva and Orlick have developed
audiotapes to facilitate psychological skill mastery.30
Healing Imagery. The value of imagery for heal-
ing is gaining acceptance in modern medicine. There
are many clinical reports of therapeutic benefits result-
ing from imagery. Whereas most are anecdotal in nature,
an increasing number of documented cases support the
healing benefits of engaging in healing imagery.1,52,72–81
In the groundbreaking work of Simonton and
colleagues,82 positive results were reported from imple-
menting a relaxation and imagery program with cancer
patients diagnosed as medically incurable. A total of
41% showed improvement, of whom 22.2% experienced
complete remission and tumors regressed in 19.1%. A
subsequent study by Hall followed up and supported this
research.83
It is most effective for clinicians to elicit relaxation in
their patients and clients before commencing with imag-
ery practice. A state of calm and quiet allows for greater
receptivity and flexibility of the mind with which to direct
and control imagery. In fact, a state of mental and bodily
relaxation is generally considered a prerequisite for all
work with therapeutic guided imagery. Common forms
of relaxation include a focus on diaphragmatic breathing,
meditation, or some form of the progressive relaxation
technique.
Knowing precisely what the healing process looks like
physiologically can enhance one’s ability to imagine it.
It is not essential that the image be realistic, but it must
symbolize positive change.30,82,84,85 Precisely what one will
imagine is determined individually. An image that works
for one person may not be as effective for someone else.
For example, among the Simontons’ cancer patients,
one patient saw her white cells as “killer sharks” attack-
ing the cancer cells, whereas another saw the white cells
as white knights.82 The important feature is to see one’s
own bodily resources as being powerful and effective.30

Table 22-4
Recovery, End Result, or Affirmation Imagery
1. Select a goal.
2. Relax.
3. See yourself with goal already met.
4. Imagine, with as many details as possible, your feelings, having reached your goal.
5. See the response of others close to you regarding your achievement.
6. Go over the steps it took to reach your goal and experience satisfaction at each level.
7. Allow yourself to feel happy about reaching your goal.
8. Gradually come back to the present.
9. Then open your eyes and commence action on that first step.

Adapted from Ievleva L, Orlick T: Mental paths to enhanced recovery from a sports injury. In Pargman D,
editor: Psychological bases of sport injuries, Morgantown, WV, Fitness Information Technology for sports injury
derived from the application for cancer treatment found in Getting Well Again by Simonton and colleagues.82
470 SECTION II • Principles of Practice
A performer recovering from a fracture might imagine
the blood flow to the injured area and “feel” the healing,
strengthening effects. Patients can become quite creative
in the process of imagining recovery. A rugby player who
after a fibula and tibia fracture had a metal plate inserted
not only fully embraced the practice of relaxation and
healing imagery, but also implemented lucid dreaming to
augment his recovery.52
While empirical evidence is limited because of the
nature of the process of documenting imagery, the com-
bination of extant research, reviews, and anecdotal evi-
dence supports the effectiveness of healing imagery in
rehabilitation.86–88
Pain-Reducing Imagery. Relaxation alone is effec-
tive in reducing one’s perception of pain and has
gained consensus approval by a panel of medical experts
(arranged by the National Institutes of Health and the
U.S. Department of Health and Human Services), which
reviewed all documented studies. Imagery is also known
to have relaxation effects, but it can be directed at specific
suggestions for reducing pain—for example, imagining
an ice-pack reducing inflammation, feeling the pain being
washed away by a rush of cool water, or envisioning cool
colors soothing and reducing inflammation.81
Imagery strategies for pain reduction fall under two
categories: those designed to divert attention away from
the pain (i.e., dissociative imagery) and those that direct
attention to the injured area (i.e., associative imagery).
The associative form is favored, first to ensure that dam-
aging pain cues are attended to and second to attain a
greater sense of control over one’s pain and rehabilitation,
which ultimately enhances the self-efficacy that is con-
ducive to compliance with treatment and rehabilitation
programs.89,90
Factors That May Affecting Healing Time
● A study with patients recovering from ACL reconstruction found
that those participants who practiced relaxation combined with
guided imagery experienced significantly reduced pain relative to
the placebo and control group at 24 weeks post surgery.91
The use of guided imagery applying associative sug-
gestions was found to be effective in lower back pain suf-
ferers. In another study by Ievleva et al.,79 listening to a
healing imagery tape92 significantly reduced pain ratings
in patients relative to baseline and a comparison group.
Moreover, the pain reduction effectiveness of the heal-
ing imagery exercise was found to significantly improve
over the 4-week period of the study. An exceptional
case in this study was a male in his 40s who had initially
been the worst case in terms of complaints and compli-
ance. Indeed, he was considered the most stubborn and
skeptical of the entire sample regarding the usefulness of
healing imagery. Upon being advised that he had nothing
to lose and encouraged to just “give it a go,” he became
the greatest advocate of the benefits of imagery. After
experiencing initial positive results, he began to practice
listening to the Inner Healing tape as often as twice per
day, seven days per week. During the first week, he never
listened to the tape; by week 2, he listened once per day,
and he listened twice per day thereafter. Whereas at first
he dwelled on his pain and the dire meaning and con-
sequences of the pain, he began to focus more on what
he had control over, which was returning to work full-
time as a retail manager. This became the most successful
case in the study in terms of return to work. The job of
a retail manager requires being on one’s feet for most
of the day—challenging for anyone experiencing back
problems. This patient attributed his success to the tape,
which provided an increased sense of control as well as
responsibility that led to his increasing belief and confi-
dence in his capacity to return to form. This result is con-
sistent with research regarding the relationship between
self-efficacy and rehabilitation.31,90
Treatment Imagery. Suggestions that chemotherapy
and radiation treatment are effective are incorporated in
the Simonton guided imagery program. The emphasis,
however, is on the body’s own resources leading the bat-
tle against cancer. This principle can be applied to the
physical therapy setting as well—for example, seeing and
feeling the treatment, minimizing scar tissue, increasing
blood flow, or strengthening the muscle or tissue.
Factors That May Affecting Healing Time
● Patients should be clearly informed about what the treatment
is designed to do so that they can imagine those effects taking
place.31
Progressive sports medicine practitioners Arnheim,93
Swearingen,94 and Steadman95 pointed out the importance
of the patient being educated about the goals and process
of healing and treatment so that meaningful detailed imag-
ery can be facilitated. The patient then can play a more
active role in optimizing rehabilitation responses and can
thereby increase feelings of control and influence.
Performance Imagery. Because injured patients
are often unable to perform physically, mental practice
becomes that much more important if they are to main-
tain a certain skill level. Performance imagery can be a
powerful tool in this respect. Not only does it provide a
medium in which to rehearse skills, it also helps patients to
prepare for situations that are infrequently encountered
in physical practice or competition. Imagery practice can
be effective in preparing injured individuals for any num-
ber of upcoming situations and thus helps them to retain
confidence in their ability and to dissipate any linger-

ing fears they may have of reinjury upon their return to
action.31 Progressive desensitization using imagery and
simulation may be necessary to help eliminate fears and
doubts that could lead to injury proneness.96
In research by Johnson,97 individuals who had engaged
in healing and performance imagery throughout their
rehabilitation were found to feel more ready to return
to action than those in the control condition. This readi-
ness was based not only on the patient’s ratings but also
on ratings by the physical therapists. This finding is sup-
ported by case studies by Evans et al.,98 who found that
the practice of guided performance imagery increased
the individual’s confidence upon returning to action and
reduced anxieties about reinjury. Such confidence may
further enable individuals to relax and be more motivated
to adhere vigorously to the rehabilitation program.91
Focusing on skill execution decreases the likelihood
of becoming reinjured. It is, nevertheless, natural to have
concerns about whether a freshly recovered body part will
hold up under performance conditions. Such fears may dis-
tract the individual, increasing the likelihood of fulfilling a
negative prophecy. These fears need to be acknowledged
and addressed before returning to competition condi-
tions. In one case, a rugby player was eagerly awaiting his
comeback to the playing field after ACL reconstruction.
The first question he was asked was, “What would best
prevent reinjury?” The player replied, “If I concentrate
well on execution.” He was then asked about the worst-
case scenario and responded, “That would be blowing out
my knee again.” He was asked to what extent he felt he
could cope with such an outcome and was then referred to
his first answer, including an assessment as to what extent
focusing on execution was within his control. To this very
talented player, staying focused on each play was not a
problem. He was then asked why he plays, to which he
exclaimed how much he loved the game, the competition,
and so on. He was then asked, considering how much he
loves to play, would he still do so even if he knew that
it could be predicted that to do so would cause reinjury
to his knee? He responded, “Absolutely!” In a few quick
short questions, this athlete’s fears were alleviated and he
was free to focus on what was within control—to channel
his dedication to preparing well including the practice of
performance imagery. Not only did this player’s knee hold
up well, but he starred in the game.52
Every effort should be made before a return to action
to have the individual feel as if he or she is a physically,
psychologically, and emotionally recovered person, as
opposed to a recovering performer. Evidence from physi-
cal tests, biofeedback, imagery, and field reports can all
contribute to this belief.
When approaching a return to training and competi-
tion, it is important to incorporate in the performance
imagery details of the use of protective devices such
as taping or braces as are required for actual activity.
CHAPTER 22 • Psychology of the Injured Patient 471
Omitting these details from the imagery may result in the
kind of pain, soreness, or discomfort that would typically
occur if one was physically performing the activity with-
out the protective device. This circumstance occurred
with a university basketball player with whom the authors
worked who habitually taped his previously injured ankles
before every practice and game in an effort to avoid sore-
ness. He had, however, inadvertently neglected to do so
in his imagery. Once the taping was included in subse-
quent imagery, the soreness did not recur.
Timing is an important consideration in an individ-
ual’s readiness to practice certain forms of imagery. For
example, it may be advisable to focus solely on relax-
ation and pain management immediately following knee
reconstruction surgery before commencing with healing
imagery. It may not be feasible to practice performance
imagery until enough healing has taken place for the
patient to feel ready to contemplate being active and per-
forming again. In some cases, the injury may have been so
dramatic or traumatic that if there has not been enough
opportunity for rest, it would be unreasonable to expect
the athlete to have sufficiently recovered psychologically,
not to mention physically, to apply the mental energy
required to implement self-directed healing.30,84,91
Summary of Imagery Application during
Rehabilitation30
● Visualizing healing taking place in the injured area
● Applying pain-reducing imagery
● Imagining treatment being optimally effective
● Imagining moving freely and efficiently through the specific motions
and situations that put the most demand on the injured area
● Reexperiencing or imagining individual skills required for best
performance—to stay sharp and mentally connected with one's sport
● Calling up the emotional and physical feelings that characterize
one's best performances
● Visualizing returning to competition and performing at one's best
again
● Imagining feeling positive, enthusiastic, and confident about
returning to training and competition
Staying Active
Exceptional patients are those who are extraordinarily
active within the limitations of their injury. Regardless
of the injury, the patient must stay active. With an upper
limb injury, the patient may cycle, walk, or use a tread-
mill, for example. A patient who has an injury of the
lower body may use an upper-body exerciser. As soon
as possible, the patient should start working out with
the nonaffected and affected limbs. Some even look to
new mediums (such as swimming pools) as vehicles for
remaining as active as possible. Not only does activity help
prevent loss of fitness and atrophy, it also is extremely
472 SECTION II • Principles of Practice

therapeutic. The therapeutic effects of regular exercise
on biochemistry and psychophysiology have been well
documented.99 These effects can be reversed if individ-
uals are kept inactive for long, and inactivity can make
them more prone than normal to depression, tension,
and frustration.
Individuals experiencing injury are especially apprecia-
tive of being able to stay active and work through some
of their frustrations through physical exercise. Benefits
such as the dissipation of excess energy, the maintenance
of a sense of control, the reduction of stress, and the
retention of one’s self-image have been identified.95,99–102
Characteristics of Peak Performers
Exceptional injury rehabilitation cases—like that of Silken
Laumann (a Canadian rower), who made a miraculous
comeback from a serious rowing accident in time to
achieve a silver medal in the 1992 Barcelona Olympics—
are reminders of the qualities of peak performers. The
attributes initially identified by Garfield103 are recognized
in top performers in many fields104 and provide a frame-
work for optimizing human potential in demanding cir-
cumstances. Table 22-5 shows the characteristics of peak
performers. These attributes and the skills involved epit-
omize attitudes of the best patients and top health care
professionals.
Exceptional patients are not exactly “patient.” They
respect medical knowledge and physiology but are proac-
tive in their pursuit of an optimal response. They serve as
inspirational models to other patients and to health care
professionals.
Health care professionals who show these attributes often
have a profound effect on the patients and professionals
around them. Their enthusiasm, professionalism, and
caring nature have a powerful influence on belief, trust,
and motivation. It is important to nurture these peak
performer attributes in patients and to model them
whenever possible.
Optimizing Rehabilitation Conditions
and Services
As a result of progressive sports medicine research, Gordon
has identified important skill areas and procedures for
trainers, therapists, and other health care professionals.105
Training in these areas can help equip professionals to
optimize patient responses to injury.
Skills
1. Clinicians are required to have effective communication
and active listening skills and are often undermined by
overloaded treatment schedules in busy clinics.
2. Clinicians could be taught to use cognitive restructur-
ing skills such as self-instruction training and stopping
thoughts thought stoppage to help patients combat
negative reasoning or to promote rehabilitation
performance.
3. Shaping behavior through schedules of positive
reinforcement can combat dysfunctional behaviors
such as moaning, arguing, lack of attention, and
nonadherence. Dealing with behavior problems in
general enhances the effectiveness of clinicians, whose

Table 22-5
Characteristics of Peak Performers
Motivated by “mission” Top performers not only have dreams and goals, they passionately invest in seeing,
feeling, and realizing them. Their sense of mission inspires focus and energy.
Action oriented Peak performers have a strong work ethic. They stay assertive, enjoy “going for it,” and
epitomize the slogan “Just do it.”
Self-mastery People who get to the top and stay there are always working on personal and situational
excellence. They want to see how good they can be and enjoy working on technical,
tactical, physical, and mental development goals.
Flexible and in control Peak performers are creative and can see solutions and maintain perspective when
others cannot. They are also mentally tough and can focus effectively and refocus when
necessary. This flexibility and control is usually due to superior preparation—physical,
mental, and emotional.
Challenged by change Top performers prepare not only for the expected but also for the unexpected. They see
demanding or changing conditions as the ultimate challenge and opportunity to test
and develop themselves. They enjoy positive rivalries and being tested, and they
believe in the slogan “Tough times don't last, tough people do.”
Team oriented Peak performers are “team” people. They care enough to encourage, challenge, and
support teammates when necessary. They remain respectful and appreciative of the many
roles of players and of the attributes necessary to create and maintain an effective team.

professional conduct is often reflected in their charac-
teristic reactions to these problems.
4. Relaxation and visualization techniques can promote
internal healing and oppose pain. Relaxation in gen-
eral also helps conserve vital energy required to fight
lengthy periods of discomfort.
5. Most individuals use goal setting, which clinicians can
readily apply to the recovery process.
Procedures
1. Peer modeling is a form of group therapy in rehabili-
tation that is known to promote performance, partic-
ularly when motivation and enthusiasm are lacking.
2. Knowledge about and explanations related to the
cause of injury, the extent of damage, and what has to
happen internally for healing to occur is an important
part of the clinician’s role. Patients should be encour-
aged to ask questions about their injury.
3. Patients appreciate it when clinicians provide sensory
information in a specific and clear (comprehensible)
manner. This information—for example, regarding
what the person will feel and for how long—reduces
feelings of helplessness and a lack of personal control
during treatment.
4. Finally, clinicians could provide all types of social sup-
port identified in the literature. These include active
listening, emotional support, emotional challenge,
shared social reality, technical application, and techni-
cal challenge. With only a little effort, clinicians could
contribute meaningfully to all types of support with-
out compromising their function of helping patients
recover as opposed to “looking after” them.
Creative, caring, dedicated health care professionals
and support people can have a tremendous effect in opti-
mizing psychological, emotional, and physical recovery
and growth. The absence of these skills and procedures
has probably complicated and limited many rehabilita-
tions in the past. In reacting to health care profession-
als who evasively said they did not want to give “false
hope,” an outstanding athlete/patient from Sweden,
Egon Oosteren, suggested, “The opposite of hope is
hopelessness, and that is totally unacceptable.” Clearly,
those facing health challenges want honesty, optimism,
and caring. Those in a position to help should not let
their schedules, fears, or backgrounds prevent them from
providing what patients really need.
Injury-Proneness and Prevention
The study of the psychophysiological dynamics during
injury rehabilitation sensitizes one to the importance
of these factors in injury prevention. Confidence,
preparation, focus, and development all can play a role
in injury prevention. Knowing one has the physical,
CHAPTER 22 • Psychology of the Injured Patient 473
technical, tactical, and mental resources to face the
demands in his or her career can help prevent stress, ten-
sion, and injury-proneness (Figure 22-3). There is no
substitute for thorough preparation and development
when one performs in the technical, tactical, physical,
and mental areas. As the demands of performance envi-
ronments grow, it is important to do better job of devel-
opment and preparation.
However, if the perceived demands in a situation
begin to exceed the perceived resources, it is fairly easy
to appreciate how the physical or psychological effects of
stress might interfere with performance and contribute
to escalating stress and injury-proneness. An adaptation
of Nideffer’s model (see Figure 22-3) demonstrates how
stress can physically or psychologically interfere with
effective functioning.106
Injury-proneness can be related to fitness, genetics,
technique, tactics, equipment, or psychological factors
such as stress, confidence, and focus. Even subconscious
needs, doubts, or fears about readiness to perform can
produce the physical and psychological effects outlined
in Figure 22-3 that can make an athlete injury-prone.
Individuals sometimes progress through their careers
virtually injury-free and carefree in their approach to
sport or work and suddenly face a frustrating and com-
plicated “injury year” in which they have one injury after
another. The initial injury sometimes triggers a com-
plex emotional and psychological reaction that involves
a heightened sensitivity to injury risk and personal fal-
libility. Individuals then often begin to overanalyze the
demands they face and any potential limitations in the
resources they bring to competition. In the process, they
Figure 22-3
Physical and psychological effects of stress on performance. (From
Botterill C, Flint FA, Ievleva L: Psychology of the injured athlete.
In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries
and rehabilitation, p 802, Philadelphia, 1996, WB Saunders. Adapted
from Nideffer R: Prevention and treatment of injury. In Nideffer R,
editor: The ethics and practice of applied sport psychology, Ithaca, NY,
1991, Mouvement Publications.)
474 SECTION II • Principles of Practice
lose the clear-minded, confident focus that helps optimize
performance and minimize injury risk.
Every effort must be made to ensure that patients are
not injury-prone when they return to action. Complete
injury rehabilitation involves psychological as well as phys-
ical, technical, tactical, and equipment considerations.
Systematic progressive simulations and performance
drills can play a critical role in the individual regaining
confidence and focus. Evidence of improved strength,
flexibility, speed, coordination, or stamina can be a pow-
erful force in changing one’s self-perception from that of
a recovering performer to that of recovered performer.
Coaches and clinicians should take advantage of every
opportunity to build confidence and provide feedback.
The patient’s personal work on the relaxation, imagery,
focusing, self-talk, and rehearsal skills described earlier
in the chapter facilitates psychological as well as physi-
cal rehabilitation. The confidence and control that come
from progressively applying these mental skills can play a
large role in preventing or overcoming injury-proneness.
Reinforcement, positive rational thinking, and a sense of
humor from those around the individual can also help to
desensitize fears, doubts, and overanalysis and encourage
an optimistic, task-relevant focus and mindset.
If there are concerns a patient may still be injury-prone,
simple biofeedback measures during real or imagined
simulations can detect complicating psychophysiological
responses. Further progressive training, desensitization,
and resensitization to an optimistic task-relevant focus
may be necessary. If it is suspected that subconscious
fears, doubts, needs, or feeling of guilt might be contrib-
uting to injury-proneness, every effort should be made to
enlist the help of someone trained in clinical psychology,
psychiatry, or hypnosis.
This same model can then be valuable in assessing if
the patient is ready to return to work or other activities
following injury. It is important that the individual feel
technically, tactically, physically, and mentally ready to
take on the demands of activity.
Fitness is an important element in injury prevention.
Stamina, flexibility, and strength all increase confidence,
reduce injuries, and increase capabilities. It is also important
to remember that fitness is a state, as well as a set of capaci-
ties, and that rest, diet, and hydration are equally important
in optimizing potential and minimizing injury-proneness.
Mental and emotional fitness also involve a “state”
as well as a set of “capacities”—mental and emotional
processing capacities—that can be masked by a “state”
of physical, mental, or emotional overload, fatigue, or
stress. Recovery can be every bit as important as prepa-
ration.107 A clear healthy “perspective” and state can be
the key to optimal performance and return to form. For
additional ideas on how to help people with perspective,
see Botterill and Patrick.48 Highly related is Life Lessons
by Kübler-Ross and Kessler.108
Mental skills, together with a rational perspective, can
help individuals “park,” or set aside, excessive demands
and pressures created by others. Recovering individuals
are wise to deliberately reduce demands and expectations
that have been irrationally escalated and exaggerated by
others. This is especially important when an individual is
returning after injury and is complemented by a primary
focus on one’s game plan and personal and situational
excellence and execution.
Malingering and Secondary Gains
For most highly motivated, take-charge patients, malin-
gering is never a problem. More often, ambitious indi-
viduals need to be held back a bit to avoid pushing
themselves too much too soon and complicating the
rehabilitation process. As the pressures and demands of
today’s world have increased, secondary gains from being
injured may subtly and subconsciously become factors in
a patient’s response.
Heil has identified increased attention from significant
others, sympathy and social support, release from day-to-
day responsibilities, escape from stressful situations, and
medication use as potential secondary gains for injured
individuals.31
Rotella and associates have identified a list of poten-
tial reasons for malingering (Table 22-6).96 For the most
part, the key to preventing malingering in sport would
seem to be maintaining enthusiasm for the primary
payoffs and the potential of effective rehabilitation and
return to action. Many of these reasons can be applied
to everyday patients. A crisp, enthusiastic, professional
environment around the clinic as well as rehabilitation
and practices can help ensure that primary motives and
proactive behavior maintain precedence over any com-
peting secondary or subconscious motives. Establishing
and reviewing long-term, short-term, and situational
goals can help prevent malingering tendencies.
Good rehabilitation environments involve a healthy
mix of empathy, support, and challenge to maximize
the patient’s rehabilitation potential. Behavioral expec-
tations for optimizing rehabilitation are made clear, and
every effort is made to maintain a high level of trust,
respect, and optimism. Tough love and professionalism
are sometimes necessary to help people through diffi-
cult phases in their lives. A mix of empathy, support,
belief, and challenge can often help people go past feel-
ing sorry for themselves and continue with effective
responses.
Honesty and openness about possible psychosomatic
influences that could complicate rehabilitation and return
to form may be necessary. At the same time, respect for
patients’ abilities to know their bodies must be main-
tained together with a trust that those involved really
want to do what is right.
 CHAPTER 22 • Psychology of the Injured Patient 475

Table 22-6
Reasons for Malingering in Sport
Using an insignificant injury to rationalize loss of starting status, reduction in playing time, and poor competitive performance
Using an injury-related disability to prevent loss of athletic scholarship
Using injury to account for apparent decrease or change in motivation for participation
Using injury to offset the personal realization of insufficient ability (talent) to compete successfully
Using injury to attract needed or desired attention from others that has not been forthcoming elsewhere
Using injury to demonstrate personal courage by “playing hurt”
Using injury to offset expectations of coaches, teammates, and parents
Using injury as a reason to desist from performing, thereby not contributing skill, talent, and ability to the team’s effort and
thus expressing hostility or anger toward coaches, teammates, or parents
Using injury to avoid the rigors of practice but still be able to compete since the coach may need the athlete’s services on game
day (athlete does not wish to “waste” his or her body)
Using minor injury to avoid play in order to save the body for intercollegiate or professional competition, in which the material
rewards are greater than those at the present level
Using injury as a way of disengaging from a dimension of life that has proved to be undesirable but also unavoidable (all males in
the family traditionally play football)

From Botterill C, Flint FA, Ievleva L: Psychology of the injured athlete. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic injuries and
rehabilitation, p 803, Philadelphia, 1996, WB Saunders. Adapted from Rotella R, Ogilvie B, Perrin D: The malingering athlete: psychological
consideration. In Pargman D, editor: Psychological bases of sport injuries. Morgantown, WV, 1993, Fitness Information Technology.

Rebuilding Confidence The mind-body relationship is a highly interactive and

The components of confidence identified by Gill provide an
excellent framework for efforts to rebuild it: (1) past experi-
ences, (2) vicarious experiences, (3) verbal persuasion, and
(4) emotional state.99 To rebuild confidence, patients can
review past successful experiences to counteract temporary
doubts and can work hard practicing activities they do con-
fidently. They can also empathize with or vicariously experi-
ence great performances by others and see and feel greatness
as they mentally rehearse and use creative imagery. Being
positive and supportive of others often leads to reciprocal
support and confidence, and every effort should be made
for performers in need of confidence to hang around ener-
gizing, confident believers.109,110 Self-talk can also be made
more positive, convincing, and persuasive if it has slipped.
Finally, becoming emotional, energized, or aroused often
leads to increased feelings of confidence and capability (fight
or flight?). Most emotions other than sadness produce
energy; thus, if one becomes passionate and engages in ener-
gizing activities or thoughts, confidence can be increased
and intensity channeled into a positive primary focus.
In summary, confidence is most related to quality
preparation. A quick review of past highlights and future
prospects is best followed by a total focus on the here
and now—the current game plan. A final phase in quality
preparation is to rehearse maintaining focus in some of
the key contrasting conditions that may occur in action.
Summary
The psychological dynamics involved in preventing
injuries and helping patients work through injury reha-
bilitation are often complex and extremely significant.
two-way connection that influences every element of
readiness for challenges and responsiveness to situations.
Injury or a physical threat to health and capability has a
profound effect on emotions and thoughts, and there is
now little doubt that thoughts and feelings can have a
profound influence on ability to perform or recover.
Factors That May Affecting Healing Time
● Treating the patient “like a performer” and mobilizing psychologi-
cal and environmental factors can make a big difference.
Informed health care professionals can be invaluable
in sensitizing patients, teammates, parents, and admin-
istrators to this powerful psychophysiology and its many
practical implications. The empathy of a parent, the
interest (and challenge) of a teammate, the caring of an
administrator, together with the skills of health care pro-
fessionals can make huge differences in the lives affected.
Psychology is not magic, but it can be a powerful part of
holistic, multidisciplinary rehabilitation.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 110 references for this chapter.

I NTEGRATION OF S TRESSES AND T HEIR
R EL ATIONSHIP TO THE K INE TIC C HAIN
Sérgio Teixeira da Fonseca, Juliana de Melo Ocarino, Paula Lanna Pereira da Silva,
and Cecília Ferreira de Aquino
Introduction
In the course of everyday activities, the human body is
constantly subjected to reaction forces as well as inertial
forces arising from the moving body segments. During
running, for example, the lumbar spine is exposed to
ground reaction forces up to 5.7 times body weight,1
while in walking, these loads are reduced to half.2 These
external forces are balanced by internal forces produced
or conserved by muscles, ligaments, tendons, fascia, and
joint structures. However, excessive external and internal
forces flowing through the body segments (kinetic chain)
(Table 23-1) must be dissipated to produce coordinated
behavior or to protect biological tissues from injury.3
Forces applied to the human tissues divided by the tis-
sues’ cross-sectional area are defined as stresses. When
stresses reaching a particular tissue or structure exceed a
critical limit, injury may occur. Consequently, dissipative
mechanisms of the kinetic chain are crucial in maintain-
ing the integrity of tissues and structures of the human
body.
The performance of any activity requires a certain capa-
bility from the musculoskeletal system to deal with the
resulting stresses caused by the flow of forces through the
kinetic chain. This intrinsic capability to generate, to trans-
fer, and to dissipate forces defines the individual’s resources.4
The relationship between the amount of stress applied on
the musculoskeletal system (i.e., demand) and the individ-
ual’s resources (i.e., capability) determines whether or not
pathology results. Therefore, an understanding of how to
optimize the individual’s capabilities or to minimize the
demand on the body tissues and structures should be the
cornerstone of musculoskeletal rehabilitation.
476
23
1
C H A PC TH EA RP T E R
Demand and Capability
The classical approach to the investigation for risk factors
of pathological processes has been the identification of
intrinsic and extrinsic factors associated with the frequency
of the occurrence of injuries.5,6 Although this approach
has offered a substantial understanding about the sources
of musculoskeletal injuries, it presents some limitations.
The multifactorial nature of these injuries prevents the
establishment of unequivocal causal relationships between
risk factors and pathology.5,7 For example, overuse injuries
are thought to be related to several possible factors such
as weakness, a decrease in flexibility, muscle imbalances,
fatigue, age, and training errors.7,8 Frequently, individu-
als within a certain group with similar physical attributes
and workloads have different outcomes in terms of injury
occurrence.5 Differences among individuals concern-
ing how limb alignment affects joint biomechanics and
arthrokinematics, muscle and connective tissue stiffness,
dynamic muscle stabilization capabilities, and movement
patterns may explain why some individuals are more sus-
ceptible to injuries than others. Thus, the understanding
of individual capabilities and the specific stress demands
applied to the body structures may prove to be a more
fruitful approach in the prevention and treatment of mus-
culoskeletal injuries. In the next sections of this chapter,
the concept of stress demand and the factors related to
individuals’ capabilities are discussed in more detail.
Stress Demand
Stress demand is defined as the amount of stress applied
to the musculoskeletal system during a given activity.
 CHAPTER 23 • Integration of Stresses and Their Relationship to the Kinetic Chain 477

Table 23-1 Energy Flow

Definition of Kinetic/Kinematic Chains Energy flow refers to the concept that forces acting at
any point on the body contribute to the observed forces
Parameter Definition
on all segments of that body, because joints transmit
Kinetic chain Mechanically coupled segments forces from one segment to the other.10 Energy transfer
in which the forces arising in among body segments and estimates of mechanical work
one segment are transferred to during different activities are important topics in biome-
other segments chanics.11,12 Energy is the ability to perform work that is
Kinematic chain Mechanically coupled segments possessed by a body by virtue of its position or motion.
in which the motion of one During any everyday activity, ground reaction forces,
segment may result in motion
joint intersegmental forces, impact forces, muscle forces,
of other segments
Open chain Coupled segments in which the
or inertial forces of moving body segments generate
motion of one segment is motions or cause changes in the position of these same
independent of the motion of segments (Table 23-3).10 Thus, in any activity, energy
other segments from one body region may apply stress to another region
Closed chain Coupled segments in which the that, because of its resulting change in position or state
motions of the segments are of motion, will change its energetic state. This continu-
interdependent ous change in the energy state of the body segments in
response to an initial event generates an energy flow.10,13
For example, Neptune et al. identified the contribution
of the action of the soleus muscle to the acceleration and
power of the leg and trunk segments.13 They found that
In biomechanics, stresses applied to a biological tis- during the midstance phase of gait, this muscle not only
sue cause a deformation (or strain) that may be either decelerates the leg to which it attaches but also deceler-
reversible (elastic deformation) or irreversible, leading to ates the thigh and accelerates the trunk even though it
a permanent change of length (plastic deformation) does not have any direct attachments to these segments
(Table 23-2).9 Although the application of continuously (Figure 23-1). In other words, the soleus action causes
increasing forces has been used to investigate the mate- an energy flow from the leg through the kinetic chain to
rial properties of biological tissues, it rarely represents the trunk during the midstance phase of gait. Although
real-life situations. In functional activities, forces from a the understanding of energy flow is crucial in biomechan-
continuous source are not normally applied to the mus- ics, the focus of the investigations has been on the indi-
culoskeletal system. Instead, a fixed amount of energy, vidual’s performance.12 However, the flow of excessive
which is represented as the area below the stress/strain energy through body segments (kinetic chain) is among
curve (see Figure 3-5), is transferred to the body and the main factors responsible for injury production.
flows through the kinetic chain.9 In this view, the amount
of energy reaching a given structure, not the stress itself,
is the main cause of injury. To understand the role of
stress demand in injury production, this chapter exam- Table 23-3
ines the concept of energy flow through the kinetic chain
Types of Forces and Definitions
and the factors that may lead to increased amounts of
energy/stress applied to the musculoskeletal system. Type of Force Definition

Ground reaction force Reactive force arising from the

ground in response to all the
forces applied to it
Table 23-2
Joint intersegmental Reactive forces that are
Stress and Strain Definitions forces transferred forces from one
Parameter Definition segment to another through the
joints
Stress Internal resistance of a body to the Impact forces Externally applied forces acting
application of an external force, as on the body segments
given by the magnitude of the force Muscle forces Forces generated internally by
divided by the area of application (N/m) the action of the muscles
Strain Deformation of a physical body under Inertial forces Forces generated by the masses
the action of applied forces, given as a and motions of the body
percentage of its initial length segments
478 SECTION II • Principles of Practice
a trunk
SOL
Vtrunk
hip 125 N
F SOL
grf
F SOL
30% Cycle
Mid Stance
Figure 23-1
Redistribution of segmental energy by SOL muscle in midstance while
at a nearly constant length. Unfilled arrows: Contribution to the hip
intersegmental force FSOLhip and the ground reaction force FSOLgrf.
The calibration bar applies to these forces. Contribution to the ankle
and knee intersegmental forces is similar to the ground reaction force
contribution (not shown). Filled arrows: Contribution to the linear
accelerations of the segments (only trunk labeled, aSOLtrunk). Magnitudes
are unscaled. Dashed arrows: Linear velocity of segments (only trunk
labeled, vtrunk). Magnitudes are unscaled. Notice that the motion of
segments is mostly forward. Because aSOLtrunk has a component collinear
with vtrunk, SOL acts to accelerate the trunk forward to cause energy
flow to the trunk (“+”). SOL-induced acceleration of thigh and shank
have a backward component to decelerate these segments (“−”; energy
flow <0). The net effect of SOL on the foot is small (“0”). Thus,
while acting nearly isometrically, SOL redistributed energy from the
leg to the trunk in midstance. (From Zajac FE, Neptune RR, Kautz
SA: Biomechanics and muscle coordination of human walking. Part I:
introduction to concepts, power transfer, dynamics and simulations,
Gait Posture 6:215-232, 2002.)
When an individual is performing a simple activity
such as walking, the ground reaction forces in every step
produce a flow of energy through the kinetic chain. At
foot contact, the laterally applied (Figure 23-2) ground
reaction force causes the foot to move into pronation.14
This pronation, because of the resulting adduction of the
talus in relation to the calcaneus, must be accompanied
by internal rotation of the tibia when the knee joint flexes
or by internal rotation of the lower extremity when knee
flexion is not sufficient to accommodate the rotational
demand produced by the foot (Figure 23-3).15 In the
Ground reaction
force
Eversion
torque
Posterior view
Figure 23-2
Torques generated by ground reaction forces at heel contact.
The lateral location of the ground reaction force on the calcaneus
produces subtalar joint eversion and, therefore, foot pronation.
(Redrawn from Adams JM, Perry J: Gait analysis: clinical application.
In Rose J, Gamble JG, editors: Human walking, ed 2, Philadelphia,
1994, Williams & Wilkins.)
presence of knee flexion, the energy produced by ground
reaction forces is dissipated or conserved (transferred) by
eccentric contraction of the quadriceps muscles, mini-
mizing the flow of energy through the kinetic chain.16 As
a result, lower levels of repetitive stress reach more proxi-
mal joints, such as the pelvis and lumbar spine, which
decrease their risk of injury. However, when this energy is
not dissipated, the resulting lower extremity internal rota-
tion produces joint reaction forces (joint intersegmental
forces) that compel the other joints in the kinetic chain
to move in response to the applied reaction force. This
process may cause compensatory or excessive motions
of particular joints of the kinetic chain. For example,
as the hip internally rotates, the pelvis may be brought
into anteversion and forward rotation, leading to lumbar
extension, rotation, and lateral flexion (see Figure 23-3).
The muscles and connective tissues of these joints will
gradually dissipate the flowing energy through the body
until no energy originating at initial contact is left to pro-
duce motions in the kinetic chain. Although these forces
are frequently of small magnitudes, they lead to increased
stresses on the tissues in the areas of compensatory or
excessive motions. Depending on the level of forces in
these areas, this may lead to macro or microtraumas.
Force Dissipation
● The musculoskeletal system is organized to take advantage of
reactive forces to protect biological tissues from injury
 CHAPTER 23 • Integration of Stresses and Their Relationship to the Kinetic Chain
E of forces through the various joints and tissues demon-
F way that minimizes the effect of the reactive forces in
D Factors Affecting Stress Demands and Shock
C ●
B G
F
E
A malities commonly seen in clinical settings may increase
Anterior view Posterior view
Figure 23-3
Effects of subtalar joint pronation on the kinetic chain. Excessive
subtalar joint pronation (A) causes the lower extremity to internally
rotate (B) and drop inferiorly (C). This, in turn, increases tensile
strain on the iliopsoas and piriformis muscles (D) and leads to a
narrowing of the greater sciatic notch (thereby predisposing the
entrapment of the sciatic nerve). Also, as the lower extremity drops
inferiorly, the ipsilateral innominate is lowered (E) and, as is consistent
with Fryette’s law, the body of L5 rotates toward the functionally
shortened leg (F). As a result, the lumbar spine attempts to straighten
itself by laterally flexing toward the long leg (G, on inset), which
compresses the lateral aspects of the discs on that side and forces
the facets on the concave side into a hyperextended or close-packed
position (stars). Over a period of years, these actions may lead to a
variety of overuse injuries. (Redrawn from Michaud TC: Foot orthoses
and other forms of conservative foot care, Baltimore, 1993, Williams &
Wilkins, 1993)
The stress demand produced during locomotion has
been well documented.17 The shock imparted to the body
during foot contact in walking and running is thought to
be related to the occurrence of degenerative and inflam-
matory musculoskeletal problems. The energy generated
at foot contact is dissipated (shock attenuation) by the
deformation of biological tissues in the body and the
eccentric action of the muscles. However, the amount of
shock attenuation is highly dependent on factors such as
the velocity of loading,18 stride length,19 or kinematics of
the movement pattern (e.g., initial knee flexion angle).20
479
Despite the influence of these factors, it has been shown
that the energy reaching the head during walking and
running is always kept at a low level.3,21 The dissipation
strates that the musculoskeletal system is organized in a
order to produce coordinated behaviors and to protect
biological tissues from injury.
Attenuation
● Structural abnormalities
Level of activity
● Movement speed
● Kinematic pattern
● Use of equipment (footwear)
● Contact surface (ground reaction force)
Structural Abnormalities
Although the musculoskeletal system presents efficient
mechanisms for energy dissipation, structural abnor-
the stress demands on the tissues and structures of the
kinetic chain. These structural abnormalities are normally
related to alterations of the lower extremity alignment
and include (but are not limited to) rearfoot and fore-
foot varus/valgus, tibia varus, tibial torsion, and femoral
anteversion/retroversion. The degree of these problems
varies from individual to individual and may be related to
several pathological processes, depending on the type of
activity performed.
A typical example of increased stress demand in
response to a structural abnormality would be a rearfoot
or forefoot varus deformity causing compensatory move-
ments or timing disruption between the motions of the
lower extremity joints during walking or running.22–24 As
mentioned previously, at foot contact, the laterally located
ground reaction force causes the subtalar and midtarsal
joints to pronate until the calcaneus and forefoot are
in total contact with the ground (see Figure 23-2). In
the presence of a varus deformity, the amount time or
excursion of calcaneal eversion or subtalar and midtarsal
joint pronation necessary to bring the foot to the ground
increases.14,15,24 The resulting excessive pronation during
walking leads to a timing disruption of the lower limb
joints (e.g., internal rotation of the talus/tibia simulta-
neously with paradoxical knee extension) that requires
compensatory motions of the knee, hip, pelvis, or spine.15
These compensatory motions generate an increased flow
of energy through the kinetic chain that will have to be
dissipated by muscle action or by the inert tissues around
joints. The repetitive actions over these structures may
480 SECTION II • Principles of Practice
lead to the establishment of pathological conditions of
the kinetic chain. This behavior can be exemplified by a
commonly found piriformis muscle tenderness caused by
the excessive action of this muscle in an attempt to con-
trol lower extremity internal rotation resulting from the
excessive subtalar joint pronation.15
Although ground reaction forces must be considered
as an important cause of increased stress demands on bio-
logical tissues, the interaction of structural abnormalities
with inertial forces generated by the moving body seg-
ments also plays a role in injury production. For example,
late pronation (subtalar and midtarsal joint pronation
during the impulsive phase of walking) causes a deviation
of the body’s line of progression toward the opposite
side during walking.15 The laterally directed body inertial
force, in combination with a contralateral rearfoot varus,
causes the foot to supinate during ground contact. The
resulting supination prevents an effective shock absorp-
tion action by the quadriceps muscles (diminished knee
flexion), allowing an increased amount of energy to reach
the laterally located structures of the lower extremity and
the joints of the hip, pelvis, or spine.15,24 To maintain bal-
ance and prevent further supination, increased action of
the ankle everters, the tensor fascia lata, and the gluteus
medius on the same side is necessary. The continuing
action of these muscles, in order to dissipate the exces-
sive energy and to stabilize frontal plane movements of
the lower extremity, may lead to overuse injuries of later-
ally located structures. This process is often related to
pathological processes such as trochanteric bursitis and
iliotibial-band friction syndrome.25 A list of potential
musculoskeletal disorders produced by excessive prona-
tion is presented in Table 23-4.
The interaction of ground reaction and inertial forces
with structural abnormalities frequently leads to an
increased stress demand on the structures of the kinetic
Table 23-4
Potential Musculoskeletal Disorders That Can Be Produced
by Excessive Pronation of the Subtalar Joint
Ipsilateral Limb Contralateral Limb
Plantar fasciitis Tendinopathies (e.g., peroneal
Calcaneal spur muscles)
Tendinopathies Patellofemoral pain
(e.g., tibialis posterior) Iliotibial band friction syndrome
Compartmental syndrome Trochanteric bursitis
Metatarsalgia
Sesamoiditis
Shin splints
Patellofemoral pain
Sacroilitis
Piriformis syndrome
chain. Although structural adaptations of the biologi-
cal tissues, such as muscle hypertrophy, collagen align-
ment, and increases in bone density, may result from this
increased demand, they may not be sufficient to prevent
the occurrence of injuries.26,27 Therefore, continuing
stresses produced by activities involving walking and run-
ning should be considered as important causes of muscu-
loskeletal problems.
Activity-Related Demands
Activities of daily living (ADL), sport, and occupational
activities involve a number of different movement pat-
terns that can impose excessive stresses on the muscu-
loskeletal system. The amount of stress reaching the
biological tissues during these activities is related to such
factors as the type of ADL activity (e.g., overhead activi-
ties, bending), level of competition (e.g., professional,
recreational), type of sport (contact or non-contact),
type of occupation (e.g., typing, load carrying), move-
ment speed, activity duration, environmental conditions,
and equipment use. Therefore, the demands are spe-
cific to the activity performed and should be analyzed
in a case-by-case basis. However, some factors, such as
locomotion speed, movement kinematic pattern, equip-
ment use, and playing surfaces, are known to increase the
amount of stresses getting to the musculoskeletal system,
regardless of the activity performed.
Movement speed is closely related to the stress
demands applied to the kinetic chain. In running, for
example, researchers have demonstrated that the amount
of shock attenuation increases linearly with running
speed.18 Although the greater demand caused by an
increase in locomotion speed affects the whole kinetic
chain, investigators have shown that increases in speed
are mainly followed by changes in stiffness at the knee
joint.28 Thus, the need for shock attenuation in running
imposes an increased demand over the lower extrem-
ity joints.18 Most of the changes in energy absorption
during dynamic activities, including running at differ-
ent speeds, are followed by changes in movement kine-
matic patterns. Researchers have demonstrated that the
amount of energy absorption in running,18 in landing
from a jump,29 or during downward stepping30 is highly
influenced by the kinematic pattern adopted during the
activity. Therefore, movement speed and kinematic
pattern are important factors related to increased stress
demands over the musculoskeletal system.
The stress demands arising from sport and occupational
activities may be modified by the use of equipment or by
the surface over which the activity takes place. Playing
surfaces and type of shoes or orthotics used have been
demonstrated to significantly affect the amount of stress
reaching the musculoskeletal system. Ferris et al. found
that runners adjust their leg stiffness to accommodate
changes in surface stiffness.31 This leg stiffness adjustment
 CHAPTER 23 • Integration of Stresses and Their Relationship to the Kinetic Chain
alters the stresses reaching the tissues of the kinetic chain
but allows an individual to maintain his or her typical
running mechanics on different surfaces (Figure 23-4).
Softer cushioning, for example, produced reductions in
leg stiffness and severity of the impact experienced by
the lower limb during controlled impacts.20 On the other
hand, harder or irregular surfaces are reported to increase
the stress demand on the kinetic chain.32 It seems that
the adjustment of subjects to different surfaces depends
not only on the stiffness of the surface but also on the
intensity of the movement performed.33 In addition,
the mechanism of adaptation varies among individuals,
probably because of differences in lower extremity align-
ment and the individual’s capabilities. This emphasizes
the necessity for clinicians to provide individualized anal-
yses of the stress demands placed on the musculoskeletal
system for each patient.34
It has been assumed that well-designed shoes can assist
in reducing the number of lower limb injuries resulting
from physical activities.35 However, the effect of sport
shoes in reducing the stresses on the lower extremity
seems to be subject specific and dependent on several
factors, including the interactions between sport shoes
and playing surfaces.36 For example, changes in the
heel material characteristics (elastic and viscoelastic) of
Soft surface Hard surface
same
kleg
A the dynamic resources available to deal with stresses.4
Hard surface Soft surface
same
kleg
B
Figure 23-4
Schematic representation of the computer simulation results. Each of
the illustrations shows the spring-mass model at three times during
stance: at initial touchdown, at the middle of the ground contact
period, and at the end of ground contact. A, When leg stiffness was
not adjusted for the hard surface, the path of the center of mass was
asymmetrical. The center of mass was at a higher height at the end of
ground contact. B, When leg stiffness was not adjusted for the soft
surface, the path of the center of mass during ground contact was
also symmetrical. However, the center of mass was at a lower height
at the end of ground contact. (From Ferris DP, Liang K, Farley CT:
Runners adjust leg stiffness for their first step on a new running
surface, J Biomech 32(8):787–794, 1999.)
481
running shoes have been associated with subject-specific
changes in oxygen consumption and in the intensities of
muscle activation before heel strike in the lower extremi-
ties.37 A similar subject-specific effect has been reported
for the use of foot orthotics.38 These studies indicate that
the effect of shoes and foot orthotics in reducing the
demand on the kinetic chain depends on factors such as
playing surface, lower extremity alignment, and the indi-
vidual capabilities.
Individual Capability
During the execution of functional activities, such as
walking or running, the musculoskeletal system has to
deal with reactive and inertial forces to produce coordi-
nated movement of body segments.39 In other words, the
musculoskeletal system has to be able not only to gener-
ate energy to move body segments40 but also to deal with
the effect of nonmuscular forces to produce the desired
movement and minimize stresses to biological tissues to
prevent them from being injured.
The interaction between inertial and reactive forces
produces transfers of energy, which, in some instances,
decrease the amount of muscle work necessary to pro-
duce the desired movement.39 On the other hand, these
nonmuscular forces might have a destabilizing effect on
the joints and body segments.39 When that is the case,
these forces must be balanced to maintain joint stability
and at the same time generate the desired movement
patterns. Thus, to produce coordinated behavior and
protect biological tissues from injury, the musculoskel-
etal system must have the capability to generate, trans-
fer, and dissipate energy.40,41 This capability constitutes
Therefore, an understanding of how the structures of
the musculoskeletal system, such as the muscles and
passive tissues (ligaments, capsules, and fascia), are
organized to fulfill these requirements would guide
rehabilitation efforts directed at improving the dynamic
capacity (strength, endurance, muscle length, and stiff-
ness) in order to prevent and treat injuries. This section
discusses factors related to the generation, dissipa-
tion, and transfer of energy and indicates interventions
that could be designed to modify the capability of the
musculoskeletal system.
Factors Related to Generation, Transfer,
and Dissipation of Energy
The ability of biological tissues to deal with the different
forces involved in the execution of functional activities,
through generation, dissipation, and transfer of energy,
depends on factors such as tissue stiffness and muscle
function. Although these factors are related to each
other, they will be described separately.
482 SECTION II • Principles of Practice
Factors Affecting Generation, Transference,
and Dissipation of Energy
● Tissue stiffness
● Muscle function/activation
Tissue Stiffness. Tissue stiffness is a mechanical
property related to the resistance offered by a tissue to its
deformation.42 This property is graphically represented by
the slope of the stress-strain curve—the greater the stiff-
ness, the steeper the slope of the curve (see Figure 3-5). The
area under this curve corresponds to the amount of energy
the tissue can absorb, which is influenced by its stiffness.
The greater this area, the greater is the potential of the
tissue to absorb energy before it tears.41 Consequently,
its susceptibility to injury is less.43 A tissue with very low
stiffness undergoes greater deformation before rupture
but withstands a very low load (Figure 23-5). Thus, it
absorbs small amounts of energy and is more prone to
injury. On the other hand, an excessively stiff tissue also
has a limited ability to absorb and dissipate energy since
it undergoes very little deformation (see Figure 23-5).
Even though an excessively stiff tissue withstands higher
forces, its low potential to absorb energy may increase
the demand on other tissues to dissipate energy, which
can increase their risk of injury. For example, Williams et
al. have shown that high-arch runners exhibited greater
leg stiffness and presented higher incidence of bony inju-
ries compared to low-arch runners.44 Thus, ideally, the
tissues should allow sufficient deformation to guarantee
normal joint mobility but have sufficient stiffness to resist
this deformation, which results in an adequate energy
absorption capability.41
Adequate levels of tissue and joint stiffness are necessary
to guarantee efficient energy transfer among segments of
the kinetic chain. This transference of energy is impor-
tant to generate appropriate movement patterns with
B Nut
C rotates
A nut
Figure 23-5
Load deformation behavior of tissues of different stiffness.
A, A low-stiffness and low-energy absorbing tissue. B, A high-stiffness
and low-energy absorbing tissue. C, A moderate stiffness and high-
energy absorbing tissue.
minimal energy expenditure while maintaining joint and
tissue stresses to a minimum. For example, an adequate
level of hip joint stiffness allows the energy generated by
pelvic rotation during locomotion to be transferred to
the lower extremity to facilitate the external rotation
of the femur and tibia and, consequently, the supination
of the subtalar joint. Since, in a kinetic chain, segments of
lower stiffness move earlier over segments of higher stiff-
ness, if the hip joint stiffness is smaller than the foot stiff-
ness, the movement of the pelvis during the stance phase
of gait causes the hip to internally rotate while maintaining
the subtalar joint in a pronated position. The relationship
between pelvic motion and subtalar joint motion can be
illustrated by a “double-threaded bolt and nuts” system
(Figure 23-6). The upper nut represents the hip joint
and the lower nut represents the subtalar joint. When
the upper nut is twisted, its stiffness increases. As soon as
the stiffness of the upper nut becomes greater than the
stiffness of the lower nut, the energy is transferred down,
causing movement in the lower nut. If the upper nut has a
low stiffness when twisted, it will dissipate most of energy
before it can be transferred to the lower one. The same
happens with the hip and subtalar joint during walking.
If the hip has a lower stiffness, a greater part of energy
generated by the pelvic movement is dissipated in the
internal rotation movement of the hip joint, decreasing
the transference of energy that is necessary to facilitate
the supination of the subtalar joint. In this case, excessive
late subtalar pronation may result, which may predispose
the individual to many dysfunctions such as metatarsal-
gia and plantar fasciitis. Therefore, adequate joint and
muscle stiffness are closely related to the capability of an
individual to deal with the stress demands of functional
activities.
Twist
Upper Stiffer Less
nut stiff
Bolt
rotates
Lower Less Stiffer
stiff
A B C
Figure 23-6
A, Double-threaded nuts and bolt system. The upper nut is twisted.
If the upper nut is stiffer than the lower nut, the bolt rotates and the
lower nut is tightened. B, If the upper nut is less stiff than the lower
nut, the upper nut is tightened (C).
 CHAPTER 23 • Integration of Stresses and Their Relationship to the Kinetic Chain
Muscle and joint stiffness are mechanical properties
that can be regulated through modifications in the inten-
sity of muscle activation. Dynamic stiffness regulation
has been reported frequently during the performance
of different functional activities, allowing individu-
als to adapt to the forces imposed on the joints during
the performance of these activities.45–47 Johansson et al.
proposed a mechanism for regulating muscle and joint
stiffness via the gamma-muscle-spindle system.48 These
authors suggested that the mechanoreceptors influence
the muscle activation level through continuous adjust-
ments of the responsiveness of the muscle spindle sys-
tem. Increases in muscle activation result in increments
in muscle stiffness and, consequently, influence joint
stiffness. Thus, this mechanism contributes to continu-
ously modifying muscle and joint stiffness according to
the functional demands required to absorb and trans-
fer energy, improving the ability of the musculoskeletal
system to deal with the energy flow through the kinetic
chain.
Muscle Function. Muscle function, in this chapter, is
defined as the ability of the muscles to generate and dis-
sipate energy through its activation. The pattern of acti-
vation is able to dynamically modify the generation and
dissipation of energy. Temporal and spatial summations
(increases in activation frequency and in the number of
fibers recruited, respectively) are physiological properties
available to increase muscular force.49 These properties
contribute to the adaptation of individuals to the varying
demands imposed on the joints during the performance
of functional activities. In addition, the arrangement of
muscle fibers within a muscle affects force production.50
For example, pennated muscles (e.g., gastrocnemius) are
adapted to generate high levels of force, while longitudinal
muscles (e.g., hamstrings) are more specialized for large
muscle excursions and higher velocity.49 Even though
muscle’s structural and physiological properties contribute
to the production of force, the interaction of the muscles
with the joints they cross can affect the manner in which
this force is utilized.51 If an internal or external force (mus-
cle force or gravity, respectively) accelerates a joint in the
direction of flexion, the contraction of an extensor muscle
dissipates the energy generated by this force. On the other
hand, if the joint is stationary, the same level of contrac-
tion generates energy to move the joint. The amount of
torque that the muscle produces to dissipate or to gener-
ate energy is proportional to the length of its moment arm
and its level of activation.49 Thus, factors such as muscle
architecture, the synchronization in the pattern of activa-
tion of the motor units, and the muscle joint interaction
directly influence muscle function.49
The concentric action of muscles is an efficient mecha-
nism of the musculoskeletal system to generate the force
(energy) necessary to perform functional activities. The
force or energy generated by a muscle directly accelerates
483
the segments to which it attaches and the joints it crosses.
However, because of the joint reaction forces produced
by the muscle action on body segments or passive tissues,
a specific muscle can also instantaneously modify the lin-
ear and angular acceleration of segments and joints far
from its attachments.13 For example, when a skilled ath-
lete throws a ball, the whole body is clearly involved in
the movement. The throwing motion involves a sequen-
tial, coordinated movement of body segments, which
results in an energy flow from the legs, to the hips, trunk,
upper arm, forearm, hand, and, finally, to the ball.52
Thus, in throwing, the legs, pelvis, and trunk, which are
the attachment sites for the larger muscles of the body,
generate a great portion of the mechanical energy neces-
sary to accelerate the ball, which is then transferred to the
smaller distal segments. In the absence of this transfer-
ence, there would be a greater demand on the joints of
the upper limbs, increasing their susceptibility to injury.
Insufficient force production in one body segment to
meet the demands of a functional activity may result in
increased stresses in the tissues of other body regions.
Therefore, not only the capability of the muscles to gen-
erate mechanical energy through concentric contraction
but also their capability to transfer the net mechanical
energy among the body segments should be considered
in the rehabilitation process.
The energy absorption capability of muscle tissue
is associated, among other factors, with its activation
level.42,53,54 When stress is applied to a muscle, the amount
of energy it absorbs is proportional to its activation level.
According to Garrett et al.,55 the area under the stress-
strain curve of an activated muscle is twice as great as the
area of a relaxed muscle (Figure 23-7). Among the types
of muscle contraction, only eccentric contractions allow
Figure 23-7
Energy absorption by passive and stimulated muscle (From Garrett
WE Jr., Safran MR, Seaber AV et al: Biomechanical comparison of
stimulated and nonstimulated skeletal muscle pulled to failure, Am J
Sports Med 15(5):452, 1987.)
484 SECTION II • Principles of Practice
a muscle to absorb energy (for example, during shock
absorption) and dissipate it as heat.26,40
This energy dissipation is possibly due to cross-bridge
breakdown secondary to chemical reactions that pro-
mote heat production.56 Biomechanical simulations have
shown that the eccentric action of lower limb muscles
dissipates 79% of the impact energy on the hip during
a fall.57 In addition, Neptune et al. have shown that in
the early stance phase of gait, during which the energy
generated by the heel strike has to be dissipated, the vasti
group of the quadriceps actively lengthens, reducing the
amount of energy possessed by the leg.13 These studies
support the role of eccentric contraction in the dissipa-
tion of forces imposed on the musculoskeletal system
during functional activities. The inability of the muscles
to generate adequate levels of eccentric force can result
in movement patterns that produce inefficient energy
dissipation. For example, during running and landing
from a jump, a decrease in knee flexion can be the result
of quadriceps weakness.58 In the presence of a more
extended knee, the impact is applied during a short time,
less force is dissipated at this joint, and more energy is
transmitted throughout the kinetic chain. Consequently,
greater dissipative demands are imposed to other tissues
and joints, increasing their susceptibility to injury. For
example, Lephart et al. have shown that women pres-
ent lower amplitudes of knee flexion during landing
from a jump.58 They have associated this factor with
the observed relative weakness of the female quadriceps
muscles normalized to body weight when compared to
males. The authors have argued that without sufficient
quadriceps strength to decelerate the body, the female
subjects evaluated tended to land in a more extended
knee position rather than absorbing the impact with con-
trolled knee flexion. In addition, the women evaluated in
this study showed greater amplitudes of hip internal rota-
tion. According to Lephart et al.,58 this increased internal
rotation of the hip, combined with a more extended knee
position, was probably associated with the greater vul-
nerability of women to anterior cruciate ligament (ACL)
injury. Therefore, inefficient dissipation of energy caused
by decreased muscle strength may result in altered kine-
matics, which seems to be related to greater incidence
of injury.58 The muscles’ capability to generate, transfer,
and dissipate mechanical energy is influenced not only by
tissue stiffness but also by other factors, such as length-
tension relationship and endurance level. These factors
are presented in the following sections.
Length-tension relationship. Modifications in mus-
cle length alter the length-tension relationship of the
muscle. In other words, the muscle changes the opti-
mal length at which it is capable of producing maximal
tension and, as a result, modifies its ability to generate
energy at certain points in the range of motion.59 When a
force is applied to a muscle at its optimal length, a greater
number of cross bridges can be formed and broken when
the muscle is actively elongated, which results in greater
energy dissipation. This can be contrasted with a muscle
that has adapted to either a shortened or lengthened
position over time. These adaptations alter the length-
tension relationship because of an addition or deletion of
the number of sarcomeres in series in any single muscle
fibril.59 Therefore, structural modifications of muscle
length leading to displacement of the length-tension
curve can decrease the muscles’ capability to generate
or dissipate energy if they have to act at an unfavorable
portion of the curve. For example, the rhomboids act
eccentrically, decelerating scapular movement during the
acceleration phase of throwing.52 In the beginning of the
acceleration phase, the scapula is adducted and the rhom-
boids are in inner range. In the presence of an increase
in length of these muscles, because of increased thoracic
kyphosis or exaggerated shoulder protraction,60 there
would be an excessive superposition of myofilaments in
the muscles, resulting in their active insufficiency. As a
consequence, the rhomboids would not be able to effi-
ciently absorb energy during the acceleration phase of
throwing, resulting in excessive scapular protraction and
loss of scapular control, which could lead to conditions
such as rotator cuff tendinopathy and anterior stress on
the glenohumeral joint.52
Endurance level. The ability of the muscles to gener-
ate, to transfer, or to dissipate energy through eccentric
contractions is influenced by their endurance level.
A muscle presenting premature fatigue may not be
able to generate adequate levels of force (concentric or
eccentric) throughout a specific activity to respond to its
demands. This fatigue may decrease the efficiency of dis-
sipative mechanisms,61,62 which could lead to greater risks
of injuries and in increased demands to tendinous struc-
tures, contributing to degenerative and inflammatory
processes.63 In addition, inefficiency in this dissipative
mechanism can result in an undesired transfer of forces to
other joints in the kinetic chain, causing excessive or com-
pensatory movements (abnormal movement patterns).61
Demand/Capability Relationship
To guarantee proper functioning of the musculoskeletal
system, the individual capabilities to dissipate, gener-
ate, and transfer energy must be sufficient to deal with
the stress demands applied to the body structures during
the performance of functional activities. Alterations in this
capability/demand relationship may result in the devel-
opment of musculoskeletal dysfunctions or pathologies.
Therefore, it is possible to treat pathological processes
or prevent their occurrence with therapeutic interven-
tions directed at the minimization of the stress demands
applied to the kinetic chain or to the optimization of the
capability of the musculoskeletal system to respond to
 CHAPTER 23 • Integration of Stresses and Their Relationship to the Kinetic Chain
these demands. Specific interventions that can be used to
increase the kinetic chain’s capability and to work on the
demand/capability relationship are discussed in the next
section.
Increasing Kinetic Chain Capability
The capability of the muscles to generate energy can be
enhanced through resistance training emphasizing their
concentric action. The inability of specific muscles to
generate force may lead to altered movement patterns
and to increased demands in other muscles and structures
of the musculoskeletal system, facilitating the develop-
ment of pathological conditions.60 For example, bicipital
tendinopathy is a pathological process that may be associ-
ated with weakness of the serratus anterior.60 This weak-
ness may decrease the amount of superior rotation of the
scapula during elevation of the arm. Since the reduced
scapular rotation may not guarantee an ideal length-
tension relationship for the anterior deltoid to generate
force, an increased demand is imposed on the biceps bra-
chialis. In this case, the bicipital tendinopathy would be
the result of this increased demand on the biceps muscle,
secondary to the weakness of the serratus anterior mus-
cle. Therefore, the identification of weaknesses in specific
muscles and modification in their capability to generate
energy through concentric training should be part of the
rehabilitation program to prevent and treat musculoskel-
etal conditions.
Resistance training that emphasizes the eccentric action
of the muscles can enhance the individual’s ability to
absorb and dissipate energy during movement and, conse-
quently, to control the amount of reactive forces flowing
through the kinetic chain.63 For example, the eccentric
action of the quadriceps muscle dissipates reactive forces
at the knee during a number of different activities, such as
walking,13 running,63 or landing from a jump.64 If the abil-
ity of this muscle to dissipate energy is altered, excessive
forces will flow to other joints, such as the hip, sacroiliac
joints, and spine, and to the quadriceps and patellar ten-
dons. Eccentric training of the quadriceps would increase
the ability of this muscle to dissipate energy at the knee
joint, decreasing the demand at other parts of the kinetic
chain during the execution of activities. Therefore, eccen-
tric training should be part of prevention and treatment
of musculoskeletal injuries, since it not only increases the
capability of the muscles to dissipate energy but also min-
imizes the stresses to the joints and connective tissues,
decreasing their dissipative demand.26
In addition to enhancing the ability of muscles to gen-
erate and dissipate energy, resistance training, resulting
in hypertrophy of the muscles, induces increases in their
stiffness, allowing a greater amount of energy absorption
and transfer by muscles.65,66 This type of training, through
increases in tissue stiffness, improves the muscle’s ability
485
to withstand the stresses imposed on the kinetic chain
during the performance of functional activities, decreas-
ing the risk of injury. Furthermore, greater amounts
of energy absorbed by muscles can be transferred to a
subsequent concentric contraction to optimize it. This
property of the muscle-tendon unit to absorb and return
energy to the system is strongly time dependent and can
be improved through plyometric training. Lindstedt et
al. have demonstrated that, within 6 weeks, this type of
training increased self-selected hopping frequency and
jump height.40 The authors have associated these gains
with an enhancement in elastic energy storage and recov-
ery when performing single or repeated jumping tasks.40
Thus, plyometric training is a way to improve energy
conservation, decreasing the force generation demand of
the contractile tissue.
Muscle training performed in specific points in the
range of motion can change the optimal length at which
the muscle is capable of generating maximal tension,
through structural modifications in muscle length.53,59
For example, strength training performed in the outer
range (Table 23-5) can result in a structural increase in
muscle length because of the addition of sarcomeres in
series, leading to a shift of the length-tension curve to
the right.67 Similarly, muscle training done in the inner
range may result in a displacement of the length-tension
curve to the left.68 Therefore, this type of training can
contribute to the treatment of pathologies influenced by
adaptive muscle lengthening or shortening.
Endurance training programs can also help to improve
the muscles’ ability to deal with forces (energy) involved
in the performance of functional activities. Muscles that
demonstrate resistance to fatigue can maintain adequate
stiffness41 and are able to produce higher forces through-
out an activity. The greater incidence of injuries at the
end of the season or toward the end of the game has been
suggested to be related to muscular fatigue in athletes
who had not been submitted to specific training regimens
to increase muscular endurance.63 Therefore, improve-
ment in muscle strength and endurance are effective ways
to optimize energy dissipation, generation, and transfer.
Table 23-5
Definitions of Working Ranges of Motion Relative
to Muscle Training
Working Ranges Definitions
Inner range Part of the range in which the
muscles work in the shortened
position
Outer range Part of the range in which the
muscles work in the lengthened
position
486 SECTION II • Principles of Practice
Working on the Demand/Capability Relationship:
Functional Training
Interventions directed at improving the kinetic chain’s
capability should be done in association with specific
functional training. Functional training can be designed
to give an individual the means to explore and use his or
her “changing” musculoskeletal properties in the context
of the demands imposed by the activity performed. This
type of training should involve the whole kinetic chain
and can lead to the development of efficient movement
patterns to guarantee adequate energy transfer during the
performance of functional activities. Additionally, move-
ment patterns can be improved to optimize the dissipa-
tion of ground reaction forces during running or landing
from a jump. For example, Hewett et al. designed a
jump training program emphasizing the correct landing
techniques to reduce the magnitude of external forces
applied to the joints.69 They instructed the athletes to
bend their knees and keep them from moving into valgus
or varus during landing. This type of functional training
produced modifications in the kinematics of jumping and
reduced the peak forces involved in this activity,69 result-
ing in a significant reduction of knee ligament injuries.70
Therefore, functional training seems to be a way to safely
and progressively impose functional stresses to the kinetic
chain in order to train the individual to use his capabili-
ties at the correct timing to respond to these stresses.
The amount of load imposed, the movement speed, and
the number of repetitions should be controlled to guar-
antee that the individual could perform using correct
and efficient movement patterns with no signs of fatigue.
This training promotes a balance between demand and
capability, minimizing stresses to biological tissues and
preventing them from being injured.
Therapeutic interventions previously discussed have
the objective of modifying the capability of the musculo-
skeletal system to dissipate, generate, and transfer energy.
These dynamic resources are essential to the performance
of functional activities. Since the whole body is involved
in these activities, a dysfunction in one segment or joint
may result in increased demands on other parts of the
kinetic chain. If these demands overcome an individual’s
capability to deal with them, injury or impaired function
may result. Therefore, rehabilitation programs should
always involve the whole kinetic chain and should be
directed to enhancing the individual’s dynamic resources
and decreasing the stress demands on the musculoskel-
etal system whenever possible.
References
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been incorporated into a CD-ROM that is provided with this text. The
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sible. There are a total of 70 references for this chapter.

A RTHROKINEMATICS AND M OBILIZATION
OF M USCULOSKELETAL T ISSUE :
T HE P RINCIPLES
Lorrie L. Maffey
Introduction
Observation of structure fosters an understanding of
movement and therefore function. This understanding
allows for a deeper exploration of dysfunction, which
enables the clinician to problem solve and often use
creative solutions. A very simple demonstration of this
type of observation and reasoning process is the child
who views and explores all aspects of a newfound toy:
twisting it, turning it, touching it, and by doing so
discovers its structure and function. A clinician uses
information drawn from a patient’s microanatomical and
macroanatomical structure regularly in assessment and
treatment to assist patients to improve their function.
This chapter is devoted to an exploration of the macro-
structure of the human body articular tissue or joints.
One of the biggest challenges in any exploration
is to obtain a detailed map. In this case the map is the
relevant terminology. Speaking the same language and
understanding and using the same nomenclature create
the map that then allows the clinician to use the rest of
this chapter’s contents, the principles of biomechanical
examination, to further explore the structure and func-
tion of the articular tissue.
Biomechanics
In assessment of a patient, the clinician uses the principles
of biomechanics to determine whether the joint complex
under examination is functioning normally. A thorough
24
C H A P T E R
understanding of the terminology and definitions of bio-
mechanical principles aids clinicians in their assessment
in addition to enhancement of future communication
regarding the patient’s diagnosis.
Planes of Motion
To apply the principles of kinesiology to joint mobility
assessment, a standard definition of movement of the body
in space is necessary. In a general sense movement can be
described under one of four headings or principles:
1. Rotation
2. Translation
3. Curvilinear (a combination of rotatory and
translatory motion)
4. The planes of motion1
All movements of the body can be described generally
as rotations or translations. Rotation describes motion
in which a rigid body moves in a circular path about a
pivot point and causes all points on the body to move
in the same direction simultaneously.2 Translation
describes movement in which all parts of a rigid body
move in the same direction and parallel to every other
part in the body.2 (See the sections Osteokinematics and
Arthrokinematics in this chapter.)
The planes of motion is a system of describing
motion borrowed from the universal three-dimensional
x-y-z coordinate system used in mathematics (Figure
24-1). Each of the three unique planes of motion has
an associated unique axis of movement that always is
487
488 SECTION II • Principles of Practice
Posterior half
Vertical or
longitudinal axis
Anterior half
Sagittal
axis
Transvers
e or Horizo
ntal plane
lan
e Frontal or Cor
ttal p
S agi
Figure 24-1
The planes of motion with their unique axis of movement that is
always found perpendicular to its associated plane superimposed on a
body in the anatomical position.
found perpendicular to its associated plane. The x coor-
dinate corresponds to the transverse or horizontal plane
that divides the body into an upper (cranial) and lower
(caudal) half. Rotational movement in this plane occurs
around a vertical or longitudinal axis (the latter term is
used when the axis passes through the shaft of a long
bone). The y coordinate corresponds to the frontal or
coronal plane that divides the body into front (anterior)
and back (posterior) halves. Rotational movement in this
plane occurs around a sagittal axis. The z coordinate cor-
responds to the sagittal plane that divides the body into
right and left halves. Rotational movement in this plane
occurs around a coronal axis.
The anatomical position is the body upright, fac-
ing forwards, with the palms of the hands also facing
forward. Although the true anatomical position of the
body has the ankle in dorsiflexion, the naming of move-
ment at the midfoot and forefoot is easiest understood
if the foot and ankle are visualized in a plantar flexed
position.
Although much nomenclature already has been
discussed, it is still inadequate to describe fully the
movement of the body and its associated joint complexes.
A terminology independent of the body’s anatomical
position and therefore independent of the viewer’s per-
Coronal axis
spective is required. These rotational or angular move-
ment terms are outlined in Table 24-1. The individual
descriptions of angular motion and the associated nor-
Cranial half
mal range of motion (ROM) will be reviewed in detail
in Chapter 25. Rotational osteokinematic motion also
can be called physiological active motion (motion that
one can produce actively under volitional control) or
physiological passive motion (PPM) (motion that if it
was done actively could be done under volitional control).
Arthokinematic motion also can be assessed as passive
accessory motion (PAM). PAM is a non-physiological
motion that a person cannot produce actively on his or
Caudal half her own and is therefore not under volitional control.
(See the sections Osteokinematics, Arthrokinematics,
and Biomechanical Assessment.)
Biomechanics is the study of mechanics of the
human body and consists of kinematics and kinetics.3
Kinematics is the study of movement without regard
to the forces that produce movement, and kinetics is the
study of these forces (Table 24-2).3 Kinematic variables
include the type and location of motion that is occur-
ring in addition to the magnitude and direction of the
onal plane
movement. Kinematics includes osteokinematics and
arthrokinematics.4
Clinicians use the principles of kinematics whenever
they analyze and treat a patient’s muscles and joints. The
purpose of the following section is to provide the reader
with the biomechanical nomenclature in relationship to
the bones and joints. An understanding of this nomen-
clature is important to apply these principles in the bio-
mechanical or mobilization assessment and treatment of
the human articular system.
In a normal functioning joint, osteokinematics and
arthrokinematics work together. One cannot occur with-
out the other following. If the joint is not free to move,
then the distal end of the associated bone cannot move.
Conversely, if the distal end of the bone cannot move in
a “normal” fashion, then the associated articular joint
surfaces are unable to move in their normal, prescribed
manner. The proportion of osteokinematics and arthro-
kinematics at each joint varies among the joints in the
human body. Understanding the principles outlined
below, in addition to the normal range of active and pas-
sive motion available at each joint, helps the reader to
interpret the results of the biomechanical examination
(e.g., joint mobility testing).
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles 489

Table 24-1
Axes and Planes of Movement 3-5
Usual Associated Physiological Usual Associated
Axis of Movement Plane of Movement Rotational (Angular) Motion Translation

Transverse Sagittal Flexion: approximation of ventral surfaces Anterior or posterior

also termed Coronal Median Extension: opposite direction to flexion
also termed Frontal Divides left/right In the wrist: volar flexion and dorsal flexion
(runs medial/lateral) In the ankle: dorsal flexion and plantar
flexion
Exception examples:
First carpometacarpal flexion and extension
Knee joint flexion and extension
Sagittal Frontal Abduction: distal lever moving away from Medial or lateral
also termed Coronal the body Lateral: right or left
Anteroposterior (runs Divides anterior/posterior Adduction: opposite direction to abduction when used for trunk
anterior/posterior) Divides ventral/dorsal Lateral flexion: term used for trunk and head and head
Divides palmar (volar)/dorsal In the wrist: radial flexion and ulnar flexion
Divides dorsal/plantar Exception example:
First carpometacarpal abduction and
adduction
Vertical Transverse Medial or internal rotation: rotation towards Vertical: compression
also termed Horizontal midline or distraction
Longitudinal Divides cranial/caudal Lateral or external rotation: opposite
(runs cranial/caudal) Divides superior/inferior direction to medial rotation
Left or right rotation: term used for trunk
and head
In the forearm: pronation and supination
In the foot: pronation (inversion) and
supination (eversion)

articular movements are discussed. This mechanical axis

Osteokinematics
is a schematic rod through the bone or line of reference
Osteokinetics is the study of the forces tending to for osteokinematic motion that replaces the bone and is
produce movement of a bone.6 In the human body, perpendicular to the joint surface. Often the bone shaft
bony shape has a great deal of variation. In addition and the mechanical axis are not in the same plane (e.g.,
to this variation, little symmetrical relationship exists to the humerus [Figure 24-2]).
bone shape and its corresponding bony end or articular Joint mobilization (see the section on Biomechanical
shape. Assessment) is performed most effectively if one thinks of
To make a kinematic discussion applicable across these always moving the proximal end of the mechanical axis
variations, the mechanical axis represents the bone when perpendicular to the joint surface, thereby following the
joint’s curvature. At the distal end of the mechanical axis
there is the outline, drawn in space, of the appropriate
Table 24-2 pathway of motion of the mechanical axis.
Osteokinematics is the study of bone movement in
Biomechanical Terminology and Definitions
space independent of any associated bony partner or
Kinematics without any reference to the forces that produce this
Latin Prefix (Movements) Kinetics (Forces) movement.7 All osteokinematic movement refers to the
physiological movements of the body (movements that
osteo-, bone Osteokinematics Osteokinetics
arthro-, joint Arthrokinematics Arthrokinetics
can be made under volitional control), with the move-
myo-, muscle Myokinematics Myokinetics ment occurring in the anatomical planes of motion (see
Table 24-1). Hip flexion and abduction are examples of
Modified from Williams P: Gray’s anatomy, ed 38, Edinburgh, 1995, osteokinematic movement. Movement of a joint com-
Churchill Livingstone. plex can be considered from two perspectives. Hip flex-
490 SECTION II • Principles of Practice

Mechanical axis
through distal end
of humeral head

Mechanical axis
through proximal end
of humeral head

Figure 24-3
The convex ball (solid line) osteokinematically spins, represented by
the top curved arrow, around the the instantaneous axis of rotation
(IAR), represented by the straight arrow. The joint arthrokinematically
spins, represented by the bottom curved arrow at the articular
surface. No osteokinematic or arthrokinematic translation occurs as
represented by the star.

Pathway of
motion
Figure 24-2
The proximal end of the mechanical axis of the humerus moves
perpendicularly to the articular surface of the glenoid fossa and
thereby follows the joint’s curvature. At the distal end of the
mechanical axis is the outline of the appropriate pathway of motion.
like a top spinning. All motion occurs around one point
so that no translation ensues. This is a rare movement in
the human body because often a spin is accompanied by a
swing. An example of an osteokinematic spin in a human
is at the proximal radius with mid range of motion prona-
tion and supination.
All movement other than a pure (cardinal) spin is
called a swing.7 Familiarity with the terms chord and arc
is a prerequisite to understand swings. The shortest dis-
tance between two points drawn on a joint surface forms
a curved line or a chord, and any longer distance repre-
sented by a line drawn on the joint surface between these
two points is termed an arc (Figure 24-4).4

A
ion can occur secondary to the femur moving anterior in
the sagittal plane on a fixed pelvis (innominate), or hip
flexion can occur secondary to the pelvis moving anterior arc chord Head of
in the sagittal plane on a fixed femur. Commonly in the humerus
upper quadrant peripheral joint movement involves the
distal bone rotating on a relatively fixed proximal bone B
and the reverse occurs in the spinal joints. In the lower
quadrant peripheral joints, movement often can occur in
either order.
Osteokinematic terms include rotation in the form
of osteokinematic spins and osteokinematic swings.7 Spins
and swings define bone movement around the mechani-
cal axis.7 Movement is described typically in one of three
planes of motion and around one of three axes of move-
ment or as an angular motion (see Table 24-1). Figure 24-4
The shortest distance between two points drawn on a joint surface
A spin is a nonlinear motion or pure rotation motion
forms a curved line or a chord, and any longer distance as represented
that occurs around the mechanical axis of a bone (called by a line drawn on the joint surface between these two points is
osteokinematic spin) (Figure 24-3).7 Always one mobile termed an arc. (Modified from Williams P: Gray’s anatomy, ed 38,
component and one stationary component exist, much Edinburgh, 1995, Churchill Livingstone.)
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
An osteokinematic chordal swing7 (also referred to
as a cardinal swing) is a pure swing, meaning the distal
end of the mechanical axis draws a chord in space; move-
ment occurs in only one plane and with no associated
spin. This type of motion is rare in the human body and
when it does occur, it is in joints that have active voli-
tional movement in at least two planes of motion; for
example, in the hip joint a chordal swing in the fron-
tal plane is femoral abduction. At any joint complex in
which two chordal swings are at an angle between 0
and 180 degrees with one another and are performed
in series or successive movements, the resulting osteo-
kinematic motion contains an associated involuntary spin
(a conjunct rotation). This type of chordal swings per-
formed in a series is termed a diadochal movement.4 A
closed diadochal movement (or ergonomic cycle) is a series
of chordal swings that move the bone from its original
position and then back again, but it does not necessarily
return to its original posture.4 An example of this in the
human body is the Codman’s Paradox5 of the shoulder,
in which movement of the arm from the side into shoul-
der flexion and neutral rotation is followed by adduction
that returns the arm back to the side of the body. When
the arm has returned to the side of the body, it is now
in external rotation. This type of conjunct rotation that
occurs as a result of a succession of movements is also
called consequential movement. Open diadochal movement
is that diadochal movement that does not return the
bone to its original position4 (e.g., performing only the
first two of the above movements).
An osteokinematic arcuate swing7 is an impure swing,
which means that the motion of the bone in space is
described by a line that is an arc. An arcuate swing has
a component of spin (conjunct rotation), which allows
movement of the mechanical axis in at least two planes
(e.g., with flexion, the first metacarpophalangeal joint
rotates medially).
In this purest definition, all movements, excluding trans-
lations, are rotations. To be more precise in description,
further clarification is required. Conjunct rotation7 is the
movement that occurs during all arcuate swings or any dia-
dochal movements. It is involuntary and is a result of the
shape of the joint surfaces in addition to the structure and
tension of the ligaments and joint capsules during move-
ment toward the close packed position. An example of this
in the human body is the external rotation of the talus that
occurs with talocrural joint dorsiflexion. All movements of
sellar joints and the majority of ovoid joints include con-
junct rotations.
Adjunct rotation7 also can accompany any arcu-
ate swing, but this type of rotation occurs under voli-
tional control created by active muscle recruitment when
movement is occurring around an independent axis of
motion. Adjunct rotation is considered a separate degree
of freedom. This type of rotation can occur only in joints
491
that can move volitionally around two or more planes of
motion, or in other words, have two or more degrees of
freedom. An example of this is the movement of flexion
and external rotation of the hip in which the rotation is
created by the piriformis and other muscles of the hip.
Flexion of the hip and external rotation of the hip can
be done separately under volitional control or combine
again under volitional control. Adjunct rotation that is
additive to the conjunct rotation (in the same direction as
the bony joint surfaces intended movement to occur) is
termed cospin7 (e.g., the peroneii muscles assisting in the
internal rotation of the cuboid in plantar flexion at toe
off in gait). Many functional movements of the human
body require some form of adjunct rotation.
An additional term often used in discussion of bio-
mechanical movement of human joints when referring
to combinations of movement is coupled movement.7
Coupled movement is any movement that consistently
occurs with another movement and is not a result of voli-
tion. For example, midcervical spine right side flexion
always is combined with right rotation.
Another important type of rotation that must occur
for normal function of a chain of bones and joints is
congruent rotation.7 With this type of rotation, a bone
or chain of bones and its associated structures rotate
in the same direction as any adjacent bones and struc-
tures. This movement is under the control of the cen-
tral nervous system. The rotation of each bone, albeit
in the same direction, does not have to be at the same
rate or amplitude. An example of this can be seen dur-
ing the swing phase of gait moving toward heel strike.
All the bones are in different amounts of external rota-
tion from the calcaneus to the hip. It is usually easier to
perform congruent rotation than to move each bony
lever and associated joint complex individually. The
opposite of congruent rotation would then be incon-
gruent rotation.7 This form of rotation involves rota-
tion of the bone and its associated structures that is not
in the same direction as other adjacent bones. This is
important because clinicians often use this principle to
create a “moveable lever” during passive mobilizations.
The clinician creates tension in a series of spinal bones
and joints, which makes a moveable lever to focus the
mobilizing force to one motion segment. For example,
the left cervical spine motion segment of C6-C7 can be
mobilized into extension, left side flexion, and left rota-
tion, whereas the adjacent bones, from the occiput to
C6, are placed into extension, left side flexion, and right
rotation. In this example, the rotations for the segment
to be mobilized (C6-C7) are opposite to the rotation
of the lever series of bones. Incongruent rotation that
occurs in other situations such as within an individual
long bone, when taken to the extreme range of motion,
is a common position for fracturing of this long bone.
For example, the fracture of the mid shaft to lower third
492 SECTION II • Principles of Practice
of the radius can occur secondarily to the supinator
muscle pulling in one direction and the pronator qua-
dratus muscle pulling in the opposite direction.
During any complete or total range of movement
that involves an osteokinematic swing, the distal end
of the mechanical axis of the bone draws a series of
chords (chordal or cardinal swing) and arcs (arcuate
swing) that join together and form what is called the
ovoid of motion (Figure 24-5).4 This ovoid of motion
describes the curved path of the joint surface, a useful
tool because it allows the examiner of the joint com-
plex to “see” the joint surface represented in space.
Osteokinematics describes movement in more precise
terms than just a description of physiological motion
such as flexion of the shoulder. This allows clinicians
to communicate more effectively what they observe to
occur with the patient during active motion in addi-
tion to what may be induced to the patient with passive
motion secondary to the effects of external forces such
as gravity or the clinicians’ hands.
Glenohumeral early range
of motion of abduction
showing ovoid of motion
Figure 24-5
The ovoid of motion describes the curved path of the joint surface. It
is a useful tool because it allows the examiner of the joint complex to
“see” the joint surface represented in space.
Arthrokinematics
Arthrokinematics is the study of joint movement of
one bony end (articular surface) on a relatively fixed
other bony end without regard to the movement of
the bone or the forces producing that movement.7
Arthokinematics also can be viewed as the study of joint
play.5 In the periphery, movement is named after the
direction of motion of the distal bony end or joint sur-
face. In the spine, the movement is named by motion of
the superior bony end. Testing the quality and quantity
in addition to the end feel of motion of this joint play
is one of the major goals of a biomechanical examina-
tion (see details in Biomechanical Examination section
of this chapter).
No arthrokinematic movement can occur without
some osteokinematic movement occurring at the same
time, and vice versa. Examination of the arthrokinematic
movements allows the clinician to determine the joint’s
structure and therefore function by feel as opposed to
seeing the osteokinematic movement. Arthrokinetics is
the study of the forces tending to produce a movement at
a joint such as traction, distraction, and shear.8
Arthrokinematic terms include arthrokinematic
slides (or glides), arthrokinematic rolls, and arthrokine-
matic spins.7 A translation defines a motion in which
all points or particles of a bone or its bony end at a
given time have the same direction of motion relative to
a fixed point.9 In pure translation no center of rotation
as movement occurs along a plane instead of through it
(Figure 24-6).4 Movement is perpendicular to the axis
of the physiological motion and is parallel to the plane
of the joint.4 A nonhuman example of this is when a
car brakes and the tires stop rotating and skid on an icy
surface, or a cross-country ski surface gliding on a snowy
surface. In a human joint this type of translatory motion
is impossible because the joint surfaces are not flat but
concave and convex. In addition they are not 100% con-
gruent in all joint positions because one surface usually
has a smaller radius of curvature than its articular part-
ner. Thus in humans all translations are impure because
some rotation occurs with the translation and is defined
as an arthrokinematic slide (or glide).7 An arthrokine-
matic slide is a translatory motion, in which one bony
Figure 24-6
The convex ball (solid line) glides to the right; the straight black arrow
represents the instantaneous axis of rotation (IAR) of the movement;
a stationary point on the planar joint partner (star). The movement
demonstrated here is a pure translation (straight, solid arrows).
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
end (joint surface) slides or glides on its relatively fixed
articular partner, bony end.
In the human joint, a slide or glide usually is associ-
ated with an arthrokinematic roll.7 An arthrokinematic
roll 7 refers to the mid range of motion and the end range
tipping or rocking motion of the mobile convex male
articular surface on its relatively fixed female partner, or a
mobile female articular surface on its relatively fixed male
partner. If it is a male mobile surface moving on a fixed
female surface, the ensuing motion is always in the oppo-
site direction to the glide, or in other words, that the roll
and glide occur in opposite directions (Figure 24-7, A).
A nonhuman example of this is a car tire rolling on
the road surface, in which the glide is in one direction
(backward), but the tire moves in the opposite direction
(forward). An example of this in a human is the hip joint
motion of abduction and adduction. If the female is the
mobile surface on a fixated male, the ensuing motion
is always in the same direction at the glide, or in other
words that the roll and glide occur in the same direc-
tions (Figure 24-7, B). An example of this in a human
is the tibiofemoral joint motion of flexion and exten-
sion. Some instructors of joint biomechanics incorrectly
refer to a mobile female moving on a fixated male as an
arthrokinematic rock instead of using the correct term
arthrokinematic roll.
Although the translation component of movement is
not always easily seen or appreciated by the clinician who
B
Figure 24-7
A, The convex ball (solid line) rolls to the right (curved arrows). The
straight arrow represents the IAR of the movement. A stationary
point on the female joint surface is represented by the star showing
that the mobile male joint surface has glided to the left in the
opposite direction. B, The concave bone (solid line) rolls to the right,
represented by the curved arrows, with the straight arrow representing
the instantaneous axis of rotation (IAR) of the movement.
A stationary point on the male joint surface is represented by the star
and shows that the mobile female joint surface also moved to the
right, which is a point on the articular surface.
493
examines the human joint mobility, it is considered such
an important component of joint mobility that White and
Panjabi added translation in the three planes of motion
to the already well understood and previously described
three planes of angular motion. This resulted in these
authors’ description of the six degrees of freedom joint
model instead of the previously described maximum
three degrees of freedom joint model.10
To understand osteokinematic and arthrokinematic
terminology concepts relies on the knowledge that the
mechanical axis of the mobile bone during movement
is termed the instantaneous axis of motion rotation
(IAR) or instantaneous center of rotation (ICR) at
the joint surface.3 This IAR forms a series of representa-
tional points on the joint surface because the IAR is mov-
ing constantly secondary to the joint shape, which causes
a combination of glides and rolls (Figure 24-8). The
greater the size difference between the joint partners,
the greater amount of glide that occurs, which causes
a greater amount of movement of the IAR. This glide
allows for joint motion in the form of a roll and ensures
that joint contact is maintained; for example, the mobile
bony end of the joint does not roll off its associated joint
partner. It is an ingenious way to increase joint mobility
and stability.
An arthrokinematic spin refers to a situation in which
one articular surface rotates on another articular surface.
The spinning motion occurs around the mechanical axis
of the moving bone, and the IAR remains stationary. An
example of this in the human body is the head of the
Anterior or palmar view of right hand
Figure 24-8
The instantaneous axis of motion rotation (IAR) forms a series
of representational points on the joint surface because the IAR
is constantly moving secondary to the joint shape and causes
combinations of glides and rolls. Enlarged view of the second
metacarpal head with the dots representing the changing
instantaneous axis of rotation for the second metacarpophalangeal
joint during flexion, resulting in anterior glides and internal rotation
of the proximal phalange (arrows).
494 SECTION II • Principles of Practice
radius spinning on the capitulum during the mid range of
motion of pronation and supination.
Accessory glide11 refers to the arthrokinematic slides
(or glides), arthrokinematic rolls, and arthrokinematic
spins that cannot occur under voluntary control but must
occur under involuntary means. For example, this occurs
when then carpals are resting on the edge of a table and
the radius and ulna are off the edge of the table, and pres-
sure (resistance) toward the floor is made actively into
the table, which creates the involuntary palmar acces-
sory glide of the distal ulna. Another form of accessory
glide occurs when the muscles surrounding the joint
complex are relaxed and one proximal end of the bone
related to that joint is fixed by an external source, and
the other bony partner’s proximal end is moved by an
external source (a passive accessory glide): for example,
when the humeral head is glided posterior on the glenoid
fossa with the scapula stabilized. This type of glide can be
labeled and graded and is discussed in the Biomechanical
Assessment section.
Osteokinematics and arthrokinematics must occur
together in perfect precision for normal mechanics of
the joint complex to occur. If the amount of movement
or timing of combined movement is not precise, then
pathology can occur, such as with excessive superior glide
of the humeral head in shoulder abduction, which results
in impingement of the subacromial bursa (Figure 24-9).
The clinician’s role during the patient biomechanical
examination is to assess if the patient has optimal osteo-
kinematics and arthrokinematics.
N
TIO
ABDUC
ROLL
S
L
I
D
E Supraspinatus
pull
A B
Figure 24-9
Arthrokinematics at the glenohumeral joint during abduction. The glenoid fossa is concave, and the humeral head is convex. A, Roll-and-slide
arthrokinematics typical of a convex articular surface moving on a relatively stationary concave articular surface. B, Consequences of a roll
occurring without a sufficient off-setting slide. (From Neumann D: Kinesiology of the musculoskeletal system: foundations for physical rehabilitation,
p 10, St Louis, 2002, Mosby.)
Arthrology
Arthrology literally means the “study of joints.”4 For the
clinician to be able to assess and treat a patient thoroughly,
an understanding of the anatomy and biomechanics of
the joint is required. Consideration of a joint relies on
an understanding of the joint’s surrounding associated
structures (e.g., nerves, blood vessels, muscles, and liga-
ments). However, this section of the book is devoted
only to the topic of joints.
An arthroses or joint is an articulation or connection
between one bone ending and its bone ending partner.4
The bone endings come in various shapes in addition
to being covered in various forms of cartilage and may
even have interarticular inclusions between the endings.
Externally the joint may be reinforced and supported with
connective tissue, a joint capsule, ligaments, and/or ten-
dons. A joint allows for movement and stability, with the
ratio, quality, and quantity of these two components being
determined by the joint’s internal and external structure.
Joints are classified based on these structural qualities.
Joint Classification
The different types of human joint classifications are
synarthroses or nonsynovial joints and diarthroses or
synovial joints (Table 24-3). Clinicians should know the
anatomical classification of the joint they are examining
because the anatomy determines the possible under-
lying pathology. For example, getting a synovitis of a
Subacromial bursa
Supraspinatus pull
ROLL
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles 495

cartilaginous joint such as the pubic symphysis joint is ulna and radius with their intervening interosseous
impossible. membrane.

Cartilaginous Joints or Amphiarthosis Joints

Synarthroses (Nonsynovial Joints)
These joints are also stable joints and allow for mini-
Synarthroses have the bony endings connected and rein- mal or little movement as a result of the individual bone
forced with specialized solid interosseus connective tissue ends connected by either hyaline cartilage or fibrocar-
in the form of fibrous or cartilaginous material thereby tilage uniting the two bony ends to one another. This
subdivided into fibrous joints or cartilaginous joints. type of structure allows for bone growth and stability and
These joints do not have a cleft between the two bony controlled mobility. These cartilaginous joints exist in
endings. If these bony junctions become fused later in humans in one of two ways, synchondrosis and symphy-
life, the joint is then termed a synostosis. Therefore the sis joints, with their differences determined by the type of
term temporary junctions is given to some examples of cartilage between the joint’s bony ends.
synarthrosis joints by some authors. 1. A synchondrosis joint has hyaline growth cartilage
between its bony ends. Examples of this type of joint
Fibrous Joints are found in the skull and in other parts of the body
These joints are stable and allow for minimal or little (e.g., the first sternocostal joint [first rib to manu-
movement between the individual bone ends, which brium], manubriosternal joint [early in life], and the
are connected by dense fibrous connective tissue. These xiphisternal joint.
fibrous joints are present in one of three ways in humans; 2. A symphysis joint has hyaline cartilage covering the
their differences are determined by the shape of the bony ends with a fibrocartilage disc in between these
bone ends. two endings. These joints can withstand large stresses
1. A suture joint has a thin layer of fibrous connective in the form of compression, tension, shear, and tor-
tissue between the two interlocking or overlapping sion. Examples of this type of joint are found in the
bony ends. An example of this type of joint is found pubic symphysis, sacrococcygeal joint, intercoccygeal
in the skull bony sutures. joints, manubiosternal joint (later in life), and inter-
2. A gomphosis joint has a peg and socket shape. An vertebral symphysis (the joint between the vertebral
example of this type of joint is found in the tooth disc and hyaline cartilages).
(peg) and mandible or maxilla (socket) articulations.
3. A syndesmosis joint has its two bony ends or com-
Diarthroses (Synovial Joints)
ponents joined by a ligament, cord, or aponeu-
rotic membrane. An example of this type of joint is Diarthroses or synovial joints developed from the break-
found in between the shaft of the tibia and fibula or down of interzonal mesenchyme tissue to form a syno-
vial cavity or a cleft between its hyaline cartilage covered
bony ends. These bony ends are contained in a collag-
Table 24-3 enous sleeve lined with synovium. This structure allows
Overview of the Joint Classification System for free movement between the bony ends. Stability is
provided intrinsically by the joint capsule and extrinsi-
Synarthroses Diarthroses (Synovial cally by the surrounding ligaments, fascia, and ten-
(Nonsynovial Joints) Joints) don/muscle tissue. Anatomical features that may be
Fibrous joints Uniaxial joints associated with synovial joints are listed in Table 24-4.
Suture joint Ginglymus/hinge joint These anatomical features increase the joint’s anatomical
Gomphosis joint Pivot/trochoid joint complexity and allow for a subclassification of synovial
Syndesmosis Modified sellar joint joints.
Cartilaginous joints Biaxial joints
Synchondrosis joint Bicondylar
Symphysis joint Ellipsoidal/condyloid joint/
modified ovoid joint The Five Characteristics of the Synovial Joint
Saddle or unmodified
sellar joint 1. Bony ends covered by hyaline (articular) cartilage
Triaxial/multiaxial joints 2. Joint cleft or cavity between two bony ends
Spheroid/ball and socket or 3. Joint capsule formed of fibrous tissue surrounding joint margins
unmodified ovoid joint 4. Synovial membrane lining the inner surface of the joint capsule
Planar joint 5. Synovial fluid
496 SECTION II • Principles of Practice

Table 24-4
Anatomical Features That May Be Associated with Synovial Joints
Anatomical Feature Function Location Examples

Ligament Restrain excessive or abnormal
movement
Fibrocartilaginous disc or Allow for increased joint surface
menisci area, increased lubrication,
increased combinations of
movement, dissipation of joint
reaction forces, increased joint
stability
Labrum or small fibrous Deepen the articular cavity and
labra thereby increase the area of
articular congruency
Adipose tissue fat pad and Proposed to help protect the
fibroadipose meniscoids joint surfaces
Bursa Decrease the friction of
structures that overlap each
other
External to joint capsule and
directly cross the joint complex
Between the joint surfaces
Inside the joint capsule at the
articular surface margins and
between thearticular surfaces
Inside the joint capsule at the
articular surface margins and
between the articular surfaces
May or may not be in
communication with the
joint cavity
Anterior talofibular ligament
of the talocrural joint
Tibiofemoral joint menisci
Distal radioulnar joint menisci
Sternoclavicular joint disc
Acromioclavicular disc
Temporomandibular disc
Glenohumeral joint labrum
Hip joint labrum
Lumbar zygapophyseal small
fibrous labra or connective
tissue rims
Superior and inferior poles of
lumbar zygapophyseal
joints
Subdeltoid bursa
Psoas bursa
Semimembranous bursa

Joint Complexity further subdivided into uniaxial, biaxial, or triaxial

The subclassification according to the synovial joints multiaxial joints. An axis is the point at which all the
complexity further subdivided into simple, compound, or net forces on the bone are zero and therefore the bone
complex joints. moves around that point. This subclassification also is
1. Simple joints have a single pair of articular surfaces: called the degrees of freedom of the joint (e.g., for each
one male, or convex, surface and one female, or con- movement of the bone and joint, motion is limited to
cave, surface (e.g., the second metacarpophalangeal one axis at a time). One synovial joint does not fit into this
joint [Figure 24-10]). classification, the plane joint. It moves in multiple planes
2. Compound joints have more than a single pair of mat- by gliding, but its axes are not situated at right angles to
ing articulating surfaces within a single joint cap- one another (e.g., the acromioclavicular joint). Synovial
sule (e.g., the ulnohumeroradial joint or elbow joint joints, other than plane joints, categorized by degrees
[Figure 24-11]).
3. Complex joints have an intraarticular inclusion within
the joint cleft that interposed between the joint sur-
faces such as a meniscus or disc that increases the
number of joint surfaces (e.g., the tibiofemoral joint
Concave surface
[Figure 24-12]).
Second
metacarpophalangeal
Subclassification of Synovial Joints joint
Synovial joints may be subclassified in numerous ways
beyond just joint complexity. Further synovial joint sub-
classfication is according to degrees of freedom, joint
shape, or joint complexity.4,7 Often the subclassifications
are combined, which gives the reader a better under- Convex surface
standing of the synovial joint structure and thereby
function.
Degrees of Freedom. The subclassification is
Figure 24-10
done according to the number of independent axes Simple joints have a single pair of articular surfaces, one male or
the bony ends of the joint can move around angularly. convex surface and one female or concave surface. This diagram is of
These axes are perpendicular to each other and can be the second metacarpaphalangeal joint.
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles 497

Humerus Medial Humerus

epicondyle Olecranon
process

Coronoid Head of
Head of radius Figure 24-11
radius process
Compound joints have more than a single pair of mating
articulating surfaces within a single joint capsule. This
Ulna
diagram is of the right ulnohumeroradial joint (elbow
Anterior Posterior joint). The dotted line represents the joint capsule.

Femur convex shapes on the same bony end, which is termed

Femur
Medial
Femoral
menisci
condyles
Medial
menisci Lateral
menisci
Tibia Head
Anterior of
fibula
Posterior
Figure 24-12
Complex joints have an intraarticular inclusion within the joint cleft
and interposed between the joint surfaces, such as a meniscus or disc,
which increases the number of joint surfaces. This diagram is of the
tibiofemoral joint.
of freedom are termed uniaxial, biaxial, and triaxial
joints (Table 24-5).
Articular Surface or Joint Shape. Synovial joints also
can be subclassified according to their shape. Typically
a synovial joint can have seven subclassifications that
describe a continuum of joint shape from nearly flat to
nearly spheroidal (Table 24-6).4 These subclassifications
are often just a variation of one of two basic forms, sellar
or ovoid (Figure 24-13).7 Sellar and ovoid joints have
an additional subclassification of being either unmodified
(pure in shape) or modified in shape.7 On the whole the
bony end shape of the joint tends to be either convex
(male), which presents a convexity to its joint partner and
thereby glides in the opposite direction to the bone move-
ment, or concave (female), which presents a concavity to
its joint partner and thereby glides in the same direction
as the bone movement. These gliding movements are
discussed in more detail in the Arthrokinematics section
of this chapter. Some joint surfaces have concave and
concavoconvex.
1. Ginglymoid or hinge joints. These joints are shaped so
that movement is restricted to one plane much like a
hinge on a door. However, unlike this inanimate object
example, in the human these hinge joints have an
associated conjunct rotation (see the Osteokinematics
section) (Figure 24-14). These joints have strong col-
lateral ligaments (e.g., the humeroulnar joint or the
interphalangeal joints).
2. Pivot (trochoid) joints. These joints are formed when
one bony end is an osseoligamentous ring and the
other a osseous peg and thereby allows the ring to
pivot around or on the peg (e.g., the median atlan-
toaxial joint [the atlas and the transverse ligament
is the ring that rotates on the peg like dens]) or the
superior radioulnar joint (the annular ligament and
ulnar notch is the ring in which the head of the radius
rotates) (Figure 24-15).
3. Condylar or bicondylar joints. These joints have one
or two convex bony ends termed condyles or knuck-
les, which articulate with one or two concave bony
ends that are in parallel and are within the same joint
capsule (e.g., in the condylar tibiofemoral joint or in
separate capsules moving as in the bicondylar pair of
temporomandibular joints [Figure 24-16]). These
condylar and bicondylar joints have conjunct and
adjunct movement (see the Osteokinematics section).
4. Ellipsoidal joints. These joints have an oval, convex
bony end that articulates with an elliptical concavity
(e.g., the radiocarpal joint or the metacarpophalan-
geal joints [Figure 24-17]).
5. Sellar or saddle joints. These joints are concavoconvex
and are stable joints that require fewer ligaments to
control movement because the joint surfaces are con-
gruent. These joints’ bony ends each have a convex
and a concave surface that fit together on the other
bony end like a rider on a saddle. These joints allow
for a conjunct spin and no cardinal movement (see the
Osteokinematics section). Unmodified sellar joint sur-
faces are purely convex in one plane and perpendicular
498 SECTION II • Principles of Practice

Table 24-5
Types of Synovial Joints and Degrees of Freedom and Their Movements
Type of Synovial Joint Degrees of Freedom Movement Example*

Uniaxial joints
Biaxial joints
Triaxial joints
One degree of freedom
Axis usually contained
near the center of the joint
Two degrees of freedom
Three degrees of freedom
Movement in three planes
around three axes with
movement usually in an
oblique plane
Movement in one plane
around one axis
Osteokinematic arcuate swing
Movement in two planes
around two axes
Either two osteokinematic
arcuate swings or one
cardinal pin with one
arcuate or cardinal swing
Two osteokinematic
cardinal swings and one
cardinal spin
Ginglymoid or hinge joint, such as
the humeroulnar joint
Pivot (trochoid) joint, such as the
median atlantoaxial joint
Modified sellar joint, such as the
talocrural joint
Bicondylar joints, such as the
tibiofemoral joint or the
temporomandibular joint
Ellipsoidal joints or condyloid joint
or modified ovoid joint, such as the
second metacarpophalangeal joint
Unmodified sellar or saddle joint,
such as the first carpometaphalangeal
joint
Spheroid or ball and socket
joint, such as the glenohumeral joint
Planar joints, such as the
acromioclavicular joint

*
Named according to their joint shape.

Table 24-6
The Seven Subclassifications of Joint Shape
Subclassification of Joint Shape Mechanical Analogy Example

Ginglymoid or hinge joint Hinge on a door Humeroulnar joint

Interphalangeal joints
Pivot (trochoid) joint Ring on a peg or finger Median atlantoaxial joint
Superior radioulnar joint with annular
ligament
Condylar joints/bicondylar joints Convex-like “knuckle” with Tibiofemoral joint
enlargement in one direction on Temporomandibular joint
shallow concave surface
Ellipsoidal joints Flattened stone in a shallow bowl Radiocarpal joint
Metacarpophalangeal joints
Sellar or saddle joints Horse rider on the saddle
Unmodified sellar joints First carpometaphalangeal joint
Modified sellar joints Tibiotalar joint
Calcaneocuboid joint
Interphalangeal joints
Ovoid or spheroid joints Mortar and pestal
Unmodified ovoid joints Glenohumeral joint
Hip joint
Modified ovoid joints Second metacarpophalangeal joint
Radiocarpal joint
Planar joints Book on a coffee table Acromioclavicular joint
Fourth and fifth carpometacarpal joints
Intermetatarsal joints
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
B or interphalangeal joints).
A 6. Ovoid or spheroid joints. These joints have one
Figure 24-13
Joint shape subclassifications are often just a variation of one of two
basic forms sellar or ovoid shape. A, The egg-shaped ovoid surface
represents a characteristic of most synovial joints of the body (e.g., hip
joint, radiocarpal joint, knee joint, metacarpophalangeal joint). The
diagram shows only the convex member of the joint. A reciprocally
shaped concave member would complete the pair of ovoid articulating
surfaces. B, The saddle surface is the second basic type of joint
surface and has one convex surface and one concave surface. The
paired articulating surface of the other half of the joint would be
turned so that a concave surface is mated to a convex surface of the
partner. (From Neumann D: Kinesiology of the musculoskeletal system:
foundations for physical rehabilitation, p 30, St Louis, 2002, Mosby.)
Humerus
Ulna
A B
Humerus
Ulna
Annular ligament
Radius
A B
499
to this joint plane is the second joint plane, which is
purely concave, allowing for two degrees of joint free-
dom (e.g., the first carpometacarpal joint [Figure 24-
18]). Modified sellar joint surfaces have the concave
and convex portions contained within the same joint
plane on the same joint surface and thereby allow only
one degree of joint freedom (e.g., the tibiotalar joint
bony end that is convex in all planes and its bony
end partner is concave in all planes. This joint shape
is sometimes referred to as a ball-and-socket joint.
The degree of curvature varies from point to point
and is usually ovoid or egg-shape rather than purely
spherical. These joints allow for much movement and
require joint inclusions and additional ligaments and
muscles to provide joint stability. The unmodified ovoid
joint or ball-and-socket shape has a degree of curva-
ture spherical enough to allow for three degrees of
joint freedom (Figure 24-19). This joint has surfaces
equally convex or concave in all directions (e.g., the
Figure 24-14
Ginglymoid or hinge joint are shaped so that
movement is restricted to one plane much like a
hinge on a door (A) or humeroulnar joint (B). The
axis of rotation (i.e., pivot point) is represented
by the pin. (From Neumann D: Kinesiology of
the musculoskeletal system: foundations for physical
rehabilitation, p 30, St Louis, 2002, Mosby.)
Figure 24-15
Pivot (trochoid) joints are formed when one bony end is an
osseoligamentous ring and the other is an osseous peg, which allows
the ring to pivot around or on the peg. A, Ring on a finger.
B, Proximal radioulnar joint with the annular ligament. The axis of
rotation is represented by the pin. (B, from Neumann D: Kinesiology
of the musculoskeletal system: foundations for physical rehabilitation,
p 28, St Louis, 2002, Mosby.)
500 SECTION II • Principles of Practice

Femur

Collateral
ligament
Tibia

Fibula

A B
Figure 24-16
Condylar or bicondylar joints have one or two convex bony ends termed condyles or knuckles that articulate with one or two concave bony
ends that are either (A) in parallel and are within the same joint capsule such as the tibiofemoral joint, or (B) separate capsules moving as
in the bicondylar pair of temporomandibular joints. (A, from Neumann D: Kinesiology of the musculoskeletal system: foundations for physical
rehabilitation, p 30, St Louis, 2002, Mosby.)

Ulna

Radius
Lunate

Figure 24-17
Ellipsoidal joints have an oval, convex bony end that Scaphoid
articulates with an elliptical concavity. An ellipsoid
joint (A) is shown as analogous to the radiocarpal
joint (B). The two axes of rotation are shown by the
intersecting pins. (From Neumann D: Kinesiology
of the musculoskeletal system: foundations for physical
rehabilitation, p 30, St Louis, 2002, Mosby.) A B

Concave

Convex

First metacarpal
Figure 24-18
A saddle joint (A) is illustrated as analogous to the Concave
carpometacarpal joint of the thumb (B). The saddle
in A represents the trapezium bone. The “rider,” Trapezium
if present, would represent the base of the thumb’s Convex
metacarpal. The two axes of rotation are shown in B.
(From Neumann D: Kinesiology of the musculoskeletal
system: foundations for physical rehabilitation, p 30,
St Louis, 2002, Mosby.) A B
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
hip or glenohumeral joint). The modified ovoid joint
or condyloid joint shape has a degree of curvature that
is not equal is all directions or, in other words, the
curvature is more pronounced in one plane than in
the other and thereby allows only two degrees of joint
freedom and allows no cardinal spin (e.g., the second
metacarpophalangeal joint or the radiocarpal joint).
7. Planar joints. These joints have such minimal curvature
to their bony ends that these usually are ignored and
considered to be primarily flat bony ends in which one
joint or more joint surfaces slides (glides) over another
joint surface with minimal rotation or angulations (e.g.,
the acromioclavicular joint, fourth and fifth carpometa-
carpal joints, or intermetatarsal joints [Figure 24-20]).
Joint Congruency
Joint congruency is a function of the joint shape and the
surrounding joint capsule and ligament structure and
tension in different ranges of normal joint movement.
Because most joints have one partner with a smaller
radius of curvature than the other, in one position the
joint is maximally congruent, the close pack position.7
Pelvis
A B
5th
Metacarpals
Hamate
Rotation
Translation
A B
501
The close pack position or locked position of a synovial
joint is the position of maximal tautness of the major liga-
ments in addition to the capsule and/or maximal surface
congruity exists, most transarticular pressure, minimal
joint volume thereby maximal stability, which allows the
least distraction or separation of the joint’s surfaces. This
is important for the clinician who is examining a human
joint because this most stable position often is used to
test ligament stability. Compressive load across the joint
surface in close pack position applies compression of the
joint’s articular surface and forces synovial fluid nutrients
out of the articular cartilage. Movement out of this close
pack position decompresses the joint’s articular surface
and allows movement of synovial fluid nutrients back
into the articular cartilage. This loading and unloading
cycle of the articular surface, much like a sponge being
wrung out and then absorbing water again repetitively, is
important for joint lubrication and joint nutrition.
If the joint cannot achieve close pack position, ground
reaction forces and gravitational forces cannot be dis-
sipated efficiently, which results in the body trying to
reachieve efficiency through additional work of the mus-
cle system, which results in the local and distal muscles
Figure 24-19
A ball-and-socket shape articulation
(A) is drawn as analogous to the
Femur
hip joint (B). The three axes of
rotation are represented by the three
intersecting pins. (From Neumann D:
Kinesiology of the musculoskeletal
system: foundations for physical
rehabilitation, p 30, St Louis, 2002,
Mosby.)
4th
Figure 24-20
A plane “joint” is formed by
opposition of two flat surfaces (A).
The book moving on the table
top is depicted as analogous to
the combined slide and spin at the
fourth and fifth carpometacarpal
joints (B). (From Neumann D:
Kinesiology of the musculoskeletal
system: foundations for physical
rehabilitation, p 30, St Louis, 2002,
Mosby.)
502 SECTION II • Principles of Practice

becoming overused and injured. This very stable position
is also the position in which the joint’s bones are most
likely to be fractured because in this position the joint’s
soft tissue is less able to absorb additional excessive load.
This stable position of close packing is not the position in
which a clinician should mobilize or manipulate a joint nor
should it be the position for resting or splinting a joint.
Habitual movement is a term used at times to
describe movement of a joint into or away from its close
packed position.7 Habitual movements always include an
arcuate swing. When habitual movement is toward close
pack, it produces a spiral twist on the joint capsule and
ligaments and thereby brings the bony ends of the joint
closer together (e.g., the screw home mechanism of the
knee when moving towards full extension, which is the
close pack position of the knee joint). Under normal
active movement, a human joint complex moves toward
or approaches the close pack position but under volunteer
movement situations is rarely in a full close pack position.
Any position in which a joint is not closed packed can
be termed loose packed.7 This loose packed position
defines the position in which the ligaments are under less
stress and the joint surfaces are not maximally congru-
ent. Often in these loose packed positions the joint is
mobilized or manipulated, acute joints are rested, and
splinting or casting occurs. The least packed, anticlosed
packed, or resting position of the joint is the maximum
loose packed position in which the major ligaments are
maximally slack and/or minimal joint surface congruency
and maximal joint volume exist, which thereby allows for
maximal joint distraction and joint play.7 See Tables 24-7
and 24-8 for a listing of all of the close pack and loose
pack positions of the human body.
Reviewing the human joint structure and kinesiology
allows the reader to see that structure dictates the motion
available at a particular joint and thereby determines the
joint’s function. Understanding these principles allows
for the understanding of the motion created actively or
passively during the biomechanical assessment, such as
joint mobility testing.
Biomechanical Assessment
The term biomechanical assessment is misleading because
it implies only an “articular” assessment. The author
prefers the term differential diagnosis assessment because

Table 24-7
Close Pack and Loose Packed Positions Described Osteokinematically in Reference to the Upper Quadrant Joint’s
Anatomical or Physiological Range of Motion7,11,12
Upper Quadrant Joints Close Pack Position Loose Pack Position

Glenohumeral joint
Acromioclavicular joint
Sternoclavicular joint
Ulnohumeral joint
Radiohumeral joint
Superior/inferior radioulnar joint
Wrist joint
First carpometacarpal joint
Second to fifth carpometacarpal joint
Metacarpophalangeal joints
Interphalangeal joints (fingers)
Full abduction and lateral rotation
30 degrees abduction
90 degrees abduction
Full elevation
Full elevation and protraction
Extension (? with pronation)
Semiflexion and semipronation
90 degrees flexion and 5 degrees
supination
90 degrees flexion and mid pronation
Full pronation or supination
Full dorsiflexion (extension)
Midcarpal: neutral flexion/extension
to full extension (serial close packing)
Intercarpal: extension
Full opposition
Full extension
Full flexion
Full extension
Semiabduction (30 degrees abduction,
30 degrees flexion, 30 degrees medial
rotation, and 30 degrees horizontal
adduction)
30 degrees abduction, 30 degrees
flexion, 30 degrees medial rotation,
and 30 degrees horizontal adduction
Arm resting at side
70 degrees flexion and 10 degrees
supination
Extension and supination
70 degrees flexion
Midposition to slight pronation
Superior joint: 35 degrees supination
with 70 degrees elbow flexion
Inferior joint: 10 degrees supinated
Semiflexion with ulnar deviation
Midcarpal: slight flexion with
ulnar deviation
Intercarpal: neutral to slight flexion
Neutral position of thumb
Semiflexion and ulnar deviation
Semiflexion and ulnar deviation
Semiflexion
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles 503

Table 24-8
Close Pack and Loose Packed Positions Described Osteokinematically in Reference to the Lower Quadrant Joint’s
Anatomical or Physiological Range of Motion7,11,13
Lower Quadrant and Spinal Joints Close Pack Position Loose Pack Position

Hip joint Extension and medial rotation and 25 to 30 degrees flexion, 30 degrees
abduction abduction, slight lateral rotation
Knee joint Full extension and external rotation 25 to 30 degrees flexion
Superior tibiofibular joint Pain with biceps contract Unknown
Talocrural joint Dorsiflexion Neutral position, 10 degrees plantarflexion
Subtalar joint End range of motion of pronation Midposition
and supination
Talonavicular joint Full supination Slight plantarflexion
Calcaneocuboid joint No conclusive evidence Slight plantarflexion
Cuneonavicular joint Full supination Semipronation
Tarsal joints Full supination Semipronation
Metatarsophalangeal joint Full extension Neutral position, 10 degrees dorsiflexion
Interphalangeal joints (toes) Full extension Semiflexion
Intervertebral joints Extension Neutral position

assessment should include investigation of the entire neu- Biomechanical Movement

romusculovasculoskeletal system. Because the following
section discusses only the principles of articular assess-
ment, the term biomechanical assessment is used.
Often the clinician’s first professional contact with
the patient is during the initial assessment. If the initial
assessment, which would include a vascular and neuro-
logical assessment, does not clearly demonstrate a disease
based on movement-based pathology, then further
assessment is necessary. In the case of significant pain
and dysfunction, the therapist should consider refer-
ring the patient back to the physician. In some cases,
the physician may refer the patient back to the clinician
for treatment, such as in the case of a frank disc lesion or
traumatic ligamentous strain. In other cases, the patient
may be demonstrating a more movement-based pathol-
ogy, which requires further examination by the clini-
cian to develop a treatment plan (e.g., the example of
decreased mobility of the glenohumeral joint complex
that results in an inflamed supraspinatus tendon). In
both of these described situations, a much more detailed
biomechanical examination must be performed before a
treatment plan for the patient is developed and initiated.
A summary of this biomechanical examination is found
in Figure 24-21.
The Purpose of the Biomechanical Assessment
● To determine which peripheral/spinal joint is dysfunctional
● To determine the presence and type of movement dysfunction
(hypomobility, hypermobility, or instability)
● From the above, to determine an appropriate treatment
Biomechanical testing may include any or all of the fol-
lowing movements and tests:
1. Active physiological movement: Assessment of the spi-
nal or peripheral joint range (osteokinematics) by
examination of the active physiological ROM avail-
able. This active movement is created volitionally by
the patient’s own muscular system.
Biomechanical Testing
● Active physiological movement
● Position tests
● Kinetic tests
● Passive mobility tests
● Stability tests
● Specific muscle testing
2. Position tests: The symmetry of the joint partners is
assessed by palpation to indicate possible areas for
passive movement testing. These tests indicate only
the position of a bone and thereby its associated
joint in space. These tests can be done in a static
position or dynamically through range (e.g., kinetic
testing).
3. Kinetic tests: A specific joint’s active movement is
assessed (e.g., pelvic step tests) while bony land-
marks often are palpated and symmetry of motion is
evaluated. These tests are used as an indication that
passive motion testing or stress testing should be per-
formed.
504 SECTION II • Principles of Practice

Active physiological range of motion with overpressure

+/- Position testing

+/- Kinetic testing

Passive physiological range of motion

(PPM or PPIVM)

Hypomobility Normal mobility Excessive mobility

Passive
accessory Normal Stability testing
motion mobility (Non-physiological
(PAM or PAIVM) motion)

Normal: Restricted: Excessive Normal

myofascial articular mobility mobility
restriction restriction

Hypermobility or
Instability
Normal

Specific muscle testing:

- Length
Figure 24-21 -Strength
Biomechanical examination flow chart. (Modified -Recruitment
from original drawing by Jim Meadows for
the Canadian Orthopaedic Division Teaching
Manuals, Canadian Physiotherapy Association.) Special tests

Kinetic Tests Passive Physiological Movement

Specific active range of motion testing: ● Single plane
● Single plane
● Combined plane
● Combined plane
● Functional plane
● Functional plane
● Repetitive movements
● Repetitive movements
● Sustained movements
● Sustained movements
● Various speeds
● Various speeds
● With distraction
● Functional testing (dependent on the patient, body part, and signs
● With compression
and symptoms)

4. Passive mobility tests: Assessment of the joint in ques-
tion is moved passively by an external force and to
assess its quantity and quality of movement (amount
of movement, resistance through range, and the resis-
tance at end ROM—the end feel) in one of two ways,
passive physiological movement and passive accessory
movement (Tables 24-9, 24-10, and 24-11).
Passive physiological movement (PPM) is assessment
of the peripheral joint range (osteokinematics) by exami-
nation of the passive physiological ROM available. Passive
accessory movement (PAM) is assessment of the periph-
eral joint arthrokinematics (non-physiological motion)
by passive motion (e.g., glides).
Passive mobility testing can assist in the diagnosis
of articular as opposed to myofascial hypomobilities.
If the active and passive physiological osteokinematic
motion is diminished but the passive arthrokinematic
motion (PAM) is present, then the resultant hypomobil-
ity (decreased movement) is not likely an intraarticular
cause but rather an extraarticular cause. In the periph-
ery the motion is described by the more distal bony
partner of the joint complex, whether this was the rela-
tively fixated or mobile lever. In the spine, the motion
is described by the more proximal bony partner of the
joint complex, whether this was the relatively fixated or
mobile lever.
 Table 24-9
Osteokinematics, Arthrokinematics, End Feel, and Joint Classification of Upper Limb Joints3,4,14-16
Upper Quadrant Joint Joint Classification Osteokinematics Arthrokinematics* Normal End Feel

Glenohumeral joint Synovial Three degrees of freedom: Distraction: above 55 degrees flexion All capsular
Simple a) Flexion/extension: cardinal spin in sagittal plane humeral anterior glide, beyond
Unmodified ovoid between 35 degreesextension and 55 degrees flexion, 35 degrees extension humeral

CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles

beyond that arcuate swing posterior glide
b) Abduction/adduction: cardinal swing in frontal plane Abduction: initial superior translation
c) Internal/external rotation: cardinal swing in then inferior glide
transverse plane Adduction: superior glide
Internal rotation: anterior glide
External rotation: posterior glide

Note that the overall goal in normal mechanics is to keep the

humeral head centered in the glenoid fossa; any movement that
occurs tries to maintain this alignment and is dependant on the
overall load imparted to the joint by the surrounding structures 16

Acromioclavicular joint Synovial Studies are inconsistent with regard to describing the Joint surfaces are mostly planar +/− All capsular
Simple (a disc or osteokinematics and arthrokinematics of this joint an intraarticular disc. Clavicle is
menisci are not complex slightly convex, and acromion is
present) Three degrees of freedom: slightly concave.
Functions as an a) Scapular elevation/depression or flexion/extension:
unmodified ovoid, scapula inferior angle of tipping anterior and posterior
often described as around a coronal/transverse axis. Arcuate swing of
a plane joint clavicle: anterior conjunct rotation of clavicle with
elevation
b) Scapular upward/scapular downward rotation or
abduction/adduction: scapula rotation about a sagittal
axis. Arcuate swing of clavicle: posterior conjunct
rotation of clavicle with abduction
c) Scapular protraction/retraction or internal/external
rotation: scapular medial border winging about a
vertical axis. Arcuate swing of clavicle: anterior
conjunct rotation of clavicle with protraction
Sternoclavicular joint Synovial Two degrees of freedom: Elevation/depression: clavicle convex All capsular
Anatomically a) Elevation/depression: arcuate swing of clavicle: Protraction/retraction: clavicle concave
complex (disc) around a sagittal axis in the frontal plane with an
Unmodified sellar anterior conjunct rotation of clavicle with elevation
b) Protraction/Retraction: arcuate swing of clavicle:
around a vertical axis in the transverse plane with an
anterior conjunct rotation of clavicle with protraction

505
(Continued)
 506
SECTION II • Principles of Practice
Table 24-9 —Cont’d
Osteokinematics, Arthrokinematics, End Feel, and Joint Classification of Upper Limb Joints3,4,14-16
Upper Quadrant Joint Joint Classification Osteokinematics Arthrokinematics* Normal End Feel

Superior/inferior Synovial One degree of freedom: Superior joint: Supination:

radioulnar joint Compound Pronation/supination: arcuate swing Supination: anterior medial glide of radius capsular
Anatomically modified with an oblique vertical axis through Pronation: posterior lateral glide of radius Pronation:
ovoid the radial and ulnar heads Inferior joint: capsular or bony
Functionally modified Supination: posterior glide of radius
sellar Pronation: anterior glide of radius
Ulnohumeral joint Synovial One degree of freedom: Flexion: anterior glide of the ulna with slight Flexion: soft
Compound Flexion/extension: arcuate swing around lateral glide tissue approxi-
Modified sellar a coronal axis with conjunct rotation of Extension: posterior glide of the ulna mation
internal rotation and abduction with with slight medial glide Extension: bony
extension, external rotation and adduction
with flexion
Radiohumeral joint Synovial Two degrees of freedom: Flexion: anterior glide of radius
Compound a) Flexion/extension: arcuate swing around Extension: posterior glide of radius
Anatomically a coronal axis in the sagittal plane Supination/pronation: distraction and at
unmodified ovoid b) Internal/external rotation: cardinal spin end ROM supination medial radius anterior
Functionally modified around an oblique vertical axis until end glide, pronation medial radius posterior
ovoid ROM where it becomes an arcuate swing glide
Wrist joint (carpals) Synovial Two degrees of freedom: Flexion: dorsal glide of the proximal carpal All capsular but
Compound a) Flexion/extension: arcuate swing row on the triangular fibrocartilage radial deviation,
Modified ovoid about a coronal axis in the sagittal plane complex (TFCC)/radius, dorsal glide of which is bony
with conjunct ulnar deviation with hamate and capitate on the proximal carpal
flexion/conjunct radial deviation with row, palmar glide trapezoid and trapezium
extension on scaphoid
b) Ulnar/radial deviation: arcuate swing Extension: palmar glide of the proximal
about a sagittal axis in a coronal plane carpal row on the TFCC/radius, palmar
glide of hamate and capitate on the proximal
carpal row, dorsal glide trapezoid and
trapezium on scaphoid
Radial deviation: ulnar glide of the proximal
carpal row on the TFCC/radius, medial
rotation (pronation) of scaphoid on radius,
radial glide of the distal carpal row on the
proximal carpal row, lateral rotation
(supination) of trapezoid and trapezium
on scaphoid
 Ulnar deviation: radial glide of the proximal
carpal row on the TFCC/radius, lateral
rotation (supination) of scaphoid on radius,
ulnar glide of the distal carpal row on the
proximal carpal row, medial rotation
(pronation) of trapeziod and trapezium
on scaphoid

CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles

Note: rotation of carpals is named
as per the direction that the palmar
aspect of the bone is moving
Note: Carpal movement can also be
referred to as a whole as fanning or
folding
Midcarpal Synovial As above As above As above
joints Compound
Modified ovoid
triquetro-hamate:
modified sellar
Intercarpal joints Synovial As above As above As above
Compound
Planar
First carpometacarpal Synovial Two degrees of freedom: swing about axis Flexion: ulnar glide of the metacarpal on All capsular
joint Simple a) Flexion/extension: arcuate an oblique that is the trapezium except adduction,
Unmodified sellar 35 degrees from the coronal plane with Extension: radial glide of the metacarpal on which is a soft
conjunct internal/external rotation with the trapezium tissue approxi-
flexion, conjunct rotation with extension Abduction: dorsal glide of the metacarpal on mation
b) Abduction/adduction: arcuate swing about the trapezium end feel
an oblique axis that is 15 degrees from the Adduction: palmar glide of the metacarpal on
sagittal plane the trapezium
Second to fifth Synovial Two degrees of freedom: Flexion: palmar glide of MC 2 on trapezoid, All capsular
carpometacarpal Simple (3 CMC) a) Flexion/extension: arcuate swing about a palmar glide of MC 3 on capitate, dorsal except adduction,
(CMC) joints Compound coronal axis sagittal plane with metacarpo- glide of MC 4-5 on the hamate which is a soft
(2, 4, 5 CMC) phalangeal (MC) 2 conjunct internal Extension: opposite to above flexion tissue approxi-
Modified ovoid rotation and MC 4-5 conjunct external Abduction: radial glide of MC 2 on trapezoid, mation
rotation with flexion, MC 2 conjunct no glide of MC 3 on capitate, ulnar glide end feel
external rotation and MC 4-5 conjunct of MC 4-5 on the hamate
internal rotation with extension Adduction: ulnar glide of MC 2 on trapezoid,
b) Abduction/adduction: arcuate swing about no glide of MC 3 on capitate, radial glide of
a sagittal axis coronal plane with MC 2 MC 4-5 on the hamate
conjunct external rotation and MC 4-5
conjunct internal rotation with abduction,
MC 2 conjunct internal rotation and MC 4-5
conjunct external rotation with adduction

507
(Continued)

Table 24-9 —Cont’d
Osteokinematics, Arthrokinematics, End Feel, and Joint Classification of Upper Limb Joints3,4,14-16
Upper Quadrant Joint
Metacarpophalangeal
(MC) joints
Interphalangeal
joints (fingers)
*Note: Only the gliding movements are listed. The associated rolling that also would be present is not described, but the reader is reminded of MacConaill’s7 concave/convex joint surface rules
for rolling.
508
SECTION II • Principles of Practice
Joint Classification Osteokinematics Arthrokinematics* Normal End Feel
Synovial Two degrees of freedom: Flexion: palmar glide of phalanx on MC All capsular
Simple a) Flexion/extension: arcuate swing about Extension: opposite to above flexion except adduction,
Modified ovoid a coronal axis sagittal plane with 2 Abduction: radial glide of second phalanx on which is a soft
phalangeal conjunct internal rotation and MC, ulnar glide of second phalanx on MC tissue approxi-
4 to 5 phalangeal conjunct external rotation Adduction: opposite to above abduction mation
with flexion, 2 phalangeal conjunct external end feel
rotation and 4 to 5 phalangeal conjunct
internal rotation with extension
b) Abduction/adduction: arcuate swing about
adduction an sagittal axis coronal plane with 2
phalangeal conjunct external rotation
and 4 to 5 phalangeal conjunct internal
rotation with abduction, 2 phalangeal conjunct
internal rotation and 4 to 5 phalangeal
conjunct external rotation with adduction
Synovial One degree of freedom: Flexion: palmar glide of distal phalanx on All capsular
Simple Flexion/extension: digits 2, 4, to 5 arcuate proximal phalanx
Modified sellar swing about a coronal axis in the sagittal plane Extension: opposite to above flexion
(digit 2 conjunct internal rotation with flexion
and external conjunct rotation with extension),
digit 4 to 5 conjunct external rotation with
flexion and internal conjunct rotation with
extension), digit 3 chordal swing about a
coronal axis in the sagittal plane
 Table 24-10
Osteokinematics, Arthrokinematics, End Feel, and Joint Classification of Lower Limb Joints3,4,17,18
Lower Quadrant Joint
Hip joint
Tibiofemoral joint
Patellofemoral joint
Superior tibiofibular joint
Inferior tibiofibular joint
Joint Classification
Synovial
Simple
Unmodified ovoid
Synovial
Compound (tibiofemoral
and patellofemoral joint in
common joint capsule)
Complex (menisci)
Bicondylar functioning as a
modified ovoid joint
Synovial
Compound (tibiofemoral
and patellofemoral joint in
common joint capsule)
Modified sellar
Synovial
Simple
Planar
Syndesmosis
Osteokinematics
Three degrees of freedom:
a) Flexion/extension: cardinal spin
in sagittal plane
b) Abduction/adduction: cardinal
swing in frontal plane
c) Internal/external rotation: cardinal
swing in transverse plane
Two degrees of freedom:
a) Flexion with internal rotation and
adduction/extension with external
rotation and abduction: arcuate
swing primarily in the sagittal
plane (conjunct rotation and
abduction/adduction)
b) Internal/external rotation: arcuate
spins primarily in the transverse plane
Nonvolitionary motion:
Abduction (valgus)/adduction (varus)
Anterior/posterior translation
Medial/lateral translation
Compression/distraction
Superior and inferior
Medial and lateral tilting
Medial and lateral rotation
With knee from extension to flexion
primary movement is medial to
lateral as well as inferior
Lacks true physiological motion
Kneeflexion: fibular head moves
posterior
Knee extension: fibular head moves
anterior
Literature is conflicting (movement
in response to the ankle)
Arthrokinematics* Normal End Feel
Distraction Flexion: soft tissue
Abduction: inferior glide approximation
Adduction: superior glide
CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
Internal rotation: posterior glide All other ROM:
External rotation: anterior glide capsular EF
Flexion: posterior roll and glide of tibia Flexion: soft tissue
with conjunct end range of motion approximation
internal rotation All other ROM:
Extension: anterior roll and glide of the capsular EF
tibia with conjunct end range of
motion external rotation
Internal rotation: posterior glide of
medial tibia condyle, vice versa for lateral
condyle
External rotation: anterior glide of medial
tibia condyle vice versa for lateral condyle
Abduction: tibia lateral glide (unproven)
Adduction: tibia medial glide (unproven)
With flexion the patellar glide Undescribed
is predominantly inferior (note this
movement does notappear to follow
MacConaill rules of sellar joints)
Ankle dorsiflexion: fibular Undescribed
head superior and posteromedial
translation with inconsistent internal
rotation
Ankle plantarflexion: fibular head
inferior and anteriorlateral translation
with inconsistent external rotation
Minimal anterior and posterior glides
(Continued)
509

Table 24-10 —Cont’d
Osteokinematics, Arthrokinematics, End Feel, and Joint Classification of Lower Limb Joints3,4,17,18
Lower Quadrant Joint Joint Classification Osteokinematics
Talocrural joint Synovial One degree of freedom:
Compound Dorsiflexion: talar arcuate swing about
Modified sellar a transverse axis with conjunct
external rotation
Plantarflexion: talar arcuate swing
about a transverse axis with conjunct
internal rotation
Subtalar joint Synovial One degree of freedom:
Compound Open kinetic chain
Anatomically two modified Triplanar motion of pronation/
ovoids supination: arcuate swing in the
Functionally modified frontal plane about an oblique axis
sellar (horizontal and vertical combination);
for example, supination is the
calcaneus doing the combined
motion of adduction with inversion
and plantarflexion
Talonavicular joint Synovial Two degrees of freedom:
Modified ovoid a) Dorsiflexion: arcuate swing
(dorsiflexion with adduction and
minimal inversion)
b) Plantarflexion: (plantarflexion with
abduction and minimal eversion)
Nonvolitionary motion:
Abduction (valgus), adduction (varus)
Calcaneocuboid joint Synovial One degree of freedom:
Simple Triplanar motion of pronation/
Anatomically unmodified supination: arcuate swing about an
sellar oblique axis
Functionally modified sellar
510
SECTION II • Principles of Practice
Arthrokinematics* Normal End Feel
Dorsiflexion: posterior glide of the talus Capsular, although
Plantarflexion: anterior glide of the talus dorsiflexion may
be a soft tissue
stretch
Open kinetic chain All capsular
Pronation: lateral glide of anterior calcaneal
facet, medial glide of the posterior calcaneal
facet
Supination: medial glide of anterior
calcaneal facet, lateral glide of the
posterior calcaneal facet
Dorsiflexion: navicular dorsal glide with All capsular
conjunct external rotation (inversion)
Plantarflexion: navicular plantar glide with
conjunct internal rotation (eversion)
Open kinetic chain All capsular
Pronation: dorsal glide of cuboid with
conjunct internal rotation (eversion) and
abduction
Supination: plantar glide of
cuboid with conjunct external
rotation (inversion) and adduction
Cuneonavicular joint
Cuneocuboid joint
Synovial Two degrees of freedom: Dorsiflexion: dorsal glide of medial All capsular
Compound a) Dorsiflexion/plantarflexion: cuneiform with external rotation
Modified ovoid arcuate swing Plantarflexion: plantar glide of medial
b) Inversion/eversion: arcuate swing cuneiform with internal rotation
Synovial (may be syndesmosis) One degree of freedom: Pronation: dorsal glide of cuboid on All capsular
Compound Triplanar motion of pronation/ lateral cuneiform
Planar supination: arcuate swing about an Supination: plantar glide of cuboid on

CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles

oblique axis lateral cuneiform
Intercuneiform joints Synovial Sliding movements in a plantar and Pronation: slight plantar glide of medial All capsular
Compound dorsal direction on middle cuneiform, slight dorsal glide
Planar of lateral on middle cuneiform
Supination: slight dorsal glide of medial on
middle cuneiform, slight plantar glide of
lateral on middle cuneiform
Metatarsophalangeal Synovial Two degrees of freedom: Dorsiflexion: dorsal glide of phalanx base All capsular
(MT) joints Simple a) Dorsiflexion/plantarflexion: arcuate on metatarsal with conjunct internal
Modified ovoid swing in the sagittal plane rotation
b) Abduction/adduction: arcuate Plantarflexion: plantar glide of phalanx
swing in the coronal plane base with conjunct external rotation
Abduction: medial glide of phalanx
1 on MT 1, lateral glide of phalanges
3-5 on respective MT
Adduction: lateral glide of phalanx 1 on
MT 1, medial glide of phalanges 3-5 on
respective MT
Interphalangeal Synovial One degree of freedom: Flexion: plantar glide of distal phalangeal All capsular
joints (toes) Simple Flexion/extension: arcuate swing base
Modified sellar about a transverse axis Extension: dorsal glide of distal
phalangeal base

ROM, range of motion. EF, end feel.

*
Note: only the gliding movements are listed. The associated rolling that would also be present is not described, but the reader is reminded of MacConaill's7 concave/convex joint surface rules
for rolling.

511
 512
SECTION II • Principles of Practice
Table 24-11
Osteokinematics, Arthrokinematices, End Feel, and Joint Classification of Midline Joints3,4,19
Midline Joints Joint Classification Osteokinematics Arthrokinematics* Normal End Feel

Temporomandibular Synovial (modified as articular Three degrees of freedom: Opening: anterior rotation of the mandibular All capsular except
joint surfaces covered with a) Opening/closing in primarily condyle on the disc followed by translation closing, which
fibrocartilage not hyaline the sagittal plane of the disk-condyle complex anterior and is teeth
cartilage) b) Protrusion/retrusion in inferior on the articular eminence approximation
Complex primarily the horizontal plane Closing: opposite to opening above
Bicondylar (right and left c) Lateral deviation (right and Protrusion: translation of the disk-condyle
ellipsoid) left) in primarily the coronal complex anterior and inferior on the
plane articular eminence
Retrusion: opposite to opening above
Lateral deviation (right): right condyle
spinning and left condyle translating
anterior or anterior, inferior, and medial
Sternocostal joint Synovial (modified as articular One degree of freedom: Inspiration/expiration: primarily small gliding All capsular
surfaces covered with Inspiration/expiration: primarily movements or costal cartilage distortion in
fibrocartilage not hyaline small gliding movements or costal the sagittal or coronal/sagittal plane
cartilage) cartilage distortion in the sagittal
Simple (joints 2-7) or coronal/sagittal plane
Modified ovoid (all other joints)
Costovertebral joint Synovial One degree of freedom: Inspiration/expiration: compression/ Undescribed
Simple (1, 10-12) Inspiration/expiration: primarily distraction (note unable to access this joint
Complex and compound (2-9) rotation in the sagittal or coronal/ so not specifically assessed)
Modified ovoid sagittal plane †
Costotransverse joint Synovial One degree of freedom: Inspiration: inferior glide of the male All capsular
Simple (1, 10-12) Inspiration/expiration: primarily costal facet
Compound (2-9) arcuate swing in the sagittal or Expiration: opposite to inspiration
Modified ovoid coronal/sagittal plane
Interchondral joint
Sacroiliac joint
Synovial membrane between
small oblong adjacent facets
of 6-9
Synovial articulation between
One degree of freedom: Inspiration/expiration: primarily arcuate Undescribed
Inspiration/expiration: primarily swing in the sagittal or coronal/sagittal plane
small gliding movements or in
the sagittal or coronal/sagittal
plane
Intricate Intricate All capsular

CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles

the sacral and iliac articular
surfaces
Note: irregular joint surfaces
with sacral surface covered in
hyaline cartilage and iliac in
fibrocartilage
Intervertebral Synovial a) Flexion/extension: primarily Flexion/extension: flexion primarily a Undescribed
zygoapophyseal Simple (cervical and thoracic) the sagittal plane superior glide of the superior facet of the
joints Complex (lumbar) b) Lateral flexion (side flexion): joint complex
Bicondylar primarily the coronal plane Lateral flexion (side flexion): primarily an
(often conjunct with rotation) inferior glide of the superior facet of the
c) Rotation: primarily the joint complex towards the convex spinal
horizontal plane (often curvature created with this movement
conjunct with lateral flexion) Rotation: primarily a posterior glide of the
superior facet of the joint complex towards
the side of spinal rotation (e.g., right
rotation: posterior glide of the right
facet joint)

*Note: only the gliding movements are listed. The associated rolling that would also be present is not described, but the reader is reminded of MacConaill’s7 concave/convex joint surface rules
for rolling.
†
Note: unable to access this joint so not specifically assessed.

513
514 SECTION II • Principles of Practice
Passive intervertebral movement (PIVM) refers to the
assessment of ROM of an intervertebral segment by pas-
sive movement. It may be either physiological (PPIVM)
or accessory (PAIVM).
5. Stability tests: Assessment of the physiological and
non-physiological passive testing for structural
integrity and stability of joint. The ratio of dis-
placement is compared with the opposite side and
throughout the ROM available. Assessment must
include the neutral zone (discussed later in this
chapter) and the end feel (discussed later in this
chapter). Stability testing is used when hypermobility
(excessive motion) is detected with passive motion
testing.
Stability Testing
● Static (tested with the muscles relaxed)
● Dynamic (tested with the muscles in some state of contraction or
tension)
6. Specific muscle testing: Assessment in detail of the
muscular tissue that is beyond the scope of the ini-
tial assessment. This testing can is used commonly to
test individual muscles or groups of muscles doing the
same action.
Methods of Specific Muscle Testing
● Isometric testing in various positions
● Concentric testing in various positions
● Eccentric testing in various positions
● Econcentric testing in various positions
● Recruitment testing in various positions
● Length testing in various positions
● Special tests: for a particular joint complex
Normal Range of Motion
Normal range of motion is individualistic, and
most ROM charts should be considered only as aver-
ages. Commonly, the normal range of motion is
similar on left and right sides but seldom equal. In
some cases, individuals may exhibit laxity, which is
considered larger than normal ROM but is within a
range in which the individual has motor control of
movement.
For normal passive osteokinematic and arthrokine-
matic range of movement to occur the following factors
must exist: intact periarticular structures, intact articular
surfaces and margins, fully extensible periarticular tissues,
intact musculotendinous tissues, and fully extensible
musculotendinous tissues.
Movement Can Be Classified As the Following:
● Normal range of motion
● Hypomobile range of motion
● Excessive motion states: hypermobility and instability
Hypomobile Range of Motion
Abnormal motion in the form of hypomobility (reduced
motion) can be secondary to the following:
1. Myofascial hypomobility caused by muscle shortening
(scars, contracture, or adaptive tissue changes result-
ing in muscular hypertonus), which creates an elastic
end feel and demonstrates a constant length phenom-
enon. If this form of hypomobility exists without any
pericapsular or intraarticular dysfunction, then a non-
capsular pattern of restriction, a normal PAM, and a
limited PPM are found.
2. Pericapsular hypomobility is caused by capsular or
ligamentous shortening (scars or adaptive), which
creates a capsular pattern of restriction that does
not demonstrate the constant length phenomenon.
A premature firm/hard capsular end feel exists if
the joint is not inflamed, or possibly a spasm end
feel if the joint is inflamed. The PPM and the PAM
are limited.
3. Articular hypomobility can be caused by intraarticu-
lar swelling or an intraarticular bleed that results in
an increased tension on the joint capsule and thereby
presents like a pericapsular hypomobility. A prema-
ture boggy, spasm, or empty end feel results. A cap-
sular pattern may be present. Intraarticular inclusions
may exist, such as a piece of cartilage, tag of a menisci,
piece of detached or stretched out ligament or joint
capsule, a piece of bone (osteochondritis dessicans)
that permanently or intermittently blocks articular
mobility. These intraarticular inclusions usually do
not present as a capsular pattern unless the joint is
acute (swollen) at the same time. A premature springy
or bony end feel occurs if the joint is not inflamed or a
spasm end feel occurs if the joint is inflamed. In both
situations outlined above the PPM and the PAM are
limited.
4. Joint fixation is a situation in which the joint is stuck
at extreme ROM. It has exceeded the physiological
barrier and cannot “go back” to its original position.
This can occur secondary to a sudden macrotrauma, a
repeated or prolonged microtrauma, or a microtrauma
imposed on an instability. The effect of the joint fixa-
tion is the limitation of gross motion (active ROM
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
and PPM) or conjunct rotation towards the limita-
tion. Also the clinician notes that the end feel away
from the fixation is abnormal and has a rather firm
capsular end feel (e.g., it feels very abrupt and hard).
The end feel towards the fixation can be normal. The
PAM into the limited ROM is abnormal.
Excessive Motion States: Hypermobility
and Instability
Hypermobility can be a result of cumulative stress (creep,
see Chapter 1) as a result of neighboring hypomobility,
a prolonged low level of overuse of local muscles and
articular tissue, or a sudden macrotrauma that is not
enough to produce instability. The results of any of these
factors is an end feel that is soft capsular if nonirritable
or an end feel of late spasm if the tissue is irritable and
inflamed.
Abnormal Motion in the Form of Hypermobility
(Excessive Motion) Can Be Due to the Following:
● Inadequate muscle control secondary to a problem with muscle
recruitment
● Inadequate muscle control secondary to a problem with muscle
strength
● Inadequate muscle control secondary to a problem with muscle
endurance
● Inadequate muscle control secondary to a problem with the
mechanics of the muscle itself
● Inadequate muscle control secondary to a problem with neuro-
logical control of the muscle
● Inadequate ligamentous support
● Inadequate articular support
Hypermobility implies that the anatomical struc-
tures (active and passive) that control movement are
still intact and are not able to control fully the joint
motion. The active elements (muscles) that control
joint movement may not be being recruited properly, or
the passive elements (ligamentous structures) that sup-
port and guide joint motion may be stretched out. An
instability is a specialized form of excessive motion that
implies that the anatomical structures such as the bones,
ligaments, joint capsules, fascia, and muscles that con-
trol movement are no longer intact. The patient often
subjectively describes signs and symptoms listed in
Table 24-12.
In spinal joints, if the PPM is normal and end feel
is normal, the joint usually can be considered normal
because the anatomical structures that control the PPM
must be intact for a normal end feel to occur. These
anatomical structures are the bones, joint surfaces,
joint capsules and ligaments, and fascia, in addition to
515
the surrounding muscles and neurological structures.
An abnormal end feel may signal either hypermobil-
ity or instability, which indicates that some change has
occurred in the anatomical structures. In the peripheral
joints, a ligamentous instability while having a normal
PPM is possible. In the peripheral joints, this occurs
because the more inert tissues such as the joint shape,
ligaments, and capsules control most of the translatory
movement, whereas the muscle controls more of the
angular movement of the PPM. For example, normal
active knee flexion and extension may be present with
an underlying lesion of the anterior cruciate ligament
that creates an increase in anterior translation. Therefore
in peripheral joints with normal PPM, joint stability still
needs to be tested to establish if any type of motion
dysfunction is present.
The types of instability that can be detected are liga-
mentous instability and articular instability. Ligamentous
instability is the condition in which excessive non-physi-
ological motion and an abnormal end feel are detected
with stability testing. Articular instability occurs with car-
tilage (hyaline or fibrocartilage) degeneration and thin-
ning, which leads to reduced congruency of the articular
surfaces and allows slipping between them when tested
in a non–weight-bearing position.20,21 This degenera-
tion permits the bone ends to move closer to each other
and thereby slacken off the capsule and ligaments, which
allows increased non-physiological motion on stability
testing with a normal end feel (Figure 24-22).
A discussion about mobility and stability must
include a discussion of some of Panjabi’s concepts.22
Panjabi postulated that efficient movement required
optimal stabilization by the interaction of three main
systems: the control subsystem (neural responses), the
passive subsystem (intact bones, joints, ligaments), and
the myofascial subsystem (efficient, coordinated mus-
cle action) (Figure 24-23). This optimal stabilization
allows for the appropriate control of the neutral zone.22
The neutral zone is a small range of displacement near
a joint’s neutral position, where minimal resistance is
given by the osteoligamentous structures (Figure 24-24).
Although this concept was used to help understand the
structures important for spinal stability, it is this author’s
contention that the concept can be just as adequately
applied to the peripheral articular system. If a dysfunc-
tion occurs in any of the three systems, then the stability
of the motion segment will be disturbed. This dysfunc-
tion eventually can lead to tissue breakdown by exhaus-
tion of its ability to sustain stress and load (e.g., muscle
tendonitis, joint instability). Panjabi has observed that
the range of the neutral zone may increase with injury,
articular degeneration, and/or weakness of the stabiliz-
ing musculature.
Panjabi defined instability as “a significant decrease
in the capacity of the stabilizing systems of the spine
516 SECTION II • Principles of Practice

Table 24-12
Subjective and Physical (Objective) Signs and Symptoms of Instability
Subjective Signs and Symptoms Physical (Objective) Signs and Symptoms

History Observational
A history of trauma Posture that is poor with a posterior or abdominal crease
A history of significant conservative treatment with only a temporary in skin often indicating the presence of a spondylolythesis
good effect The presence of spinal ledging
Aggravating Factors Spinal angulation on full range of motion
Repeated unprovoked episodes or episodes following minor ROM Related
provocation “Catching” or “blip” of motion during active or
Aggravation by trivial movement but the specific movements vary passive ROM
(inconsistent symptomatology) A decreased willingness to move
Aggravation with sustained postures An inability to recover normally from a full range motion
Symptom Presentation Excessive active range of motion
A feeling of instability or giving way Neurological
Minor aching for a few days after a sensation of giving way Often negative neurological signs
Compression symptoms (vascular for example vertebrobasilar, Muscular
spinal cord, peripheral or spinal nerve) that are not associated with A muscle imbalance found locally and more globally
a disc or stenotic like history (i.e., throughout the body)
Consistent clicking or clunking noises Atrophy of local muscles
Protracted pain (with full range motion) Special Tests
Grumbling pain, morning stiffness, often eased by rest
Positive stability tests
Inability to efficiently and effectively perform functional
tests involving the region under examination

Ligament
Joint capsule

Hyaline cartilage on
A joint surface
Figure 24-22
Articular instability. A, Normal joint with normal stability. Glides and
Lax ligament non-physiological mobility will be limited by the joint surfaces and
Lax tension in the ligaments and joint capsules. B, Degenerative joint with
joint capsule articular instability. Note the degeneration permits the bone ends to
move closer to each other and thereby slacken off the capsule and
ligaments. This allows increased non-physiological motion on stability
Thinning of testing with a normal end feel. Glides and non-physiological mobility
hyaline cartilage are less limited by the flattened joint surfaces and slackened ligaments
B on joint surface and joint capsules.

CONTROL SUBSYSTEM
Neural
Figure 24-23
Stabilizing systems. Passive system includes the joint surfaces,
ligaments, and bony structures. Myofascial system represents the
muscles and their investing fascial bands. Control system represents
the motor planning programs that the body utilizes to produce
movement. This is greatly influenced by descending control from
PASSIVE ACTIVE the brain. (Modified from Panjabi M: The stabilizing system of
SUBSYSTEM SUBSYSTEM
the spine. Part II. Neutral zone and instability hypothesis, J Spinal
Spinal Column Spinal Muscles
Disord 5:390-396, 1992.)
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles 517

Load used Panjabi’s theories of mobility and stability and

Neutral
Zone
Displacement
Figure 24-24
Panjabi’s neutral zone. (Modified from Panjabi M: The stabilizing
system of the spine. Part II. Neutral zone and instability hypothesis,
J Spinal Disord 5:390-396, 1992.)
to maintain the intervertebral neutral zones within
physiological limits so that there is no neurological dys-
function, no major deformity, and no incapacitating
pain.”22 White and Panjabi defined clinical instability as
the loss of the ability of the spine, under physiological
loads, to maintain relationships between the vertebrae in
such a way that neither damage nor subsequent irritation
to the spinal cord or nerve roots occurs. Furthermore,
incapacitating deformity or pain resulting from structural
change does not develop.10 Hypomobility and excessive
motion states often can coexist in the same joint complex
on opposite sides of the joint. For example, the gleno-
humeral joint can be anteriorly hypermobility/instability
with a posterior hypomobility present. Lee has brilliantly
conceptualize additional diagrams to demonstrate these
points in Figures 24-25 and 24-26.19,23
To determine if the joint has normal or abnormal
mobility the clinician must know the normal active
and passive ROM for the joint being examined (see
Chapter 25). An exploration of a patient’s joint mobility
requires assessment of the quantity and of the move-
ment quality. The quality of the joint mobility is assess-
ment with passive mobility testing, the PPM, and the
PAMs. Did the patient express any signs or symptoms
of pain during the testing? What did the examiner feel
was the quality of the resistance through ROM (both
the neutral zone and on either side of this zone)? What
did the examiner feel was the resistance felt at the end
of range, the end feel? If the joint mobility was limited,
was the pattern of limitation characteristic of a capsular
or noncapsular pattern?
End Feel
The end feel is what the clinician perceives as the physical
limitation of a joint. It is the sensation imparted to the
examiner by the resisting tissues at the end of the avail-
able range of the joint. Dr. James Cyriax first described
this phenomenon and created the original list of end
feels (EF).13 Table 24-13 lists the various end feels that
have undergone refinement and expansion by health

NZ NZ

A B

NZ NZ

C D

NZ

E F
Figure 24-25
Neutral zone and its changes and effect of motor control deficits. A, Normal neutral zone (i.e., normal joint complex). B, Increased neutral
zone (i.e., loose/hypermobile joint). C, Decreased neutral zone (i.e., stiff/hypomobile). D, Normal joint with decreased neutral zone (i.e., a
myofascially compressed joint, passive system intact and neutral zone limited by excessive muscle). E, Abnormal joint with decreased neutral
zone (i.e., the passive restraints have been affected, which results in a joint fixation that is overly compressed by the muscle activation).
F, Fixated motor control deficit. Inability of the body to control movement, resulting in an abnormal neutral zone. Passive testing of the joint
will feel normal, but active tests, which load the joint, show dynamic instability. Motor control errors are due to a compromise in spinal stability
secondary to a short and temporary reduction in activation to the intersegmental muscles.19 (Modified from Panjabi M: The stabilizing system
of the spine. Part II, Neutral zone and instability hypothesis, J Spinal Disord 5:390-396, 397, 1992; Lee D: The pelvic girdle, ed 3, Edinburgh,
2004, Elsevier Science.)
518 SECTION II • Principles of Practice

Painful Pain-free Neutral Pain-free Painful of the body would be constructed so that the muscular
Zone Zone Zone Zone Zone tissue would be the first line of defense for protection
of the capsules and ligaments during normal range of
motion. Further evidence that the muscle is the first
limitation to angular motion is the fact that when one
Figure 24-26 passively extends an elbow joint before and after the
Analogy of the neutral zone with passive movement and/or stability patient undergoes a general anesthetic. Significantly
testing. (Modified from Lee D: The pelvic girdle, ed 3, Edinburgh, more movement of the patient’s elbow into extension
2004, Elsevier Science.) occurs during the effects of a general anesthetic. Clearly
the patient’s bony anatomy has not changed before
and after the general anesthetic, therefore the the pre
care providers working with patients since Cyriax’s general anesthetic end feel for elbow extension could
first published list. Often what is perceived initially as not have been a true bony end feel as Cyriax initially
an end feel of any type is more likely a true muscular claimed. For a clearer view of the inert structures of
limitation. For example, often if the clinician does a the joint, assessment and treatment must get past this
muscular release technique such as proprioceptive neu- muscle barrier. This may be why research into the area
romuscular facilitation, more movement is gained and of end feels and capsular patterns (see following section
the end feel changes. It makes sense that the anatomy on Capsular Pattern) has been so inconclusive.24-28

Table 24-13
End Feels
Type of End Feel Characteristics Example

Capsular Produced by capsule or ligaments Normal: wrist flexion (soft)

Various degrees of stretch without elasticity
Solid, well-defined end point
Described as leathery
Impression that further displacement will tear
something
Amount of resistance dependent on the
thickness of the tissue:
Strong capsular or extracapsular ligaments
produce a hard capsular end feel
Thin capsule produces a softer end feel
Bony Produced by bone to bone approximation
Abrupt and unyielding
Impression that further forcing will break
something
Soft-tissue Produced by contact of two muscle bulks on
approximation either side of a flexing joint, in which the joint
range exceeds other restraints
Forgiving end feel with impression that further
normal motion possible if enough force applied
Elastic Produced by muscle-tendon unit
May occur with adaptive shortening
Stretch with elastic recoil end feel
Exhibits constant length phenomenon
Further loading feels as if it will snap
Springy Produced by articular surface rebounding from
an intraarticular meniscus or disc
Impression is that if forced further, something
will collapse
Rebound sensation as if pushing off from
a rubber pad
Normal: elbow flexion in supination (medium)
Normal: knee extension (hard)
Abnormal: inappropriate amount of
resistance for a specific joint.
Too hard: hypertrophy resulting from arthrosis
Too soft: hypermobility
Abnormal: end point too early in the range
of motion
Normal: elbow extension
Abnormal: cervical rotation (may indicate
osteophytosis)
Normal: knee flexion or elbow flexion in
extremely muscular subjects
Abnormal: elbow flexion with the obese
subject
Normal: wrist flexion with finger flexion or
the straight leg raise with ankle dorsiflexion
as well as the knee extended
Abnormal: dorsiflexion of the ankle with
the knee flexed
Normal: axial compression of the cervical spine
Abnormal: knee flexion or extension with
a displaced meniscus
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles 519

Table 24-13 —Cont’d

End Feels
Type of End Feel Characteristics Example

Spasm Produced by reflex and reactive muscle contraction Normal: none

in response to irritation of the nociceptors Abnormal: significant traumatic arthritis;
predominantly in articular structures and muscle recent traumatic hypermobility; grade 2
Forcing it further feels as if nothing will give muscle tears
Abrupt and twangy end feel that is unyielding
while the structure is being threatened but
disappears when the threat is removed
Early in range of motion: joint inflammation
Late in range of motion: hypermobility
Apparent in grade two muscle tears as the muscle
is passively lengthened and is accompanied by
painful weakness of that muscle
Boggy Produced by viscous fluid (blood) within a joint Normal: none
“Squishy” sensation as the joint is moved Abnormal: hemarthrosis at the knee
towards its end range
Further forcing feels as if it will burst the joint
Empty Produced solely by pain Normal: none
Frequently caused by serious and severe Abnormal: acute subdeltoid bursitis; causes
pathological changes that do not affect the joint of the sign of the buttock
or muscle and so do not produce spasm
If present, with the exception of acute subdeltoid
bursitis, evidence of serious pathology
Limitation of motion has no tissue resistance
component
Examiner stops movement at patient’s insistence,
although free movement still feels possible
Not the same feeling as voluntary guarding but
rather it feels as if the patient is both resisting
and trying to allow the movement simultaneously
Further forcing simply increases the pain to
unacceptable levels

Modified from Cyriax J: Textbook of orthopaedic medicine. Volume I: Diagnosis of soft tissue lesions, ed 8, London, 1982, Bailliere Tindall.

Capsular Pattern 1. Ligamentous adhesions: The joint is limited only in

A capsular pattern of movement restriction is a char-
acteristic pattern of restriction for a synovial joint that
occurs in the presence of an arthritis or an arthrosis.13
Each joint has its own capsular pattern, and this pattern
is universal among all patients for that joint (Tables 24-
14 and 24-15). However, different joints show differ-
ent patterns of limitation. The proportions of limitation
designate whether the pattern is capsular; therefore the
medical examiner must measure all joints with a limi-
tation of movement to be sure the pattern is actually
capsular.
Noncapsular Pattern
If, on examination, it is revealed that the joint mobility
limitation does not fit into a capsular pattern of limitation,
then the limitation may be secondary to any of the fol-
lowing:
the direction that stretches the ligament, whereas all
other movements will be full and pain free.
2. Internal derangement: This is the development of
an intraarticular cartilaginous or bony fragments
(e.g., loose bodies, meniscal tears). The limitation
amount depends on where the fragment lies in the
joint.
3. Extraarticular lesion: This lesion occurs in the tis-
sue that crosses the joint extraarticularly or that lies
nearby the joint and therefore can affect the joint’s
mobility (e.g., acute bursitis [subdeltoid bursitis
results in marked decreased abduction, with external
rotation fairly free]), myofascial restriction—referred
signs from the neck (commonly C5 dysfunction
causes spasm in the infraspinatus muscle, result-
ing in decreased internal rotation with abduction
and external rotation remaining free), neural tissue
520 SECTION II • Principles of Practice

Table 24-14
Capsular Patterns of the Upper Quadrant and Spine*
Upper Quadrant and Spine Capsular Patterns

Glenohumeral Limitation of lateral rotation greater than abduction greater

than medial rotation (approx 2:1)
Acromioclavicular Pain at extreme ROM
Sternoclavicular Pain at shoulder girdle extreme ROM
Elbow Limitation of flexion much greater than extension with
pronation and supination full or slightly limited
Superior and inferior radioulnar Equal limitation of supination and pronation
Wrist Equal limitation of opposite movements
First carpometacarpal Limitation of abduction and extension
Second to fifth carpometacarpal Limitation of flexion greater than extension
Metacarpophalangeal Limitation of flexion greater than extension
Interphalangeal (fingers) Limitation of flexion greater than extension
Temporomandibular Limitation of mouth opening
Atlanto-occipital Extension and side flexion equally limited with a query in the
literature whether there is a limitation of flexion greater than
extension
Atlanto-axial Equal limitation of rotation, with a query in the literature
whether there is a limitation of flexion or extension
Rest of the spine Equal limitation of rotations and side flexions greater than
extension greater than flexion
Sacro-iliac Pain when joints are stressed

*The movements listed first have the largest amount of ROM limitation
Adapted from Cyriax J: Textbook of orthopaedic medicine. volume I: diagnosis of soft tissue lesions, ed 8, London, 1982, Bailliere Tindall.

Table 24-15
Capsular Patterns of the Lower Quadrant*
Lower Quadrant Capsular Patterns

Hip Limitation of flexion, abduction, medial rotation (order may vary)

Slight limitation of extension, little or no limitation of adduction
and lateral rotation
Early capsular pattern usually detectable with limitation of medial
rotation and extension
Knee Limitation of flexion much greater than extension, rotations full or
slightly limited
Tibiofibular Pain when joints are stressed
Talocrural Limitation of plantar flexion greater than dorsiflexion
Talocalcaneal Limitation of supination greater than pronation
Midtarsal Alternative pattern limitation of dorsiflexion, plantar flexion,
adduction and medial rotation with abduction and lateral rotation
full
First metatarsophalangeal Limitation of extension greater than flexion
Second to fifth metatarsophalangeal Variable but eventually fix in MTP extension (flexion greater than
extension)
Interphalangeal (toes) Variable but eventually fix in IP flexion (extension greater than
flexion)

MTP, metatarsophalangeal. IP, interphalangeal.

*The movements listed first have the largest amount of ROM limitation
Modified from Cyriax J: Textbook of orthopaedic medicine. Volume I: Diagnosis of soft tissue lesions, ed 8, London, 1982, Bailliere Tindall.
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
pathology (decreased neural mobility of the median
nerve in the carpal tunnel can result in decreased
wrist mobility in flexion or extension with radial and
ulnar deviation), or skin scarring (i.e., from a burn,
surgery).
Articular Mobilization Techniques
The clinician uses many different definitions of mobi-
lization and manipulation. They all have a common
theme and emphasis but their own nuances. Four influ-
ential practitioners of orthopedic manual therapy who
each had their own school of thought on this subject
matter were Cyriax,13 Kaltenborn,11,29 Maitland,30,31
and Mennell.32,33 For the purpose of communication in
this chapter, the Canadian Physiotherapy Association
definition is used; it describes mobilization as the
rhythmic passive movements of graded amplitude
applied to a joint within its physiological range of
motion with the intent to restore optimal motion,
function, and/or reduce pain.8 This same organiza-
tion describes manipulation as a passive, high-velocity,
low-amplitude thrust applied to a joint beyond its
physiological limit of motion but within its anatomical
limit with the intent to restore optimal motion, func-
tion, and/or reduce pain.8 Articular mobilization and
manipulation are the passive therapeutic maneuvers a
clinician applies to a joint that demonstrate dysfunction
(hypomobility) to restore or improve arthrokinematics
and thereby osteokinematics and function. Two basic
methods of mobilization exist:
1. Distraction: A force applied perpendicular to
the joint surface to create separation of the joint
surfaces
2. Gliding: A force applied to one of the two joint sur-
faces to create movements parallel to each other
Table 24-16
Passive Mobilization Technique Selection
Pain/Resistance* Acuteness
Pain, no resistance Empty end feel (serious)
Constant pain Hyperacute (pure chemical)
Pain greater than or earlier than Acute (mainly chemical)
resistance
Pain at the same time or equal to Chronic/subacute (mechanochemical)
resistance
Pain less than or later than resistance Chronic (mechanochemical)
Resistance Stiff (mechanical)
*To determine the aggressiveness of therapy, the relationship between the tissue resistance and the onset of pain can be assessed.
521
Mobilization Grades
Joint mobility assessment uses a grading system to com-
municate the amplitude of movement applied to the joint
complex. In addition to this amplitude information, the
examiner must be aware of the relationship between the
amount of motion available to the amount and quality of
pain and onset of resistance in addition to the end of these
tissues. The amplitude of treatment mobilization is graded
using either Kaltenborn11 or Maitland31 grading systems.
When either mobilization grading system is used with
decreased range of motion present in a joint, the remain-
ing available range is still divisible into the three or four
grades described. It is always important to start to grade
the movement from the rest position of the joint and fre-
quently return to this “start position” to prevent poten-
tially harmful excessive loading into higher mobilization
grades or “winding up” of the joint. Consideration of the
relationship between resistance and pain response assists
the clinician in the correct choice of grade to use in either
mobilization assessment or treatment (Table 24-16).
In different parts of the world, Australia, for example,
the term manipulation refers to mobilization grade I to
V (Maitland), whereas in North America the term mobi-
lization refers to grade I to IV (Maitland) techniques and
manipulation refers to grade V (Maitland) techniques.
Mobilizations and manipulations using passive physi-
ological movements (PPM) help to restore osteokinemat-
ics, whereas those that use passive accessory movements
(PAM) help to restore the joint’s arthrokinematics. To
achieve greater success with mobilization, the ovoid of
motion must be considered in relationship to the joint
plane of motion. The effects of mobilization are outlined
in Tables 24-17 and 24-18. Research is ongoing and adds
to the scientific evidence that supports the effects of mobi-
lization and manipulation, rather than just attributes these
effects to known anatomy and physiology principles.34-46
Technique (Maitland Grading
System Used)
None, refer back to doctor
RICE
Very gentle mobilization Grade I (II)
specific traction
Gentle mobilization Grade I-II
Moderate mobilization Grade III-IV
Aggressive prolonged stretch Grade
IV (V)
522 SECTION II • Principles of Practice

Kaltenborn Grades (Traction and Gliding Mobilization) Maitland Grades of Movement

Grade I “Piccolo” distraction: neutralize joint pressure with tissue Grade I Small amplitude at start of range
neither maximally tightened nor stretched Grade II Large amplitude, from start of range to mid range
Grade II “Take up the slack”: move joint partner only as far as soft Grade III Large amplitude, mid to end range
tissue will allow (tissue is tightened but not stretched) Grade IV Small amplitude, end range
Grade III Once slack taken up, further “stretch” the soft Grade V Small amplitude, high velocity thrust at end range
tissue by applying more traction
Note: End range is referring to the patient’s end of available range of motion,
Gr I: Loosen Gr III: Stretched
not necessarily the end of normal physiological range of motion for that
tissue.
Modified from Maitland G: Peripheral manipulation, London, 1991,
Gr II: Tightened Butterworth-Heineman.
Modified from Kaltenborn F: Manual therapy for the extremity joints, ed 2, Modified from Maitland G: Vertebral manipulation, ed 5, Toronto, 1986,
Oslo, 1976, Olaf, Norlis Bokhandel. Butterworths.

Range of Motion Joint Complexes

Example of a Normal Range of Motion Joint Complex Showing Example of a Hypomobile Range of Motion Joint Complex
Maitland’s Mobilization Grades

Grade I Grade III Grade III+

Grade II

Grade III Grade IV+

Grade IV
Grade IV
Grade V Grade V

A B A R B

Example of a Hypermobile Range of Motion Joint Complex

Grade I

Grade III

Grade II

Grade IV

A B H

A = start of range of motion

B = end of average normal range of motion
R = hypomobile ROM
H = hypermobile (excessive) ROM
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles 523

Table 24-17
Mobilization and Postulated Cellular Level Effects
Mobilization Effect Postulated Effects

Mechanical effect: connective tissue remodeling Cellular modulation

Release of enzymes to breakdown cross links
Stimulation of fibroblast synthesis of collagen proteoglycans
Realignment of old fibers (piezoelectric current)
Increase interfiber distance (break cross links)
Increase interfiber lubrication (proteoglycans bind with H2O)
Alignment of new fibers (piezoelectric current)
Stretching articular capsule/segmental muscle
Breaking intraarticular adhesions
Vertebral movement—definite motion of vertebra in cadavers returns to same
position; not well studied in patients
Articular cartilage changes Alter joint lubrication
Enhance cartilage nutrition
Movement of joint inclusions (meniscoids) or loose bodies (cartilage
fibrillation)
Shift hard fragment of intervertebral disc
Neurological effect8,26-28,31,35,47-49 Stimulate Type I and Type II mechanoreceptors
Inhibit transmission of nociceptive impulses
Decrease pain perception
Relieve mechanical irritation of nervous system
Activation of articular mechanoreceptors
Stimulation of sympathetic nervous system
Neuromuscular response36,37,40,42 Alter afferent input to effect efferent output (gamma bias)-relax muscle
Stimulation of muscle spindle
Stimulation of the Golgi tendon organ (GTO) causes reflex inhibition of
segmental muscle
Alter segmental (and more distal) muscle activity
Reflex muscle response locally and at a distance
Decrease spinal segmental facilitation
Alter circulation Increase supply of materials required for healing
Remove chemical irritants, hence decrease nociceptor stimulation
Physiological43,49 Increased beta-endorphin levels
Immune system effects
Joint tissue response Increase capsule elasticity
Improve articular cartilage nutrition
Improve circulation
Restoration of joint play/accessory glides
Restoration of passive/active movement
Decrease pain perception

Mobilization and Reliability

Reliability of any tool is based on the tool’s accuracy, con-
sistency, and reproducibility of the “examination tech-
nique.”50 In a review article of accessory motion of spinal
and peripheral joints by manual therapists, Riddle51 states
that few studies have examined the validity and reliabil-
ity of such assessments, and the reliability of judgments
based on accessory motion techniques performed on
spinal joints has not been studied adequately. He suggests
that study of the predictive value of positive and negative
accessory motion test results in addition to the sensitiv-
ity and specificity of the many tests manual therapists use
would be valuable.51 Based on the existing literature, a
review of manual therapy mobilization and manipulation
techniques in the literature revealed that these techniques
often have moderate to poor interrater reliability.1,6,51-60
524 SECTION II • Principles of Practice
Table 24-18
Mobilization and Postulated Effects
Grade of Mobilization
Grade I, II, III
Grade IV
Grade V
Technical Summary of Mobilization Treatment
Application
● Patient consent received (informed about nature and purpose of
mobilization, alternate forms of assessment, associated risks and
benefits)
● Select starting position of the patient, ensuring that they are
relaxed, comfortable, and well supported
● Select starting position of the clinician (see following box)
● Select treatment grade
● Select a sustained or oscillatory technique
● Select duration and speed of oscillatory technique (shorter for
acute conditions)
● Increase the intensity and duration of treatment only when
evidence exists that increased dose will not exacerbate pain
● Select reassessment technique to use before, during, and after
treatment
● Select home program to maintain treatment effects
Some research supports the statement that better
manual therapy interrater reliability results occur with
training and practice doing identical performance and
interpretation of tests (e.g., first clearly clarifying and
defining the features to be tested).6,61,62 Some possible
factors that may affect reliability of mobilization tech-
niques are the following:
The stress applied to tissue usually is not quantified
● use of mobilizations in clinical practice. In the cervi-
(i.e., amount of pressure on palpation amount of
compression/traction applied).
The patient reports rely on the patient’s attention
● and resistance to movement. These findings were
being consistent.
Over the time of the study, a change occurs in the
● tion was made between the two testing procedures,
clinician’s and the patient model’s tissues.
The late Vladimir Janda, one of the leaders in the
field of musculoskeletal medicine, once remarked,
“Just because we cannot always prove a hypothesis
Postulated Effects
Neurophysiological effect
Vascular effect
Mechanical effect
As per Grade I, II, III with possible greater:
Mechanical mobilizing effect
Enhancement of joint lubrication
As per Grade I, II, III with possible greater:
Mechanical mobilizing effect
Neurophysiological effect
Cavitation
Enhancement of joint lubrication
Technical Summary of Therapist Position and
Application of Mobilization Treatment
● Must be in a comfortable position (grip must be relaxed and
efficient body mechanics employed)
● To determine the joint end feel, bunch up skin to give some
“slack” in the skin
● To avoid potentially harmful compression to the joint the following
are necessary:
● Place the hands as close to the joint line as possible
● Find the joint plane, thereby gliding perpendicular to the
mechanical axis of bone/traction and compression along
mechanical axis of bone
● Fix one bony end and move the other
● Therapist’s forearms should always be inline with the plane of
joint movement
● Concentrate on end feel and amount of range of motion
● Allow recoil to neutral in between mobilizations
does not mean that we cannot or should not think
about it.” This advice is useful in this discussion
because it means that researchers need to develop a
different methodology to examine what many clini-
cians already believe to be true: when correctly used,
mobilizations are a useful assessment and treatment
tool. Some evidence currently exists that supports the
cal spine, a physiotherapist can locate a symptomatic
facet joint on a patient via tenderness on palpation
compared with diagnostic blocks, and 100% correla-
which gives evidence that mobilization is a valid form
of assessment.63 On cervical facet joint examination
to identify decreased passive intervertebral motion,
studies show fair intrarater reliability and poor inter-
 CHAPTER 24 • Arthrokinematics and Mobilization of Musculoskeletal Tissue: The Principles
rater reliability of the studies’ examiners.17,64 Studies
also exist in the lumbar spine to show that clini-
cians, specifically physiotherapists, are skilled in the
diagnosis of symptomatic facet joints,65 symptomatic
intervertebral discs,66 and lumbar instability.13
With regard to treatment, evidence is continually
mounting that mobilization and manipulation alone or
combined with exercise and patient education are effec-
tive for treating joint hypomobilities.67-75 Other studies
reveal spinal mobilization as a treatment method has
Factors Involving the Clinician and Patient
Relationship to Consider as a Contraindication for
Mobilization or Manipulation
● Insufficient subjective assessment of the patient, that is, inad-
equate information about coexisting conditions, disease, and/or
medication or in general the patient has an inability to communi-
cate or is an unreliable historian
● Poor appraisal of the patient as a reliable historian
● Patient is intoxicated or heavily medicated
● Patient age: children (skeletal maturity, consent issues)/elderly
(tissue health/integrity issues)
● Failure to discuss the assessment findings and treatment options
with patient
● Failure to receive or to agree with patient consent
● Insufficient scanning examination or detailed biomechanical
examination
● Inappropriate findings, end feel, or patient response with the following:
● Scanning examination
● Biomechanical testing
● Stress testing (positive for level desire to treat or cautionary if
above or below joint/level treating)
● Dizziness reproduction testing
● Clinician’s insufficient awareness of contraindications and
conditions requiring extra care and gentleness
● Clinician’s physical limitations for the technique (e.g., their size,
strength, speed, fatigue)
● Lack of clinician’s confidence for the technique
● Lack of proper equipment for the technique (e.g., not using a
high/low plinth)
● Pain in the position of the technique
● Patient’s joint placed in a fully closed packed position
525
good outcomes in terms of reduced pain levels and bet-
ter physical function.9,76-79
Cautions and Contraindications to Consider with
Articular Mobilization or Manipulations
As with any technique, patient safety always must be con-
sidered. Some of the cautions and contraindications to
consider with articular mobilization or manipulations are
outlined in the accompanying boxes.80-85
Factors Involving the Patient’s Anatomy
or Physiology to Consider as a Caution or
Contraindication for Mobilization or Manipulation
● Bony elements
● Fractures (presently healing)
● Dislocations (presently healing)
● Past or present cancers that metastasize to bone (e.g., breast,
bronchus, prostate, thyroid, kidney, bowel, lymphoma)
● Active bone infection (cautionary with past bone infections;
e.g., osteomyelitis, tuberculosis, congenital anomalies)
● Gross foraminal or spinal canal encroachment on x-ray or other
imaging examination
● Vascular elements
● Vertebral artery insufficiency
● Vascular disease (e.g., aneurysm, atherosclerosis)
● Signs of vascular insufficiency in that region
● Bleeding disorders
● Aortic graft
● Neurological elements
● Central nervous system disease or signs and symptoms of its
injury
● Spinal cord disease or signs and symptoms of its injury
● Cauda equina disease or signs and symptoms of its injury
● Multiple/bilateral level nerve root involvement
● Soft tissue elements
● Collagen disease (e.g., Ehlers-Danlos syndrome)
● Connective tissue instability
● Acute posttraumatic stage of healing
● Metabolic disease (e.g., bone disease, such as osteoporosis)
● Systemic disease/condition (e.g., asthma, hemophilia, pregnancy)
● Inflammatory diseases (e.g., acute active inflammation such as
rheumatoid arthritis or inactive inflammatory disease)
● Medications patient may be taking
● Anticoagulants (e.g., heparin/caution with ASA)
● Any medication that affects collagen (e.g., corticosteroids or
tamoxifen or any medication that is linked to osteoporosis)
● Antidepressants
526 SECTION II • Principles of Practice
Summary
With the information presented in this chapter, the reader
has become more familiar with the nomenclature and the
principles of articular macrostructure, which allows for
better understanding and assessment of function. These
concepts are intended to allow the reader to be ultimately
more successful in the treatment of dysfunction using
biomechanical technique principles. The reader is now
encouraged to read the individual chapters devoted to
the assessment and treatment of each of the specific
articular complexes while keeping the principles of this
chapter in mind.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 85 references for this chapter.

R ANGE OF M OTION AND F LEXIBILITY
James E. Zachazewski
Introduction
Movement dysfunction and any subsequent physical
disability suffered by patients who have incurred some
type of musculoskeletal injury may be caused by a number
of factors. The alteration or loss of normal joint motion
and soft tissue flexibility are two of these critical factors.
Clinicians seek to develop rehabilitation programs that
allow the patient to return to their highest level of physical
activity. In order to develop this program the clinician
has a responsibility to determine which factor or factors
are the cause of this movement dysfunction that alters
the patients’ level of physical ability. The clinician also
must determine the physiological basis for these factors
to determine the most appropriate method of clinical
intervention.
The purpose of this chapter is to present the
physiological considerations that should guide the
clinician in determining why the patient has suffered a
compromise in joint motion and soft tissue flexibility
available; and the impact of this loss on the patients’
ability to move freely and easily for all activities of daily
living (ADLs) and recreational activities. This understand-
ing allows the clinician to choose the most appropriate,
efficient, and effective methods of clinical intervention to
assist patients in regaining the fullest level of function.
Definitions
The terms range of motion and flexibility often are used
synonymously and interchangeably by clinicians, yet they
are not the same. An understanding of the differences
and interrelationship between these terms is critical for
clinicians and for their ultimate success in working with
patients with musculoskeletal dysfunction.
The term range of motion (ROM) most typically
refers to the amount of measured joint motion available
in any single joint in a single plane. This range usually is
25
C H A P T E R
measured in the clinical arena with a goniometer, an incli-
nometer, or some other similar type of device. The ROM
about any joint depends ultimately on and is limited by
that particular joint’s arthokinematics, soft tissue contact,
or approximation and bone-to-bone contact. An example
would be the limitation of elbow extension imposed by
contact between the olecranon and the olecranon fossa
and the limitation of elbow flexion by approximation of
the soft tissues in the antecubital fossa.
The term flexibility has been defined by many authors
in many ways.1-4 Most of these definitions share com-
monalities originally proposed by deVries, who stated,
“Flexibility may be most simply defined as the range of
motion available in a joint, such as the hip, or a series
of joints, such as the spine.”5 The definition posed by
deVries takes into consideration the joint ROM and
its limiting factors as described above and the ability
of the periarticular and musculotendinous tissues to be
deformed or lengthened.
However, the accuracy of this definition has been
questioned by Holt et al. based on the concept that flex-
ibility in this type of definition is not seen as correspond-
ing to some particular measure but as the measurement.
Range of motion should be not be considered the same
as, but demonstrative of, the flexibility of the periarticu-
lar connective tissues and musculotendinous tissues that
cross that joint or series of joints. Based on this concept,
Holt et al. have proposed that flexibility be defined as
“the intrinsic property of body tissues which determine
the range of motion achievable without injury at a joint
or group of joints.”6 Table 25-1 summarizes these defini-
tions and some of the clinical concepts that are relative
to the definitions.
Holt’s definition and concept of flexibility is perhaps one
of the most clinically relevant. The maximum potential ROM
(which is what is clinically measurable) possible that may be
available at any single joint is governed by the joint’s anatom-
ical shape and orientation (arthrokinematics)7 and the ability
527
528 SECTION II • Principles of Practice
Table 25-1
Definition and Clinical Concepts of Flexibility5,6
Definition
Flexibility6 The intrinsic property of body tissues that
determines the range of motion achievable
without injury at a joint or group of joints
Static Flexibility5 Measured ROM available about a joint or
series of joints
Dynamic Flexibility5 Measure of the resistance to active motion
about a joint or series of joints
of the tissues that surround that joint or series of joints. This
measured ROM should be considered equivalent to deVries’
definition of “static flexibility” (see Table 25-1).
The clinician always must remember that functionally,
the ability to move through or into a specific ROM
is dependent upon the flexibility of the tissues. This
flexibility is dependent upon the intrinsic viscoelastic and
neurophysiological characteristics and properties of the
periarticular connective tissues and musculotendinous tis-
sues that cross that joint, to be deformed or lengthened
and return to their original length.8-14 These are the
intrinsic properties described by Holt et al. and are also
integral to deVries, definition of “dynamic flexibility”
(see Table 25-1).
To assess the motion available in a joint, the clinician
measures ROM. This measurement also, at times, may be
considered an indirect assessment of the flexibility of the
periarticular and musculotendinous connective tissues
associated with the joint, because these tissues must be
deformed for the joint to move into or through a specific
ROM. While clinicians measure ROM, they must influ-
ence flexibility of the tissues associated with the joint to
alter the ROM measured. This is true for any single joint
or a series of joints (such as are found in the spine) from
both a static and dynamic perspective.
Clinical Concepts
Intrinsic Properties: viscoelastic and neurophysiological
Able to be modified (increased or decreased) through
exercise, lifestyle, injury, or aging
Properties have limits
Exceeding these properties may lead to dysfunction or
injury
Body Tissues
Include muscle, tendon, fascia, capsule, ligament, bone,
and nervous system components such as muscle
spindle, Golgi tendon organ, and central mechanisms
Tissue hierarchy exists for each joint, joint group, and
individual
Range of Motion
Influenced by arthrokinematics
Limited by soft tissue approximation, bone-bone
contact, periarticular connective tissue tension
Injury
May result if attempts are made to increase or augment
ROM if restriction is due to normal ligament or
capsular limitations or bony contact
Motion available without consideration of time or
dynamic requirements to obtain that position
Periarticular and musculotendinous connective tissue
must be able to deform in the time required for
activity to take place
Clinical Example of ROM Measurement
● A patient in the supine position may have full-knee flexion ROM
demonstrated by the ability of the patient to touch his or her heel
to the buttocks but lacks 5 degrees of extension ROM. When
performing the flexion measurement, the clinician has the patient
positioned in 90 degrees of hip flexion and when performing the
extension measurement, the hip is fully extended.
● However, if the patient is positioned prone, the knee flexion
available may be limited to 130 degrees. In the prone position, the
limitation of the knee flexion ROM is due to flexibility of the rectus
femoris (musculotendinous tissues). ROM of the joint is full and
uncompromised as demonstrated by full range being achieved in
the supine position, limited only by the approximation of the
hamstring and quadriceps mass. No restriction is due to
periarticular connective tissues.
● Lack of full knee extension with the patient supine and the hip
in full extension demonstrates that the restriction in ROM is due
to a limitation of the periarticular connective tissues such as the
posterior joint capsule. In this position the musculotendinous
tissues (hamstrings) are not on tension and cannot contribute to
this limitation. If knee extension is measured with the hip flexed to
90 degrees and if the loss of extension increases to –20 degrees
then a limitation of hamstring flexibility further compromises
extension.

The velocity of human movement varies from
slow and methodical (walking) to high and explosive
(gymnastics). Although good dynamic flexibility is
important for general activities, it is critical for athletics.
Periarticular and musculotendinous connective tissues
must be able to deform in the time required for the
sports activity to take place. Dynamic flexibility often is
limited by the ability of the connective tissues to deform
quickly and easily and the necessary integration of the
neuromuscular system.
If it is deemed that a problem exists with the patient’s
flexibility or ROM, the clinician must be careful to
understand the underlying causes of the patient’s
movement dysfunction. Does the patient suffer from
a true loss of joint range of motion because of a joint
effusion, changes in bony architecture, or alignment
of the articular surfaces? Is the alteration in the ROM
measured from a loss of flexibility of the periarticular
connective tissue structures, musculotendinous tissues,
or both? How does the loss of ROM or flexibility affect
the patient functionally? Often clinicians strive for full
ROM when patients desire or require only a ROM
that allows them to be functional and pain free in their
everyday activities. Identifying the source of the problem
and its extent assists the clinician in developing the most
efficient treatment plan. The appropriate restrictive tissue
component (contractile, noncontractile, or neural) must
be addressed.
The clinician should reserve the term range of motion
to describe what happens concerning the joint’s ability to
move through its anatomical range of motion but use the
term flexibility to describe what happens regarding the
ability of the periarticular and musculotendinous connec-
tive tissues to deform. When evaluating or describing the
range of motion, the clinician should make certain that
any musculotendinous tissue associated with a particular
joint, and that may cross two or more joints, is not on
stretch because this tends to limit flexibility of the joint
Table 25-2
Contribution of Tissue Resistance to Joint Motion: Midposition*
At Extension
−0.5 Radian
g-cm % Total
Skin −58 19
Muscles −133 43
Tendons −25 8 17
Capsule −92 30
Total −308 100
*Frequency of rotation 0.1 cycles per second.
†
Skin reduced the torque required to flex the joint.
‡
Torque in the intact joint.
From Johns RJ, Wright V: Relative importance of various tissues in joint stiffness, J Appl Physiol 17:824-828, 1962.
CHAPTER 25 • Range of Motion and Flexibility 529
being assessed. This renders a false impression of that
joint’s actual ROM.
Structures Limiting Range of Motion
and Flexibility
Joint Surfaces
As previously stated, the ROM available at any joint ulti-
mately depends on the bony architecture and alignment
of joint surfaces (arthrokinematics). If the architecture
and alignment of the articular surfaces are normal,
then the limiting components of any joint’s motion
(before reaching limits imposed by articular alignment
and architecture) must be the periarticular connective
tissues and musculotendinous tissues that are in close
proximity or cross the joint. The impact of these tis-
sues may vary depending upon the joint’s position in
space. Limitation of motion in the midrange has been
attributed primarily to the joint capsule, with further
limitations provided by the surrounding musculature
and finally the tendons that cross that joint according
to studies completed by Johns and Wright with use of
an animal model (Table 25-2).15 At the end of the ROM
available at a particular joint or series of joints, espe-
cially in the more physically active individual or in ath-
letes, muscle may play a larger role in limiting motion
and creating stiffness. deVries,5 in a recalculation of the
data developed by Johns and Wright, has stated that
the primary factor limiting movement at the end of the
range of motion may be muscle and the fascial sheath
associated with it, followed by the capsule and finally
the tendon (Table 25-3).
Knowledge of these facts and appropriate clinical
assessment of the individual patient allow the clinician
to prioritize treatment considerations and interventions
that would be most effective for the patient based upon
where the limitation of motion lies and what the tissues
At Flexion Peak to Peak
0.5 Radian† 0.5 Radian‡
g-cm % Total g-cm % Total
−50 −38 8 2
49 37 182 41
13 42 10
117 88 209 47
133 100 441 100
530 SECTION II • Principles of Practice

Table 25-3
Contribution of Tissue Resistance to Joint Motion: End Range of Motion
Torque Required at Torque Required at Torque Required at
Extension −48 degrees Flexion +48 degrees Peak to Peak
g-cm % Total g-cm % Total g-cm % Total

Skin −70 11.2 −45* −8.7 25 2.2

Muscles
Extensors −35 42.4 0 36.9 35 40
Flexors −230 190 420
Tendons −70 11.2 170 33 240 21
Capsule −220 35.2 200 38.8 420 36.8
Total −625 100 51 100 1140 100

*Note: Skin aided in flexing joints.

From deVries HA: Flexibility. In deVries HA: Physiology of exercise for physical education and athletics, ed 4, p 463,
Dubuque, 1966, Wm C Brown; calculated from data of Johns RJ, Wright V: Relative importance of various tissues in joint
stiffness, J Appl Physiol 17:824-828, 1962.

primarily responsible are. The focus of the intervention
and tissues addressed may need to change as the motion
available changes. Beginning, mid range, and early end
range stiffness and restriction would require the clinician
to focus on the periarticular connective tissues such as
the joint capsule. As the motion available changes, the
focus may need to shift to the musculotendinous tissues
that cross that joint. As an example, the patient with a
restriction in shoulder elevation may require a significant
amount of joint mobilization when the range of motion
available for glenohumeral flexion and abduction are
limited and below 100 to 120 degrees. However, as the
glenohumeral motion available increases, more clinical
attention should be devoted to increasing the flexibility
of the musculotendinous tissues that cross that joint to
obtain a greater functional elevation.
Although the clinician should not ignore regaining full
glenohumeral motion because of restrictions of capsular
structures, more attention should be paid to stretching
the muscles of the rotator cuff that are below the spine
of the scapula and joints center of rotation (infraspina-
tus, teres minor), latissimus dorsi, teres major, pectoralis
major, and pectoralis minor. The impact of the flexibil-
ity of these muscles in allowing the patient to achieve
full ROM often is underappreciated as the glenohumeral
joint’s ROM increases.
Connective Tissue
The connective tissues of the body are composed of
the same basic cellular and extracellular components.
Fibrocytes, chondrocytes, and osteocytes and osteoblasts
are responsible for the synthesis of the fibers and extra-
cellular components associated with fibrous connective
tissue, articular cartilage, and bone, respectively. These
components are summarized in Figure 25-1.

Figure 25-1
Components of connective tissue.
(From Culav EM, Clark CH,
Merrilees MJ: Connective tissues:
matrix composition and its relevance
to physical therapy, Phys Ther
79:308-319, 1999.)
 CHAPTER 25 • Range of Motion and Flexibility 531

Collagen and elastin are extracellular fibers that Table 25-4

complement each other from a functional perspective. Collagens of Connective Tissue
Collagen enables the connective tissues to resist tensile
Tissue Collagen Type*
forces and deformation, providing a skeletal structure
held together by connective tissue, whereas elastin Skin I, III
assists in the recovery of a tissue from deformation.11,16-20 Bone I
Overall, collagen may be compared with a fibrous sus- Hyaline cartilage II
pension bridge. The structural properties of this fibrous Pericondrium I, II
suspension bridge depend on the material properties of Basement membrane IV
the collagen fibrils (physical and mechanical properties), Granulation tissue I, III
Annulus fibrosus I, II
the size of the collagen fibril (area and length), and the
Nucleus pulposus II, I
organization and alignment of the fibrils (Figure 25-2).
Muscle
Influencing the ability of collagen to be deformed with- Epimysium I, III, IV
out being injured should therefore be the focus of the Perimysium I, III, IV
clinician working with the patient with some type of loss Endomysium I/III, IV, V
of ROM or flexibility.11,12,21 Tendon
Although collagen is the common building block, Bundles I
the type of collagen that makes up the different connec- Endotendinium III, IV
tive tissues varies and has been well summarized for the Joint capsule I, III
clinician by various authors.16,17,22-26 Although 19 differ- Fascia I
ent types of collagen have been identified,25 the clinician
*The type listed first is the most abundant found in that tissue.
involved with musculoskeletal rehabilitation is concerned
From Zachazewski JE: Improving flexibility. In Scully R, Barnes ML,
primarily with tissues that are composed mainly of types editors: Physical therapy, Philadelphia, 1989, JB Lippincott.
I through V. Table 25-4 summarizes these tissues and the
types of collagen they comprise.
As viewed in this table, type I collagen is the most collagen does. As healing proceeds it is replaced by stron-
abundant in the tissues with which the rehabilitation cli- ger collagen such as type I.27
nician is primarily concerned. It is responsible primarily Elastin is found in higher concentrations of tissues (e.g.,
for a tissue’s strength and resistance to injury forces and the skin, lungs, and blood vessels) that must be able to
its ability to withstand tensile stress and deformation. withstand repeated stretching and deformation and return
type II collagen is found primarily in hyaline cartilage. to their original state. The arrangement of these fibers var-
type III collagen may be considered a more “imma- ies depending upon the strength and direction of forces
ture” type of cartilage, whose synthesis is triggered by an applied to the tissues in which they are found. Although
injury and resultant healing process.27 Type III collagen the exact mechanism of their extensibility is not clearly
is prominent in the early stages of healing and scar tissue understood, the quantity of elastin found in tissue usually
formation. This type of collagen does not have the ten- is reflective of the amount of mechanical strain imposed
sile strength and ability to resist deformation that type I on it and the need for that tissue to return to its original

Figure 25-2
Collagen: Fibrous suspension
bridge. (From Akeson WH,
Woo SLY, Amiel D et al: The
chemical basis of tissue repair:
the biology of ligaments. In
Hunger LY, Funk FJ, editors:
Rehabilitation of the injured
knee, St Louis, 1984,
CV Mosby.)
532 SECTION II • Principles of Practice
state.16 These fibers are able to increase their length to
150% yet still return to their previous configuration.28
The biosynthesis of collagen is a complicated intra-
cellular and extracellular process (Figure 25-3).17,24,26,29-32
Collagen contains certain amino acids regardless of
its genetic type. Within the cell, these amino acids are
sequenced into a single chain termed a protocollagen.
These amino acid chains are formed from a chain of
repeating tripeptides that most often have a sequence of
glycine: X – Y. X is frequently proline and Y is frequently
lysine. During this intracellular process, three chains of
progeoglycans are synthesized individually and simultane-
ously. Proline and lysine residues within this protocollagen
are hydroxylated to form hydroxyproline and hydroxy-
lysine. In the presence of the enzyme transferase, select
hydroxylysines are then glycosylated. It is during these two
steps that these three proteoglycan chains spontaneously
are bound together to form a right-handed triple helix and
stabilized by intramolecular hydrogen bonds. This triple
helix, the common structural feature of all collagens, is
termed procollagen. Procollagen is then transported out-
side the cell membrane. Outside of the cell membrane extra
peptides are removed from the procollagen and transform
it into tropocollagen. Intermolecular cross-links form
between the tropocollagen molecules. Five tropocollagen
molecules come together, held together by these inter-
molecular cross-links to form a quarter-staggered array.
Figure 25-3
Collagen biosynthesis. A, Intracellular process. (From Zachazewski JE: Improving flexibility. In Scully R, Barnes ML, editors: Physical therapy,
pp 704-705, Philadelphia, 1989, JB Lippincott.)
The intermolecular cross-links that are usually present are
dihydroxylysinonorleucine (DHLNL), hydroxylysinonor-
leucine (HLNL), and histodonohydroxymerodesomine
(HHMD).33 It is the triple helix procollagen and its quar-
ter stagger formation in association with its intermolecular
and intramolecular cross-links that ultimately provide the
connective tissue with its characteristic mechanical proper-
ties to withstand tensile load and deformation.
Tropocollagen fibrils band together to form a microfibril
in a characteristic pattern. Microfibrils then come together
to form subfibrils and these subfibrils come together to
form collagen fibrils. The collagen fibril is the basic load-
bearing structure of connective tissue (Figure 25-4). In
its relaxed state, collagen has a characteristic crimp struc-
ture on a microfibrillar basis.34 The strength and integrity
of this fibril are dependent upon the intramolecular and
intermolecular cross-links as detailed above (Figure 25-5).
The best analogy would be to compare this to the forma-
tion of a rope in which strand upon strand comes together
to form the rope and give it strength.
The collagenous fibrils of any tissue are embedded
in the interstitial spaces between the cells along with
soluble macromolecules, called proteoglycans (PG)
or glycosaminoglycans (GAG), and water. This space
often is termed the ground substance. One of the criti-
cal functions of the PG or GAG is hydration of the matrix
by binding water to the area, which creates a viscous gel
(Continued)

Figure 25-3—Cont’d
B, Extracellular process. (From Zachazewski JE: Improving flexibility.
In Scully R, Barnes ML, editors: Physical therapy, pp 704-705,
Philadelphia, 1989, JB Lippincott.)
that probably serves to provide lubrication and spacing
between the collagen fibers at intercept points where they
cross. The space provided between the fibrils may pre-
vent excessive cross-links between the fibrils that could
decrease tissue mobility and deformation.35 An example
of this would be changes found in the connective tissue
as a result of a joint contracture or arthrofibrosis.
The ability of collagen to withstand tensile stress and to
allow or prohibit motion is primarily dependent upon the
strength of the intramolecular and intermolecular cross-
links as described earlier. However, the fibrils’ direction of
orientation also must be taken into consideration (Figure
CHAPTER 25 • Range of Motion and Flexibility 533
TROPOCOLLAGEN
MICROFIBRIL
3.5 nm
staining sites
SUBFIBRIL
Fibroblast
Fascicular
FIBRIL membrane
Waveform of
FASCICLE crimp structure
Reticular
TENDON membrane
(cut edge)
Figure 25-4
Formation of tendon.
25-6). Collagen tends to be oriented along lines of stress.
Because of this arrangement it is capable of tolerating
significant tensile stress but cannot support significant
shear or compressive stress.10 Collagen fibrils of tendon
have the most parallel orientation and are therefore the
most tolerant of tensile stress. A less parallel orientation is
evident with ligament and joint capsule. Therefore these
tissues are more tolerant of stress in different directions
but still primarily along their lines of orientation.
Tendon, ligament, capsule, fascia, and aponeurosis are
classified as dense regular connective tissues.20 Collagen
fibrils of the tendon have the most parallel orientation;
therefore the tendon is primarily resistant to tensile stress.
Ligament and capsule have a less distinct parallel orienta-
tion, whereas the fascia and aponeurosis are arranged in
multiple sheets or lamella (although the collagen fibrils
associated with these sheets or lamella follow a parallel
and slightly wavy course within each layer, the direction
of orientation of each layer may differ slightly).10,11,36
Because of this arrangement, stress tolerance is allowed
in multiple directions but still primarily along the col-
lagen fibrils lines of orientation. Loose connective tissue,
with its abundant, highly hydrated ground substance,
commonly is found between muscles and in other sites
where mobility is advantageous.20
Limitations of flexibility and range of motion that
result from noncontractile structures (muscle) are a result
of an increase in the stiffness and limitation of the con-
nective tissues to be deformed along their lines of stress.
These are the types of changes that are seen commonly
with joint contractures and arthrofibrosis. The changes
associated with these structures are described in greater
detail later in this chapter.
534 SECTION II • Principles of Practice
Figure 25-5
Intramolecular and intermolecular cross-links.
Muscle and Contractile Elements
Flexibility and range of motion may be limited by tissues
in close proximity to joints that act as passive restraints
(e.g., joint capsule, ligament, fascia, aponeurosis) and
by muscle and its ability to be lengthened. Muscle has
an anatomically complex arrangement of contractile and
noncontractile elements whose ability to deform and
recover from deformation is dependent upon the com-
plex arrangement.37,38 These collagenous elements make
up the series and parallel elastic components of muscle
and provide functional stiffness to enhance the transmis-
sion of tension. The limitation of muscles, ability to be
deformed and stretched is predominantly dependent on
these noncontractile protein components integrated into
Figure 25-6
Direction of collagen fibril orientation. (From Nordin M, Frankel
VH: Biomechanics of collagenous tissues. In Frankel VH, Nordin M,
editors: Mechanics of the musculoskeletal system, Philadelphia, 1980,
Lea & Febiger.)
a viscoelastic network of connective tissue. However,
some resistance to deformation and tension may be attrib-
utable to crossbridge activation between actin and myo-
sin filaments.39-42 In summary, it appears that for muscle,
contractile and noncontractile elements limit deforma-
tion and “flexibility.” The contribution supplied by the
contractile elements appears to be related to the velocity
of deformation early in the range, whereas the farther a
muscle is stretched, the greater the contribution of the
noncontractile elements to the resistance to deformation
and stretch. (Matzkin et al. present a complete descrip-
tion and discussion of muscle and its ability to undergo
deformation and what happens when its tolerance defor-
mation is exceeded in Chapter 5 of this text. Readers are
encouraged to review this chapter in its entirety.)
The neurophysiological impact of muscle stretch-
ing has been well summarized by Stanish et al.43
These key structures, the muscle spindle and the Golgi
tendon organ (GTO), are illustrated in Figure 25-7.
The two characteristic types of muscle fibers impor-
tant in the neurophysiology of stretching are the intra-
fusal and extrafusal fibers. The primary contractile fibers
of any muscle are the extrafusal fibers, which are inner-
vated by alpha motor neurons. The intrafusal fibers may
be considered the sensory elements of muscle deforma-
tion and signal length change and the rate of change
in length of a muscle. As part of the muscle spindle,
the intrafusal fibers are innervated by gamma and beta
 CHAPTER 25 • Range of Motion and Flexibility 535

Extrafusal Spindal branch The GTOs, or type Ib afferent fibers, are located pre-
muscle fiber of intramuscular dominantly at the transition from the muscle to the
nerve trunk
Gamma tendon or from the muscle to the aponeurosis. Only a
efferent fiber small number lay in the tendon.44 These afferent fibers
Motor are sensitive to force production via muscle contrac-
end-plate tion. Upon firing, the GTO inhibits alpha motoneuron
11 Sensory activity to the active muscle (agonist) while facilitat-
fiber
ing the antagonist. Sensitivity to tension varies among
Capsule
GTOs and appears to be correlated inversely with the
Flowerspray 1A Sensory
ending mechanical stiffness of the muscle tendon unit in which
fiber
Nuclear it lies.14 Fukami and Wilkinson have demonstrated that
bag region the greater the stiffness of the muscle tendon unit, the
Lymphatic less the sensitive the GTO to tension and the less likely
space
Annulospinal
it is to fire and inhibit alpha motoneuron activity. A
ending “tight or inflexible” muscle may be more resistant
Extrafusal to recruitment and firing of the GTO. The strain or
muscle fiber deformation of the GTO is most important, not the
Tendon force applied.
A From a practical clinical perspective during any type
Golgi tendon organ
of stretching activity or exercise, the clinician should
Sensory neuron
attempt to minimize or inhibit the input from the type
Ia and II spindle afferents and maximize the input or
influence from the GTO.

Alpha
motoneuron inhibited
B ated with the musculoskeletal tissues are metabolically
Figure 25-7
A, Muscle spindle. B, Golgi tendon organ.
motor neurons. Afferent impulses generated by a change
in muscle length are perceived and transmitted by the
type Ia and type II sensory nerves. The perception of
these afferent signals may activate alpha motoneurons
and supply the extrafusal fibers, which causes the extra-
fusal fibers to contract through a monosynaptic stretch
reflex. Contraction of the extrafusal fibers relieves the
stretch or deformation of the spindle and decreases the
afferent discharge. The Ia and II afferent impulse rate
is a function of muscle length, movement, and efferent
fusimotor activity, all of which are modified by higher
central nervous system commands or spindle activ-
ity. The ability of the muscle spindle to continuously
perceive and signal changes in muscle length (and the
velocity of this change) as it shortens during muscle con-
traction is accomplished by gamma efferent fibers that
continuously reset the spindle.
The muscle tendon junction area also contains
structures that are sensitive to forces produced by
muscular contraction, the Golgi tendon organ (GTO).
Homeostasis
Flexibility of the tissues associated with the musculo-
skeletal system and adequate range of motion of joints
are required for optimal function. The collagens associ-
active elements that are constantly undergoing change
and turnover. Deformation of connective tissue, which
is facilitated by movement and motion, is necessary for
homeostasis.21,39 The response of the tissues may be cat-
egorized as cellular modeling, ground substance, and
collagen response and tissue response. These are sum-
marized in Figure 25-8.
Cellular Modeling
The forces and stress imposed upon the tissues by move-
ment and motion stimulate the fibroblasts to modulate
collagen and glycosaminoglycan (GAG) synthesis,21,45
whereas collagen and GAG that are no longer needed
are removed through enzymatic degradation.46-48 The
rate of turnover and change is much faster for GAG
than for collagen.
Ground Substance and Collagen
Response
GAG (synthesized by the fibroblasts) binds with water
and forms the ground substance that subsequently
provides lubrication for the collagen fibrils. This assists
536 SECTION II • Principles of Practice
Joint Motion Deformation of Connective Tissue
Active
Passive
Tissue Response
Maintain strength of tissue
Maintain flexibility
Maintain joint range of motion
Figure 25-8
Periarticular connective tissue homeostasis. (From Burkardt S: Tissue healing and repair, National Athletic Trainers Association Professional
Preparation Conference, Nashville, 1979.)
in minimizing excessive cross-linking by maintaining
the distance from collagen fibril to collagen fibril. The
development of anomalous cross-links is prevented by
motion occurring,45 whereas the orientation and dispo-
sition of newly formed cross-links along lines of tensile
stress are influenced by stress and motion.21,45 Thus con-
trolled motion during tissue healing can have a positive
outcome in the alignment of these cross-links and in
collagen restoration in general.
Tissue Response
Flexibility of the soft tissues and joint range of motion
are maintained for the range through which movement
usually occurs. The connective tissue maintains its integ-
rity and strength and enables it to appropriately resist the
stresses imposed upon it.
Properties of Connective Tissue
Collagenous tissues exhibit various mechanical and phys-
ical properties when undergoing deformation. It is these
properties that allow connective tissues to respond to
load and deformation appropriately and give the tissues
their ability to withstand high tensile stresses that may
be imposed upon them. The three mechanical properties
exhibited by collagen are elasticity, viscoelasticity, and
plasticity. The three physical properties are force relaxation,
creep, and hysteresis.
Mechanical Properties
Elasticity is a springlike behavior through which elonga-
tion produced by tensile load is recovered after the load
is removed. This property may be best symbolized by a
spring. Viscoelasticity is a viscous or fluid-like property
that allows slow deformation with an imperfect recov-
Cellular Modelling
Synthesis and lysis of
collagen and glycosaminoglycans
Ground Substance and Collagen Response
Aggregation of soft collagen molecules
Appropriate chemical cross-linking to form collagen fibers
Alignment of collagen in direction of stress
Formation of proteoglycan and water complexes in the matrix
ery after the deforming force is removed. The recovery is
a result of the tissue’s elastic property, whereas the imper-
fection is the result of the viscous property. This change
is not a perfect one. The property of viscoelasticity is best
symbolized by a spring and dashpot in parallel. The spring
represents the elastic response and the dashpot represents
the viscous response. The final property is plasticity. With
this property, residual or permanent change caused by
deformation is maintained. Plastic change, which is dif-
ficult to achieve, may be best symbolized by the coulomb
element of dry friction. The viscous properties of tissues
permit permanent plastic deformation. These properties
do not occur separately in the tissues. All three properties
are affected when the tissue is deformed. These proper-
ties are depicted in Figure 25-9.
Physical Properties
Butler et al. have reviewed extensively the physical prop-
erties of collagen in a classic reference.10 The three physi-
cal properties of connective tissue—force relaxation,
creep, and hysteresis—are time-dependent properties.
These are depicted in Figure 25-10.
Force relaxation is defined as the decrease in the
amount of force required to maintain a tissue at a set
amount of displacement or deformation over time. The
rate at which the force is applied affects the resulting
relaxation of the tissue. Generally, the more rapid the
rate of tissue deformation, the larger the resultant peak
force, and the greater the tissues’ subsequent relaxation.
Therefore less force is required to maintain the tissue at a
set displacement. However, one potential problem exists
in attempting to influence the force relaxation response.
Time is required to facilitate viscoelastic and plastic
deformation. The greater the velocity of deformation,
the shorter the amount of time available for change, and
the greater the chance of exceeding the tissue’s ability to
 CHAPTER 25 • Range of Motion and Flexibility 537

Figure 25-9
Mechanical properties of collagen.
(A through C from Viidik A: Func-
tional properties of collagenous
tissues, Rev Connect Tissue Res
6:144, 145, 149, 1973; D from
Frankel VH, Burstein AH: Ortho-
pedic biomechanics, Philadelphia,
1970, Lea & Febiger.)

undergo viscoelastic and plastic change. If the capacity
for viscoelastic and plastic change is exceeded, injury
may occur.
In contrast to force relaxation, the creep response of
the tissue is the ability of the tissue to deform over time
while a constant force is being applied. This constant
force causes the tissue to lengthen over time. Viscoelastic
and plastic deformation occur as a result of the creep
response.
The hysteresis response is the amount of relaxation
a tissue has undergone during any single cycle of defor-
mation and relaxation. It is an indication of the viscous
response of the tissue.
is termed the load-deformation curve (Figure 25-11).10
To assist the reader in understanding the relationship of
the physical and mechanical properties of collagen, the
properties affected in each portion of the curve have
been added to the normal load deformation curve.
In zone I, or the “toe” region of the curve, the crimp
structure or wavy pattern normally found in collagen
fibrils changes to a more parallel arrangement. Little
force is required to do this; a elastic type response occurs.
The further the elongation in this region, the greater
the stiffness and the force required to attain or maintain
this elongation. This region accounts for 1.5% to 4.0%
of the total collagen elongation possible. Unloading

Load Deformation and Stress

Strain Curve
STRESS (LOAD)

The physical and mechanical properties of any tissue have Linear

end point
a direct impact on the tissue’s ability to tolerate load and
deform without a loss of integrity. The curve developed

0% 2% 4% 6% 8% 10%
STRAIN (DEFORMATION)

A B C D

Zone Toe Linear Primary Total

stretch failure failure
Collagen
Fibril

Properties Elasticity Elasticity Viscoelasticity Influenced to

Affected Viscoelasticity Plasticity failure
Plasticity Force
Force Relaxation
Relaxation Creep
Figure 25-10 Creep
Hysteresis
Physical properties of collagen. (From Butler DL, Grood ES, Noyes
FR et al: Biomechanics of ligaments and tendons, Exerc Sports Sci Rev Figure 25-11
6:126-282, 1979.) Load deformation curve.
538 SECTION II • Principles of Practice
the collagen within this region restores the crimp struc-
ture and length. The mechanical property of elasticity is
affected in this portion of the curve.
In zone II, or the linear region, collagen has lost its
crimp structure and is now parallel in its orientation. The
load required to produce further deformation increases
in a linear manner. All mechanical and physical proper-
ties of collagen are affected within this zone. The specific
velocity at which force was applied, or the length of time
that the force is applied, may determine which specific
property is affected. Although all of these properties are
time dependent, the velocity of the deformation also
influences force relaxation. A group of collagen fibrils
being tested will tolerate a deformation of 2% to 5%. The
end of the linear zone is characterized by the linear end
point. That is also the starting point for zone III.
Zone III is the region of primary failure. Once the
linear end point (yield point) has been reached, isolated
collagen fibrils begin to fail. Failure occurs in an unpre-
dictable manner. In this region, if the load has been
applied too quickly, not allowing for viscoelastic and
plastic change, the force relaxation response is affected
in such a manner that the collagen fibril fails. Excessive
viscoelastic and plastic change may cause collagen failure
by allowing too much deformation via the creep response.
Once the maximum tolerable load is reached, complete
failure occurs. This occurs when the collagen fibril has
been deformed by 6% to 10% of its total resting length.
The maximum strain at failure of collagen fiber bundles
in human patellar tendon, lateral collateral, anterior cru-
ciate, and posterior cruciate ligaments has been demon-
strated to range from 13% to 15%. This is thought to be
a result of organization of the fiber bundles within the
whole structure and the support that they provide one
another.49
Impact of Aging, Immobilization,
and Remobilization
Aging
Aging is a normal and continual process of the human
body. Collagen and elastin, the connective tissue ele-
ments that make up tendon, capsule, muscle, fascia, and
aponeurosis, undergo change with age. The changes
within these elements influence the response of these tis-
sues to stress, the amount of deformation possible, the
ability of the tissue to return to its original length, and
how forces are transferred within the tissues.
Total collagen content of tendon,50 capsule,51 and
muscle52 increases, in addition to the collagen fibril diam-
eter.50 These changes increase the stability of the collagen
fibril.50,53,54 This increase in stability is a result in the total
collagen of these tissues and a result of the maturation and
development of stable and more complex intermolecular
cross-links between tropocollagen molecules.53-55 These
changes are summarized in Table 25-5.
With age, associated changes also are evident through
a decrease in the components of the ground substance of
muscle52 and tendon.50 The decrease in these components
results in a reduction the gel-fiber ratio. The gel-fiber
ratio assists in keeping the collagen fibrils separated. A
reduction in this ratio, which allows binding between
collagen and GAG molecules that envelop the fiber, may
be one reason for the increase in stiffness that results
from aging.50,56
Physical properties of the crimp structure of the
collagen fibril also change with age. The wavelength of the
crimp increases while the wave-crimp angle decreases.57
These changes allow the collagen fibril to reach the linear
zone of the load-deformation curve sooner. This results
in a steeper curve, or increased tissue stiffness, which
translates clinically into the tissue reaching its available
limits of deformation sooner.
During the aging process the stiffness of a tissue and
its resistance to deformation may result in an alteration
of flexibility (see Table 25-1). This alteration may make
it difficult for individuals to move easily into ranges
required for daily activities (e.g., reaching overhead) or
obtaining adequate hip extension for an efficient gait
cycle. This alteration or loss may be a result of altered
joint range of motion, soft tissue deformation, or muscle
flexibility. These changes may be static or dynamic in
nature. The challenges to the clinician are to determine
what these changes are from, can they be altered through
rehabilitation intervention, and if so, which methods of
intervention are most effective and efficient.
Aging and Joint Motion
The tendency exists for normal joint range of motion
and muscle flexibility to change with age.57-65 These
changes vary by joint. A comparison of the average joint
range of motion available in males ranging in age from
birth to 85 years is presented in Table 25-6 based on
data from Boone and Azen58 and Walker et al.64 These
comparisons for joint motion by age demonstrate a
decrease in range as males age. Data are consistent
with other studies.62,63 Similar data for females have not
been found in the literature, but the clinician should
Table 25-5
Age-Related Changes in Connective Tissues
Increased with Age Decreased with Age
Total collagen content Water
Collagen fibril diameter Elastin
Collagen crosslink maturation Glycosaminoglycans
Collagen crosslink stability
Number of elastic cross-links
 CHAPTER 25 • Range of Motion and Flexibility 539

Table 25-6
Comparison of Range of Motion by Age in Males58,64
0 – 19 yr58 N = 53 20 – 54 yr58 N = 56 60 – 85 yr64 N = 30
Degrees of Motion
Mean SD Mean SD Mean SD

Shoulder
Abduction 185.4 3.6 182.7 9.0 155 22
Flexion 168.4 3.7 165.0 5.0 160 11
Extension 67.5 8.0 57.3 8.1 38 11
Medial rotation 70.5 4.5 67.1 4.1 59 16
Lateral rotation 108.0 7.2 99.6 7.6 76 13
Elbow
Beginning flexion 0.8 3.5 0.3 2.7 6 5
Flexion 145.4 5.3 140.5 4.9 139 14
Forearm
Pronation 76.7 4.8 75.0 5.3 68 9
Supination 83.1 3.4 81.1 4.0 83 11
Wrist
Flexion 78.2 5.5 74.8 6.6 62 12
Extension 75.8 6.1 74.0 6.6 61 6
Radial deviation 21.7 4.0 21.1 4.0 20 6
Ulnar deviation 36.7 3.7 35.3 3.8 28 7
Hip
Beginning flexion 3.5 4.3 0.7 2.1 11 3
Flexion 123.4 5.6 121.3 6.4 110 11
Abduction 51.7 8.8 40.5 6.0 23 9
Adduction 28.3 4.1 25.6 3.6 18 4
Medial rotation 50.3 6.1 44.4 4.3 22 6
Lateral rotation 50.5 6.1 44.2 4.8 32 6
Knee
Beginning flexion 2.1 3.2 1.1 2.0 2 2
Flexion 143.8 5.1 141.2 5.3 131 4
Ankle
Plantar flexion 58.2 6.1 54.3 5.9 29 7
Dorsiflexion 13.0 4.7 12.2 4.1 9 5

From Zachazewski JE: Flexibility for sports. In Saunders B, editor: Sports physical therapy, Norwalk, 1990, Appleton and Lange.

expect similar types of changes with age. These types of
data should remind the clinician that “normal” range
of motion varies by age and that rehabilitation goals
should be set with these considerations in mind.
Aging and Muscle Flexibility
Studies in the literature on muscle flexibility tend to
use composite scores of the individual’s ability to move
through a range of motion in which two-joint muscles
(e.g., hamstrings over hip and knee; rectus femoris over
hip and knee) are put on stretch. One of the reasons
that the flexibility of these muscles is studied to such a
degree is that these muscles most frequently to suffer
muscle strain injury.
Kendall and Kendall published one of the first and
largest studies (N=5115; Figure 25-12) in 1948 of
how “flexibility” changes according to age in healthy
individuals between the ages of 1 to 22 years.60
Flexibility of the hamstrings (measured by the ability to
touch fingers to toes in long sitting) decreased in both
males and females between ages 1 to 12 or 13. After this
age the ability of the subjects to touch their toes again
increased. Similar findings have been demonstrated by
Hunter et al. in high school athletes between the ages
of 12 and 18.
It appears that healthy, growing children and ado-
lescents gradually lose flexibility until after puberty.
Flexibility regained at the time of adulthood appears to
then be gradually lost.57-64 These changes are not irre-
versible, however, as it has been demonstrated that flex-
ibility and range of motion may be regained through
the use of a specific exercise program.66 Whenever
flexibility (joint range of motion or muscle) is consid-
ered in relation to age, the clinician must always take
into consideration the general activity pattern or level
of the individual.
540 SECTION II • Principles of Practice
Figure 25-12
Age and ability to reach toes in
long sitting. (From Kendall HO,
Kendall FP: Normal flexibility
according to age groups, J Bone
Joint Surg 30A:690-694, 1948.)
Questions can be raised regarding whether certain
changes, seen in the composition and physiology of the con-
nective tissues associated with aging may be secondary to
decreased physical stress. Individuals who maintain a healthy,
active lifestyle that requires their joints to go through large
ranges of motion and their muscles to be stretched though
various motions may retain motion and minimize the effects
of hypokinesis (lack of movement/motion) and subsequent
movement dysfunctions to a greater degree than those indi-
vidual who are more sedentary and do not tend to push the
limits of their range. Viidik has summarized the effect of
activity on connective tissue and the need for maintaining a
physically active lifestyle very well.53
Effect of Activity on Connective Tissue*
“Connective tissues have a capacity to react to physical exercise by
a retardation of the normal temporal changes. Moderate life-long
training keeps the connective tissues ‘younger.’ The retardation
is achieved in the time period before maturity and in the years
thereafter. The age changes seem to occur with the same speed
in training as in sedentary individuals, all the time at a parallel, but
‘younger’ level.”
*According to Viidik.53
In summary, age-related changes in the connective tis-
sues result in a tendency for there to be a loss of flexibility
and motion. The binding between collagen fibrils increases
because of a loss of the tissues’ normal gel-fiber ratio. The
cross-links present become more stable, which causes an
increase in the slope of the normal load deformation curve
and the tissue reaching its limits of deformation sooner.
Immobilization
Immobilization of one or more joints and their sur-
rounding tissues, whether absolute (as may be imposed
by some type of casting or internal or external fixation),
or relative (as may be imposed by an individual no longer
going through a previously available range of movement
because of age, injury/pain, or an alteration in physi-
cal activity or lifestyle) causes changes at a tissue level.
These changes are a result of a lack of or alteration in the
deformation of the periarticular connective tissues from
restricting their ability to move freely. The restriction of
motion at a joint may be due to contracture of the cap-
sule, muscle, and/or the proliferation of fibrofatty tissue
within the joint space.67-69
Numerous investigations have examined the effect of
immobilization on the periarticular connective tissues
(i.e., tendon, joint capsule, capsular ligaments, and
fascia).21,35,45,68,70-82 These changes, summarized in Figure
25-13, may be divided into those that occur at a cel-
lular level (cellular modeling), the response within the
ground substance and collagen, and responses at a tis-
sue level. From a clinical perspective, after injury it does
not appear that rigid immobilization is required. These
changes occur even if the joint does not move through a
full normal range of motion, which stretches periarticu-
lar connective tissue and muscle to its fullest extent. The
time required for these changes to take place is shorter
than the time required for recovery from the changes
imposed by immobilization.35,78 Thus immobilization
must be imposed only when absolutely necessary and
that motion, in total or in part, must be maintained and
encouraged throughout the process of injury, repair,
rehabilitation, and return to maximal functional level.
 CHAPTER 25 • Range of Motion and Flexibility 541

Figure 25-13
Changes from immobilization—connective tissue and synovial joints. (Modified from Burkhardt S: Tissue healing and repair, National Athletic
Trainers Association Professional Preparation Conference; Nashville, 1979; and Olson VL: Connective Tissue Response to Immobilization and
Mobilization. Current Concepts in Orthopedic Physical Therapy – Home Study Course 11.2.1; Alexandria, 2001, American Physical Therapy
Association.)

Cellular Modeling present. If an inflammatory process is present, type III

No significant change has been demonstrated in the
total collagen content measured from periarticular con-
nective tissue after 9 weeks of immobilization.35,68,70-74,78
Despite the fact that no change in total collagen content
occurs with immobilization, an increase is apparent in
the turnover rate (increased synthesis and degradation)
of collagen, based on animal models using ligament and
tendon for study.72 A difference exists in how ligament
and periarticular connective tissue respond to immobi-
lization. With immobilization, ligament loses stiffness,
whereas periarticular connective tissue gains stiffness. No
alteration occurs in the type of collagen produced during
a period of immobilization if no inflammatory process is
collagen is still predominantly formed early during the
inflammatory period when new collagen is laid down
compared with type I and IV collagen that is formed
later as the scar and collagen matures.35,75,78,83,84 The lack
of any significant increase in quantity of collagen con-
tent indicates that other mechanisms more subtle than
fibroplasias and scar formation that affect the quality of
the collagen and its ability to deform are involved in the
contracture process as a result of immobilization.45
Ground Substance and Collagen Response
A profound response of the extracellular matrix, or
ground substance, to immobilization occurs. There is
542 SECTION II • Principles of Practice
significant loss of water and glycosaminoglycans (GAG)
from the ground substance. This loss results in an altera-
tion of the gel-fiber ratio and a decrease in the viscosity,
lubrication, and the interfiber distance between collagen
fibrils.68,71-73 The loss of GAG is correlated significantly
with joint stiffness. The reduction of this GAG buffer,
in conjunction with the continued synthesis of collagen
and the absence of mechanical forces, facilitates the syn-
thesis of increased cross-links at strategic points between
adjacent collagen fibrils (Figures 25-14 and 25-15) and
an alteration in the collagen weave pattern.21,35,68,71,73
Cross-links become more stable and mature over time,
which results in an increase in the stiffness of periarticu-
lar connective tissues thus restricting movement.19,35 The
biochemical and biomechanical changes described gen-
erally result in a qualitative rather than a quantitative
change in the collagen structure within the connective
Figure 25-14
Collagen fibril cross-linking. A and B, Preexisting fibers. C, Newly
synthesized fibril, D, Cross-links as the fibril joints the fiber. X, Notal
point where the fibers romally slide past one another freely. (From
Akeson WH, Amiel D, Woo SLY: Immobility effects of synovial joints:
the pathomechanics of joint contracture, Biorheology 17:95, 1980.)
Figure 25-15
Restriction from excessive
crosslinking. A, Collagen fibril
arrangement. B, Collagen fiber
cross-links. C, Normal stretch.
D, Restricted stretch resulting
from cross-link. (From Woo
SLY, Matthew JV, Akeson WH:
Connective tissue response to
immobility: Correlative study of
the biomechanical and biochemical
measurement of normal and
immobilized rabbit knees, Arthritis
Rheum 18:257-264, 1975.)
tissue. The qualitative change is attributable to a quanti-
tative and qualitative change in the number and matu-
rity of cross-links. For this reason, motion must continue
to occur whenever possible to maintain the GAG buf-
fer between collagen fibrils to prevent hypomobility and
joint dysfunction.
Tissue Response
With the passage of time, the formation and accumu-
lation of new collagen are important regardless of how
small that accumulation is.71 A loss of free gliding of
these tissues occurs, and collagen may be laid down ran-
domly, which leads to a haphazard arrangement and the
formation of adhesions within the connective tissues,
interfering with proper joint mechanics and tissue defor-
mation.21,68,74 A summary of the responses from the spe-
cific tissues is detailed in Figure 25-13 based on a review
by Olson.82
One of the most significant changes that can occur
at a tissue level occurs in muscle. Atrophy and a loss
of strength occur, and the ability of the muscle to be
lengthened or stretched also is altered. The changes that
occur with muscle that has been immobilized have been
well summarized by Olson82 and Gossman et al.85 and
are reviewed briefly for the reader. Interested rehabilita-
tion clinicians are encouraged to review Gossman’s clas-
sic review and reference in total in the journal Physical
Therapy.
Immobilization with Muscle Lengthened
Adaptation to immobilization begins within 24 hours.
The exact method of adaptation appears to vary with age
in the animal model. In the “adult” animal model when
muscle is immobilized in a lengthened position, muscle
 CHAPTER 25 • Range of Motion and Flexibility 543

fibrils adapt by adding sarcomeres at the end of the fibril
while at the same time decreasing the length of each sar-
comere. However, in the “young” animal model it is not
muscle but tendon that elongates. This effectively places
the muscle in a shortened position. This “shortened” posi-
tion then causes a reduction of the number of sarcomeres
in series to occur. This change is similar to what happens
when a muscle is immobilized in a shortened position.
Immobilization with Muscle Shortened
The changes that occur in muscle that has been immobilized
appear to be the most profound when muscle is immobilized
in a shortened position. A decrease of up to 40% of the num-
ber of sarcomeres occurs with immobilization in a shortened
position. In conjunction with the decrease in number of
sarcomeres, an increase occurs in the length of the remain-
ing sarcomeres. With passive immobilization these changes
appear to begin after 5 days, whereas with a decrease in
length that may be imposed by more “active” means (spas-
ticity or electrical stimulation), changes may be seen in as
few as 12 hours. These changes have been demonstrated in
muscles that have undergone prolonged immobilization in
addition to muscles that have been required to function con-
tinuously although in a chronically shortened range.86 Upon
termination of the immobilization, the number and length
of sarcomeres return to normal. As with muscle immobi-
lized in a lengthened position, the change in the number
of sarcomeres is also related to age for muscle immobilized
in a shortened position. In the “young” animal model, the
rate of addition decreases; however, in the “adult” animal
models, an absolute loss occurs. Recovery takes longer in the
adult than in the youth. Shortened muscle also demonstrates
steeper passive tension curves (greater stiffness). This change
appears to be a reflection of connective tissue loss occurring
at a slower rate than muscle contractile tissue loss. The ensu-
ing increase in connective tissue results in increased muscle
stiffness and a reduction in extensibility of the muscle.87,88
The thickness of the endomysium and perimysium also may
affect the extensibility of the muscle.
Olson has recommended considering “immobiliza-
tion injury” as part of the clinical construct, examination
process, and rehabilitation planning (Figure 25-16).82
Immobilization and its effects on connective tissue result
from absolute immobilization (casting, splinting, internal
or external fixation) but also from “relative” immobilization
(restriction of ROM) as has been discussed earlier. Based
on the body’s ability to respond to change by adaptation
and remodeling, the clinician should strive to minimize
the effects of immobilization to the greatest degree pos-
sible. In doing so, the clinician attempts to shorten the
slope and magnitude of the changes caused by immobi-
lization and maximize the efficiency and effectiveness of
rehabilitation and the ability to return patients to their
normal lifestyle as soon as possible.

Pre-Injury/Normal
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High Probability for Normal Function/Injury Prevention

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INCAPACITATING
INJURY
Figure 25-16
Immobilization “injury” and early intervention. (From Olson VL: Connective Tissue Response to Immobilization and Mobilization. Current
Concepts in Orthopedic Physical Therapy – Home Study Course 11.2.1; Alexandria, 2001, American Physical Therapy Association.)
544 SECTION II • Principles of Practice
In summary, immobilization affects the musculosk-
eletal connective tissues of the body in multiple ways.
The clinician should strive to maintain the motion and
extensibility of all tissues to the maximum degree pos-
sible throughout the healing stages and rehabilitative
course by striving to prevent or minimize the impact of
immobilization.
Remobilization
The changes that are a result of immobilization are
reversible. The extent to which these changes can be
reversed is influenced by the age of the patient, the
length of time of immobilization, and the overall
health and quality of the tissues. These are summarized
in Figure 25-17.
Cellular Modeling
Synthesis and lysis of collagen continue to occur while
motion stimulates the production of GAG.21,74,79
Ground Substance and Collagen Response
The ground substance, which suffered a loss of water and
GAG during the immobilization process, regains these
valuable components with remobilization. The gel-fiber
ratio, which increases the lubrication and interfiber dis-
tance, returns to normal. The rate of recovery is faster
than the rate at which the fiber lubrication and interfiber
distance were lost. A good correlation is demonstrated
between the biomechanical and biochemical results. As
the components of the ground substance increase, joint
stiffness decreases.
Contracture/Adhesion Stress Imposed by Exercise
Return of Range of Motion and ADL
Tissue Response
Increased flexibility
Restored joint play
Improved gliding
Loss of adhesions
Increase or decrease of number and
length of sarcomeres as appropriate
Restored length-tension relationship
Figure 25-17
Remobilization. (From Burkhart S: Tissue healing and repair, National Athletic Trainers Association Professional Preparation Conference,
Nashville, 1979.)
Tissue Response
As a result of motion, new collagen fibrils are oriented
along their lines of stress,21,45,74 and previously formed
collagen fibrils are reoriented along their proper lines of
stress. Muscle fibrils respond by increasing or decreasing
their number of sarcomeres in series within each fibril,
correcting the length-tension relationship that may have
been altered by shortening or lengthening of the mus-
cle. Flexibility is increased and joint mechanics return
to normal, which breaks the negative cycle and connec-
tive tissue changes imposed by immobilization. Normal
movement and function are restored.
Factors Influencing Connective
Tissue Deformation
From a rehabilitation perspective, the major factors influ-
encing the ability of connective tissue to undergo some
type of deformation are temperature of the tissue, the mag-
nitude and velocity of the force applied, and the time
over which the force is applied. The rehabilitation spe-
cialist can manipulate each of these variables in an effort
to achieve an efficient and effective gain in flexibility and
joint range of motion.
Temperature
The physical and mechanical properties of connective
tissue may be affected by an alteration in the temperature
of the tissue or collagen. The mechanical properties of col-
lagen are temperature independent below 37°C (98.6°F),
whereas above this, temperature changes occur that allow
Cellular Modeling
Synthesis of glycosaminoglycans
Synthesis and enzymatic
degradation of collagen
Ground Substance and Collagen Response
Glycosaminoglycans
Water
Lubricating action
Interfiber distance
Inappropriate chemical cross-links
 CHAPTER 25 • Range of Motion and Flexibility 545

the cross-links between collagen fibrils to be broken more 15.0

easily and more rapidly. The most profound changes are Tendon samples
compared at full load
capable of occurring above 40°C (104°F)89-91 with an upper 12.5
limit of therapeutic temperatures of 45°C (113°F).92-94 The Experiment 1
greatest amount of residual change in length occurs with 10.0 9.13
39˚C vs 45˚C
p = 0.003

Time (minutes)
the use of low-load, long-duration forces applied to tissues !6.60 Experiment 2
41˚C vs 43˚C
when they are at their highest temperatures.92-94 This type 7.5 p = 0.028
of loading is thought to have a larger impact on the vis- Experiment 3
cous elements of collagen than high-load, short-duration 43˚C vs 45˚C
5.0 p = 0.024
stress used to affect elastic elements.95 4.78
!2.66 2.86
When considering the effect that temperature has on
2.5 !1.11 1.70
collagen, clinicians should keep these key points in mind !1.00 1.48
0.81
!0.49
and use these principles to their advantage: !0.33
1. The amount of force required to attain/maintain 0
39˚ 41˚ 43˚ 45˚
a desired deformation decreases as temperature A Temperatures evaluated
increases (Figure 25-18).
2. The time required to deform collagen to the point
of failure is inversely related to temperature (Figure
25-19A).
3. The higher the temperature, the greater the load colla- 500 Tendon samples
compared at
gen is able to tolerate before failure (Figure 25-19B). 403 full load
400
4. The higher the temperature, the greater the amount of !89
Load (grams) Experiment 1
deformation possible before failure (Figure 25-19C). 300 341 299 39˚C vs 45˚C
In isolated tissue models (rat tail tendon), less tissue dam- 238 !67 !77 p = 0.001
age occurs at higher temperatures, and changes appear to !60 Experiment 2
200 155 41˚C vs 43˚C
occur more rapidly or efficiently. Clinicians should consider 125 !45 p = 0.002
methods of increasing tissue temperature, within therapeutic 100 !46 Experiment 3
limits (37° to 42°C; 99° to 108°F) tolerable to the patient 43˚C vs 45˚C
p = 0.014
through the use of appropriate modalities. The depth of 0
39˚C 41˚C 43˚C 45˚C
the tissues that the clinician is trying to influence should Temperatures evaluated
be taken into consideration. Superficial heating modalities B
such as hot packs, paraffin, and warm water whirlpools may
be sufficient to increase the temperatures of connective tis-
sues that are relatively superficial (e.g., as in the hand) but
insufficient to influence deeper tissues associated with the 15 Tendon samples
shoulder, hip, or spine. For deeper tissues, modalities such compared at
full load
as ultrasound or diathermy should be considered.96-98 12
Elongation (percent)

Figure 25-18
Effect of temperature on force relaxation response. (From Lehmann
JF, Masock AJ, Warren CG et al: Effect of therapeutic temperatures
on tendon extensibility, Arch Phys Med Rehab 51:481-487, 1970.)
Experiment 1
9 39˚C vs 45˚C
p = 0.001
6 Experiment 2
41˚C vs 43˚C
p = 0.024
3 Experiment 3
43˚C vs 45˚C
0 p = 0.006
C 39˚C 41˚C 43˚C 45˚C
Figure 25-19
A, Effect of temperature on time of elongation to failure. Time to
achieve 2.6% strain with the treatment procedures using full load and
comparing the temperatures of 39° vs. 45°, 41° vs. 43°, and 43° vs.
45°C. B, Maximum load at rupture subsequent to treatment procedures
incorporating the application of full load and temperatures compared at
39° vs. 45°, 41° vs. 43°, and 43° vs. 45°C. C, Effect of temperature on
percent elongation to failure. Maximum strain at rupture subsequent
to treatment procedures incorporating the application of full load and
temperatures at 39° vs. 45°, 41° vs. 43°, and 43° vs. 45°C. (From Warren
CG, Lehmann JF, Koblanski JN: Elongation of rat tail tendon: effect of
load and temperature, Arch Phys Med Rehab 52:465-474, 1971.)
546 SECTION II • Principles of Practice
The combination of heat and stretching allows the great-
est deformation of the tissue while using the lowest and saf-
est amount of force, in the shortest amount of time. This
combination allows maximum residual gain from elonga-
tion. Allowing the tissue to “cool” while in the elongated
or deformed state may enhance this residual gain.12
Along with the use of therapeutic modalities to
increase tissue temperature, exercise also may be used
to increase intramuscular temperature.99,100 However,
these temperatures appear not to be able to be increased
above approximately 39°C (102°F) (Figure 25-20). The
inability to exceed 39°C is due to the body maintaining
temperature equilibrium between heat production and
dissipation in normal instances. Therefore the increase
in intramuscular temperature from exercise may not be
sufficient to influence viscoelastic behavior and passive
energy absorption of the connective tissue associated
with muscle during stretching exercises.101 Although
a small contribution may be based on some increase in
intramuscular temperature, it may not play as significant
a role as previously thought regarding “warm-up” pre-
ceding stretching exercises.102-104
Consideration of the effect of temperature on a
muscle’s ability to be “stretched” must accompany con-
sideration of the impact on the neurophysiological char-
acteristics of the muscle-tendon unit. The sensitivity of
the GTO to sustained stretch appears to increase with
increased temperatures of the muscle tendon junction.14
Figure 25-20
Effect of exercise on intramuscular temperature. (From Asmussen E,
Boje OVE: Body temperature and capacity for work, Acta Phys Scand
10:1-22, 1945.)
Force: Magnitude, Velocity, and Time
Although increased tissue temperature may prove a
valuable tool to gain tissue flexibility in the absence of
a deforming force, heat alone does not cause a change
in collagen deformation. However, a deforming force,
even without the elevation of tissue temperature, causes
a change in collagen length.92 The key factor for any
change in flexibility is the deforming force.
When considering the magnitude and velocity of the
force applied to shortened tissues, and the time that the
force will be applied, the clinician should consider all fac-
tors presented and discussed thus far in this chapter. What
will be the effect on the physical and mechanical proper-
ties of the collagen and tissue that must be influenced?
The most common method that the clinician should
consider is the application of low-load, long-duration
forces. These will result in the greatest long-term gains
with minimal risk of injury to the patient by an attempt
to influence the viscoelastic properties of the collagen.
The clinician also should consider the effect of tissue
temperature to gain any further advantage possible.
At times, however, despite the clinician’s best efforts,
more aggressive means may be needed to gain flexibil-
ity and range of motion. In these instances manipulation
under anesthesia or surgical release is required. These
more aggressive techniques also require follow-up reha-
bilitation. Should these types of procedures be required,
the clinician’s primary responsibility now becomes main-
taining the flexibility and range of the tissue gained by
these procedures.
Clinical Management Considerations:
Muscle Flexibility
Injury Prevention and Physical Performance
Having good muscle flexibility is considered an integral
component of health and fitness. Flexibility and stretch-
ing programs historically have been stated to enhance the
tissue and bodies ability to dissipate impact shock, accom-
modate stress, and absorb abnormal or excessive forces to
thereby reduce injury102,105,106 and improve physical per-
formance.107 The most common arena for study of the
impact of flexibility on injury and injury prevention has
been athletics, because an estimated 30% to 50% of all
sports injuries are musculotendinous in origin, with the
majority being acute muscle strains.108-111 Because of this
high incidence, flexibility and stretching programs are a
common part of athletics in an effort to reduce the fre-
quency and severity of injury. Historically, hundreds of
articles have been written regarding this topic area. As
with all research, the reader must critically review the
article for relevance, design and methodology, data and
statistical accuracy, whether the conclusions are supported

appropriately by the data and the ability to provide an
appropriate comparison to other published literature.
Unfortunately, as with much of the rehabilitation litera-
ture, these factors may be subject to question, leading to
questions and concerns regarding the conclusions made.
Because of these factors, a number of recent studies and
substantial, well-designed reviews of the literature have
challenged these commonly held beliefs on stretching
and flexibility programs.112-116 Others feel that for certain
sports with a high percentage of ballistic, bouncing, or
jumping activities with high-intensity stretch–shortening
cycles (e.g., soccer, sprinting, hurdles), some evidence
may suggest that stretching may assist in the prevention
of injury.117, 118
These challenges to existing historical beliefs are
perhaps best summed up in a meta-analysis review pro-
vided by Thacker et al.116 and a review of literature by
Shrier.118,119
Thacker et al.116 identified 361 papers published
between 1966 and 2002 that reported on flexibility (its
underlying physiology and relation to stretching), risk
factors for injury and methods for prevention, alterna-
tive approaches to stretching, the effects of stretching
on performance and injury prevention, and the adverse
effects of stretching. Of the 361 papers identified, only
six reports compared stretching with other methods
to prevent injury. According to Thacker et al. the 361
papers reviewed clearly demonstrated that stretching can
increase muscle and joint flexibility (usually measured as
short-term static flexibility); however, extremes of inflex-
ibility and hyperflexibility increase the risk of injury.
What cannot be determined from their well-designed
meta-analysis and review of the literature is any relation-
ship between flexibility programs and injury prevention.
Based upon the fact that out of 361 studies reviewed
only six met their full analysis criteria, Thacker et al.
state that sufficient evidence does not exist to endorse
or discontinue routine stretching before or after exer-
cise to prevent injury among competitive or recreational
athletes. This is a critical point for all involved in physi-
cal rehabilitation of patients and athletes to remember.
The question has not yet been fully answered regard-
ing the true value of stretching and flexibility exercises.
The need is for further research with well-controlled,
randomized controlled trials to truly determine whether
Impact of Stretching on Sports Injury Risk*
“There is not sufficient evidence to endorse or discontinue routine
stretching before or after exercise to prevent injury among competi-
tive or recreational athletes.”
*According to Thacker et al.116
CHAPTER 25 • Range of Motion and Flexibility 547
flexibility and stretching programs aid in the prevention
of injury.
Shrier118 reviewed 293 citations retrieved from an
extensive Medline search concerning whether or not pre-
exercise stretching prevents injury. Only 17 of the 293
articles published between 1996 and 2001 used a con-
trol group for comparison purposes. Of these 17 arti-
cles, seven suggested that preexercise stretching may be
beneficial for injury prevention (Table 25-7);120–126 three
suggested it was detrimental (Table 25-8);127–129 and six
suggested that no difference occurred (Table 25-9).130–136
Details of these articles regarding risk, odds, and hazard
ratios relative to injury are summarized in Figure 25-21.
Shrier also has completed a second critical review of the
literature related to stretching and performance (or per-
formance testes) between 1966 and 2002.119 Questions
asked were the following: What is the impact of stretch-
ing on physical performance? Does a difference exist from
a short-term/acute bout to long-term/regular routine
perspective? This review has led him to conclude that an
acute bout of stretching does not improve force or jump
height and that results for running speed are contradic-
tory. Regular stretching, however, improves force, jump
height, and speed, although no evidence exists that it
improves running economy.
Considering these large literature reviews and meta-
analyses, significant room exists for further contribution
to the body of knowledge regarding stretching with well-
controlled and well-designed studies. Data must be col-
lected and studies completed that continue to explore the
risks, benefits, and methods of stretching relative to injury
prevention, management, and human performance.
Based on the literature published to date, the clinician
should be asking the question “why stretch?” Stretching
before, during, or after an activity or event histori-
cally has been prescribed as a method of minimizing
the chance of or avoiding an injury. However, a critical
view of the literature provokes questions regarding the
efficacy of stretching relative to injury prevention. The
“gain” from stretching, perceived or real, appears to be
specific to the individual. The impact of this on an indi-
vidual patient’s sense of well-being, progress, or physical
need should not be discounted. Performing stretching
exercises has been shown in some cases to increase pain
threshold,137-139 allowing Shrier119 to present and concep-
tually discuss that stretching may act like an analgesic,
and that any subsequent increase in ROM or flexibility
from stretching is due partially to this analgesic effect.
All individuals vary in what they specifically feel that they
require relative to stretching. Some feel that they require
a significant amount of time to stretch to obtain satis-
faction and a gain (perceived or real) in their flexibility,
whereas others feel that they require minimal or none.
Stretching should perhaps be considered an individual-
ized preference and activity based upon the individual
 548
SECTION II • Principles of Practice
Table 25-7
Brief Summary of Clinical Studies That Suggest Stretching Immediately Before or After Exercise May Prevent Injury
Reference Population Study Design Results Comments

Ekstrand, Gillquist, 180 Elite male soccer RCT intervention of warm-up, The group receiving the The multiple interventions prevent
Liljedahl120 players stretching, leg guards, pro- combination intervention the conclusion that preexercise
phylactic ankle taping, controlled had a RR of 0.18 (0.6 in- stretching is beneficial
rehab, information and juries/month vs. 2.6
supervision injuries/month)
Bixler and Jones121 5 High school football Pseudo RCT intervention of half Intervention group had If an intervention team did no stretch
teams time stretching and warm-up 0.3 injuries/game vs. 0.8 at half time they were considered part
injuries/game for control of the “control data.” No numbers
group were given for changes in exposure.
With increased exposure and constant
risk, frequency of injuries is expected
to increase. Therefore risks cannot be
calculated. Also, a co-intervention of
warm-up occurred.
Ekstrand, Gillquist, 180 Elite male soccer 1-year prospective cohort study All seven quadriceps strains No real analysis of stretching before
Moller, et al.122 players affected players of teams in exercise. Multiple co-interventions.
which shooting at the goal
occurred before warm-up
(p<.0.058). Hamstring
strains were most common
in teams not using special
flexibility exercises (t=2.1).
Wilber, Holand,
Madison, et al123
Cross and Worrell124
Hilyer et al.125
Hartig and Henderson126
For the relative risk (RR) or odds ratio (OR), a value above 1 means a higher rate of injury in people who stretch
From Shrier I: Does stretching help prevent injury? In MacAuley D, Best T, editors: Evidence-based sports medicine, London, 2002, BMJ Publishing Group.
518 Recreational cyclists
195 Division III college
football players
469 Firefighters
298 Basic training recruits
Survey of overuse and other
related factors
Chart review, pre and post stretch-
ing intervention using historical
controls
Stretching immediately before
exercise
Cluster randomization by fire
district
Stretching at work
Obviously not possible
immediately before fire
Cluster randomization by company
Only results available are
“Stretching before cycling
(1 vs. 2 minutes, p<0.007)
had a significant effect on
those female cyclists who
sought medical treatment for
groin/buttock conditions.”
43/195 injuries preinter-
vention and 21/195 post-
intervention (p<0.05)
48/251 injuries in stretching
group and 52/218 injuries
in control group (RR = 0.82,
95% CI 0.57, 1.14); $950
per injury for lost time in
stretching group and $2838
in control group (p<0.026)
25/150 injuries in stretching
group and 43/148 in con-
trol group (RR:0.57, 95%
CI: 0.37, 0.88)
Response rate of 518/2500. Associations
between stretching and injuries to other
body parts (knees, back) was not
reported, even thought data available.
It is unclear if people stretched before
injury or because of injury. The effect
occurred only in women and not in men.
Use of historical controls is poor design.
Likely to have had high rate of injuries
and decided to introduce stretching.
If true, results are likely by chance the
result of “regression toward the mean.”
Reviewed exercises with subjects but not
clear how closely. Medical cost
difference also was greater in control
group but not significantly (p=0.19).
Because medical costs were more similar
than lost time costs, total cost was not
significantly different (p=0.56).
Stretching group more flexible before
training and not controlled for in
analysis. Almost twice the loss to
follow-up in stretch group, which means
less people available to be injured.
CHAPTER 25 • Range of Motion and Flexibility
This would appear to make stretching
more effective.
549
550 SECTION II • Principles of Practice

Table 25-8
Brief Summary of Clinical Studies That Suggest Stretching Immediately Before Exercise May Be Detrimental
and Provoke Injury
Reference Population Study Design Results Comments

Howell127 17 Elite Cross-sectional Stretching associated with Not clear if people stretched before
women injuries injury or because of injury
rowers
Jacobs and 451 10K race Survey of past ∼90% of injured people Response rate 451/550. Not clear how
Benson128 participants injuries and stretched compared to 550 were chosen from potential of
related factors ∼80% of noninjured people 1620. Univariate analysis only. Not
clear if people stretched before injury or
because of injury
Kerner and 540 people Survey of past Only results available are Response rate of 540/800. No data
D’Amico129 buying injuries and “A comparison of subjects available to determine clinical relevance.
running other related who warmed up prior to Not clear if people stretched before
shoes factors running (87.7%) and those injury or because of injury
who did not (66%) revealed
a higher frequency of pain
in the former.”

For the relative risk (RR) or odds ratio (OR), a value above 1 means a higher rate of injury in people who stretch
From Shrier I: Does stretching help prevent injury? In MacAuley D, Best T, editors: Evidence-based sports medicine, London, 2002, BMJ
Publishing Group.

patient and their perceived needs. The role of the clinician
may be to assist the patient in determining what they
actually need in a flexibility and stretching program.
Although the majority of recent studies and critiques
of the existing literature presents facts and discussion
that stretching demonstrates minimal effect relative to
the prevention of injury, the clinician cannot ignore the
patients’ perceived value relative to the level of comfort
and preparation that they feel stretching provides them
relative to physical activity. This relative “perceived”
value may be more important on an individual basis
than scientific basis. This impact, of a stretching and
flexibility program on quality of life outcome scores and
bodily pain scores in certain populations, has been dem-
onstrated by King et al.140 Improvement in these two
scores was demonstrated in a patient population over
the age of 65 at the conclusion of a 12-month com-
munity-based program that incorporated stretching and
flexibility exercises. In this situation, the primary role
of the clinician is to educate the individual and provide
proper instruction, methods, and an environment for
that individual to maximize the gain in flexibility sought.
For patients who present with a loss of ROM or flex-
ibility after injury, the role of the clinician is to assist the
patient to regain the ROM and flexibility lost.
Important Questions
How long should a stretch be held? Multiple studies and
articles exist in the literature that have examined how
long a stretch should be held.141-161 The time for which
the stretch was held in these studies have ranged from 6
to 120 seconds. While they reported the duration that
stretch was held, many of these studies also assessed
the effectiveness of a specific method of stretching
(e.g., PNF),145-152 or the effectiveness of combining
various modalities (e.g., heat, cold, massage) with
static stretch.153-158 Direct comparisons between dura-
tion of stretch times during static stretch have been
completed by Madding et al.162 Stretch times compared
were 15, 45, and 120 seconds in Madding’s study and
15, 30, and 60 seconds by Bandy et al. During a sin-
gle session of stretching, Madding et al. reported that
15 seconds of stretch was as effective as 45 or 120
seconds to increase hip abduction. Bandy et al., when
assessing the effectiveness and statistical significance
of these stretch times over a 6-week period, demon-
strated that the most effective duration for holding a
stretch was 30 seconds. Based on these two studies, it
should be recommended to patients that positions that
place a stretch on a muscle be held for between 15 and
30 seconds.
How long does it take to cause an increase in muscle
flexibility? Because the ability of a muscle to stretch and
alter its length can be changed within any single session,
this is an exceedingly difficult question to answer and
is truly unknown. No studies to date have been able to
fully answer this question. Factors that would affect the
answer to this question are the muscle in question (e.g.,
different muscles may respond to the same duration
 CHAPTER 25 • Range of Motion and Flexibility 551

Table 25-9
Brief Summary of Clinical Studies That Suggest Stretching Immediately Before Exercise Does Not Prevent Injury
Reference Population Study Design Results Comments

Pope et al.130 1538 Male 12 weeks RTC Univariate HR = 0.95 Large sample size used. Military recruits
military (95% CI: 0.77, 1.18) do not perform same activities as elite
recruits Multivariate HR = 1.04 athletes, but the activity is probably
(95% CI: 0.82, 1.33) very similar to recreational athletes.
Compliance and follow-up are easy in
this group.
Pope et al.131 1093 Male 12 weeks RTC HR = 0.92 (95% CI: Although stretching did not reduce
military stretch calves 0.52, 1.61) risk, there was a fivefold increased
recruits ankle injury if ankle ROM was only 34
degrees (p<0.01).
Van Mechelen 421 Male 16 week RTC RR: 1.12 Intervention was warm-up and
et al.132 recreational matched on preexercise stretching. Each group
runners age and weekly experienced a lot of “noncompliance.”
running distance
Burnet et al.133 1501 Road Survey of past Similar frequencies of Response rate unknown. Cross-sectional
race and injuries and injuries among those study design but injury profile was
recreational other related who stretch and those “any injury” and not recent injury. Not
runners factors who do not clear if people stretched before injury
or because of injury.
Macera et al.134 583 Habitual 1 year prospective OR for men = 1.1, for Response rate of 966/1576. Stretching
runners cohort women = 1.6 data were controlled only for age.
Stretching was not included in the
multiple regression analysis because
it was insignificant in the original
univariate analysis.
Blair et al.135 438 Habitual Survey of past Only results available Response rate of 438/720. This article
runners injuries and are “frequency of comprises three studies. Only the
other related stretching . . . were not cross sectional study directly looked at
factors associated with running stretching habits. Not clear if people
injuries.” stretched before injury or because of
injury.
Walter et al.136 1680 1 year prospective Comparison group is To be consistent with other articles, the
Community cohort people who always RR was converted so that the numbers
road race stretch. reflect the risk of people who always
runners RR: Never stretched: stretch. These numbers are controlled
1.15, 1.18 for running distance and frequency,
Sometime stretched: type of runner and use of warm-up,
0.56, 0.64 injuries in past year
Usually stretched: 1.05,
1.25

For the relative risk (RR) or odds ratio (OR), a value above 1 means a higher rate of injury in people who stretch
(From Shrier I: Does stretching help prevent injury. In MacAuley D, Best T, editors: Evidence-based sports medicine, London, 2002, BMJ
Publishing Group.)

and frequency of stretching differently), the group
being used, initial flexibility of the person, and muscle
group). Controlling these factors would be extremely
difficult. Clinical experience dictates that the response
time is a function of the individual, his or her specific
initial flexibility, response to stretching, and a host of
other factors.
How long does an increase remain after stopping
a stretching program? The duration of a change in a
muscle’s ability to deform/lengthen from a stretching
program has been stated to be between 30 and 60 min-
utes according to human subject data from Magnusson
et al.101,162 Usually, the goal of any flexibility program
is to increase the muscle’s ability to stretch during the
552 SECTION II • Principles of Practice
Hartig 1999
Hilyer 1990
Figure 25-21
Pope 1998
The relative risk, odds or hazard
ratios (±95% confidence interval)
from prospective studies are shown. Cross 1999
Data for men are demonstrated by
closed circles; data for women by
open circles. Values greater than 1 Walter et al, 1989 (sometimes)
mean an increased risk for people
who stretch before exercise. Values
less than 1 mean a decreased risk of
injury for people who stretch before
exercise. (Redrawn from Shrier I:
Does stretching help prevent injuries?
In MacAuley D, Best T, editors: Ekstrand et al, 1983
Evidence-based sports medicine,
London, 2002, BMJ Publishing
Group.) 0.1
session and immediately after it but to maintain gains
achieved over time. How long gains remain is uncer-
tain. Once a flexibility program is stopped, gains made
will be lost over time (unless the range gained is main-
tained through use). Zebas and Revera163 have studied
the gains and losses of muscle flexibility as a result of a 6-
week flexibility training program using static, modified
ballistic, and PNF stretching. After 6 weeks, a significant
increase was demonstrated in flexibility about the ankle,
shoulder, hip, trunk, and neck (p<0.05). A statistically
significant loss (p<0.05) occurred in all muscle groups 2
weeks after cessation of the program. A further gradual
loss was measured at the end of 4 weeks. Even with the
loss after 4 weeks, the flexibility retained was greater
than the start of the stretching program. Functionally, it
would appear that the level of muscle flexibility achieved
and maintained is based on the flexibility and range of
motion required by a specific individual for the tasks and
activities that they commonly participate in. Perhaps in
educating the patient regarding the need of gaining/
maintaining flexibility it might be best to quote a com-
mon saying “If you don’t use it, you lose it.”
How often must one stretch? The study by Wallin
et al.164 suggests that pursuing a flexibility program one
time per week may be sufficient to maintain flexibility
gained, whereas engaging in a program three to five
times per week increases flexibility.
How many repetitions are necessary to gain flexibility?
The viscoelastic properties and behavior of muscle fibers
undergoing repeated stretching have been studied in an
animal model by Taylor et al.165 Their data demonstrate
that the greatest amount of change in length, force-relax-
ation, and hysteresis response of muscle occurs in the first
few repetitions of stretch. (See Chapter 5 of this text for
a full discussion of this study and the viscoelastic behav-
ior of muscle undergoing deformation.) Based on these
Stretching at times not before exercise
Pope 2000
Walter et al, 1989 (usually)
Walter et al, 1989 (never)
van Mechelen et al, 1993
Macera et al, 1989
1 10
in vitro results from isolated tissue preparations, from a
clinical perspective, the clinician and patient should con-
sider paying special attention to the initial cycles/rep-
etitions of any stretching program. The majority of the
benefits during any one session may be obtained during
the initial few stretches.
Magnusson et al., in clinical studies examining
hamstring flexibility of subjects, have demonstrated
similar findings that resistance to stretch and the sub-
sequent change or decrease in this resistance with
holding the stretch are greatest in the first few repeti-
tions.162,166 Although Magnusson et al. originally attrib-
uted these changes to the viscoelastic response of the
hamstrings,166,167 they subsequently have attributed the
response to greater stretch tolerance of their subjects.168-
172
This change is based upon an alteration of their testing
methodology from their initial studies. The methodology
used by Magnusson et al. allows the clinician to examine
changes in a muscle resistance to stretch in a clinical set-
ting. Although the studies by Magnusson et al. begin to
answer some initial questions regarding the viscoelastic
behavior of muscle using methods available in the clinic,
further investigation is warranted based upon what is
known from bench research.
What is the best method of stretching? Although enhanced
flexibility achieved through stretching promotes greater
compliance of the muscle-tendon unit, clinicians must deter-
mine what method of muscle stretching is the best method
to gain the desired compliance, flexibility, and range of
motion. Three common methods of stretching muscle gen-
erally are used in an attempt to gain an increase in flexibility.
These methods are stretching through the use of proprio-
ceptive neuromuscular facilitation (PNF) techniques, mus-
cle energy, static stretching, and ballistic stretching.
The three techniques of PNF commonly used for
increasing joint ROM and muscle flexibility are contract-

relax (CR), hold-relax (HR), and contact-relax with ago-
nist contraction (CRAC). Historically these techniques
have been used to facilitate the GTO to inhibit the mus-
cle in which it lies and to use the principles of recipro-
cal inhibition.173 Muscle energy, a technique developed
by osteopaths, is based on the same physiological prin-
ciples of PNF. The principles of application are similar
to PNF with two important differences. Using muscle
energy to stretch involves isolating the muscle through
the use of a submaximal isometric contraction (compared
with a maximal isometric contraction using PNF tech-
niques) and making sure that the muscle that has been
contracting is completely relaxed before proceeding into
a new range. Because muscle energy techniques involve
a lighter contraction, they are used commonly earlier in
the healing continuum to restore range. Using them at
this time is easier for the patient and causes less pain.
However, no studies have compared the effectiveness of
muscle energy over PNF. However, clinically they appear
to be just as effective.
Various authors and studies have concluded that PNF
techniques are effective in increasing flexibility. However,
there appears to be no consensus regarding which is the
single best technique to accomplish this.* In many cases
the stretching force was not controlled, with the excep-
tion of one study.148 Controls such as this are vital for
valid, well-designed research to answer questions appro-
priately as can be appreciated based upon the reviews dis-
cussed earlier in this chapter.116-119
As stated, the historical premise of the PNF tech-
niques was that the GTO would be facilitated in the
muscle that was to be stretched and that reciprocal inhi-
bition would occur if that muscle’s antagonists were
activated. This, however, has not been demonstrated to
be the case in a number of studies. In these studies acti-
vation of the contractile elements of the muscle under-
going stretch was increased as demonstrated through
the use of surface EMG.138,148,177,179,180 This fact may
lend further support to the concept of PNF stretch-
ing producing an “analgesic” effect as put forth by
Shrier118 or the impact of “stretch-tolerance” presented
by Magnusson et al.138
Results of studies on PNF stretching using surface
EMG have been challenged by Entyre and Abraham,
however.181 These authors having reported that tracings
from surface electrodes having the appearance of activ-
ity between antagonistic muscles were actually cross-talk
between the electrodes. No activity was seen from fine
wire electrodes supporting the use of antagonistic muscle
contraction during stretching to inhibit contraction of
the muscle being stretched. Minimal EMG activity also
has been demonstrated by Magnusson et al.138 during
*References 138,148,149,154,163,164,173-178.
CHAPTER 25 • Range of Motion and Flexibility 553
their studies using isometric contractions in association
with stretching.
Static and ballistic stretching are the methods used by
most athletes because they can be completed individually,
without the use of a partner (as is often required using
PNF stretching). Although both methods are effective,
advantages and disadvantages exist to static and ballistic
stretching.
During static stretching, a stationary position is held
for a period of time during which specific joint(s) are
placed and held in a position that places the muscles
and connective tissues that surround that joint at their
greatest length. Advantages of static stretching are that
less danger exists of exceeding the limits of extensibil-
ity of the tissues being stretched; energy requirements
are lower; and less chance exists of developing muscle
soreness, and in fact, muscle soreness often is relieved.47
The advantages offered by static stretching are reason-
able because the connective tissues have a high resistance
to a suddenly applied force of a short duration (as would
be imposed by ballistic stretching), while demonstrat-
ing viscoelastic responses when placed under prolonged
stretch.95 Static stretching also minimizes the impact of
Ia and II spindle afferent stimulation and attempts to
maximize the impact of the GTO.
Ballistic stretching usually involves some type of cyclic,
rhythmic motion(s) that impose movement and a change
in length of the muscles and/or connective tissues that
surround a joint.46,47 Ballistic stretching movements are
initiated by muscles that are antagonistic to those that are
being stretched. The use of ballistic stretching has not
been recommended by multiple well-respected exercise
physiology textbooks.182-184 Ballistic stretching, although
effective, may pose a threat of causing microtraumatic
injury. A place, however, does exist for ballistic stretching
for activities performed at a high velocity. Before con-
sidering the use of ballistic-type stretching, the clinician
must consider all factors associated with the patient such
as pathology, stage of healing, age, comorbid factors rela-
tive to their general medical history, and type of activ-
ity in which they are involved. This type of higher velocity,
dynamic stretching would appear to be appropriate for
athletes involved in high-velocity dynamic activities
such as hurdles or any other type of athletic activity that
require high-velocity movements at the extremes or at
the available ROM.
For the general patient population, static stretching
exercises are the most often prescribed. These exercises
can be completed by the individual without the need for
a partner (e.g., PNF) and are generally safe and effective.
Ballistic stretching exercises are generally not appropriate
for the general patient population, sedentary individual,
or geriatric patient. Ballistic stretching, however, may
play an integral role in the conditioning and training of
athletes because athletic activities are ballistic in nature
554 SECTION II • Principles of Practice

or for individuals performing ballistic functional move-
ments at the end of their range of motion.
For the athlete, static stretching exercises should make
up the baseline of their flexibility program. These should
be used throughout the season but certainly predominate
in the early season. Increasing the proportion of ballistic
to static stretching should be considered based on posi-
tion and activity, where athletes are regarding their pro-
cess of warm-up and preparation for practice/play and as
the athletes’ level of fitness and conditioning increases.185
If ballistic stretching exercises are to be used, they should
be preceded by static stretching and confined to a small
range of motion, perhaps no more than 10% beyond the
individual’s static end range of motion. Ballistic stretch-
ing should be used to assist in the development of the
dynamic flexibility of the athletes end range of motion.
Any ballistic or dynamic flexibility program should be
progressive in nature. Zachazewski has previously pro-
posed the concept of a progressive velocity flexibility pro-
gram (PVPF; Figure 25-22).104 The PVFP requires that
the muscle group being stretched while undergoing an
eccentric contraction and controlling movement of the
limb segment and the amount of stretch being placed
upon it. A transition from antagonist to agonist also may
be required depending upon the stretching exercise.
These types of transitions and potentially dyssynergistic
contractions have been implicated as one potential cause
of muscle strain injury.186,187 The individual must work
on his or her neuromuscular coordination through this
type of activity. A motor learning response may be set up
as the individual stretches at a higher and higher velocity
over time, simulation and integration functional activity
necessary for sport or high-level end-range activity.
A general activity warm-up and static stretching should
precede the PVFP. The PVFP is initiated over a period
of days or weeks depending upon the individual’s activity
level and physical status. The PVFP takes the individual
through a series of stretching exercises in which the veloc-
ity and range of stretch are combined and controlled on a
progressive basis. The individual progresses from control
to activity simulation and from slow methodical activity to
higher velocity functional activity. Control and range are
the responsibility of the individual. The clinician acts as a
“coach.” No outside force is exerted by anyone else.
Muscle Stretching Program Considerations
The ultimate goal of any stretching and flexibility pro-
gram is to enable the muscle to be lengthened through
the necessary range of motion to allow injury-free func-
tion in the most efficient manner. As just discussed, the
stretching program prescribed for an athlete versus a
more sedentary patient would differ primarily based on
their type and level of activity. However, regardless of
the type of patient the clinician is working with, the basic
components of the sequence of activities are the same:

C
Anatomic limit of
flexibility prior to
injury
B
"Stretch pain"
limit of flexibility

Perception of
"stretch or
A
stiffness"
Static stretching

SSER FSER
"Flexibility
Slow SFR Fast FFR
zone"
Short Slow Short Fast
End Full End Full
Range Range Range Range
Slope of velocity Slope of velocity Slope of velocity Slope of velocity
of stretch = t of stretch = 2 t of stretch = 1/2 t of stretch = 1/2 t

Time
Figure 25-22
Progressive velocity flexibility program. Line A represents the point where the individual first perceives stretch or stiffness. Few individuals push
significantly past this point when performing static stretch activities. Line B represents the point of “stretch pain” where individuals usually stop
stretching because of pain or discomfort associated with the stretch. Line C represents the anatomical limit of flexibility before injury occurring.
The goal of the PVFP is to get the individual to push beyond the self-imposed limit represented by Line A. Using controlled ballistic type
stretching activity allows individuals to push to or beyond their “stretch pain” represented by Line B. Each time an attempt is made to push
farther into the available range the ballistic movement completed is shortened for control purposes. (Modified from Zachazewski JE: Flexibility
for sports. In Saunders B, editor: Sports physical therapy, Norwalk, 1990, Appleton and Lange.)

(1) a general “warm-up” activity; (2) participation in an
exercise/stretching program; and (3) some type of “cool-
down” or post-participation period. The number and
complexity of these steps differ with each individual based
on multiple factors, such as general level of health-fitness-
flexibility, age, activity level, and individual perception of
what feels “right” for them regarding type-amount-fre-
quency-duration of stretch. All individuals differ in their
own perceived needs, and clinicians must recognize this.
Any or all of these steps could be altered or eliminated
based on the individual patient and their perceived needs.
The following are given as examples for two distinctly
different patient populations.
The Athlete
The most efficient sequence of the following five activi-
ties should be considered for athletes:
1. General warm-up: This type of general warm-up con-
sists of repetitive nonfatiguing exercise of the muscle
groups to be stretched. This type of exercise occurs
in the athlete’s readily available ROM. Examples such
as cycling have been studied clinically and have been
demonstrated to be effective in increasing flexibility
up to 15 minutes after the activity.154,188
From animal model studies it is known that physi-
ological warming (preconditioning) has been dem-
onstrated to prevent muscular injury by increasing
the force to failure, length to failure, and elasticity
of the muscle-tendon unit.11 However, it appears
that the increase in intramuscular temperature from
exercise may not be sufficient to influence viscoelastic
behavior and passive energy absorption of the con-
nective tissue associated with muscle during stretch-
ing exercises.101 Although a small contribution may
be based on some increase in intramuscular tempera-
ture, it may not play as significant a role as previously
thought regarding “warm-up” preceding stretching
exercises.102-104 Therapeutic modalities also can be
used as a method of increasing tissue temperature as
has been discussed previously in this chapter.
Because of these facts, the question should be asked
why a general activity warm-up should continue to
be considered as part of an athlete’s preparation to
stretch and exercise. Part of this reason may be histor-
ical, cultural, or traditional for athletics (i.e., “because
that’s the way it has always been done”). From a clini-
cal perspective, this type of general, cyclic warm-up
activity, occurring in the athlete’s readily available
range of motion begins to prepare the athlete for
participation. An initial, cyclic phase or building up
process of deformation within the connective tissues’
tolerable limits of deformation may be most efficient
before the addition of a residual stationary stretch. In
this cyclic phase, the connective tissue that makes up
muscle is deformed in its readily available limits. This
CHAPTER 25 • Range of Motion and Flexibility 555
deformation may be progressively increased because
discomfort decreases as a result of the increase in
“stretch-tolerance” described by Magnusson et al.138
or the analgesic effect of stretching as described by
Shrier.118
2. Preparticipation stretching: Slow static stretching
is begun in this phase of the cycle. Maintenance
of the stretch allows the viscoelastic properties of
the tissues to be influenced or a further increase
in “stretch-tolerance” as described by Magnusson
et al.138 Slow static stretching also may result in
decreased facilitation of the spindle afferents
and facilitation of the GTO. After static stretch-
ing, ballistic/cyclic type stretching could be
considered using a slow velocity, progressively con-
trolled deformation at the athlete’s end range of
motion.
3. “Neuromuscular” warm-up: The purpose of this
part of the cycle is to begin to simulate the ath-
lete’s activity. The velocity of the activity chosen,
the ROM through which it is carried out and the
vigor of the activity should be increased progres-
sively over a series of repetitions to functional levels
for that athlete. This progressive increase in veloc-
ity and ROM influences the viscoelastic properties
of the tissues by further conditioning them to tol-
erate the stress to be imposed at the velocity and
deformation necessary for training and competition.
The repetition of activity at increasing velocities also
imposes the motor learning and skill necessary for
competition. It is during this neuromuscular warm-
up that the PVFP may be incorporated. An example
of a neuromuscular warm-up is the process that a
pitcher would go through before taking the mound
at the start of the game.
4. Activity participation: The athlete is now ready to
participate in his or her chosen activity.
5. Post-participation stretching: Post-participation
stretching capitalizes on any possible effect that
an increase in intramuscular temperature may have
toward maintaining or gaining further flexibility.
Post participation also has been demonstrated to
assist in a decrease or prevention of muscular sore-
ness commonly present after strenuous activity.142,189
Consideration also may be given to “cooling-down”
with the muscle in an elongated position to capital-
ize on any possibility of gaining further change at
a tissue level.12,93,94 For maximal gain after exercise,
the muscle/muscle groups being stretched should
not be fatigued because fatigue has been dem-
onstrated to facilitate the spindle and inhibit the
GTO.190,191
The Sedentary Individual or Geriatric Patient
Both of these groups of individuals have a great need for
appropriate flexibility and ROM to minimize the amount
556 SECTION II • Principles of Practice
of stress imposed during general life and ADL. Neither
of these groups has a great need for dynamic flexibility
for general daily needs. The general cycle of sequence
of stretching activities for these types of patients is simi-
lar. Neither needs ballistic stretching or a neuromuscular
warm-up type of activity.
1. Warm-up: Some type of general activity/warm-up
activity is beneficial if possible. The goals are the same
as outlined above, and activity is carried out in the
immediately available range. The range in which the
activity is accomplished is increased as tolerated by
the individual. Modalities also may be used to assist in
this process; however, the progressive cyclic activity is
the key consideration.
2. Flexibility exercises: Concentration is on static stretch-
ing activity. Minimal to no need exists for ballistic
type stretching exercises in this patient population.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever pos-
sible. There are a total of 191 references for this chapter.

T HE U TILITY OF O RTHOPEDIC C LINICAL
T ESTS FOR D IAGNOSIS
Daniel J. Cipriani and Jeffrey B. Noftz II
Introduction
Clinicians rely on physical diagnostic tests along with
other assessment findings to make decisions about inter-
vention and guidance for their patients. These diagnostic
tests, coupled with a comprehensive history intake and
other assessment findings, including movement testing,
functional testing, sensation testing, and palpation, are
part of a whole intended to provide the clinician with
the necessary information to guide the decision-making
process, which can include decisions about the presence
or absence of disease, treatment intervention, treatment
modification, treatment discontinuation, and patient
education. None should be used in isolation.
As with any physical measure, a diagnostic test must
meet certain standards for it to be clinically useful. These
standards are similar to the standards imposed on all mea-
sures. Diagnostic tests must yield reliable data and infer-
ences that are valid. In other words, the clinician must be
confident that the use of a diagnostic test will result in
accurate and consistent information for a given patient,
and that this information permits useful interpretation.
Diagnostic tests are divided into two main catego-
ries: tests that result in a discrete outcome and tests that
result in a continuous outcome. A discrete outcome is a
result that permits interpretation as present/absent, dis-
eased/not diseased, mild/moderate/severe. A continu-
ous outcome is a result that provides data on an interval
or scale of measurement, such as millimeters of displace-
ment or degrees of range of motion. Results from labora-
tory tests on blood are recorded as continuous, whereas
results from the evaluation of a radiograph as either frac-
ture or no fracture fall in the discrete outcome category.
In either case, however, the primary goal is to determine
26
C H A P T E R
some level of diseased/healthy, injured/uninjured, or
stable/unstable, for example.
Diagnostic Test Categories
● Discrete outcome tests
● Continuous outcome tests
When a patient presents to a clinician after an injury
to the knee, the clinician first obtains a comprehensive
history, including basic demographics, past medical con-
ditions, and the conditions related to the current injury.
The mode of injury and the initial physical presentation
then guide the clinician to the rest of the examination,
including the use of appropriate physical tests. The patient
reports that he or she experienced a palpable and audible
“pop” sensation in his or her knee while rebounding a
basketball. In addition, the patient experienced imme-
diate pain and swelling. These symptoms prevented the
patient from returning to the basketball game. The clini-
cian, based on this information, will likely have formed
several pretest probabilities regarding the nature of the
injury. By pretest, we mean that the clinician has formed a
likely hypothesis as to possible diagnoses before perform-
ing any physical examination. These are often termed the
initial differential diagnoses.
In this case, given the history of an audible and pal-
pable “pop” sensation, as well as swelling and pain and
the inability to return to activity, the clinician may con-
sider several pathologic etiologies, including patellar
dislocation, anterior cruciate ligament (ACL) tear, or
557
558 SECTION II • Principles of Practice
osteochondral fracture at the knee. Given these possi-
bilities, the clinician will choose from a variety of physi-
cal tests as part of the examination to rule in (confirm)
or rule out (reject) the possible diagnoses.
Again, in this example, the clinician may decide to
perform a patellar apprehension test and Lachman’s test,
and request an x-ray. Each of these tests results in discrete
outcomes. In addition, the clinician might submit the
patient to a test using an instrumented knee arthrometer
to measure the anterior displacement of the tibia relative
to the femur (in millimeters). This results in a continuous
outcome. Interpreting the outcomes of these tests will
likely assist the clinician to rule in or rule out the diag-
noses of patellar instability, tear to the ACL, or fracture
at the knee.
For the clinician to formulate an appropriate interpre-
tation and accurate final diagnosis, the tests chosen must
be useful. Several criteria must be met to consider a diag-
nostic test to be useful. These criteria are based on the
concepts of reliability and validity.
Reliable diagnostic tests will yield similar outcomes
each time the test is administered, regardless of the indi-
vidual administering the test. In other words, not only
must the test yield consistent information for each repeat
of the test by a single clinician, it must be consistent when
administered by different clinicians on the same patient.
In addition, the results of the test must be valid. To be
valid, the test must yield accurate results.
This chapter describes the methods used to test the
reliability and validity of physical diagnostic tests, and
provides examples of how the clinician can use the mea-
sures of validity to assist with decision making. In addi-
tion, the chapter highlights some of the potential biases
associated with the estimates of utility of a diagnostic
test because these estimates are certainly not perfect esti-
mates. It is important for clinicians to be aware of the
potential weaknesses in the estimates of the usefulness of
any diagnostic test.
Reliability of Diagnostic Tests
The reliability of the data obtained from a diagnostic test
is influenced by three primary factors: patient factors, cli-
nician factors, and instrument factors. The patient must
be able to permit the test to be performed without influ-
ence. Patient factors include the levels of pain and appre-
hension the patient is experiencing at the time of the test
and the patient’s degree of sincerity. Clinician factors
include the experience and skill level of the individual
administering the test, and the environment in which the
testing occurs in (e.g., on-field examination versus clinic-
based examination). Finally, instrument factors affect reli-
ability. The instrument must be precise and sensitive to
the physical entity it is to measure. It must have adequate
calibration that is stable across all conditions.
Factors Affecting Relliability of Diagnostic Tests
● Patient factors
● Clinician factors
● Instrument factors
Given that so many variables affect reliability, it is inac-
curate to refer to any diagnostic test or instrument as
“reliable.” Rather, it is the data obtained from the appli-
cation of that instrument that are reliable. The instru-
ment, the administrator, and the object of measure (i.e.,
the patient) all influence the accuracy and stability of the
data obtained from any procedure.
There are several measures of reliability commonly
used in health and physical medicine. Two common
approaches are the intraclass correlation coefficient
(ICC) and the kappa statistic. These measures depend on
the level of data obtained from a procedure.
For procedures that result in continuous data, the
intraclass correlation coefficient is the method of choice
to test the inter-rater (i.e., comparison of interpretation
between different clinicians) and intrarater (i.e., repeat
use by the same clinician) reliability. The ICC results in a
correlation coefficient value that ranges from 0.0 to 1.0,
with values approaching 1.0 deemed desirable. Although
no empirical cut point has been established for a neces-
sary value of the ICC, common agreement is that ICC
values should be greater than 0.75 for any level of confi-
dence that a measure results in reliable data. In the case
of high-stakes decision making (e.g., should a patient
undergo surgery), the ICC value should exceed 0.95.1,2
A second form of reliability is the kappa statistic,
which is a measure of rater agreement. This measure,
also bounded by the values of 0.0 and 1.0, is an indica-
tion of how well two raters (or how well a single rater
performing a measure more than one time) agree on
a discrete outcome. In this case, when the measure
results in a decision that a condition is absent/present,
a diagnosis is confirmed/ruled out, or a joint is mildly,
moderately, or severely unstable, then the kappa statistic
can provide a measure of agreement for this decision-
making process. Once again, kappa statistics should
approach the value of 1.0, and values below 0.75 are
considered questionable in terms of the reliability of the
interpretation. Numerous interpretations of the value
of the kappa statistic are available; however, Sim and
Wright3 recently recommended values between 0.61 and
0.80 be defined as substantial values, and those greater
than 0.80 as almost perfect agreement. An advantage
of the kappa statistic is that it takes into account the
possibility of chance agreement—that is, two raters
are likely to have some amount of agreement strictly
because of chance. Hence, the kappa statistic is actually
 CHAPTER 26 • The Utility of Orthopedic Clinical Tests for Diagnosis
the proportion of actual agreement, controlled for by
the proportion of chance agreement:
k = Po − Pc / 1 − Pc
where Po is the proportion of observed agreement and Pc
is the proportion of chance agreement. Many studies on
the utility of diagnostic tests report either a kappa statis-
tic as a measure of agreement or the ICC as a measure
of reliability.
Validity Measures of Diagnostic Tests
The accurate interpretation of a diagnostic test is a func-
tion of the validity of the test. In other words, if a clini-
cian decides that, based on the observed outcome of a
test, a patient has a given condition, the accuracy of this
interpretation is a direct reflection of the validity of the
diagnostic test. Thus, test validity is a vital component in
interpreting test results.
There are two main indicators of diagnostic test valid-
ity, based on whether the validity measure is directed
toward the outcome of the test or toward the inference
of the test. In other words, a diagnostic test might be
reported as being very sensitive to a given condition,
which is a measure of the validity directed toward the
outcome of the test. This test accurately identifies indi-
viduals with a known diagnosis. The clinician would
have confidence that this test is sensitive to a certain
condition. However, the clinician will also need some
degree of confidence that, given a positive result on this
sensitive test, a patient in fact has the condition that
was being tested, which is validity directed toward the
actual interpretation.
Four terms must be understood in order to describe
validity. Two of these terms apply to validity of the test
and two apply to validity of the interpretation. Validity
directed toward the test comes in the form of two mea-
sures, test sensitivity and test specificity.4 Validity
directed toward the interpretation also comes in the form
of several measures, namely, predictive values and likeli-
hood values.4 We examine sensitivity and specificity in
greater depth first, and then consider predictive values
and likelihood values.
Measures of Validity
● Validity of the test
● Sensitivity
● Specificity
● Validity of the interpretation
● Predictive values
● Likelihood values
559
Sensitivity and Specificity
As mentioned earlier, the ability of a diagnostic test to
correctly classify a person as diseased or not diseased,
healthy or sick, is of paramount importance to the test’s
usefulness. Diagnostic tests are designed to discriminate
between persons of different levels of health or disease.
In the special case in which the diagnostic test produces
the binary outcome of positive/negative or diseased/
healthy (for example), these properties are referred to as
the sensitivity and specificity of the test.
Sensitivity is the proportion of individuals correctly
identified (by the diagnostic test) as positive when the
disease/condition is present, a true-positive result.
Specificity is the proportion of individuals correctly
identified (by the diagnostic test) as negative when the
disease/condition is not present, a true-negative result.5
For example, a test such as Lachman’s test of the knee is
considered to be very sensitive because it is able to detect
a tear of the ACL in individuals with a torn ACL. Hence,
Lachman’s test will be positive for individuals with a torn
ACL (sensitivity). Lachman’s test is also quite specific
in that it is positive only in the event of a torn ACL. If
an individual does not have a torn ACL, the test will be
negative (specificity).
Tests that accurately identify a person with a disease
or dysfunction possess sensitivity. A test that is 100%
sensitive correctly identifies all persons with the disease.
Tests that accurately identify a person as healthy (i.e., dis-
ease/dysfunction free) possess specificity. A test that is
100% specific will correctly identify all persons without
the disease. A test that is both 100% sensitive and 100%
specific correctly discriminates between individuals with
the disease or condition and those without the disease or
condition, in all cases.
Sensitivity and Specificity
● Level of ability to discriminate between or correctly identify
persons with different levels of a condition
● Determine a test’s usefulness
● Remain constant regardless of prevalence of condition
To study the sensitivity and specificity of any diag-
nostic test, and thus provide the clinician with necessary
information about the usefulness of the test, all such tests
must themselves undergo testing for validity. To estimate
the sensitivity/specificity of any diagnostic test (i.e., to
examine the validity of a diagnostic test), the test must be
compared with a test of established validity, also referred
to as a gold standard. Estimating the sensitivity and
specificity of a diagnostic test is essentially comparable
with establishing concurrent validity evidence—that is,
560 SECTION II • Principles of Practice
how well the diagnostic test performs when compared
with a perfect diagnostic test.
The perfect diagnostic test is the gold standard with
which all other tests are then compared.4 Gold standards,
by definition, have a sensitivity of 100% and a specificity
of 100%. That is, the gold standard will correctly classify
those individuals with the disease or condition as positive
100% of the time, and correctly classify those without
the disease or condition as negative 100% of the time.
Although the 100% rate is ideal, even gold standards are
subject to error, resulting in imperfect gold standards.
The imperfect gold standard is discussed later in this
chapter. Gold standards are usually invasive and expen-
sive, hence the need for other forms of diagnostic test-
ing. For example, the gold standard to confirm a tear
to the ACL is invasive surgery.6 Thus, before subjecting
all patients with a suspected tear of the ACL to surgery,
clinicians can perform less invasive procedures to deter-
mine the integrity of the ACL, such as Lachman’s test, a
pivot shift test, or an instrumented ligamentous test. The
test of interest is then compared with the gold standard.
Ideally, the outcomes from the test of interest will match
the gold standard in all cases. However, and more likely,
the test of interest will possess some error, resulting in
sensitivity and specificity values less than 100%.
When the test of interest correctly identifies a person
with the diagnosis (i.e., when it agrees with the gold
standard), the result is referred to as a true positive.
When the test of interest incorrectly identifies a person
with the diagnosis as not having the condition, the result
is referred to as a false negative. Similarly, when the test
of interest correctly identifies a person as healthy (i.e., it
agrees with the gold standard), the result is referred to
as a true negative; when the test of interest incorrectly
identifies a healthy person as actually having the disease
or condition, the result is a false positive.
Although a perfect test will have no false-negative or
false-positive outcomes, most tests possess at least some
proportion of error. It is important to note that as sensi-
tivity or specificity decrease (i.e., deviate from 100%), this
is an indication that the diagnostic test is producing too
many false outcomes. Hence, a test with low specificity
identifies too many cases as positive (both true-positive
Table 26-1
2×2 Table for Calculation of Diagnostic Test Performance Measures of Sensitivity and Specificity
Positive
(Gold Standard)
Test is positive True positive
Test is negative False negative
Marginal totals Total known positive
Sensitivity = true positives/total known positives (i.e., the proportion of all positive results the test correctly classified as positive).
Specificity = true negatives/total known negatives (i.e., the proportion of all negative results the test correctly classified as negative).
and false-positive results), making a positive outcome
with this test less meaningful. This test then would not
be specific to the diagnosis of interest.
For example, the Hawkins impingement test has been
reported to have a sensitivity of 92% and specificity of 25%
for the diagnosis of shoulder impingement.7 In this case,
the Hawkins test correctly labels individuals who have
an impingement 92% of the time; however, it also labels
75% of individuals without an impingement as actually
having an impingement (the specificity is 25%, indicating
that only 25% of healthy people are correctly identified
as healthy, resulting in 75% of the healthy subjects being
diagnosed as positive). Thus, a positive outcome on the
Hawkins test must be considered only with other sup-
porting information, and the test should not be used in
isolation when making a diagnosis.
In general, sensitivity and specificity are attractive mea-
sures of a diagnostic test’s usefulness because these values
are inherent characteristics of a test. Thus, the values of
sensitivity and specificity should hold constant regardless
of the prevalence of the disease or condition.8 In other
words, a test’s sensitivity and specificity should not be
influenced if the condition in question is either rare or
very common. The estimation procedure for sensitivity
and specificity values is based on the standard 2 × 2 table
shown in Table 26-1.
As an example, consider a hypothetical situation in
which a particular diagnostic test has a sensitivity of
80% and a specificity of 90%. Further, consider that a
particular disease is present at a proportion of 50% in a
population of 1000 persons. Thus, 500 persons have this
particular disease (Table 26-2). In the case of sensitivity,
80% (400/500) of those in the population with the dis-
ease, or 400 cases, will be correctly labeled as diseased,
whereas 100 will be incorrectly labeled as disease free. In
the case of specificity, 90% (450/500) of these persons
will be labeled correctly as disease free (i.e., 450 persons
will be correctly labeled as disease free), whereas 50 per-
sons will be incorrectly labeled as diseased.
These proportions remain constant, even in the event
of a rare disease. For instance, consider the previous
example, only in this case the disease is a rare one, affect-
ing only 1% of the population. The test’s sensitivity will
Negative
(Gold Standard) Marginal Totals
False positive Total positive by test
True negative Total negative by test
Total known negative
 CHAPTER 26 • The Utility of Orthopedic Clinical Tests for Diagnosis 561

Table 26-2 the value of the test in the event of a negative result; this
Example Using a Population of 1000 Persons test finds most healthy knees to be negative, but it also
and a Prevalence of 50% finds ACL-injured knees to be negative in over 30% of
cases (sensitivity is only 70%, resulting in a 30% false-
Known Known Marginal
negative rate).13 Clinicians are strongly advised to use
Positive Negative Totals
diagnostic tests that have been tested for both sensitivity and
Test positive 400 (TP) 50 (FP) 450 specificity. Relying on only one value, typically sensitivity,
Test negative 100 (FN) 450 (TN) 550 may provide the clinician with a false sense of security for
Marginal totals 500 500 1000 decision making. Relying on sensitivity alone does not
take into account whether a diagnostic test yields too
TP, true positive; FP, false positive; FN, false negative; many false-negative results (poor specificity); it is only
TN, true negative.
an indication of the proportion of true- and false-posi-
tive results. A highly sensitive test (yields true-positive
results) may also have poor specificity (yields additional
again be 80%, correctly labeling 80% of the persons with false-positive results), making a positive outcome unsta-
the disease as diseased and incorrectly labeling 20% as ble or unreliable.
disease free. Given the same population (i.e., 1000 per- An additional problem with sensitivity and specificity
sons), this would result in 8 correct cases (true positives) is based on the quality of the gold standard on which
and 2 incorrect cases (false negatives); 10 of 1000 per- these estimates are based. Typically, the gold standard
sons actually have the disease (Table 26-3). does not undergo the same level of scrutiny because it is
Sensitivity and specificity are only as valuable as the often the definitive test (e.g., surgery, in which the clini-
data from which they are derived. Unfortunately, many cian can visualize the tissue). An imperfect gold standard
studies designed to evaluate the usefulness of a partic- results in inaccurate estimates of sensitivity and specific-
ular diagnostic test report only the sensitivity value of ity. The problems associated with an imperfect reference
the test. This occurs in situations in which only subjects standard have been reported throughout the literature
with the condition in question are used in the study. For on diagnostic test performance assessment.5,14-25 As noted
example, in several studies designed to examine the use- by Green and colleagues,17 an imperfect reference test
fulness of the anterior drawer test for diagnosing a torn (i.e., one lacking 100% sensitivity/specificity) leads to a
ACL, the studies involved only individuals who actually biased estimate of the sensitivity and specificity for the
had a tear to the ACL.9-12 In these cases, the sensitivity of test of interest.
the test was determined by the proportion of individuals Imperfect standards may be due to a faulty instru-
correctly identified with a torn ACL. However, without ment or to the fact that not all patients receive a defini-
also performing the anterior drawer test on persons with tive assessment for disease status.5 In fact, as noted by
healthy knees, it is not possible to determine if the test Begg and Greenes,5 imperfect gold standards result from
can incorrectly identify healthy people as having a torn the bias that arises when only those patients most likely
ACL (false-positive results). to have the disease are subjected to the definitive test.
The anterior drawer test, although fairly sensitive (i.e., In other words, many patients do not receive the defini-
values approaching 70% in the acute, alert individual), tive test, particularly if the clinician has determined the
may not be very specific for ACL tears because it could probability to be low that the disease is actually present.
give a positive result in a healthy knee as well as an injured The test may be avoided for reasons of cost efficiency
one. Hence, a positive result on the anterior drawer test or because of its invasiveness (e.g., surgical intervention,
might not be useful without additional data. As it turns painful procedures). In any case, the gold standard often
out, one study found that the specificity of the anterior is administered only to select patients, those presenting
drawer test is very high (>97%), which actually decreases with a history sufficient to justify the use of the gold stan-
dard test. These patients may not be a true representa-
tion of all individuals with a given diagnosis.26
Table 26-3 In the event that the diagnostic utility of a procedure
Low Prevalence of Disease has been estimated using an imperfect gold standard,
the estimates of sensitivity and specificity must be used
Known Known Marginal
with caution. And, as is demonstrated in the following
Positive Negative Totals
sections, additional measures of test validity are suspect
Test positive 8 9 17 on this same issue: the estimates of predictive value and
Test negative 2 891 893 likelihood ratios are also based on the quality of the
Marginal totals 10 990 1000 gold standard. These estimates may also be biased in the
absence of a perfect gold standard.
562 SECTION II • Principles of Practice
Predictive Value of Diagnostic Tests
Although sensitivity and specificity provide useful infor-
mation regarding the proportion of individuals that the
test will correctly classify as either diseased or healthy,
clinicians often are interested in the probability that a
person with a positive test result is, in fact, diseased. And
given the difficulty associated with decision making, in
the presence of a positive or negative test result with a
test of questionable sensitivity or specificity, the clinician
needs a measure of confidence as to whether a condition
is in fact present or absent. In other words, given a posi-
tive test result, the clinician wishes to know the probabil-
ity that the person actually has the disease of interest.
Recall that most diagnostic tests are not 100% sensi-
tive or specific. Therefore, a positive or negative response
remains suspect without a confirmed diagnosis. The predic-
tive power of a diagnostic test provides information regard-
ing the probability that a subject is diseased or healthy.4
In ascribing probability, predictive values are used.
Predictive values are reported as either positive or neg-
ative, such that a test with a high positive predictive
value (PPV) indicates that a positive outcome on the test
indicates a high probability that the condition is present,
and a test with a high negative predictive value (NPV)
indicates a high probability that the condition is absent
in the event of a negative test. Predictive values are cal-
culated based on the same 2 × 2 table as for sensitivity
and specificity (see Table 26-1). Predictive values are cal-
culated as the proportion correctly identified from the
number of total positive or negative results identified by
the test of interest.
Calculation of Predictive Values
● Positive predictive value = True positives/all positives by the test
(true positives + false positives)
● Negative predictive value = True negatives/all negatives by the
test (false negatives + true negatives)
In this case, the PPV is based on the proportion of
true-positive results (correct decisions) relative to all the
positive results obtained with the test (correct and incor-
rect decisions). The NPV is based on the proportion of
true-negative results (correct decisions) relative to all the
negative results obtained with the test (correct and incor-
rect decisions). In the previous example (see Table 26-2),
the PPV of the test of interest would be 89% (400/450
= 88.8). Thus, the probability that a person, testing as
positive, actually has the condition is 89%. Similarly, the
NPV of this test would be 82% (450/550), indicating
that the probability that a person does not have the con-
dition, given a negative test outcome, is 82%.
Unfortunately, predictive values are very dependent
on the prevalence of a condition in a given population.
Thus, unlike sensitivity and specificity, which are stable
across prevalence rates, predictive values change depend-
ing on the prevalence of disease in any population, mak-
ing comparisons difficult. This is of particular concern
when the predictive values of tests have been estimated
from studies that did not account for the true prevalence
rate of a condition in the design of the study.
Predictive Values
● Probability that a condition is present (positive) or absent (negative)
● Dependent on prevalence of condition in a given population
Riegelman8 demonstrated how the prevalence rate
affects the predictive value of diagnostic tests. Table 26-4
shows a continuum of predictive values as influenced by
different prevalence rates of a condition. In all cases, the
sensitivity and specificity values remain constant at 80%
and 90%, respectively. Tables 26-5 through 26-8 show
data for disease prevalence rates of 1%, 10%, 50%, and
90%, respectively.
The predictive values, while providing useful informa-
tion about the effectiveness of a diagnostic test, can vary
dramatically depending on the prevalence of the disease
of interest. For a predictive value to be meaningful in
terms of a positive value, the frequency of the disease
must be high (e.g., diabetes in a sample of obese individ-
uals). Negative predictive values become more useful in
populations with a low frequency of the disease of inter-
est (e.g., certain forms of cancer).27 This is an impor-
tant issue when designing a study to examine the utility
of a diagnostic test. If the test design artificially inflates
the prevalence rate to assure a sufficient sample size of
patients with a rare condition, the resulting predictive
values will be overestimated or underestimated.
In an empirical study, Lauder and colleagues28 dem-
onstrated the instability of predictive values while sensi-
tivity and specificity remained relatively unchanged. In
Table 26-4
Changes in the Predictive Values of Diagnostic Tests as
Prevalence Rate Changes
Prevalence Rate
1% 10% 50% 90%
Positive 7.5% 47.1% 88.9% 98.6%
predictive value
Negative 99.8% 97.6% 81.8% 33.3%
predictive value
 CHAPTER 26 • The Utility of Orthopedic Clinical Tests for Diagnosis 563

Table 26-5
Prevalence of Disease at 1%
Known Known Marginal
Positive Negative Totals

Test Positive 8 99 107 (PPV = 7.5%)

Test Negative 2 891 830 (NPV = 99.8%)
Marginal Totals 10 (Sn = 80%) 990 (Sp = 90%)

PPV, positive predictive value; NPV, negative predictive value; Sn, sensitivity; Sp, specificity.

Table 26-6
Prevalence of Disease at 10%
Known Known Marginal
Positive Negative Totals

Test Positive 80 90 170 (PPV = 47.1%)

Test Negative 20 810 830 (NPV = 97.6%)
Marginal Totals 100 (Sn = 80%) 900 (Sp = 90%)

PPV, positive predictive value; NPV, negative predictive value; Sn, sensitivity; Sp, specificity.

Table 26-7
Prevalence of Disease at 50%
Known Positive Known Negative Marginal Totals

Test Positive 400 50 450 (PPV = 88.9%)

Test Negative 100 450 550 (NPV = 81%)
Marginal Totals 500 (Sn = 80%) 500 (Sp = 90%)

PPV, positive predictive value; NPV, negative predictive value; Sn, sensitivity; Sp, specificity.

Table 26-8
Prevalence of Disease at 90%
Known Positive Known Negative Marginal Totals

Test Positive 720 10 730 (PPV = 98.6%)

Test Negative 180 90 270 (NPV = 33.3%)
Marginal Totals 900 (Sn = 80%) 100 (Sp = 90%)

PPV, positive predictive value; NPV, negative predictive value; Sn, sensitivity; Sp, specificity.

their investigation, they examined the effectiveness of
sciatica symptoms in correctly classifying persons with L5
radiculopathy. In one study, the reference standard was
electromyography, which yielded a prevalence of radicu-
lopathy of 11%. In another study, the reference standard
was lumbar surgery, which yielded a prevalence of 57%.
In the first case, sensitivity and specificity values were
60% and 55%, respectively, for the prevalence rate of 11%.
These values were relatively similar in the second case
(prevalence of 57%), with sensitivity and specificity of
55% and 69%, respectively. However, the predictive val-
ues changed dramatically between the two studies. PPVs
increased from 27% to 70% when comparing the study
with an 11% prevalence rate with the 57% prevalence rate
study. In addition, NPVs decreased from 92% to 54%
when comparing the 11% prevalence rate study with the
57% prevalence rate study. Thus, although sensitivity and
specificity hold constant across prevalence rates, predic-
tive values are highly dependent on the prevalence of the
disease.
564 SECTION II • Principles of Practice
Likelihood Ratios
To overcome the variability of predictive values, as well as
the confusion over interpretation of sensitivity and speci-
ficity, likelihood ratios were established to facilitate com-
munication about a diagnostic test.29 As noted by Fritz and
Wainner,29 although sensitivity and specificity allow one to
infer the probability of a correct test result, given the result
of the reference standard, they do not provide information
about the probability that the disease is actually present.
Similar to the predictive value of a test, likelihood ratios
are based on the odds that a given disease or health status
is present. A positive outcome on a test with a high likeli-
hood ratio can be interpreted as strong probability that the
person has the condition of interest.
A benefit of likelihood ratios is that this measure com-
bines sensitivity and specificity to provide a useful mea-
sure of the likelihood of a condition. Thus, likelihoods
are not dependent on the prevalence of the condition;
sensitivity and specificity alone can be combined to pro-
vide this information. Calculations of likelihood ratios
are based on the sensitivity and specificity values (see
Table 26-1). A positive likelihood ratio will likely result
in a value greater than 1.0 and a negative likelihood
ratio will likely result in a value less than 1.0. These two
ratios result in values that should deviate from a value
of 1.0. A value of 1.0, when multiplied against the odds
of a condition being present or absent, results in no
change in those odds. However, values greater than or
less than 1.0 will result in a change in the odds that a
condition is present or absent.
Calculation of Likelihood Ratios
● Positive likelihood ratio = sensitivity/1 − specificity
● Negative likelihood ratio = 1 − sensitivity/specificity
Likelihood Ratios
● Level of ability to correctly identify persons with or without a
condition
● Combines sensitivity and specificity
● Not dependent on prevalence of condition in a given population
Based on this relationship, a positive likelihood ratio
(LR+) of 1.0 indicates that the test result does nothing to
change the odds of a person actually having the disease of
interest. Likelihood ratios greater than 1.0 increase the
odds favoring the condition. Negative likelihood ratios
(LR−) of 1.0 also do not provide any useful informa-
tion. However, negative likelihood ratios less than 1.0
decrease the odds favoring the condition.
Small negative likelihood ratios correspond to high
sensitivity values, yielding a measure that is useful for rul-
ing out a condition. Likewise, large positive likelihood
ratios correspond with high specificity, indicating a mea-
sure that is useful for ruling in a condition.29
For example, in the previous case (see Table 26-2),
the positive likelihood ratio would be 8.0 (0.8/1 − 0.9
= 8.0). Thus, the odds favoring the condition are eight
times greater in the event of a positive outcome on a test
with sensitivity of 80% and specificity of 90%. Further, the
negative likelihood ratio becomes 0.22 (1.0 − 0.8/0.9
= 0.22). The odds favoring the condition are decreased
approximately 4.5 times (1/0.22) in the event of a nega-
tive test outcome.
Clinicians may use likelihood ratios at face value.
That is, given a positive test result that has a high posi-
tive likelihood ratio, the clinician can simply inform the
patient of the high likelihood a condition is present.
However, in the event the clinician wishes (or needs)
to provide a more definitive decision, based on the his-
tory and physical presentation, along with the outcome
of a test, the clinician can apply the likelihood ratio to
the preconceived notion of whether a condition is pres-
ent/absent.
To apply likelihood ratios, clinicians must first esti-
mate the odds that a condition is either absent or present,
based on a hypothesis formed before actually running
a particular test—known as the pretest probability of
a particular disease or condition. Once a pretest prob-
ability has been established, clinicians can then apply the
likelihood ratio to the pretest probability to obtain an
estimation of a post-test probability for the disease. Many
clinicians apply the nomogram proposed by Fagan30 as an
application of Bayes’ theorem for interpretation of likeli-
hood ratios. Fritz and Wainner29 provide an example of
this application in their review of diagnostic test inter-
pretations.
A second, more accurate method for applying likeli-
hood ratios is presented by Sacket and colleagues.31 This
process involves three simple calculations. The first cal-
culation is to convert the pretest probability to odds; the
odds is then multiplied by the likelihood ratio, resulting
in post-test odds. The post-test odds can then be con-
verted back to a probability, resulting in the post-test
Calculation of Probabilities
● Pretest odds = pretest probability/(1 − pretest probability)
● Post-test odds = pretest odds × likelihood ratio
● Post-test probability = post test odds/1 + post-test odds
 CHAPTER 26 • The Utility of Orthopedic Clinical Tests for Diagnosis
probability that a condition is either present or absent.
The clinician can than compare the pretest and post-test
probabilities to demonstrate the level of confidence pro-
vided by the diagnostic test.
Consider the original example at the beginning of this
chapter, in which a female athlete has reported a history
consistent with a tear to the ACL. In this example, the
clinician may have established a pretest probability of
75% that the ACL is torn. This pretest probability has a
pretest odds of 3.0 (0.75/1 − 0.75). The odds of a tear
are three times the odds of no tear to the ACL, given
the patient’s history and physical presentation. The next
step is to multiply the pretest odds by the likelihood ratio
value of a diagnostic test. Consider the positive likelihood
ratio values of a positive Lachman’s test (LR+ = 16) and
a negative Lachman’s test (LR− = 0.21), based on esti-
mates from research.11,13 For each test, the post-test odds
would be 48 (3 × 16) or 0.6 (3 × 0.2) for, respectively,
a positive or negative result of Lachman’s test. The final
step is to convert these odds to post-test probabilities
using the third formula. Thus, the post-test probability
given a positive Lachman’s test result, and based on a
pretest probability of 75%, would be 98%. The post-test
probability of an ACL tear in the event of a negative
Lachman’s test result would decrease from 75% to 38%.
Before administering Lachman’s test, the clinician may
have been 75% certain the ACL was in fact torn. Given
a positive result on Lachman’s test, that clinician is now
be 98% certain the ACL is torn. Given a negative result
on Lachman’s test, the clinician will feel less confident
of a tear because the probability of a tear has decreased
to 38%. Further testing is necessary. Thus, Lachman’s
test created a shift in the probability that an ACL tear
Evidence-Based Case Example
History
A 44-year old man presents after a recent onset of
posterior ankle pain. The symptoms came on abruptly
while he was playing basketball with his daughter.
He reports feeling a sudden “electric”-type jolt in
his posterior ankle area, followed by severe pain and
weakness. The incident occurred last evening and he
has reported to the clinic for evaluation. He suspects
he sprained his ankle. He reports no significant past
medical history. He is mildly obese (height, 5’ 10’’;
weight, 210 lbs), relatively inactive during the week
(he works as an appliance salesperson), and is a recre-
ational drinker and smoker.
Pretest Probability
Given the description of the onset of symptoms and
the patient’s physical and activity history, the clini-
565
occurred in this patient, resulting in greater confidence
in the final diagnosis.
One difficulty associated with using likelihood ratios
applied to pretest probability estimates is the fact that
pretest estimates are biased based on the clinician’s
level of experience. Such estimates are based on clini-
cal experience, clinical knowledge, and confidence of
the clinician—all of which are subjective components
of this estimate. Several investigations report the sub-
jective differences between practicing clinicians in the
application of diagnostic test performance assessment
and utility.31-34 Timmermans34 found that clinicians’
level of experience influenced their effectiveness in
estimating probabilities of disease. Less experienced
clinicians provide less effective estimates than more
experienced clinicians. Thus, clinical experience plays
an indirect role in the utility of a diagnostic test based
on a clinician’s initial estimation of the probability of a
disease. The fact that clinical experience affects prob-
ability estimates introduces bias into the performance
measures of diagnostic tests.
In addition, variability within subjects plays a role
in the sensitivity and specificity estimates of diagnostic
tests. Hlatky and colleagues32 reported on the variations
in sensitivity and specificity for exercise electrocardiogra-
phy. They note that clinical history, a key component in
the estimate of pretest probability of disease, varies con-
siderably among patients. This variation then affects the
overall predictive value or post-test probabilities associ-
ated with diagnostic test measures. The clinical picture of
many conditions varies considerably among patients with
the same diagnosis, and this variability affects the ability
to generate an accurate pretest probability estimate.
cian suspects a possible tear of the Achilles tendon.
An experienced clinician estimates this probability to
be 70%, whereas a second-year student estimates the
probability at 50%. Likelihood ratios will be used to
demonstrate how to determine the post-test prob-
ability using the sensitivity (Sn) and specificity (Sp)
values in Table 26-9. The clinician selects the three
following tests, because of the diagnostic value of
these tests reported in the literature: the gap sign (Sn
= 73%, Sp = 89%, LR+ = 6.6, LR− = 0.3), calf squeeze
(Thompson test; Sn = 96%, Sp = 93%, LR+ = 13.7,
LR− = 0.04), and Matle’s sign (Sn = 88%, Sp = 85%,
LR+ = 5.9, LR− = 0.14). Matle’s sign is negative,
but the gap sign and calf squeeze are both positive.
Given these results, the pretest probability to post-
test probability will have shifted as follows, for the
clinician and student, respectively:
566 SECTION II • Principles of Practice

Evidence-Based Case Example—Cont’d

Pretest Probability and Odds
Clinician probability = 70% Student probability = 50%
Clinician odds = 2.33 (0.70/1 − 0.70) Student odds = 1.0 (0.50/1 − 0.50)
Post-Test Odds
Gap test Clinician odds 2.33 × 6.6 = 15.18 Student odds 1.0 × 6.6 = 6.6
Squeeze test Clinician odds 2.33 × 13.7 = 31.51 Student odds 1.0 × 13.7 = 13.7
Matle’s sign Clinician odds 2.33 × 0.14 = 0.32 Student odds 1.0 × 0.14 = 0.14
Post-Test Probabilities (post-test odd/1 + post-test odd)
Gap test Clinician = 15.18/16.18 = 94% Student = 6.6/7.6 = 87%
Squeeze test Clinician = 31.51/32.51 = 97% Student = 13.7/14.7 = 93%
Matle’s sign Clinician = 0.32/1.32 = 24% Student = 0.14/1.14 = 12%

The clinician decides to trust the squeeze test and gap sign,
given that both were positive. The clinician also knows that
Matle’s sign is suspect in an awake patient, being more
effective when the subject is under anesthesia. Thus, the
clinician rules that the patient has a tear to the Achilles ten-
don and refers the patient to an orthopedic surgeon. The
student also feels comfortable with this decision based on
his or her post-test probabilities. The clinician and student
began with pretest probabilities that the Achilles was torn
of 70% and 50%, respectively. After running the diagnostic
tests, the probability of a tear increased to greater than 90%
for the clinician and greater than 85% for the student.

Table 26-9
Examples of Tests Used for Specific Conditions
Diagnosis Test Gold Standard Sn Sp LR+ LR−

Meniscus injury35-39 Joint line tenderness Arthroscopy 55%-85% 29%-67% 1.7-2.6 0.67-0.22
McMurray test 16%-58% 77%-98% 2.5-29.0 0.86-0.43
Apley grind test 13%-16% 80%-90% 1.3-1.6 0.93-1.07
Anterior cruciate Anterior drawer sign Surgery 22%-70% >97% 7.3-23.3 0.8-0.31
ligament Lachman’s test 80%-99% >95% 16.0-19.8 0.21-0.01
injury9-11,13,40,41 Pivot shift 35%-95% 98% 17.5-47.5 0.66-0.05
Achilles tendon Gap sign Surgery 73% 89% 6.6 0.30
injury/rupture42 Calf squeeze 96% 93% 13.7 0.04
Matles sign 88% 85% 5.9 0.14
Carpal tunnel Phalen test Electrodiagnosis 34%-75% 71%-74% 1.3-2.6 0.86-0.35
syndrome43,44 Tinel’s sign 27%-64% 83%-91% 1.6-7.1 0.88-0.40
Night pain 96% 59% 2.3 0.07
Superior labral Biceps load test Arthroscopy 91% 97% 30.3 0.09
anterior-posterior Speed test 9%-32% 75% 0.36-1.3 0.91-1.2
(SLAP) lesion45-47 Yergason’s test 12%-43% 79%-96% 0.57-10.7 0.92-0.59
Jobe relocation test 36% 63% 1.0 1.0
Anterior apprehension 30% 63% 0.81 1.1
Shoulder anterior Anterior apprehension Arthroscopy 53% 99% 53.0 0.47
instability48 Relocation test 46% 54% 1.0 1.0
Surprise test 64% 99% 64.0 0.36
Rotator cuff Supraspinatus test Surgery
pathology49,50 Partial-thickness tear 62% 54% 1.35 0.89
Full-thickness tear 41% 70% 1.36 0.84
Massive tear 88% 70% 2.93 0.40
Painful arc 97.5% 10% 1.08 0.25
Weakness with 64% 65% 1.83 0.55
abduction
Weakness with 76% 57% 1.77 0.59
exterior rotation
Acromioclavicular Horizontal adduction Surgery 77% 79% 3.67 0.29
joint lesion51 Resisted extension test 72% 85% 4.80 0.33
Active compression 41% 95% 8.20 0.62

Sn, sensitivity; Sp, specificity; LR+, positive likelihood ratio; LR−, negative likelihood ratio.
 CHAPTER 26 • The Utility of Orthopedic Clinical Tests for Diagnosis
Conclusion and Recommendations
Diagnostic tests, to be useful, must possess some level of
reliability and validity. The outcome of the test should be
repeatable among clinicians or for a single clinician doing
the same test several times. The interpretations resulting
from the outcomes should be based on some level of con-
fidence. This confidence is established by the sensitivity of
the test to a given condition as well as the specificity of the
test for that condition. Based on sensitivity and specificity,
the likelihood of the presence/absence of the condition
can be estimated to assist the clinician with the decision-
making process. Because there are no known cut-off val-
ues established for sensitivity and specificity (i.e., there is
no established minimum value of sensitivity or specificity
that indicates the usefulness of a test), the final decision
regarding the patient is left to the clinician, based on mul-
tiple forms of evidence (e.g., history, physical presenta-
tion, results of tests, clinician experience). The following
recommendations are provided to assist the clinician in the
selection and use of diagnostic tests:
1. Seek clinical studies that subject both involved as well
as healthy subjects to the diagnostic test, thus provid-
ing both necessary estimates of a test’s utility, that is,
sensitivity and specificity. Avoid studies that report
only on sensitivity, which is an insufficient estimate of
a test’s usefulness.
2. Avoid the use of predictive values because these val-
ues are highly dependent on the prevalence of the
condition in the population. If a study sample does
not accurately represent the condition’s prevalence in
the general population, the predictive values will be
567
inaccurate. Rather, rely on likelihood ratios; if likeli-
hood ratios are not provided, estimate the ratios using
sensitivity and specificity.
3. Scrutinize the gold standard (reference standard) that
is used to estimate the usefulness of any diagnostic
test. The gold standard should be 100% sensitive and
specific. Any study demonstrating the sensitivity and
specificity of a particular diagnostic test should pro-
vide evidence of the quality of the gold standard. The
study should report how accurate (sensitive and spe-
cific) the actual gold standard is, before it was used to
test the quality of a new diagnostic test.
4. Scrutinize the criteria used by the study to deter-
mine if a diagnostic test is positive or negative; scru-
tinize the criteria used by the study to determine if
the outcomes of the gold standard are positive or
negative. For any given diagnostic test, the deter-
mination of a positive or negative result should be
clearly stated; these criteria should be consistent
with the expectations of the reader. For instance,
the criteria for a positive Lachman’s test result are a
sensation of increased translation as well as the lack
of a firm end feel. Such criteria should be clearly
stated in any study that is testing the quality of a
diagnostic test.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever pos-
sible. There are a total of 51 references for this chapter.

I MAGING J OINTS AND
M USCULOSKELETAL T ISSUE :
P ATHOANATOMIC C ONSIDERATIONS
J. Bradley Barr and Robert E. Berg
Objectives
This chapter presents a basic understanding of how
diagnostic images are produced by plain film radiography,
computed tomography, magnetic resonance imaging,
diagnostic ultrasound imaging, and nuclear medicine
imaging and explores the safety issues related to the use
of each of the imaging modalities. Modalities used for
musculoskeletal imaging are compared and contrasted,
taking into consideration the diagnostic strengths and
weaknesses of each. In addition, the chapter introduces
the holistic process one should use for assessing a
conventional radiograph series and understanding how
clinical decision rules are utilized to help practitioners
decide when conventional radiographs are necessary
and should be requested. Lastly, the chapter describes
the principles for using diagnostic imaging to evaluate
the following types of musculoskeletal pathology: frac-
tures and fracture/dislocations, periarticular injuries,
intervertebral disc injuries, neoplasms, and arthritides.
Types of Diagnostic Imaging
● Plain film radiography (x-rays)
● Computed tomography (CT)
● Magnetic resonance imaging (MRI)
● Diagnostic ultrasound
● Nuclear medicine (e.g., bone scan)
568
271
C H CA H
P TA EP RT E R
Overview
Diagnostic imaging affords clinicians the opportunity to
evaluate the musculoskeletal system in a way not pos-
sible through interview and physical examination alone.
Modern imaging equipment can create remarkably clear
and detailed images of what lies beneath the skin. Imaging
should not be used in isolation but as an integral and often
necessary part of an examination. Imaging information
can confirm or disprove those diagnostic hypotheses
generated during the clinician’s examination.
All clinicians involved in the rehabilitative management
of patients should possess basic knowledge about the field
of radiology and be able to converse intelligently with other
practitioners concerning diagnostic imaging. They should
also be able to recommend an appropriate imaging study
when necessary. Professional education for rehabilitation
disciplines such as physical therapy is often completed at
the clinical doctorate level, many states allow such profes-
sionals to see patients directly without physician referral,
and, within the foreseeable future, rehabilitation profes-
sionals may have privileges to order radiological studies.
Rehabilitation specialists can benefit greatly from
reading a radiologist’s report and applying the information
to a patient’s plan of care. Clinicians can gain a wider
perspective of a patient’s problem when they are able to
look at an imaging study and, along with the radiologist’s
report, understand what they are seeing. Finally, they
have an opportunity to use a patient’s imaging films for
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 569

patient education, an important dimension of a compre- Modern computed tomography (CT) also uses radiation,
hensive rehabilitation program. but instead of a unidirectional beam, both the radiation
This chapter guides the reader through some of the basic source and the detector systematically encircle the body.
principles of diagnostic imaging. The reader will find infor- Information gathered is reconstructed by a computer uti-
mation regarding the science behind the various imaging lizing a complex Fourier analysis, resulting in the creation
modalities used in musculoskeletal imaging (in other words, of a series of two-dimensional “slices” of a subject’s body
how the images are created and which tissues are best visual- part. When necessary, information on multiple adjacent
ized by each modality). The chapter stresses the importance slices can be summated to form three-dimensional images
of examining diagnostic images in a holistic fashion so that that make complex anatomy or pathology easier to com-
serious pathology is not overlooked. Some basics regard- prehend. Like plain film radiographs, the appearance of
ing imaging of the immature skeleton are also presented. tissues on CT depends on the amount of radiation they
Of direct relevance to the practicing clinician, the chapter absorb. Within the musculoskeletal system, CT excels at
introduces the application of decision-making guides, which identifying fractures (Figure 27-2), bony articular degen-
clinicians can use to determine the need for imaging under erative changes, and calcification within tumors.
particular circumstances. Finally, the most substantive por- Although there are no definite contraindications
tion of the chapter focuses on imaging various types of mus- to plain film radiography or computed tomography,
culoskeletal pathologies by using many examples to help the these studies utilize ionizing radiation and so con-
reader to understand which imaging modalities are useful for tribute to the total radiation exposure of the indi-
a given problem and to visualize the pathology in compari- vidual and the population. Radiation effects are
son to the normal condition. grouped into deterministic and stochastic catego-
ries. Deterministic, or dose-related, effects increase
Basic Scientific Principles of Imaging in severity with increasing dose and include cataracts,
decreased sperm count, skin erythema, marrow fail-
Techniques ure, gastrointestinal failure, and fatal cerebral edema.
Plain Film Studies and Computed Tomography With the possible exception of some long or com-
Plain film (conventional) radiographs (x-rays), the most
common imaging examination, require the unidirectional
passage of x-radiation through part of the body. X-rays
are a form of electromagnetic radiation, lying between
ultraviolet light and gamma rays on the electromagnetic
spectrum. Radiation that is not absorbed or scattered as
it passes through a body part is detected either electroni-
cally or by radiographic film. The amount of radiation
absorbed as it passes through the body part depends on
the tissues’ radiodensity, which is determined in part by
atomic weight and in part by thickness.
Radiation that passes through the body without being
absorbed ultimately strikes radiographic film or a detector.
The resulting image is created either on film (hard copy)
or digitally and appears to a clinician on a special diagnos-
tic monitor. Either presentation of a radiographic image
should be referred to as a “radiograph” (not “x-ray”).
Radiographic images appear in various shades of gray,
depending on the tissues’ varying radiodensities. More
radiodense objects, such as metal orthopedic hardware
and bone, appear relatively whiter in radiographs whereas
less radiodense objects, such as soft tissue, fat, and air in
the trachea, appear blacker (or more radiolucent). Figure 27-1
Plain film radiographs excel at displaying bony Radiodensity differences. This is a glass of water and the author’s
anatomy, and, to a lesser extent, soft tissue structures. hand. Why are the soft tissues of the index finger visible whereas the
soft tissues of the middle finger are not? The middle finger is in the
Because a difference in radiodensity is necessary for two
cup of water, while the index finger is behind the water. The electron
structures to appear different on resultant radiographs, density of the water nearly matches that of the soft tissues, so no
adjacent soft tissues often cannot be separated because interface is visible. The index finger is outlined by air, the interface
they have similar radiodensities (Figure 27-1). between tissues and air clearly visible because of the density difference.
570 SECTION II • Principles of Practice
Figure 27-2
Calcaneal fracture. A, Plain film. This lateral view of an ankle shows subtle loss of Bohler’s angle, loss of cortical continuity at the inferior aspect of
the calcaneus, and loss of trabecular continuity within the calcaneus, all suggesting fracture. B, Sagittal reconstruction of axial CT–Calcaneal fracture
is confirmed. Fracture lines, lines of demarcation between muscular soft tissues and fat, and edema are all more clearly demonstrated on CT.
plicated angiographic studies, doses high enough to
cause deterministic effects are not commonly achieved
in medical imaging studies. Stochastic, or non-dose-
related effects of radiation include germ line muta-
tions and cancer induction. Although the severity of a
stochastic effect is independent of exposure, the prob-
ability of suffering a stochastic effect is increased by
increased exposure without any threshold. Avoidance
of stochastic effects, especially cancer induction, is
the main reason radiation exposure from radiological
studies is minimized. Specific cancers linked to radia-
tion exposure include some breast cancers, thyroid
cancers, and leukemias.
Classifications of Radiation Effect
● Deterministic (dose related)
● Stochastic (nondose related)
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) has become the
standard modality for differentiating among soft tissues
in the musculoskeletal system. MRI uses a very high
magnetic field, electronic radiofrequency pulses, and
sophisticated sensing devices to generate two- and
three-dimensional images of the body much like
computed tomography. Unlike CT radiation, the mag-
netic field utilized in MRI has been shown to have no
long-term adverse effects.
Contraindications to magnetic resonance imaging
include pacemakers, cardiac defibrillators, and implanted
electronic devices. Severely claustrophobic or obese
patients may not tolerate MRI scanners.1 Most implanted
metal prostheses, prosthetic heart valves, and aneurysm
clips and coils are MRI safe. When unsure, the safety
of implanted metal devices must be individually con-
firmed. Patients in high-risk occupations (e.g., welders)
or patients who have been injured by metallic debris
may need preliminary plain films of the area of concern
to ensure that a previously unknown metallic structure
is not moved or heated by the magnetic field, causing
injury. The area of most concern is the orbit. Even if safe,
metal devices usually do degrade imaging quality in the
anatomical region local to the metal device.
“Open MRI” refers to MRI units with a larger bore.
These are useful for patients with severe claustrophobia
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 571

(FSE), and fat saturation sequences further complicate

Cautions/Contraindications to MRI
● Pacemakers
● Cardiac defibrillators
● Implanted electronic devices
● Claustrophobic patients
● High-risk occupations (e.g., welders)
● Pregnancy (if intravenous contrast used)
and those too large to fit into a standard MRI. Open
MRI utilizes much lower magnetic field strength
(0.2-0.3 Tessla) than standard MRI (1.5-3.0 Tessla).
Because image quality is proportional to field strength,
these studies offer considerably less diagnostic infor-
mation, and patients who do not absolutely need open
technique should be strongly encouraged to undergo
standard MRI when possible.
A review of MR images requires some understand-
ing of how various normal structures appear. The
simplest descriptions of MRI tissue signal characteristics
are given in terms of T1 and T2 signal. T1 and T2 are
biological parameters unique to each tissue. Different
MRI sequences can make different tissues more or less
conspicuous by weighting the MR image toward either
the tissue’s T1 or T2 value. In addition to basic T1 and
T2 sequences, specialized sequences such as proton
density (PD), gradient recall echo (GRE), fast spin echo
the understanding of MR images.
Although discussion of the physics underlying the
main MRI sequences is beyond the scope of this chapter,
some generalizations can be made. On T1-weighted
images, fat is bright (including marrow fat), cerebrospinal
fluid is dark, and structures with high fibrous tissue con-
tent such as tendons, ligaments, and cortical bone are dark.
On T2-weighted images, fat signal varies. Fluid including
cerebrospinal fluid, synovial fluid, and edema is bright, and
fibrous structures such as tendons, ligaments, and cortical
bone are again dark. Muscular tissue and central nervous
system gray matter signal are intermediate on T1 and T2
images (Figure 27-3). Flowing blood creates a dark signal
void on both TI and T2 images. Hemorrhagic blood sig-
nal varies with age on both T1 and T2 images. Fat satu-
ration sequences, which turn fat dark, can be combined
with either T1 or T2 image sequences (Figure 27-4). The
most common MRI contrast agent is gadolinium, which
is bright on T1. Giving intravenous contrast during an
MRI exam causes blood in vessels and hypervascular struc-
tures, such as most tumors and some normal structures, to
appear very bright on MR images subsequently obtained.
These appearances are summarized in Table 27-1.
Ultrasound
Diagnostic ultrasound, which utilizes an extremely
high-frequency sound wave and the detection of echoes

Figure 27-3
MRI T1 versus T2. Coronal (A) fat saturated T2 and (B) T1 MR images of the pelvis and hips in an adolescent show slipped capital femoral
epiphysis on the right (arrow). Note that on the T1 image, normal marrow is white. On the T2 image, the right epiphysis and femoral neck show
high T2 signal and are dark on T1, because of marrow edema. Also noted is a small hip joint effusion. The synovial fluid is high signal (white) on
T2. One advantage MRI has over CT is the ability to obtain images in any plane.
572 SECTION II • Principles of Practice

Figure 27-4
MRI fat saturation. Sagittal (A) T1 and (B) fat saturated T2 images of an ankle show a tear of the Achilles tendon. On the T1 image, marrow fat
and subcutaneous fat are bright. On the fat saturation image, fat is dark. T2 images show the fluid within the posterior ankle joint and the edema
within the swollen Achilles tendon as bright. Normal fibrous tendons and ligaments are dark on both T1 and T2 sequences.

returned from the body’s tissues, is sometimes used to Because of increasing availability, superior resolution,
image the musculoskeletal system. Ultrasound has no and higher interpretation accuracy,2 MRI has largely
known adverse effects. In contrast to MRI, ultrasound is supplanted ultrasound for musculoskeletal diagnostic
relatively inexpensive, is more portable, can image soft tis- purposes. However, ultrasound continues to be utilized
sues near metal prostheses, and can easily be used to guide for certain indications such as evaluation of rotator cuff
percutaneous biopsies or drainages. However, ultrasound and biceps tendons, ankle tendons, joint effusions, pediat-
is extremely dependent on operator training, experience, ric developmental hip dysplasias, carpal tunnel syndrome,
and technique. In the hands of experienced operators, and in the evaluation of some soft tissue masses such as
ultrasound provides valuable diagnostic information. ganglion cysts at the wrist.2 Figure 27-5 shows examples
of normal anatomy about the shoulder and knee using
diagnostic ultrasound imaging.
Table 27-1
Appearance of Common Structures on Basic Uses of Diagnostic Ultrasound
MRI Sequences*
● Rotator cuff and biceps tendons
T1 Bright T1 Dark T2 Bright T2 Dark ● Ankle tendons
Fat Fluid Fluid Fibrous tissue
● Joint effusions
Bone marrow Ligaments Fat Ligaments
● Pediatric hip dysplasia
Subacute blood Menisci Marrow Menisci
● Carpal tunnel syndrome
Gadolinium Moving Edema Moving
● Soft tissue masses (e.g., ganglion)
Melanin blood blood

Diagnostic ultrasound has no known contradictions,

*Of note, fat saturation can be used with either T1 or T2 sequences,
and the use of fat saturation renders all fat-containing tissues although color doppler is not advisable when directed at
(subcutaneous, marrow, intra-abdominal, etc.) dark on resultant a living fetus as it may cause mild thermal effects within
images without changing the remainder of the image. imaged tissue.
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 573

Biceps tendon
Patellar tendon

Patella

Tibia
Bicipital 2
groove

A B
Figure 27-5
Normal ultrasound imaging. These static images were captured using diagnostic ultrasound imaging. A, Normal anatomy of the long head of the
biceps tendon within the bicipital groove is demonstrated. B, A normal infra-patellar tendon can be visualized, extending from the patella to the tibia.

physiological metabolism. A small amount of radiation

Nuclear Medicine is emitted, detected, and used to form an image showing
Nuclear medicine imaging involves intravenous admin- the radiopharmaceutical’s distribution. Examples of
istration of radioactive compounds, which distribute nuclear medicine procedures include bone scanning with
themselves within a patient’s body according to Technetium-99 m MDP (Figure 27-6) or performing

Ant Post 3Hr bone delays

Rt lat Lt lat

R
L
i e
g RAO LPO
h f
t
t

LAO RPO

10/13/04

Figure 27-6
Bone scan. Whole-body bone scan following intravenous administration of technetium 99 m MDP shows diffuse skeletal uptake of
radiopharmaceutical. Low-level activity within soft tissues and urinary collecting system is normal. Focal intense uptake at the T6 vertebral body
is present. This was later confirmed to be the result of breast cancer metastasis (same patient as Figure 27-48, CT and MR images).
574 SECTION II • Principles of Practice
osteomyelitis or abscess localization with Gallium-
67. Positron emission tomography (PET) is a form of
nuclear medicine study that utilizes a positron-emitting
isotope, usually Flourine-18 Flourodeoxyglucose (F-18
FDG). F-18 FDG is a glucose analog that is taken up
and retained by cells that normally metabolize glucose,
and the resulting emitted radiation is detected and used
to form a diagnostic image. PET is frequently combined
with CT (PET/CT). The combination allows detailed
simultaneous anatomical and physiological evaluation.
Imaging of the Pregnant Patient
Care must be taken in radiological evaluation of the
pregnant patient. Radiation exposure to the fetus is
minimized by judiciously minimizing plain film and
CT exams. Computed tomography contrast is some-
times given in pregnancy, and the decision to utilize CT
contrast is made on a case-by-case basis. Although no
controlled blinded study has been performed on pregnant
patients to confirm MRI safety, the use of this modality
in pregnancy is widespread, with no worldwide reports of
adverse effect. Use of gadolinium MRI contrast is abso-
lutely contraindicated during exams of pregnant patients
as it crosses the placenta and undergoes repetitive cycles
of fetal renal excretion into amniotic fluid followed by
fetal swallowing and resorption into fetal circulation.
This cycle greatly prolongs fetal exposure, with possible
adverse outcomes.
Figure 27-7
Humerus tumor. A, Chest x-ray obtained for unrelated symptoms of coughing demonstrated unexpected irregularity of the right humerus.
Additional (B) AP and (C) lateral views of the humerus obtained subsequently showed a large expansile lytic tumor involving the humerus. This
case again stresses the importance of examining every structure on a study.
Overriding Principles of Conventional
Radiography
Clinical indications for various radiology examinations
are important for clinicians to understand, as are condi-
tions under which certain examinations are appropriate or
inappropriate. Although radiologists formally read most
imaging studies performed, it is important for all clinical
practitioners to be familiar with the basic anatomy and
interpretation of imaging studies. Even in practice settings
where diagnostic imaging is not readily available, muscu-
loskeletal clinicians are frequently asked to review imaging
studies with their patients and will need to communicate
effectively about imaging with other practitioners.
The ordering physician or health professional must review
the result of every examination ordered and take the appro-
priate action. Clinically unsuspected abnormalities are fre-
quently identified on radiographic studies, and it is crucial that
all available information included in the study be identified
(Figure 27-7). Failure to identify a serious condition such as
a bone tumor on a radiograph, even though the radiograph
was performed for another reason, is a source of major patient
morbidity and can be a source of considerable medicolegal
liability.
There are a few overriding principles that will assist all
clinicians when recommending or looking at radiographic
images. Adhering to these principles will help prevent over-
sight and enhance understanding of the images. Figures
27-8 through 27-21 demonstrate normal plain film radio-
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 575

Figure 27-9
Normal pelvis. AP view of pelvis shows normal osseous and soft tissue
anatomy.

Figure 27-8
Normal elbow. Anteroposterior (AP) and lateral views of elbow show
normal osseous and soft tissue structures. By convention, the AP view
is obtained with the elbow fully extended and the lateral view shows
the elbow flexed 90°.

Figure 27-10
Normal cervical spine. AP (A), lateral (B), and open-mouth odontoid (C) views of the cervical spine show normal osseous and soft tissue
anatomy. The airway, epiglottis, and soft tissues are well assessed on the lateral view. This study was obtained with patient lying supine because of
recent trauma, causing loss of the normal cervical spine alignment. Although normal in this example, spasm can cause a similar appearance.
(Continued)
576 SECTION II • Principles of Practice
Figure 27-10—Cont’d
graphic studies in various body regions by illustrating both
normal appearance of anatomical structures and the typi-
cal views obtained in each region.
Plain film radiographs provide a two-dimensional
image of a three-dimensional body part. A single radio-
graphic image essentially “collapses” all of a patient’s
tissues in the area of interest upon one another into a
flat picture. Therefore, two radiographic views from two
different angles are always recommended when order-
ing or performing a radiographic study (Figure 27-22).
A second view allows an abnormality to be limited to
a specific three-dimensional location. Specific shapes
can be described more accurately. Also, fractures and many
other abnormalities are often only visible on one view; views
from another angle may appear normal (Figure 27-23).
Figure 27-11
Normal hip. AP views of the hip joint with hip in neutral (A) and abducted positions (B). Because of the external rotation associated with hip
abduction, the abducted view shows the proximal femur and especially the femoral head from a different angle that simulates a lateral view.
Clinicians may be forced to evaluate a radiograph
or study without the benefit of a radiologist report.
In this instance, it is advisable to follow a consistent
approach to evaluation of images. For example, when
looking at plain films of an extremity, many people first
evaluate osseous anatomy, followed by joint alignment,
then local soft tissue structures, and finally all subcuta-
neous fat interfaces with muscular soft tissues (Figure
27-24). Although different professionals may take dif-
ferent formal approaches, it is important that each indi-
vidual uses a consistent and systematic method of image
interpretation to avoid neglecting important details
(Figure 27-25). A common saying among radiologists
is “The most common missed abnormality is the second
one on the film.” The search for radiographic abnor-
malities must not be satisfied when an abnormality is
identified. Having a routine for film analysis prevents
missing additional, possibly unsuspected abnormalities
(Figure 27-26).
What to Look for When Evaluating Plain
Radiographic Film
● Osseous anatomy
● Joint alignment
● Local soft tissue structures
● Subcutaneous fat interfaces
● Muscle soft tissues
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 577

Figure 27-12
Normal knee. AP (A) and lateral (B) views of the knee show normal osseous and soft tissue anatomy.

Figure 27-13
Normal foot. PA (A), oblique (B), and lateral (C) views of foot show normal osseous anatomy.
578 SECTION II • Principles of Practice
Figure 27-14
Normal leg. AP (A) and lateral (B) views of the leg show normal osseous and soft tissue anatomy. The demarcation between muscular soft tissues
and subcutaneous fat is usually seen well in this area and can be a valuable clue when absent in areas of edema or cellulitis.
Decision-Making Principles
A crucial aspect of using of diagnostic imaging appropri-
ately in practice concerns the clinician’s initial decision about
whether imaging is warranted in a particular case (Tables 27-
2 and 27-3). Imaging modalities can yield important infor-
mation in the investigation of differential diagnoses when the
nature or extent of an injury is unclear. But many times the
clinical examination data are sufficient to reveal the diagnosis
and lead a clinician to choose appropriate interventions.
To summarize this important decision, if the results of
the imaging study could potentially change patient man-
agement, then the study is necessary.3 If interventions or
outcomes are unlikely to be altered as a result of the imag-
ing results, then the study is not needed. Clinicians should
remember that radiologists can always lend their expertise
to the decision about whether a particular diagnostic imag-
ing modality is appropriate.
Need for Radiographs3
If the results of an imaging study will potentially change how a
patient is treated, then the imaging study is necessary.
Ordering or recommending imaging studies
imposes significant costs on both the patient and the
health care system. Unfortunately, diagnostic imaging
is probably overused by most clinicians. 4,5 Reasons for
the excessive use of imaging include institutional rou-
tine, patient expectation, or protection against legal
action. 6 Ultimately it is the responsibility of all prac-
titioners who may influence decisions about patient
management to weigh the value of a diagnostic imag-
ing study against the cost that will be imposed on the
health care system. Rehabilitation specialists should
share this responsibility with referring physicians and
radiologists.
Clinicians who are in a position to influence imag-
ing decisions should know the relative diagnostic
value of the imaging results (see Table 27-3). For
example, each imaging modality has strengths and
weaknesses in helping clinicians to visualize different
types of pathology. Also, the results from an imaging
study are not always consistent with a patient’s pre-
sentation. When this occurs, clinicians should never
rely completely on the result of an imaging study;
rather they should rely on the complete clinical pic-
ture created by all available information when decid-
ing how to proceed.
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations
Figure 27-15
Normal forearm. AP and lateral views of the normal radius and ulna
show normal osseous and soft tissue anatomy.
Clinical Decision Rules
Clinical decision rules (CDRs) are decision-making
guides developed to assist clinicians faced with making
judgments about ordering or recommending diagnostic
imaging. These guides are particularly helpful for clini-
cians functioning in primary care roles, but they can also
assist those who see patients through referral if they are
in a position to recommend imaging. The CDRs men-
tioned here (Table 27-4) are published in the literature
and have been validated for accuracy and analyzed for
clinical impact in terms of patient outcomes and costs.
Guides for Knee Trauma
There are two sets of clinical decision rules to help cli-
nicians decide whether to obtain plain film radiographs
following acute knee injuries. Seaburg et al. reported that
radiographs were ordered for 85% of patients who sus-
tained trauma to the knee, when only 6% to 12% of those
patients actually had a fracture.7 The Pittsburgh decision
rules and Ottawa knee rules were created to promote
more efficient and cost-effective use of radiography fol-
579
Figure 27-16
Normal immature hand. Single PA view of the hand in a young
adolescent shows normal osseous anatomy.
lowing such trauma.8 Both rule sets are similar in that
they use clinical examination findings to guide the clini-
cian toward a decision about whether to use plain film
radiography to screen for fractures about the knee.
Pittsburgh Decision Rules. The Pittsburgh decision
rules call for plain film radiographs when a patient has had
blunt trauma or a fall as a mechanism of injury plus either of
the following: (1) age younger than 12 years or older than
50 years; or (2) inability to walk four weight-bearing steps
in the emergency department.7-9 The guide’s sensitivity and
specificity values for identifying knee fractures are 99% and
60%, respectively.7,8 Seaberg et al. suggested that application
of the Pittsburgh decision rules could decrease the use of
radiographs in this patient population by 52%.7
Pittsburgh Rules for Knee Trauma
● Blunt trauma or fall
● Patient younger than 12 years
● Patient older than 50 years
● Inability to walk four weight-bearing steps
580 SECTION II • Principles of Practice

Figure 27-17
Normal hand. AP, lateral (A), and oblique (B) views of the hand in a skeletally mature patient demonstrate normal osseous and soft tissue
anatomy.
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 581

Figure 27-18
Normal ankle. AP, mortise (A), and lateral views (B) of left ankle show normal osseous and soft tissue structures. The mortise view is taken with
the leg in slight internal rotation relative to the x-ray beam to allow the examiner to evaluate the symmetry of the ankle joint.

Figure 27-19
Normal lumbar spine. AP (A) and lateral (B) views of
the lumbar spine in an adult show normal vertebral
alignment, normal osseous anatomy, and normal soft
tissues.
582 SECTION II • Principles of Practice
Figure 27-20
Normal shoulder. The usual shoulder series includes AP views
of the shoulder with the humerus in both internal (A) and
external (B) rotation. The additional axillary lateral view (C)
shows the relationship of the humeral head to the glenoid,
excluding dislocation.
Ottawa Knee Rules. The Ottawa knee rules are
intended to be used following knee trauma in patients 18
years of age and older.7,8,10 They recommend plain film
radiographs whenever any of the following conditions are
met: (1) the patient is older than 55 years, (2) there is
tenderness at the head of the fibula, (3) there is isolated
tenderness of the patella, (4) the patient is unable to flex
to 90°, or (5) the patient is unable to walk four weight-
bearing steps immediately after the injury and in the
emergency department.7,8,10 This CDR’s sensitivity and
specificity are 97% and 27%, respectively.7,8 Seaberg con-
cluded that use of the Ottawa Knee Rules could reduce
the use of radiographs in patients following knee trauma
by 23%.7
Ottawa Ankle Rules
The Ottawa Ankle Rules11,12 includes two sets of radiog-
raphy decision-making guides following trauma to the
Ottawa Rules for Knee Trauma
● Knee trauma
● Patient older than 55 years
● Tenderness at head of fibula
● Isolated tenderness of patella
● Patient unable to flex knee to 90°
● Patient unable to walk four weight-bearing steps immediately
after injury and when examined
ankle, one for use with patients complaining of ankle
pain and the other for patients complaining of midfoot
pain. Concerning the ankle, the rules state that plain
film radiographs should be ordered only if there is pain
surrounding one or both of the malleoli and one of the
following: (1) tenderness at the posterior aspect or tip
of the lateral malleolus, (2) tenderness at the posterior
CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 583

Figure 27-21
Normal wrist. AP and lateral views
of the wrist allow the examiner to
evaluate the distal radius and ulna,
the carpals, and the metacarpals. The
relationships among the distal radius,
lunate, and capitate are optimally
demonstrated on the lateral view.

Figure 27-22
Importance of multiple views. A, AP and
oblique views of the wrist appear near
normal with the exception of a mildly
abnormal lunate shape, which would be
easy to disregard. B, Lateral view of the
wrist shows a clear perilunate dislocation
(arrow), with the capitate dislocated
posteriorly relative to the lunate.
584 SECTION II • Principles of Practice

Figure 27-23
Importance of multiple views. AP, oblique (A), and lateral (B) views of hand show a subtle nondisplaced fracture of the diaphysis of the third
metacarpal. Extremely subtle on the AP view, the fracture line is much more apparent on the oblique view.
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 585

Figure 27-24
Unexpected finding on plain film. Two
views of the leg obtained for knee trauma
showed a normal knee but abnormally
thick cortical bone within the tibia.
Such an appearance can be caused by
tumor or benign conditions, in this case
melorheostosis.

aspect or tip of the medial malleolus, or (3) inability
to bear weight both immediately and in the emergency
department.11,12
When the primary area of concern is the foot, the
rules state that plain film radiographs should be ordered
only if there is pain about the midfoot and one of the
following: (1) tenderness at the fifth metatarsal base,
(2) tenderness at the navicular bone, or (3) inability to
bear weight both immediately and in the emergency
department.11,12
Sensitivity and specificity values for the Ottawa ankle
rules, reported for the ankle and foot rules used together,

Figure 27-25
Lytic bone lesion. Two views of shoulder show a lucent region within the proximal humerus. Lesions with this appearance are referred to as
“lytic” and can be caused by bone cysts, myeloma, or metastases most commonly. Note that the defect is more evident on the view in which the
humerus is externally rotated. Incidentally, note the surgical clips projecting over the neck. Thyroid cancer metastases are a classic cause of lytic
bone metastases.
586 SECTION II • Principles of Practice

Ottawa Rules for Ankle Trauma

● Pain on one or both malleoli
● Tenderness at posterior aspect or tip of lateral malleolus
● Inability to bear weight immediately and in department

Ottawa Rules for Foot Trauma

● Pain in midfoot
● Tenderness at base of fifth metatarsal
● Tenderness at navicular bone
● Inability to bear weight immediately and in department

are 100% and 40%, respectively.11 Stiell et al. suggested that

application of the Ottawa ankle rules could reduce the use
of plain film radiography following ankle trauma by 30%.11

The Canadian C-Spine Rule

This clinical decision rule is for application to alert and
medically stable patients who have sustained cervical
spine trauma. It is designed to help clinicians to decide
whether plain film radiography of the cervical spine
is necessary following traumatic injury involving the
head or neck. More specifically, the CDR is meant to
identify patients at risk for clinically important cervi-
cal spine injury, defined as any fracture, dislocation,
or ligamentous instability demonstrated by diagnostic
imaging.13
Figure 27-26
Importance of examining entire film. Single AP view of pelvis shows
mildly displaced fractures of the right superior and inferior pubic
rami. Adjacent obturator internus margin is displaced, suggesting an
additional obturator hematoma. Unless the examiner has a routine for
examining the entire film, the second major finding of diastatic left
sacroiliac joint may be missed.

Table 27-2
Imaging Modality Summary
Modality Advantages Disadvantages

Computed Bone detail Contrast toxic to kidneys

tomography (CT) Calcification Poor soft tissue separation
Acute blood Ionizing radiation
Very fast
Moderate cost

Magnetic resonance Soft tissue resolution Expense

imaging (MRI) Intra-articular structures Poor bone/calcification
detail

Nuclear medicine Poor spatial resolution Expense

(bone scan and PET) Sensitive, not specific

Plain films Bone detail Ionizing radiation

Calcification
Inexpensive
Diagnostic Portable Operator dependent
ultrasound Inexpensive Often require MRI anyway
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 587

Table 27-3
Value of Various Modalities in Demonstrating Pathology
Structure/Lesion MRI CT US Plain Films

Meniscus or labrum tear Excellent Poor Poor Poor

Fracture Excellent Excellent Poor Good
Articular cartilage lesion Good Poor Poor Poor
Muscle tear Good Fair Fair Poor
Tendon tear Excellent Fair Fair Poor
Ligament tear Excellent Poor Fair Poor
Joint effusion Excellent Excellent Good Good (large joints)
Lipohemarthrosis Excellent Excellent Good Fair
Muscle edema Excellent Good Poor Poor
Bone edema Excellent Poor Poor Poor

The rule is based on answers to three questions:13 (1)
Are there any high-risk factors that mandate radiography?
Examples include age greater than or equal to 65 years,
a dangerous mechanism of injury, or paresthesias in the
extremities. If the answer is yes, then radiographs should
be obtained. (2) Are there any low-risk factors that allow
safe assessment of range of motion? Examples include a
simple rear-end motor vehicle accident, a normal sitting
position, a patient being ambulatory at any time, delayed
onset of neck pain, or absence of midline cervical spine

Table 27-4
Clinical Decision Rules for Plain Film Radiography
Sensitivity and
CDR Criteria for Radiography Specificity

Pittsburgh decision rules
(knee)5-7
Ottawa knee rules5,6,8
Ottawa Ankle Rules (ankle
and foot)9,10
Canadian C-Spine Rule11
Blunt trauma or fall plus: 99% and 60%
—age younger than 12 years or older than 50 years, or
—inability to walk four weight-bearing steps in the emergency department
For patients >–18 years old following knee trauma, radiography is 97% and 27%
warranted if:
—the patient is older than 55 years
—there is tenderness at the head of the fibula
—there is isolated tenderness of the patella
—the patient is unable to flex to 90°, or
—the patient is unable to walk 4 weight-bearing steps immediately after the
injury and in the emergency department
Ankle: pain surrounding one or both malleoli and: 100% and 40%
—tenderness at the posterior aspect or tip of the lateral malleolus
—tenderness at the posterior aspect or tip of the medial malleolus, or
—inability to bear weight both immediately and in the emergency
department
Foot: pain about the midfoot and:
—tenderness at the fifth metatarsal base
—tenderness at the navicular bone, or
—inability to bear weight both immediately and in the emergency
department
For alert and medically stable patients following cervical spine trauma, 100% and 43%
address the following:
—Are there any high risk factors that mandate radiography? If yes,
radiography is warranted
—Are there any low risk factors that allow safe assessment of range of
motion? If yes, go to the following step. If no, radiography is warranted
—Is the patient able to actively rotate the neck at least 45° to the right and
left? If no, radiography is warranted
588 SECTION II • Principles of Practice
tenderness. If the answer is no, then radiographs should be
obtained. If the answer is yes, then the clinician can move
to question 3. (3) Is the patient able to actively rotate the
neck at least 45° to the right and left? If the patient is
unable to do so, then radiographs should be obtained. If
the patient is able, then no radiographs are necessary.
Canadian Rule for Cervical Spine Trauma
● Trauma (i.e., mechanism of injury)
● Age greater than or equal to 65 years
● Paresthesia in extremities
● If range of motion cannot be assessed, imaging required
● Rotation cannot actively rotate neck at least 45°
Stiell et al. reported that the Canadian C-spine rule
has a sensitivity of 100% and specificity of 43%.13 In their
prospective study of the CDR’s effectiveness, the authors
concluded that the radiography ordering rate would have
been 58% using the rule, compared to the actual rate of
almost 70%.13
Diagnostic Imaging Guidelines for Acute Low Back
Pain
The utility of plain film radiography and advanced imaging
in cases of acute low back pain is questionable. Particularly
with this patient population, plain film radiographs are
overutilized.14 For the majority of patients complaining of
acute low back pain, ordering imaging studies is unneces-
sary because their symptoms are likely to resolve within
4 weeks with proper conservative management.14-16
A critical literature review by Jarvik and Deyo,17
including the years 1966 to 2001, examined the diag-
nostic accuracy of clinical information and imaging for
patients with acute low back pain. Based on the evidence,
the authors suggested the following diagnostic strategy:
(1) for adults younger than 50 years of age with no signs
or symptoms of systemic disease, symptomatic therapy
without imaging is appropriate; (2) for patients 50 years
and older or those whose findings suggest systemic dis-
ease, plain film radiography and simple laboratory tests
can almost completely rule out underlying systemic dis-
ease; and (3) advanced imaging should be reserved for
patients who are considering surgery or those in whom
systemic disease is strongly suspected.17
Diagnostic Imaging Guidelines for Acute Low
Back Pain
● Patients older than 50 years (plain films)
● Patients with signs/symptoms of systemic disease (plain films)
● Patients considering surgery (plain films and/or advanced imaging)
Basics of Growth and Development
Understanding basic skeletal maturation and the appear-
ance of an immature skeleton on a radiograph provides
insight into the nature of traumatic, neoplastic, and
infectious processes. The named portions of a typical
long bone are diaphysis, metaphysis, physis or growth
plate, and epiphysis (Figure 27-27). Long bones elon-
gate through activity at the growth plates, or physes.
Radiographically, physes appear as linear radiolucent
(light) structures between metaphysis and epiphysis.
Apophyses are equivalent to epiphyses but are adjacent
to muscles instead of joints. Whereas an epiphysis is near
a joint, where compression is applied to it, an apophysis
is adjacent to soft tissues, where traction may be applied
to it. Epiphysis examples include the articular ends of
long bones such as the head of the femur, radius, ulna,
metacarpals, and phalanges. Apophysis examples include
the iliac crest, ischial tuberosity, greater trochanter, and
medial and lateral epicondyles.
Different injuries, tumors, infections, and other prob-
lems may preferentially affect a certain part of imma-
ture bone. For example, childhood sarcomas typically
arise at the most mitotically active regions of growing
bone, which are the metaphyses of the femur, tibia,
and humerus. Whereas infections can cross the physis
in infants and adults, the physis in a child often acts as
a barrier to the spread of infection to the epiphysis or
apophysis. Sesamoid bones are considered epiphyseal/
apophyseal equivalents, thus processes affecting epiphy-
ses also can affect sesamoids.
Clinicians who are familiar with the radiographic
appearance of growing bone can avoid mistaking nor-
mal structures for pathology because the appearance
of some normally developing structures can look very
alarming on radiographs to inexperienced viewers.
For example, the apophysis of the growing calcaneus
Diaphysis
Metaphysis
Physis
Epiphysis
Figure 27-27
Parts of a typical growing long bone.
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 589

frequently looks abnormally dense and can appear frag-

mented. Now known to represent a normal variant,
this condition was initially (and incorrectly) believed
to represent avascular necrosis and named Sever’s dis-
ease (Figure 27-28). Pain in symptomatic children
may actually come from bone bruising or microscopic
stress fractures of the metaphyseal bone adjacent to
the apophysis.18 Another example of a normal struc-
ture that can have an alarming appearance on radio-
graphs of children is ischiopubic synchondrosis, in
which the inferior pubic ramus and the ischial ramus
are in the process of fusing. It is normal for this region
to appear irregular and even asymmetric side to side,
and it is often mistaken for fracture by inexperienced
clinicians, especially when the patient’s pain complaint
is local to it.
Sometimes the physis is the weakest link in the kinetic
chain formed by muscle and tendon, and injury or vig-
orous athletics can separate the bone at the physis line, Figure 27-29
creating a physeal avulsion. This is most common where Single AP view of the pelvis. This athlete felt a “pop” while sprinting
and experienced immediate severe hip pain. The lesser trochanter
bone is exposed to large lever arms and strong weight- on the right is avulsed and retracted proximally. The right greater
bearing muscles, such as the origin of hamstring, adduc- trochanter is normally positioned.
tor, rectus femoris, or sartorius muscles or at the insertion
of the iliopsoas or hamstring muscles (Figure 27-29). As
physeal avulsion can be subtle on plain radiographs, a CT tem (Figure 27-30), different classes of fractures carry-
study may be warranted if initial images appear normal ing different ramifications pertaining to future growth
and clinical suspicion remains high. and complications (Table 27-5). Salter-Harris type I frac-
Fractures involving the physis (approximately 10% tures account for only 6% of epiphyseal plate injuries and
of all fractures in patients under age 16) in a skeletally involve complete separation of epiphysis from metaphy-
immature patient are classified by the Salter-Harris sys- sis. Prognosis for future growth is good, as these tend
either to self reduce or be relatively easy to reduce, and
the physeal germinal matrix, or region of growing carti-
lage, is usually intact.
Salter-Harris type II fractures are the most com-
mon type of growth plate injury, accounting for 75%
of such injuries (Figure 27-31). The fracture line
runs through the metaphysis and through the phy-
sis, removing a piece of metaphysis. The potential for
future growth is excellent providing blood supply is
not damaged.
Eight percent of physeal fractures are type III, extend-
ing through the epiphysis to the physis and involving the

I II III IV V

Figure 27-28
Normal calcaneal apophysis. Lateral view of the foot shows normal
osseous anatomy. The calcaneal apophysis often looks very dense and
can even appear fragmented; however, this is normal. When in doubt,
films of the contralateral foot can be obtained to confirm a relatively Figure 27-30
symmetric appearance. The Salter-Harris classification system.
590 SECTION II • Principles of Practice

Table 27-5 articular joint surface to the physis and an additional

Salter-Harris Fracture Summary fracture line runs from the physis through the metaphy-
sis, these frequently require open reduction and fixation.
S-H Prognosis for
Classification Location Growth
Future growth and joint surface alignment and integrity
are concerns. There is a relatively high risk of new bone
Type I Physis separation Good bridging the growth plate, which prevents future sym-
Type II Metaphysis side of Good metric growth.
physis The least common type of physeal fracture, and the
Type III Epiphysis side of Fair; may require most difficult to identify and treat, is the Salter-Harris
physis surgery; joint type V fracture. This involves crushing of both the
surface often growth plate and its blood supply. As there is no associ-
damaged
ated fracture of metaphyseal or epiphyseal bone, this is
Type IV Through metaphysis, Fair; may require
physis, and epiphysis surgery; physis
difficult to diagnose and sometimes is misdiagnosed as a
often fuses sprain. Premature growth arrest is common.
Type V Physis crushed Physis often fuses

Fractures and Fracture/Dislocations

joint surface. Open reduction may be required and, in
addition to concerns regarding future growth, damage to
the joint surface is possible, so prognosis is less favorable
with this type.
Salter-Harris type IV fractures account for 10% of all
physeal fractures. As the fracture runs from the intra-
Fractures are among the most common indication for
radiographic evaluation. Clinical decision-making guides
discussed above, such as the Ottawa Ankle Rules and
Ottawa Knee Rules help clinicians decide whether suf-
ficient clinical evidence exists to suspect a fracture, and
thus, to warrant radiographic evaluation.

Figure 27-31
Salter type II fracture. AP, mortise (A), and lateral (B) views of ankle show a fracture of the posterior tibia in the distal diaphysis/metaphysis
region, which extends to the physis but not into the physis or epiphysis.
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations
An initial fracture workup consists of radiographic
plain films of the area in question in at least two differ-
ent planes. Extremity radiographs may be compared to
radiographs of the contralateral (presumably normal) side
to clarify whether an abnormality represents an injury or
normal variation. On plain films, a fracture may be repre-
sented by a step-off of cortical bone, discontinuity of tra-
becular bone, an avulsion of a small piece of bone (usually
in an area of tendinous or ligamentous insertion) (Figures
Figure 27-32
Avulsion fracture. AP, lateral (A), and mortise (B) views of ankle show
small avulsion fracture involving medial malleolus. The demarcation
line between subcutaneous fat and muscular soft tissues is lost adjacent
to this because of edema associated with acute avulsion. The talocrural
joint is wider laterally than medially, suggesting severe ligament
damage with compromised joint integrity.
591
27-32 and 27-33), or an obvious separation of two por-
tions of bone (Figures 27-34 and 27-35). Occasionally
fractures are occult, meaning that they are not appar-
ent initially on plain film radiographs. In cases in which
plain film radiography is normal but nonvisualized or
occult fracture is suspected on clinical grounds, plain
Figure 27-33
Avulsion fracture. AP, lateral (A), and oblique (B) views of the hand
show a subtle avulsion fracture involving the proximal aspect of the
first proximal phalanx. Called a gamekeepers thumb, this fracture
involves avulsion of the metacarpophalangeal joint and ulnar collateral
ligament. Although subtle, this is a significant injury that often
requires surgical fixation.
592 SECTION II • Principles of Practice
Figure 27-34
Displaced fracture. This single view of the humerus shows a
complete fracture of the humeral diaphysis with displacement of the
distal segment laterally and a small amount of bayonet apposition
(overriding).
radiographs may be repeated after several days as frac-
tures will show resorption of bone along fracture edges,
improving fracture conspicuity and allowing identifica-
tion of previously unappreciated fractures (Figure 27-36).
In addition, a bone scan will show increased uptake of
radiotracer at the site of fracture, making this area bright
on imaging (called a “hot spot”). Alternatively, CT or
MRI may be performed without delay and will likely
demonstrate the occult fracture if one exists.
Fractures may be described or classified according to
how they appear radiographically. In adults, fractures are
usually complete rather than incomplete, meaning they
involve the entire thickness of bone and disrupt the entire
cortical circumference. Fractures may also be described
as transverse (across the bone) (Figure 27-37), oblique
(diagonal to the long axis of bone), or spiral. A commi-
nuted fracture involves multiple fragments and may also
be termed complex. A fracture extending to the articu-
lar surface of a bone is also considered complex, regard-
less of how many fracture fragments there are. A simple
fracture, on the other hand, consists of no more than
two fracture fragments and does not involve an articular
surface. “Closed” fractures are not associated with skin
disruption, whereas “open” fractures imply disruption of
overlying skin and carry a higher risk of subsequent infec-
tion or osteomyelitis.
Fractures in Children
Because the bones of children are more flexible than
those of adults, children are susceptible to incomplete
fractures in addition to those fractures experienced by
adults (Figure 27-38). Incomplete fractures in children
include buckle, greenstick, and bowing fractures. Buckle
fractures involve a “bending” of cortex on one side of
a bone. When this involves the entire circumference
of the bone, it is termed a torus fracture, although the
terms “buckle” and “torus” fracture are often used inter-
changeably. Greenstick fractures involve a linear fracture
through one cortical surface and a flexing deformation of
the opposite cortical surface. The third type of childhood
incomplete fracture is the bowing fracture, in which the
entire bone is bent with persisting, often minimal, defor-
mity. Bowing fractures actually involve countless micro-
fractures along a long segment of the bone.
Children are also susceptible to fractures involving the
physis, or growth plate, which constitutes the weakest
portion of growing bone (see Figure 27-31). Physeal
injuries, discussed previously, are significant in that they
may affect subsequent growth.
Stress and Insufficiency Fractures
Stress fractures and insufficiency fractures can be diffi-
cult to identify. Although similar in concept, these are
very different entities. Stress fractures occur in normal
bone as a result of abnormal stresses, whereas insuffi-
ciency fractures occur in abnormal bone as a result of
normal stresses. Common locations of stress fractures are
the femoral neck or tibial shaft in runners, the metatar-
sals in athletes or military recruits, or the wrist region
of gymnasts. Stress fractures may initially appear normal
on plain films, but with time they often show indistinct
sclerosis and periosteal reaction (indistinct thickening of
the outside border of the bone). Untreated, these can
progress to complete fracture.
Insufficiency fractures occur in bone that is abnormal.
Osteoporosis and osteopenia are two examples of abnor-
mal bone. Osteoporotic bone is normally mineralized but
the quantity of bone is decreased, leading to decreased
ability to tolerate stress. Osteoporosis can be associated
with hormonal changes following menopause, prolonged
immobilization, Cushing’s disease, exogenous steroid
administration, and many other factors. Osteopenic bone
is abnormal in quality, usually because of an underlying
CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 593

Figure 27-35
Shoulder dislocation with Hill-Sachs fracture. A, AP of view the
shoulder showing an abnormal relationship between the humeral
head and the glenoid fossa. It is impossible to determine from this
view whether the humeral head is anterior or posterior to the glenoid.
Either an axillary lateral (requiring the patient to abduct the shoulder)
or a scapular Y view is necessary to assess the relative position of these
structures. B, Postreduction scapular Y view showing the humeral
head properly positioned relative to the glenoid fossa.
C, Postreduction AP view of the shoulder shows the humeral head
cortex defect consistent with Hill-Sachs fracture. Hill-Sachs fractures
are best visualized with the humerus internally rotated.
594 SECTION II • Principles of Practice

Figure 27-36
Occult elbow fracture. Initial AP (A) and lateral (B) views of elbow show no fracture. However, both the anterior and posterior intra-articular
extra-synovial fat pads are superiorly displaced (arrows), indicating a joint effusion or hemarthrosis. In the setting of trauma and pain, this
appearance almost always represents a radial head fracture in adults. In children, the most common occult elbow fracture is supracondylar.
Additional views confirmed a radial head fracture in this case.

abnormality in metabolic mineralization of the osteoid

matrix of developing bone. Osteopenia is associated with
rickets, metabolic abnormalities in vitamin D metabolism,
hyperparathyroidism, and many other factors. Common
locations for insufficiency fractures include the vertebrae,
which may show frank compression fractures or subtle
end plate fractures, the hips, and the pelvis. Identifying
insufficiency fractures is often difficult because of under-
lying bone osteopenia. When suspicion of stress or insuf-
ficiency fracture is high and plain films are normal, CT,
MRI, or bone scan may demonstrate the abnormality.

Figure 27-37
Impacted fracture. AP and lateral view of the wrist show irregularity
of the radial metaphysis cortex and trabecular bone consistent with
impacted transverse fracture.
Fracture Healing
To make accurate prognoses and appropriate clinical
decisions, it is important to be able to gauge chronic-
ity of any fractures identified. Acute fractures show sharp
margins, adjacent soft tissue edema or hematoma, and no
sign of bony healing. Subacute fractures show resorption
of bone along fracture edges, adjacent periosteal reaction,
and eventual bridging bone. Healed fractures may show
bone deformity with no adjacent soft tissue abnormality
or with adjacent joint degenerative changes. Nonunited
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 595

Figure 27-38
Supracondylar fracture. AP and lateral views of the elbow show a supracondylar fracture with disruption of the anterior cortex and mild posterior
angulation of the distal fragment. Elevation of the anterior and posterior fat pads at the elbow joint signifies an elbow effusion.

fractures or chronic avulsion fractures show well-corti-
cated adjacent bone edges, no adjacent soft tissue edema,
and no periosteal reaction. Figure 27-39 shows a healing
fibula fracture at various stages of the process.
Fracture healing rates vary depending on the location
and type of fracture. Most young patients show complete
fracture healing for uncomplicated fractures in 6 to 8
weeks. Some regions, such as the tibia, may take slightly
longer.
Some areas of the body are prone to fracture com-
plications. Because of their tenuous blood supply, the
scaphoid bone of the wrist, the talus, and the femoral
head are prone to avascular necrosis (AVN) following
fracture. Although initial plain films often appear nor-
mal, with time these regions appear sclerotic and even-
tually associated articular surfaces become irregular, and
subchondral bone may collapse. Whereas CT may have
the advantage in demonstrating occult fracture, MRI is
superior for demonstrating marrow abnormality associ-
ated with AVN.
A number of factors other than fracture type and
location affect healing rates. Generally speaking, frac-
ture healing is slower in the elderly, smokers, patients on
corticosteroids, and patients who continue to experience
motion across the fracture.
After fracture healing, angular deformity across a fracture
site usually persists indefinitely in adults (Figure 27-40). In
children, angular deformity in the anterior-posterior plane
usually decreases and may even completely normalize with
subsequent growth. Valgus, varus, and rotational deformi-
ties after fracture healing in children often decrease with
time and growth but may not fully normalize.
596 SECTION II • Principles of Practice

Figure 27-39
Healing fracture of the fibula. A, Acute phase. Fracture edges are well
defined, bony angles are sharp, and adjacent soft tissue swelling is
present. B, 3 weeks. Resorption has occurred along the fracture edges
and early periosteal new bone formation adjacent to the fracture site is
visible. C, Early bridging bone across the fracture site is present.

examination data have been obtained, diagnostic imaging

Periarticular Injuries
Acute injuries to periarticular structures typically occur
in response to a single, traumatic incident. To a lesser
extent, these injuries may result from the application of
abnormally high forces to a joint over a period of time. In
either case, because of the traumatic nature of the injury
there are a number of potential diagnoses affecting struc-
tures around joints that must be considered before clini-
cians can make a definitive diagnosis.
A few examples of differential diagnoses include fractures,
articular cartilage injuries, meniscus or labrum injuries, and
musculotendinous unit injuries. The patient’s mechanism
of injury and clinical presentation usually help to narrow
the potential diagnoses to a few, but often the picture can
remain unclear in terms of either the exact structure involved
or the extent of the injury. Once the interview and physical
can help clinicians differentiate among these joint-related
injuries and define the injury more completely.
Conventional radiographs can be helpful when investi-
gating some of these differential diagnoses. For example,
radiographs usually visualize a fracture occurring near a
joint. They may also show joint effusion and soft tissue
swelling around a joint that may be indicative of intra-
articular lesions, such as osteochondral injuries, meniscus
and labrum injuries, and subtle fractures that may not
be readily apparent. For soft tissue injuries such as carti-
lage and ligament lesions, however, the indirect evidence
offered by conventional radiography may not be enough
to confirm a diagnosis or characterize it sufficiently.
Because injuries to soft tissue structures can be dif-
ficult to evaluate fully using only conventional radiog-
raphy, MRI is the diagnostic modality of choice in cases
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 597

Figure 27-40
Impacted fracture with angulation. AP, lateral, and oblique views of wrist show an impacted fracture of the distal radius with dorsal angulation of
the distal fragment. The alteration in radiocarpal joint biomechanics can have major long-term implications if not recognized and addressed.

in which the structural integrity of hyaline cartilage,
fibrocartilage, tendons, ligaments, menisci, labral struc-
tures, bursae, muscle, and neurovascular structures is
in question.
Because of their high association with both acute and
chronic injury, the knee and shoulder are the two most com-
monly evaluated peripheral joints with MRI. Spine evalua-
tion is discussed elsewhere in this chapter. Other joints, such
as the ankle, elbow, and hip, are also frequently evaluated
but will not be specifically discussed here because general
concepts are similar to those of the knee and shoulder.
Diagnostic Imaging of the Knee and Shoulder
MRI of the knee is able to demonstrate the joint and
periarticular soft tissues with unparalleled detail. Synovial
fluid, especially high volumes associated with joint effu-
sion, and edema of soft tissue structures appears bright
on T2 images. Hemorrhage within the joint (hemarthro-
sis) shows varying T1 and T2 signal intensity depending
on the age of the blood, whereas lipid material within
the joint (lipohemarthrosis) appears bright on T1 images
and dark on fat saturation images.
Cartilage injuries (chondral) or bone and cartilage
combination injuries (osteochondral) may be nondis-
placed, showing only synovial fluid extension below the
surface of articular cartilage into the defect, or completely
displaced, in which case a segment of cartilage with or
without underlying bone is missing. Bone edema, bright
on T2 images, will be seen deep to the defect in acute
stages. A loose chondral or osteochondral fragment is
often identified within the joint.
Menisci are composed of fibrocartilage and appear
dark on both T1 and T2 images. Meniscal tears (Figure
27-41) appear as regions of high T2 intensity within the
substance of the meniscus, and may be associated with
displacement of a portion of meniscus, as occurs with
bucket handle tears.
598 SECTION II • Principles of Practice
Figure 27-41
Meniscus tear versus normal. Sagittal T2 fat saturation images show the posterior horn of the medial meniscus both (A) without and (B) with a
tear. The tear communicates with the inferior articular surface of the meniscus.
Anterior cruciate ligament (ACL) tears are more
common than posterior cruciate ligament (PCL) tears,
but both appear as disruptions in the continuity of the
ligaments, often with associated edema and hemorrhage
(Figures 27-42 and 27-43). Partial ligament tears often
show regions of high T2 signal within the substance of
the ligament, with or without thinning or attenuation of
the ligament itself. Medial and lateral collateral ligament
tears, identified as discontinuity of the ligaments and
often retraction in the direction of maintained attach-
ment, are often visible.
Marrow signal within the subchondral bone must be
carefully evaluated, as edema frequently gives a clue as
to the nature of injury. For example, edema underlying
the medial aspect of the patella accompanied by edema
of the lateral aspect of the lateral femoral condyle often
indicates a lateral patellar dislocation has occurred, even
though no other abnormality may be present currently.
The musculotendinous structures about the knee are eas-
ily evaluated with MRI, as is the patellar tendon and asso-
ciated bursal structures.
The shoulder is a particularly complex joint, and MRI
is uniquely suited to its evaluation. The musculotendi-
nous structures most likely to sustain injury include the
rotator cuff (supraspinatus, infraspinatus, teres minor,
and subscapularis) and biceps brachii tendons (long
and short heads). Rotator cuff tears appear as regions of
T2 and often T1 brightness within the otherwise dark
fibrous tendons of the rotator cuff muscles. Joint effu-
sions are often seen.
The glenoid labrum, composed of fibrocartilage,
appears dark on both T1 and T2. Labral tears appear
bright on T2 images and may involve separation of the
labrum from the underlying glenoid. In cases of adhe-
sive capsulitis, the glenohumeral joint capsule will appear
thickened and often show a bright signal following con-
trast administration.
Edema and Joint Effusion
Soft tissue abnormalities are often visible on plain film
radiographs. Many joints show characteristic changes
when an effusion or hemarthrosis is present. The glenohu-
meral joint or hip joint may appear normal or slightly wid-
ened because of extra intracapsular fluid. An intracapsular
but extrasynovial fat pad is present at the anterior aspect
of the elbow joint (Figure 27-44). This may be visualized
on lateral plain film projections of the elbow in normal
individuals; however, with an increase in joint fluid the
fat pad is pushed cephalad and assumes a triangular posi-
tion. The posterior fat pad, which lies in the olecranon
fossa and is not normally visible, is also pushed cephalad
and made visible with increased elbow joint fluid. Elbow
fractures are often occult, and in the presence of trauma,
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 599

Figure 27-42
Anterior cruciate ligament tear. A, T1-weighted sagittal image of knee shows disruption of the anterior cruciate ligament (ACL). B, fat saturated
T2-weighted sagittal image shows same. Because fat saturation pulse was used on this image, the marrow fat signal is suppressed, making the
marrow appear dark.

Figure 27-43
Normal anterior and posterior cruciate ligaments. A, T1-weighted sagittal image of knee shows normal low signal anterior cruciate ligament
(ACL) and, partially visible in plane of section, posterior cruciate ligament (PCL). Typical of T1-weighted images, the fat within femur, tibia,
infrapatellar fat pad, and subcutaneous tissue fat are high signal; muscle tissue is intermediate, and patellar tendon is low signal, similar to cruciate
ligaments. B, T2-weighted image shows normal low signal patellar tendon, ACL, and PCL. Synovial fluid, typically a high signal on T2 images, is
visible in the suprapatellar bursa, indicating a joint effusion within the knee.
600 SECTION II • Principles of Practice
Figure 27-44
Olecranon fracture. AP and lateral views of elbow show a mildly
displaced olecranon fracture with elevation of both the anterior
and posterior fat pads of the elbow joint, indicating a large joint
hemarthrosis or effusion.
a new elbow effusion is considered hemarthrosis because
of occult fracture (see Figure 27-36). The most common
occult fracture in a child’s elbow involves the supracon-
dylar humerus (see Figure 27-38), whereas adults often
suffer occult radial head fractures. At the knee, an effusion
distends the suprapatellar pouch and creates a soft tissue
density that displaces the quadriceps tendon anteriorly
and flattens the normal fat against the distal femur.
Edema may be present in cellulitis or injury. Sometimes
edema adjacent to an occult fracture may be the only clue
that the fracture is present and may prompt closer evalu-
ation. Edema adjacent to sprains or strains may also be
a clue to injury mechanism. On plain films, edema fluid
infiltrates the soft tissues, and the planes of demarcation
between soft tissues and between muscle and subcuta-
neous tissue are lost. On T2-weighted MRI, edema is
bright because of high water content.
Intervertebral Disc Injuries
In patients with recent-onset uncomplicated back
pain, radiological evaluation is frequently not per-
formed because the majority of such back pain resolves.
Evaluation is generally indicated in cases of complicated
back pain associated with neurological deficit, bowel or
bladder function changes, possible spinal infection, sus-
pected spinal cord compression, or postoperative compli-
cation. Findings of radiographic studies must be strictly
correlated with patents’ age and physical examination.
Because of the expense associated with MRI, MRI
should not be performed unless a treatment decision,
such as the decision to operate, hinges on its result.
Studies have shown that up to 22% of spinal MRIs have
been performed for inappropriate indications.19 Several
studies have shown a high prevalence of spinal stenosis,
facet degeneration, disc bulges, and disc herniations in
asymptomatic patients.20-23 In patients under 40 years of
age, these abnormalities occur in up to 30% of asymp-
tomatic patients, and prevalence increases with advanc-
ing age. Further confusing the relevance of imaging
findings to actual patient symptoms, Boos et al. evalu-
ated lumbar spine MRI in 46 patients without current or
prior back pain, identifying disc abnormalities in 76%.24
The researchers subsequently followed these patients for
5 years. Physical characteristics of the patient’s job, job
satisfaction, and shift work were more likely to predict a
future low-back-pain medical consultation than were the
abnormalities identified on MRI.24 Given the high preva-
lence of imaging abnormalities in asymptomatic patients,
a careful clinical correlation between imaging findings
and clinical exam is crucial.
Plain film radiographs are usually the first step in
evaluating suspected spinal disorders. Clinicians can
readily assess vertebral degenerative changes such as
disc space height loss, end plate sclerosis, osteophyte
formation, end plate defects (Schmorl’s nodes), and
hypertrophic facet changes. Spondylolisthesis severity
is easily assessed, and oblique views can demonstrate
pars interarticularis fractures. Compression fractures
are easily identified. Vertebral alignment, traumatic and
degenerative changes, and evidence of metastatic dis-
ease or malignancy can be identified. Nonmineralized
soft tissue structures, such as discs, paraspinal soft tis-
sues, and supporting ligaments, cannot be directly
evaluated.
CT is the most sensitive modality for evaluating pos-
sible occult spinal fractures. CT myelography, requiring
direct injection of radiographic contrast into the thecal
sac before imaging, improves the sensitivity of CT in
detection of disc bulges and other processes impinging
on the central canal. Nonetheless, MRI has largely sup-
planted CT in spinal imaging because of MRI’s superior
ability to demonstrate soft tissues.
Spinal MRI allows exquisite, noninvasive evaluation
of the spine and associated structures. The vertebral col-
umn, spinal cord, discs, supporting ligaments, and adja-
cent muscles and soft tissue structures can all be assessed
(Figure 27-45). Cord edema, local cord demyelination,
and abnormal cord fluid collections such as cysts, hydro-
melia, or syringomyelia appear bright on T2 images.
Vertebral alignment can be assessed on sagittal images.
In processes such as vertebral metastases, the normal
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 601

Figure 27-45
Degenerative lumbar disc with spondylolisthesis. A, T1-weighted lumbosacral MRI shows narrowing of the L3-L4 disc space with end plate
irregularity, Schmorl’s node within the superior end plate of L4, and grade 1 spondylolisthesis of L3 on L4 because of the degenerative changes.
B, T2-weighted image shows high signal subjacent to the inferior end plate of L3 and the superior end plate of L4, which are caused by the
severely degenerative disc. Marked degenerative changes such as this can be caused by infection or trauma as well as the usual degenerative
mechanisms. The L4-5, L5-S1, and T11-12 discs show low T2 signal, suggesting less severe degenerative changes.

marrow fat may be replaced, decreasing the T1 bright-

ness of affected marrow. Intravascular gadolinium con-
trast causes hypervascular structures and those structures
with concentrated blood to turn bright on T1. This may
improve conspicuity of lesions in the spinal canal and
paraspinal soft tissues; however, vertebral tumors that
contrast enhance may be less conspicuous on non-fat-
saturated T1 images as they may appear closer in signal
to the normally bright marrow fat.
Disc bulges may be visible on both sagittal and axial
MR images, and their location (central, paracentral, neu-
ral foraminal, lateral), severity (bulge, protrusion, extru-
sion, sequestration), and association with cord and nerve
roots can readily be assessed (Figures 27-46 and 27-
47). Annulus fibrosis fibers are dark on both T1 and T2
images, whereas annular tears are usually bright on T2
images and often show contrast enhancement because of
granulation tissue. Nucleus pulposus material is bright
on T2 in young patients because of its high fluid con-
tent. With age, normal disc desiccation decreases this T2
brightness.
Neoplasms (Tumors)
Tumors of bone may be suspected when a patient experi-
ences significant pain at night, pain unrelated to physical
position or activity, pain or deformity out of proportion to
an inciting incident, or when a pathological fracture occurs.
Metastases to bone are approximately 25 times more
common than primary bone tumors. Eighty percent of
bone metastases arise from primary breast, prostate, lung,
or kidney cancers (Figure 27-48). Other slightly less com-
mon sources of bone metastases are gastrointestinal, thy-
roid, and round cell malignancies (Figure 27-49).
The most common primary malignancy of bone in
adults is multiple myeloma, followed in frequency by
osteosarcoma and chondrosarcoma. In children, Ewing’s
sarcoma is most common in the first decade, whereas
osteosarcoma followed by Ewing’s sarcoma is most com-
mon in the second decade. The importance of early diag-
nosis of bone malignancy cannot be overstated, as these
malignancies are most treatable when identified early.
The effects of delayed diagnosis can be devastating, as
602 SECTION II • Principles of Practice

Figure 27-46
Disc herniation. A, Sagittal T2-weighted MR image of cervical spine shows posterior herniation of the C6-C7 intervertebral disc. B, Axial
T1-weighted image shows the disc herniation to be eccentric to the right and demonstrates the degree of spinal canal narrowing it causes. By
convention, all axial CT and MR images are oriented with the patient’s right side toward the left side of the image.

Figure 27-47
Degenerative lumbar disc with protrusion. A, Sagittal T1-weighted MRI of lumbosacral spine shows loss of disc height at the L5-S1 disc as well as
posterior extension of disc material into the spinal canal. B, T2-weighted image of same patient shows low signal within the L5-S1 disc because of
the loss of disc fluid related to degeneration. Because cerebrospinal fluid within the thecal sac is high signal on T2 images, the impression made by
the disc upon the sac is easily seen as well. The remaining discs show normal high T2 signal.
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 603

Figure 27-48
Lytic metastasis (same patient as Figure 27-6). A, Axial CT of a thoracic vertebral body shows a lytic lesion affecting the left posterolateral
vertebral body and the left pedicle. Axial (B) and sagittal (C) T1-weighted MR images of the same lesion show loss of the normal vertebral
marrow fat signal within the affected vertebra and demonstrate that the lesion is confined to the vertebrae and does not yet compress the spinal
canal. D, T2-weighted axial MRI at same level confirms the previous findings.
604 SECTION II • Principles of Practice
Figure 27-49
Blastic metastasis. AP (A) and lateral (B) views of lumbar
spine show the L3 vertebral body to be very sclerotic.
Additionally, the vertebra has lost height, likely the result of
softening caused by the underlying process. When a tumor
causes this type of appearance, it is described as blastic, and
common malignancies associated with blastic metastases
include lymphoma and prostate cancer. Some malignancies,
such as breast cancer, can cause lytic or blastic metastases.
Some benign processes, such as Paget’s disease, can also
cause this appearance.
many tumor types, such as osteosarcoma and chondro-
sarcoma, tend toward early metastasis.
For all types of bone tumors, plain film radiography is
the initial imaging modality. On plain film, clinicians can
assess the size and location of the lesion, the pattern of
bone destruction, the extent of soft tissue involvement,
the presence of tumor matrix, and the aggressiveness of
the lesion. Taken into consideration along with patient
age, gender, and relevant medical history, a short list of
differential diagnostic considerations can be generated.
If a tumor such as osteosarcoma or chondrosarcoma is
suspected, plain film or CT of the lungs may be desirable
because of the propensity for these tumors to metastasize
to lung early.
To evaluate multifocal primary or metastatic bone
tumors, radionuclide bone scans utilizing intravenous
technetium 99 m are utilized. Although bone scans are
very sensitive to any disease process involving bone,
they are extremely nonspecific, and differentiating bone
tumors from traumatic lesions, degenerative or arthritic
changes, or metabolic disease involving bone may be
impossible. Also, bone scans are insensitive to myeloma.
To identify or follow myeloma lesions, Short tau inver-
sion recovery (STIR) protocol MRI or plain films of the
axial and appendicular skeletons are necessary. Positron
emission tomography (PET) shows promise for identify-
ing and possibly even grading bone lesions and tumors
in the future.
Because the visualization of calcification with CT is far
superior to MRI or plain film, CT is utilized primarily for
characterizing the bone matrix of a tumor and identify-
ing subtle pathological fractures. Primary osseous tumors
(osteosarcoma) and primary cartilaginous tumors (chon-
drosarcoma) differ in their calcific tumor matrix, and addi-
tional types of dystrophic or reactive calcification can often
be identified. Soft tissue extent of tumor cannot be reliably
evaluated with CT.
MRI allows unparalleled evaluation of the soft tissue
extent of a tumor, including the extent of adjacent edema
(Figure 27-50). MRI allows imaging in multiple planes
including oblique planes, making a thorough evaluation
in three dimensions possible. Contrast injection is often
used to improve lesion conspicuity. Involvement of neu-
rovascular bundles and local lymph nodes can often be
evaluated. Hematoma, hemorrhage, or inflammatory
change adjacent to tumor may make exact identification
of tumor margins impossible. Following surgical resec-
tion of a tumor, MRI is usually the modality of choice
to evaluate tumor bed residual or recurrence.
Arthritides
Recognizing degenerative changes is important
because outcome expectations or treatment plans may
be affected by chronic joint pathology. Osteoarthritis
is the most common form of arthritis and may be
 CHAPTER 27 • Imaging Joints and Musculoskeletal Tissue: Pathoanatomic Considerations 605

Figure 27-50
Soft tissue tumor. Axial T2 (A), axial STIR (B), and sagittal (C) fat
saturated contrast enhanced T1 images of the thigh show a large
mass within the anterior thigh soft tissues that is intensely contrast
enhancing. The small regions of T1 high signal on the skin are vitamin
A tablets, often used on MRI studies to provide markers so palpable
abnormalities can be localized on the study. Mass was later shown to be
malignant fibrous histiocytoma.

either primary (no known cause) or secondary (caused
by trauma, vascular insult, infection, or other factors).
Osteoarthritis is associated with a nonuniform loss
of articular cartilage. This is seen as decreased joint
space between two adjacent bones on radiographs.
Deep to the cartilage surfaces, cysts, or geodes, form
in the bones as a part of the degenerative process.
Osteophytes form at the margins of degenerative joints
and usually align themselves along ligamentous ten-
sion lines. The ends of the bones deep to the cartilage
become sclerotic. Often a joint affected by osteoar-
thritis undergoes extensive reactive bone formation,
an example of which is buttressing, or thickening of
the inferior femoral neck, which is seen in cases of
severe hip arthritis. Figure 27-51 demonstrates com-
mon radiographic features of osteoarthritis affecting
the wrist and hand.
Many disease processes can cause degenerative changes.
Rheumatoid arthritis can cause severe bilateral joint
degeneration and deformity, which is usually symmetric
606 SECTION II • Principles of Practice

Figure 27-51
Hand osteoarthritis. PA (A), lateral (B), and oblique (C) views of the hand show degenerative changes in a distribution classic for osteoarthritis.
The most pronounced changes occur in the first carpometacarpal joint and lateral intercarpal joints.

Figure 27-52
Juvenile rheumatoid arthritis. AP (A) and lateral (B) views of
wrist in a 17-year-old female with juvenile chronic arthritis show
advanced loss of carpal articular spaces as well as prominent
subchondral cyst formation. Findings were symmetric bilaterally.

bilaterally (Figure 27-52). Psoriasis, lupus, Reiter’s syn-

drome, ankylosing spondylitis, septic arthritis, gout, and
a host of other processes can cause severe monoarticular
or multiarticular degenerative changes. Many of these
also affect the sacroiliac joints and spine, and many are
asymmetric bilaterally.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 33 references for this chapter.
 28
C H A P T E R

F RACTURE M ANAGEMENT
Sachin K. Patel, Bruce H. Dick, and Brian D. Busconi

external environment) or closed (they do not communi-

Introduction
Fractures are an inevitable consequence of the anthro-
pological evolution of a rigid skeletal frame. Before the
development of modern surgery, minor fractures com-
monly led to disfigurement and loss of function, whereas
major fractures, such as those of the femur, pelvis, and
spine, frequently led to death. The acute and long-term
management of fractures, like the mechanisms that cause
them, has evolved. As a result of war and the Industrial
Revolution, fractures and their sequelae have proven to
be a major social and economic concern.1,2
Deciding the mode of fracture treatment is mul-
tifactorial, requiring the input of the patient, family,
and physician to provide an optimal plan within the
patient’s realm. To most efficiently treat fracture dis-
ease, medical professionals must first understand the
mechanism behind injury, the biology of the disease,
nonoperative and operative treatment options, and
ultimately rehabilitation.
cate with the external environment) (Figure 28-1). The
mechanism of injury as well as the amount of energy
imparted to bone in the process of injury determine the
resultant fracture patterns.3 Lower energy injuries result in
simple fracture patterns (i.e., transverse, spiral, or oblique)
(Figure 28-2). Higher energy injuries (i.e., automobile
versus pedestrian injuries) tend to be due to severe direct
violence and often result in comminuted fractures with
butterfly fragments (Figure 28-3). This method of describ-
ing fractures is useful in communicating the nature of frac-
tures among medical professionals, as well as in assessing
the nature of associated soft tissue injury.
Fracture Descriptions
● Nondisplaced versus displaced
● Location
● Epiphyseal (periarticular)
● Metaphyseal

● Diaphyseal

Fracture pattern
Knowledge Required to Offer Fracture Management
●

● Transverse

● Short oblique and oblique

● The mechanism of injury
● Spiral
● The biology of the “disease”
● Butterfly
● The ways fractures heal
● Comminuted
● Operative or nonoperative treatment options
● Complications of fractures
● Soft tissue (condition of skin)
● Open versus closed
● Rehabilitation guidelines and precautions
● Edema
● Realistic expectations, functional outcome
● Presence of blisters

Fracture Patterns Biomechanics

Typical fracture patterns include stress, transverse, short Before discussing the specifics of the management of frac-
oblique, oblique, spiral, butterfly, and comminuted. They tures, we review basic biomechanical concepts. Various
may also be open (because they communicate with the types of forces deform bone in predictable ways. These

607
608 SECTION II • Principles of Practice
Figure 28-1
Open (A) and closed fractures (B). (From Connolly JF: DePalma’s
the management of fractures and dislocations, pp 8-9, Philadelphia,
1981,WB Saunders.)
include compressive forces that shorten bone, tensile forces
that elongate bone, bending forces that cause bowing in
the center of long bones, and torsional forces that deform
a bone around its long axis. Forces acting on bones include
gravity, muscular contraction, and external “traumatic”
forces from an object outside the body such as a motor
vehicle. These forces can be described by vectors that have
both magnitude and direction. Forces acting on the center
of a bone’s rotation result in translation. Moment arms,
forces acting on a bone away from its center of rotation,
result in rotation. Equilibrium is a state in which all force
vectors acting to translate or rotate a bone sum up to zero,
resulting in no net movement.
Figure 28-2
Low-energy fracture patterns. A, Transverse. B, Oblique. C, Spiral.
(From Connolly JF: DePalma’s the management of fractures and
dislocations, pp 9-10, Philadelphia, 1981,WB Saunders.)
Bufferfly
fragment
Figure 28-3
High-energy fracture patterns. A, Comminuted. B, Segmental. (From
Connolly JF: DePalma’s the management of fractures and dislocations,
pp 10-11, Philadelphia, 1981,WB Saunders.)
Forces Affecting Bone
● Compression (shortening)
● Tensile (elongating)
● Bending (bowing)
● Torsional (deformation on long axis)
Biomechanical and Structural Properties
Stress and strain are biomechanical properties used to
describe what may happen to any material when placed
under load independent of that material’s size or shape.
Load applied to any bone results in certain stress and strain
that can deform bone independent of shape or size. Stress,
analogous to pressure, refers to a force applied over a spe-
cific area. Strain refers to elongation or shortening of bone
normalized to its original length. Structural properties are
used to describe the behavior of bone when standardized
deformations are applied. The relationship of these prop-
erties can be demonstrated graphically in stress-strain dia-
grams (Figure 28-4). When force is applied to a sample of
bone, some type of deformation results. When the force
is released, the bone tends to return to its original shape.
This property is referred to as elastic deformation. When
the force is sufficient to deform bone permanently, plastic
deformation has occurred. The point at which elastic
behavior goes to plastic behavior is termed yield point.
The slope of the stress-strain curve in the elastic range is
called modulus of elasticity or Young’s modulus. This
parameter is specific to individual materials (i.e., bone,
titanium or plastic) and characterizes their stiffness.

Figure 28-4
Stress-strain diagram. The slope of the curve in the elastic range
represents the elastic (Young’s) modulus of a material. (Adapted from
Lujan B and White R: Human Physiology in Space, private printing,
1994 as it appears in Vaccaro A, editor: Orthopaedic knowledge
update 8, p. 46, Rosemont, American Academy of Orthopaedic
Surgeons, 2005.)
Bone is strongest in compression and weakest in ten-
sion. When a deforming force is applied to bone, the
region of the bone under tension will fail first. Pure tension
results in a stepped transverse fracture. When subjected to
pure bending, one side of the bone is under tension while
the other is under compression. With persistence of the
force, a transverse fracture originates on the tensile side
and propagates to the compression side. Torsional forces
on bone also produce fractures as a result of failure in ten-
sion. As an example, consider a solid cylinder subjected to
torsion. The diagonal line drawn between two corners of
a square on the surface of the cylinder tends to elongate
as it is subjected to a twisting, torsional force, creating
surface tensile forces (Figure 28-5). A crack originates
perpendicular to the direction of tension, propagating
around the cylinder, resulting in a spiral fracture. Pure
compression crushes bone, leading to a comminuted
fracture. Compressive forces can also result in fracture of
bone by shear. Bone is significantly weaker in shear than
in compression. As bone fails in shear, fractures propagate
at 45° to the applied load, leading to an oblique fracture.
Another major factor contributing to the biomechanics
of fracture disease is bone density.4 Because the stiffness
of trabecular bone varies with bone density, osteoporo-
sis decreases the magnitude of force required to fracture
bone. In addition, the fracture patterns seen in osteo-
porotic bone differ from those in young, dense bone.
Osteoporotic insufficiency fractures are common in the
vertebrae, distal radius, and proximal femur.
CHAPTER 28 • Fracture Management 609
Figure 28-5
Mechanism of long bone fractures: transverse and torsional. (From
Bucholz R, Heckman J, editors: Rockwood and Green’s fractures
in adults, ed 5, p 16, Philadelphia, 2001, Lippincott Williams &
Wilkins.)
Classification of Fractures
Recognition of common fracture patterns has led to
many classification systems. These systems allow more
reliable communication among orthopedic surgeons.
Historically, certain fractures or fracture patterns were
assigned eponyms, usually after the individual who origi-
nally described them. Colles’s fractures (1814) refer to
distal radius fractures, Pott’s fractures (1769) refer to
distal fibula fractures with lateral subluxation of the talus
(ankle fracture), and Malgaigne’s fractures (1847) refer
to vertical shear injuries to the pelvis.1 Eponyms often
refer to a gross deformity, since many of these types
and classifications of fractures were described before the
advent of x-rays. Specific fracture types that cause similar
gross deformities but are very different radiographically
are sometimes lumped into eponymic fracture types. This
often leads to confusion and errors in communication.
Fractures are now routinely assessed with x-rays, com-
puted tomography, and magnetic resonance imaging
(MRI). The additional information provided by these
imaging modalities allows more complex classifications
based on anatomical fracture patterns and associated soft
tissue injury. Some systems may reflect the importance an
individual surgeon places on injury and treatment. The
explosion of research and descriptions in the literature
of various fracture types have left clinicians with numer-
ous classification systems that may or may not be clinically
610 SECTION II • Principles of Practice
useful.5 Discussion of every fracture type is out of the scope
of this text; the reader is referred to a dedicated fracture
text.3,6,7 The AO/Association for the Study of Internal
Fixation (ASIF) has developed a way to describe fractures
of long bones (Comprehensive Long Bone Classification
System)3 (Figure 28-6). Each fracture segment is divided
into three types: A, B, or C. Each type is then subdivided
into three groups. As necessary, further subgroups are then
designated to more accurately define fracture fragments or
displacement. Developed by the AO/ASIF, this system is
intended for international use as well as to be compatible
with research database development.
Not all of these systems are clinically useful. To be used
on a daily basis for communication and decision mak-
ing, the system must be validated.8 A valid classification
system must accurately assess what it purports to assess,
have acceptable intraobserver reproducibility, and have
acceptable interobserver agreement.5 The variability of
image quality (i.e., accurate views and good resolution),
experience in interpretation, and the need for statisti-
cal analysis make normalization of fracture classification
Figure 28-6
AO/ASIF Comprehensive long bone classification system applied to proximal humerus fractures. (From Bucholz R, Heckman J, editors:
Rockwood and Green’s fractures in adults, ed 5, pp 41-42, Philadelphia, 2001, Lippincott Williams & Wilkins.)
systems a formidable task. Furthermore, by using valid
classifications to guide treatment and ultimately evaluate
their efficacy with outcomes assessment, the clinicians’
ability to treat fractures will likely improve.9
Fracture Management
The management of fractures begins with emergency
medical service. Whether in the form of a makeshift sling
for a child with a distal radius fracture or the coordina-
tion of firefighters and emergency medical technicians in
the extraction of a patient from a massive motor vehicle
accident, early attention paid to bony and soft tissue inju-
ries helps prevent further medical deterioration.10 Early
stabilization of fractures minimizes blood loss. This can
be particularly important in patients with long bone frac-
tures (i.e., femur) or pelvic fractures. Early stabilization
is essentially a form of fluid management.11 In addition,
reduction of a fractured bone resets muscle tension,
decreasing muscle spasm and pain. This type of “field”
care helps the surgeon to optimize definitive treatment.
 CHAPTER 28 • Fracture Management 611

28-7). Fractures of the epiphysis often involve dis-

Early Fracture Management placed articular fragments that usually need surgical
● Stabilization minimizes blood loss intervention to achieve an anatomical reduction and
● “Resets” muscle tension restore normal articular relationships. The ultimate
● Decreases spasm and pain goal of fracture care is to restore form and function as
● Decreased soft tissue injury promptly as possible. Although many upper extremity
● Identification of open injuries fractures can be treated nonoperatively (e.g., midshaft
and proximal humerus and some distal radius frac-
tures), others require operative treatment to restore
Splinting a fractured extremity in the field helps make function (e.g., radial shaft fractures). Lower extremity
patients more comfortable. These splints are often rudi- fracture management has the additional challenge of
mentary—cardboard or dedicated arm/leg boxes with weight bearing for mobility. Nonoperative treatment
Velcro straps usually suffice. Femur fractures can be sta- does not subject the patient to the additional risks of
bilized temporarily in a Thomas splint. In the emergency anesthesia, infection, and bleeding associated with
room, the availability of local anesthesia or conscious operative fixation.3,12 Nonoperative treatment is usu-
sedation allows reduction and stabilization with a well-
Joint capsule
molded splint or cast. Epiphysis
The importance of the condition of the soft tissue Articular
injuries associated with fractures, particularly identifying cartilage
open fractures, cannot be emphasized enough. Fractures
associated with a break in the skin are considered open
(see Figure 28-1). The deformity of a fractured extremity Epiphysial
plate or physis
seen in the emergency room does not accurately repre-
sent the energy imparted to the patient during the injury. Metaphysis Cancellous
bone
The shortening and angulation of a long bone during the
injury can be severe; the sharp ends of the fractured bone
Artery to
certainly may traumatize nearby skin, muscle, blood ves- periosteum
sels, and nerves. The lacerations of the skin may actually
be some distance from the fracture and can potentially
Periosteum
lead to a missed open injury. Open injuries are signifi-
cantly more prone to long-term complications including Marrow cavity
infection, nonunion, and amputation.10 Identification of Diaphysis Cortical
open injuries is an important component of the primary bone
and secondary surveys.
Nutrient artery
Gentle compression and elevation can help control
local edema and hematoma development. The condi-
tion of the skin (internal as well as external injury) and Osteon
amount of edema that develops factor into definitive
treatment decision making. Once all injuries have been
assessed by physical exam and imaging, a management
plan is formulated. This section examines various forms
of nonoperative as well as operative treatment.

Nonoperative Management
Most fractures can be managed without surgery. Once
the clinician has achieved an acceptable reduction by
closed means, various devices can be used to main-
Epiphyseal
tain the relative position of a fractured bone. Many plate
metaphyseal and diaphyseal fractures can be treated
conservatively. Special attention should be paid to
epiphyseal fractures. Anatomically, the epiphysis is
Figure 28-7
considered the portion of a long bone between the Zones and types of bone. (Modified from Gardner E, Gray DJ,
articular surface and the physis (growth plate) or phy- O'Rahilly R: Anatomy: a regional study of human structure,
seal scar (remnant of the physis in an adult) (Figure Philadelphia, 1975, WB Saunders.)
612 SECTION II • Principles of Practice

ally reserved for nondisplaced fractures with a low risk
of displacement, for displaced fractures thatare stable
after acceptable reduction is achieved, or for patients
for whom anesthesia and surgery are contraindicated.
Candidates for Nonoperative Treatment of Fractures
● Nondisplaced fractures with a low risk of displacement
● Stable displaced fractures after acceptable reduction
● Patients in whom anesthesia and surgery are contraindicated
Splints, fracture braces, casts (Figure 28-8), and
skeletal traction are all nonoperative devices that can
be used to treat fractures (Table 28-1). These devices
provide relative stability rather than absolute stability.
Absolute stability is achieved with internal fixation,
allowing no motion about the fracture site, whereas
braces and splints reduce gross motion about the frac-
ture site, providing relative stability. Relative stability
results in a larger callus during healing. Fracture align-
ment should be carefully assessed, usually weekly, until
the fracture is sufficiently healed with callus to provide
some inherent stability.
Splints and Fracture Braces
Splints and fracture braces are noncircumferential coap-
tive devices that lie along one or more surfaces of an
extremity. With a splint, the supporting slats, made of
a prefabricated material (molded plastic) or plaster, are
secured with an elastic bandage. With a fracture brace,
a padded moldable piece of plastic is strapped in place.
Without some mechanism to keep it in place (bandage or
Velcro), a splint will not maintain its position. As such,
the splint is much more adaptable; it can be molded
to specific contours or to provide corrective forces.
Prefabricated splints are usually designed to fit everyone
but often no one.13 Thus, custom-molded splints, usually
made of plaster, should be used when possible. Splints
and fracture braces have the advantage that they can be
easily removed for local wound care.
Splints can be used to either immobilize or passively
correct fractures. These devices cannot reliably or actively
correct and maintain unstable fractures. The deforming
muscular forces usually overpower the stabilizing capac-
ity of splints. In addition, immobilization of the joints
proximal and distal to the fractured bone helps prevent
displacement. Splints are usually temporary, used for
days to a few weeks. If effective, plaster or plastic splints

Figure 28-8
A, Humeral fracture brace. B, Air cast for certain nondisplaced lateral malleolus (ankle) fractures. C, Walking boot for certain foot fractures.
(A, from Browner BD, Jupiter JB, Levine AM, Trafton PG: Skeletal trauma, vols 1 and 2, p 1185, Philadelphia, 1992, WB Saunders. E, from
Bucholz R, Heckman J, editors: Rockwood and Green’s fractures in adults, ed 5, p 677, 2001, Philadelphia, Lippincott Williams & Wilkins.)

Figure 28-8—Cont'd
D, Fiberglass cast. E, Various finger splints.
CHAPTER 28 • Fracture Management 613
are replaced by fracture braces. Excellent results for
transverse or short oblique midshaft humerus fractures
and certain midshaft tibia fractures can be obtained with
fracture bracing.14
Cast Immobilization
Like effective splinting or bracing, casting is an art that
takes considerable experience to perform.15 Casting more
effectively immobilizes fracture fragments than either
splinting or bracing by providing rigid circumferential
support into which appropriate molds and three-point
fixation can be incorporated. Three-point molding is a
method to help the fracture resist deforming forces. The
three points are points of contact by the cast that apply a
resistant force opposite in direction to a deforming force.
Well-applied casts are strong, rigid, light, and comfort-
able. Plaster is usually used when extensive molding is
required. Fiberglass can also be used but is more often
reserved for the second cast and beyond, when the
fracture site is more stable.
Once a fracture has been acceptably reduced and that
reduction confirmed radiographically, a plaster cast can be
rolled, molded, and allowed to dry. Cast padding is used
to prewrap the extremity to both protect the extremity
from the exothermic (heat) reaction of the plaster and
water and prevent ulcers during the few weeks the patient
remains in the cast. In particular, extra cotton padding or
felt should be applied to bony prominences (e.g., olecra-
non process, calcaneus, fibular head, anterior iliac spine).
Underlying abrasions and lacerations are usually dressed
with a petroleum-impregnated gauze. Additionally, a hole
or “window” can be cut into casts over the area of the
wound to allow access for wound care. This cast cutout
would then be replaced over the dressed wound and ban-
daged in place to prevent herniation of the edematous tis-
sue below. The clinician then applies the cast in a snug
manner, being careful to not apply it too tightly as neu-
rovascular compromise, and the possibility of an acute
compartment syndrome, can result. In addition, care must
be taken to prevent finger indentations, as local pressure
points may result in ulceration. When edema is present
or anticipated, the cast can be split or bi-valved once dry.
When the edema stabilizes or decreases, the cast can then
be reapplied or overwrapped.15
Casts are particularly useful for maintaining reduc-
tions of ankle, tibia, pediatric forearm, and distal
radius fractures. In infants and toddlers, hip spica
casts can be applied to manage femoral fractures.
Shoulder spica casts are sometimes used for humerus
fractures when compliance with a splint or brace is
questionable.15
Patients should be thoroughly counseled in cast care.
Unless specifically constructed to allow it, weight bearing
on lower extremity casts is not recommended. Acute frac-
tures should be iced and elevated. Dependent edema can
614 SECTION II • Principles of Practice

Table 28-1
Nonoperative Treatment of Fractures
Treatment Advantages Disadvantages Can Be Used For

Splinting Removable for hygiene Poor to moderate stability 5th metacarpal

Accommodates swelling Phalanx (hand)
Lightweight Carpal bones
Inexpensive and easy to make with
plaster
Bracing Removable for hygiene No absolute stability Midshaft humerus
Moderate to good stability Expensive, often needs Scaphoid
Accommodates swelling customized molding Metacarpal
Lightweight Carpal bones
Adaptable to allow joint motion Nondisplaced ulna, midshaft
tibia
Calcaneus and tarsal bones
Metatarsals
Casting Moderate to good stability Difficult to access soft tissue Metacarpals
Inexpensive and easy to make with wounds Distal radius
plaster or fiberglass Typically heavier than splints and Oblique nonarticular distal
Excellent method for initial braces humeral metaphyseal
treatment of displaced fractures No absolute stability Pediatric femoral shaft
requiring reduction Nondisplaced tibial shaft
Some distal fibula (ankle)
Calcaneus and tarsal bones
Metatarsals
Traction Allows longitudinal traction Requires routine adjustment Femoral shaft
Takes advantage of ligamentotaxis Requires expensive and lengthy Tibial shaft
Good for temporizing long bone hospital stays Humeral shaft (rarely)
fractures in unstable patients Risk of pin tract infection Acetabulum
Pelvis

cause an entire limb to swell to the point of neurovascular

compromise. When a cast is too tight and neurovascular
symptoms are present, the cast should be split imme-
diately. Plaster and fiberglass casts are not waterproof.
Immersion in water will soak the underlying padding and
cause maceration and predispose to ulceration and infec-
tion. When Gore-Tex cast padding is used, patients can
immerse fiberglass casts in water. They come, however,
at great expense.

Skeletal Traction
Longitudinal traction has long been recognized as a
method for reduction of long bone fractures. Hippocrates
devised a traction table known as a scamnum (Figure 28-9)
to provide traction to reduce fractures.1 Sufficient traction
must be applied either manually or via weights and pul-
leys to overcome the powerful shortening force of muscles
across a fracture site. Sustained traction was not possible in
Hippocrates’ era, as the ropes used would shear and ulcer-
ate through the skin. Patients were suspended on incline
tables with weights bandaged to the tibia in the hope that Figure 28-9
gravity would help provide the sustained traction. It was Hippocrates’ scamnum, from Sculetus’ 17th-century book. (From Rang
not until the start of the Civil War that Gurdon Buck M: The story of orthopaedics, p 20, Philadelphia, 2000, WB Saunders.)

devised a method of applying longitudinal traction using
bandages around the length of the leg to disperse the trac-
tion forces and reduce the risk of shear injury to the skin.
Robert Hamilton Russell, in 1924, described a method
of balanced traction for femur fractures that opposed
both the deforming force of the rectus femoris and the
hamstring muscles. Fritz Steinmann, in 1907, described a
method of driving a nail, under anesthesia and sterile con-
ditions, through the femoral condyles and applying lon-
gitudinal traction through the nail. Variations of Russell’s
and Steinmann’s traction are still used.
Before the aseptic surgical technique, skeletal traction
proved a valuable method of reducing and maintain-
ing fractures. Because gravity and muscle tension both
deform fractures, a balanced traction must be used.16 The
configuration of traction will vary with the specific bone
involved. For the femur, weights attached to a sling under
the fracture oppose the effects of gravity, whereas longi-
tudinal traction through a Steinmann pin through the
distal femur or proximal tibia helps maintain the fracture
reduction (Figure 28-10). How much traction weight
is necessary? The answer is empirical—enough to main-
tain opposition of the fracture ends without producing a
significant gap.
Indications for treatment of fractures in traction have
diminished since the 19th and 20th centuries. With
Figure 28-10
Proximal tibial traction with balanced suspension. (From Schmeisser G: A clinical manual of orthopedic traction techniques, p 37, Philadelphia,
1964, WB Saunders.)
CHAPTER 28 • Fracture Management 615
the successful development of surgical reduction and
internal fixation, traction is now usually reserved as a
temporizing measure. Patients with massive head inju-
ries may need to be stabilized before they can tolerate
the physiological stresses of intramedullary fixation of
long bones.17 Under the care of experienced orthopedic
nursing, balanced traction can be maintained with rela-
tive ease. Even since the mid-1990s, traction has been
routinely used to maintain pediatric femur fractures.
Traction requires a lengthy stay in the hospital, often
from 3 to 6 weeks, and is very costly. Improved tech-
niques using flexible intramedullary nails have nearly
eliminated the need for traction in children. In proxi-
mal pediatric femoral fractures, the iliopsoas tends to
flex and externally rotate the proximal fragment, unop-
posed. A modified form of femoral traction can be used
to maintain a pull in the axis of the femur with the
hip flexed at 90° and the leg suspended at 90° of knee
flexion (90°-90° traction) (Figure 28-11).
Traction setups requires regular attention. First, the
pin sites need to be cleansed two to three times a day
with a solution of hydrogen peroxide and saline and
dressed with petrolatum-impregnated gauze.18 Second,
the weights, pulleys, and lines need to be adjusted regu-
larly to account for patient movement. Third, for lower
extremity traction, the heel needs to be suspended to
616 SECTION II • Principles of Practice

Figure 28-11
90°-90° traction. (From Schmeisser
G: A clinical manual of orthopedic
traction techniques, p 44,
Philadelphia, 1964, WB Saunders.)

prevent development of sores over the posterior calcaneus.
Prolonged bed rest required of patients in traction often
leads to bedsores, pneumonia, and thromboembolic dis-
ease.19 Prolonged hospital admissions are also a major
economic burden.20
Halo traction is commonly used in the treatment of upper
cervical fractures (Figure 28-12). Angular and rotatory con-
trol of fractures of the dens, the atlas (first cervical vertebra),
and the axis (second cervical vertebra) can be achieved with
a halo ring. The halo ring is fixed to the cranium by a series
of pins that are screwed through the ring and into the cra-
nium. The pins are tightened to the cranium with 8 ft-lbs of
torque in an adult. The ring is rigidly attached to a vest worn
by the patient through a series of suspension bars. A similar
form of traction can be used while the patient lies supine
in a bed; however, the halo traction allows patients lies be
mobile. This form of traction requires regular maintenance
of the pin position and the skin around the pins, requiring
serial x-rays to evaluate fracture healing.
Operative Management
Before the development of aseptic technique and anes-
thesia, the cumulative attempts at open reduction and

Figure 28-12
The halo device is the most effective
means of externally immobilizing the
cervical spine. The patient can resume
near normal activities during its use.
(From Browner BD, Jupiter JB, Levine
AM et al: Skeletal trauma, vols 1 and
2, p 659, Philadelphia, 1992, WB
Saunders.)

internal fixation were disastrous, resulting in ampu-
tation as well as death by sepsis.1 Wiring techniques
using bronze and silver wire were commonplace in
the early 19th century. Once anesthesia provided bet-
ter pain control and bought the surgeon more time
to operate, more extensive surgeries developed. In the
late 19th century, the earliest plates and screws were
developed. These were made of ordinary steel and pre-
dictably corroded, causing severe soft tissue reactions.
Early in the 20th century, better stainless-steel alloys
were developed, and these plates were the standard for
nearly 50 years. In 1963, the Swiss Arbeitsgemeinschaft
für Osteosynthesefragen (AO) Manual was published,
championing the current concept of compression across
fractures and describing, in detail, modern methods of
fracture fixation using plates, taps, and screws. The late
20th century saw vast improvements in the methods and
metallurgy for intramedullary rod fixation. The newest
form of fracture fixation using locking plates became
popular in the 21st century.
The immediate advantage of operative treatment is
the anatomical reduction of fracture fragments and early
mobilization. The long periods of rest and immobiliza-
tion are obsolete in all but a select few situations. The
incidence of cardiorespiratory compromise, thrombo-
embolic disease, and bedsores has significantly decreased
with early mobilization and physical therapy.3,19
Despite the success of the various forms of nonopera-
tive treatment described here, some fractures, particularly
periarticular fractures, require operative fixation (Figure
28-13). Some long bone fractures (i.e., femur) are better
suited for operative treatment to allow early mobilization
and weight bearing. Closed reduction with percutaneous
pinning, external fixation, open reduction and internal
fixation, and intramedullary nail fixation will be covered
(Table 28-2).
Percutaneous Pinning
Percutaneous pinning is a minimally invasive form
of internal fixation. Without the use of some type of
internal fixation, distal radius fractures reduced in a
closed fashion may remain unstable, despite appropri-
ate casting techniques; or in the case of osteoporotic
bone, fractures can be extremely comminuted and tend
to collapse and angulate dorsally. To maintain optimal
alignment, the fractures are pinned percutaneously
using Kirschner wires. The pins are driven through
the skin and cortex, across the reduced fracture, and
into the opposite cortex. This technique is common
in the hand, distal radius, proximal humerus, and foot
(Figure 28-14). Careful wound care is necessary to
prevent pin-site infections. Fractures treated with per-
cutaneous pinning usually require cast immobilization
to protect the pin sites and to help prevent them from
backing out. Pin migration can also be a frustrating
CHAPTER 28 • Fracture Management 617
complication. Pins are typically removed when the
fracture heals. However, larger bones are subject to
forces too great for the pins to withstand, resulting in
pin breakage. Larger bones require different types of
fixation techniques.
External Fixation
The external fixation of fractures maintains traction and
alignment without the need to confine the patient to
a bed in a traction device. Threaded traction pins are
inserted into the bone proximal and distal to the fracture
site (Figure 28-15). The fracture is manually reduced
and fixed in position with carbon-fiber bars spanning
the fracture site outside the skin. The rigidity of fixation
depends on the configuration of the pins, connectors,
and bars. External fixators can be used for definitive fixa-
tion. However, with improved intramedullary and open
techniques, external fixators have assumed the role of
temporary stabilizers in preparation for delayed definitive
fixation. External fixation can be accomplished with rela-
tive speed and ease, making this type of fixation ideal in
multiply injured patients. Though some advocate using
these fixation systems in the emergency room under local
anesthesia, they are usually applied in the operating room
under anesthesia.21 Almost any fracture can be tempo-
rarily stabilized with an external fixator, including all
long bones and the pelvis. Hybrid variations have been
developed to allow fixation of periarticular metaphyseal
fractures such as the tibial plateau and weight-bearing
area of the distal tibia (pilon). Thin, flexible wires are
crossed in the subchondral metaphysis to form a trampo-
line. These pins are then stabilized to an external fixation
frame further down the shaft across the fracture site. This
method allows the clinician to fixate smaller fragments
without having to span and immobilize a joint.
Open Reduction and Internal Fixation (ORIF)
The goal of formal open reduction and internal fixation
(ORIF) is to anatomically reduce and provide absolute
stability to as many of the fracture fragments as possi-
ble. ORIF requires exposing the fracture through a skin
incision and safe intermuscular and internervous planes.
Upon exposing the fracture site, the fracture hematoma
is typically evacuated and the fracture ends cleared of any
debris including periosteum. Excessive stripping of peri-
osteum is discouraged, as this eliminates a major source
of blood supply to the healing fracture. The fracture
fragments are manually reduced and temporarily held in
place with bone clamps or Kirschner wires. When possi-
ble, lag screws are inserted to provide compression across
fracture planes. Some long bone spiral fractures may
be treated solely with a series of strategically placed lag
screws. Usually a plate is applied to the tensile cortex and
fixed with screws. Compression across fracture sites allows
for primary fracture repair, without callus formation.
618 SECTION II • Principles of Practice

Figure 28-13
Examples of fractures requiring operative fixation. A, Fracture of proximal middle phalanx treated with open reduction and lag screw fixation.
B, Displaced scaphoid fracture. This particular fracture would require open reduction, bone graft, and internal fixation with a screw.
C, Segmental, displaced both bones forearm fracture (radius and ulna) treated by open reduction and internal fixation with plates and screws.
D, Distal one-third humeral shaft fracture treated by open reduction and internal fixation with plates and screws. (From Bucholz R, Heckman J,
editors: Rockwood & Green’s fractures in adults, ed 5, pp 699, 787, 883, 987, Philadelphia, 2001, Lippincott Williams & Wilkins.)
 CHAPTER 28 • Fracture Management 619

Table 28-2
Implants for Internal Fixation
Type of Fixation Can Be Used For Advantages Disadvantages Precautions

Percutaneous pins Phalanges Minimal or no incision Can bend or break Must prevent adjacent
Metacarpals required within bone joints from becoming
Distal radius Can be incorporated Risk of pin track stiff (e.g., wrist, elbow)
Proximal humerus into casts infection Must prevent motion
Metatarsals Easy removal in clinic No absolute stability at fracture
Screws (alone) Phalanges Can achieve Cannot provide May need to prevent/
Carpal bones (i.e., scaphoid) compression across rotational stability; limit torsional forces
Pelvis fracture site may need to be during rehab
Distal femur Low profile supplemented by a
Proximal tibia May be performed neutralization plate
Spiral tibial shaft percutaneously or or bracing (i.e., distal
Distal fibula only require small fibula)
Metatarsal incision
Tarsal navicular
Plates and screws Phalanges (hand) Can achieve accurate May require large Prevent adjacent joints
Metacarpals reduction with exposure from becoming stiff
Distal radius absolute stability May involve periosteal Weight bearing usually
Radius/ulna Compression stripping not possible until
Olecranon across fracture site Potential for implant fracture unites
Distal humerus (intra- promotes healing failure (breakage or
articular) without callus screw pullout)
Humeral shaft
Humeral neck
Clavicle
Scapula
Pelvis
Intertrochanteric femoral neck
Femoral shaft
Distal femur
Proximal tibia
Tibial shaft
Distal tibia (intra-articular,
pilon)
Distal fibula
Calcaneus
Tarsal bones
Metatarsals
Intramedullary Femoral shaft Provide relative May disrupt endosteal Weight bearing may be
nails Tibial shaft stability (intramedullary) allowed depending on
Humeral shaft Can lock to provide blood supply presence of locking
Radial shaft rotational stability Some entry points are screws, cortical
Ulnar shaft intra-articular (distal contact, fracture
Clavicle femur and proximal pattern, surgeon
tibia) preference
External fixators Phalanges (hand) Typically easy to apply Provide only relative Weight bearing is
Distal radius in an emergency for stability usually not possible
Olecranon unstable patients Risk of pin track Often bulky
Humerus Allow longitudinal infection May allow early
Pelvis traction adjacent joint motion
Femoral shaft
Distal femur
Proximal tibia
Tibial shaft
Distal tibia (pilon)
620 SECTION II • Principles of Practice
Figure 28-14
An unstable distal radius in a 33-year-old
patient. AP (A) and lateral (B) radiographs
demonstrate the displaced fracture. Closed,
manipulative reduction and percutaneous
pin fixation were accomplished using image
intensification (C and D). (From Browner BD,
Jupiter JB, Levine AM et al: Skeletal trauma,
vols 1 and 2, p 1078, Philadelphia, 1992,
WB Saunders.)
Figure 28-15
External fixation of the femur. A, Stacked lateral one-half pin frame
(unilateral frame). B, Wagner external fixation. (From Browner BD,
Jupiter JB, Levine AM et al: Skeletal trauma, vols 1 and 2, p 1554,
Philadelphia, 1992. WB Saunders.)
Screwing the plate flush to bone provides sufficient fric-
tion to add significant rigidity to the construct. In the
midshaft of long bones (e.g., the radius), the plates are
applied in compression (Figure 28-16). In oblique distal
fibula fractures, the compression is usually provided by a
lag screw. A lateral plate is then applied to impart rotation
stability to the fracture (neutralization). In the proximal
tibia, plates and screws can be used to buttress the lat-
eral tibial plateau and resist translation along the fracture
plane (shear) (Figure 28-17). In severely comminuted
fractures, the fragments may be too small to lag, and the
ends of the bone may be noncontiguous. In these cases,
the length of the bone is restored with traction. The cli-
nician bridges the fracture ends with a plate in neutral
mode, using the remaining comminuted bone to fill the
gap. In cases of severe bone loss, bone graft may be neces-
sary. Careful hemostasis with electrocautery is important
to prevent postoperative hematomas. The wound is care-
fully irrigated and closed in layers. Postoperatively, rig-
idly fixed fractures are splinted for comfort. Subsequent
application of a cast is left to surgeon preference, but it is
usually recommended to protect the repair, particularly
in the lower extremity.
 CHAPTER 28 • Fracture Management 621

Figure 28-17
Tibial plateau fracture fixed with a medial buttress splate and screws.
(From Canale T, editor: Campbell’s operative orthopaedics, ed 10,
Philadelphia, 2003, Mosby.)

Figure 28-16
Schematic representation of the technique of applying a DC plate to
an oblique forearm shaft fracture. A, The plate is recontoured to sit
1 mm off the shaft over the fracture site. The fracture is reduced, the
plate is held with a clamp, and a screw is applied in a neutral mode in
the fragment, which has its obliquity facing away from the plate.
B, The gliding hole for an interfragmentary lag screw through
the plate can next be drilled with a 3.5-mm drill bit. C, A screw is
next applied in the “load” or compression position in the opposite
fragment, which will allow this fragment to be “pulled into” the plate
when compression is applied. D and E, The interfragmentary lag
screw is then placed through the plate by drilling the far cortex with a
2.5-mm drill bit, tapping it with a 3.5-mm tap, and placing
an appropriate length screw. The remaining screws are applied
through the plate. (From Browner BD, Jupiter JB, Levine AM
et al: Skeletal trauma, vols 1 and 2, p 1106, Philadelphia, 1992, WB
Saunders.)

Intra-articular fractures pose a formidable challenge Figure 28-18

(Figure 28-18). Failure to anatomically restore articu-
lar surfaces, particularly in weight-bearing joints, results
in posttraumatic arthritis and severe disability. Often,
impaction of trabecular bone underneath the articular
surface requires elevation and reduction of the articular
fragments and buttressing with a bone graft.
Locking Plates
The introduction of locking fracture plates has changed
the way many fractures are treated. Locking plates have
Drawing of an intra-articular distal humerus fracture fixed with
plates and screws. Anatomical reduction of the intra-articular fracture
components is essential to restore normal motion and prevent
posttraumatic arthritis. (From Canale T, editor: Campbell’s operative
orthopaedics, ed 10, Philadelphia, 2003, Mosby.)
threaded holes into which screws with threaded heads
can engage and form a rigid scaffold (Figure 28-19).
These plates do not, by themselves, provide compression
at the fracture site. They are often called “internal exter-
nal fixators,” as they do not have to lay flush against bone
622 SECTION II • Principles of Practice

Threaded locking portion

(combination hole)
Non-locking portion
(combination hole)

Figure 28-19
Locking compression plate. The screw on
the right has a threaded head that screws
into threads in the locking portion of the
combination hole. The screw has a rounded
head and can be inserted at an angle
through the nonlocking portion of the
combination hole.

to provide stability. Newer versions of locking plates have immediately after locked intramedullary nail fixation of
combination holes, giving the surgeon the option of femoral fractures.17 Early mobilization of patients after
locking or compressing. Long-term studies using these femoral and tibial rodding is a major advance compared to
plates still need to be performed. They do show great the prolonged immobilization in traction, but not all frac-
promise in the treatment of osteoporotic bone, as this tures are amenable to this technique. The major advantage
construct provides additional rigidity and stability. of intramedullary nails in the upper extremity (i.e., radius,
ulna, humerus fractures) is avoidance of a large incision and
Intramedullary Nailing risk to neurovascular structures. Fractures near the articu-
The idea to stabilize long bone fractures with an lar surface still need to be fixed with pins, screws, plates,
internal splint is not new. The type of intermedullary or a combination thereof. As described earlier, fractures
fixation devices available to the surgeon has changed and
improved throughout history. Aztecs used sticks in the
bony canal in the 16th century. Eventually, silver, brass,
and ordinary steel pegs were all inserted into the medul-
lary canal to improve alignment. In 1916, Hey-Grove
used long metal rods with limited success. Rush intro-
duced the concept of filling the intramedullary canal with
numerous slender, prebent rods in 1936 and Kuntscher
successfully used slotted nails in the German army in
1940. Rush ultimately published a pioneering text on the
three-point fixation principle in 1955. As improved met-
allurgy increased the rigidity and endurance of intramed-
ullary implants, devices such as the locked nail became
popular in the 1980s.22 Intramedullary nails have been
developed for a multitude of fractures that include the
humerus, radius, ulna, femur, tibia, and even the spine
(Figure 28-20).
Fracture fixation with intramedullary nails provides
relative stability. Unless the nail is locked proximally and
distally and has tight fixation at the fracture site, the fixa-
tion may have rotational and angular instability. This lack
of stability may lead to displacement of the fracture or
nonunion. Factors that affect fracture healing with use of
intramedullary nails include the use of locking screws, nail
diameter and rigidity, intramedullary reaming, and post- Figure 28-20
Schematic representation of second-generation femoral locking nails and
operative weight bearing. The current state of metallurgy
their primary indications. A, Fixation of a comminuted subtrochanteric
and operative techniques allows greater advantages for fracture. B, Fixation of an ipsilateral neck and comminuted shaft
early range of motion (ROM), weight bearing, and reha- fracture. (From Browner BD, Jupiter JB, Levine AM et al: Skeletal
bilitative intervention. Weight bearing can be permitted trauma, vols 1 and 2, p 264, Philadelphia, 1992, WB Saunders.)

through the articular surface can lead to posttraumatic
arthritis. Accurate reduction improves cartilage healing
and restoration of joint surfaces.
Stress Fractures
A stress fracture is one of the most common forms of
overuse injuries. First described by the Prussian military
physician Breithaupt in 1885, who called stress fractures
of the metatarsal shaft “march fractures,”23 stress frac-
tures develop when excessive, repetitive loads are placed
on the bone without adequate periods of rest. This
causes an increase in osteoclast activity, which creates an
imbalance between bone resorption and bone formation.
The metabolic imbalance between osteoblasts and osteo-
clasts results in what is termed a fatigue fracture. Stress
fractures are more common in weight-bearing activities,
especially running and jumping (Figure 28-21). To be
certain, athletes are particularly prone to these fractures.
More than 90% of stress fractures occur in the lower
extremities.23 In nature, other than humans, only two
types of animals develop stress fractures: racehorses and
racing greyhounds.
Risk Factors
Extrinsic risk factors include training regimens, footwear,
and training surfaces, whereas intrinsic risk factors for
developing stress fractures include body type and indi-
vidual physiology. High training volumes and abrupt
increases in the duration, frequency, or intensity of train-
ing increase the risk of stress fractures. This commonly
CHAPTER 28 • Fracture Management 623
occurs when athletes make the jump from junior varsity
to varsity or from high school to college-level sports.
Improper program design and training errors are the
most frequently encountered causes of stress fractures.23
Poor footwear is another culpable factor. Athletes should
change their running shoes frequently (every 6 months)
and choose shoes with sufficient shock-absorbing soles.
Hard training surfaces (e.g., cement, asphalt, pavement)
and uneven terrain increase one’s risk of developing
a stress fracture.
Even more numerous are intrinsic risk factors. Age,
race, foot structure, and nutrition status are some exam-
ples. Women are more prone to stress fractures than are
men, particularly when associated with menstrual irreg-
ularity and eating disorders. Military data suggest that
black individuals are less likely than white individuals to
develop stress fractures. Bone mineral density (BMD),
bone geometry, and foot structure are some biome-
chanical risk factors accounting for these differences.
Low BMD in the lumbar spine, femoral neck, hip, and
foot is a significant risk factor for development of stress
fractures in both male and female track and field ath-
letes. Bone geometry refers to the amount of force a
bone can withstand based on its cross-sectional area and
cross-sectional moment of inertia. In one study, military
recruits with narrower medial to lateral tibial widths were
more likely to sustain stress fractures in the femur, tibia,
or foot than one with a wider tibia.23 A high arched (pes
cavus) foot absorbs less stress and transmits greater force
to the tibia and femur. A low arched (pes planus) foot
absorbs more stress in the foot itself, placing the meta-
tarsals and tarsal bones at greater risk for stress fracture.
Figure 28-21
A, X-ray demonstrating a suspected stress fracture
on the compression (medial) aspect of the
femoral neck. B, Healed stress fracture; note the
sclerotic medial femoral neck. (From Canale T,
editor: Campbell’s operative orthopaedics, ed 10,
Philadelphia, 2003, Mosby.)
624 SECTION II • Principles of Practice
There is a correlation between pronated feet and tib-
ial stress fractures, while cavus feet are associated with
metatarsal and femoral stress fractures.
Nutrition
Athletes with a lower intake of calcium have been shown
to sustain relatively more stress fractures.24 One rea-
son is that decreased calcium intake can lead to lower
BMD.25 The recommended daily allowance for calcium
is 1000 mg per day, but for athletes there is much debate
about whether or not this amount is too low. Athletes
should aim for 1200 to 1500 mg of calcium per day, as
well as for 400 to 800 IU of vitamin D per day.
Female Athlete Triad
The female athlete triad consists of amenorrhea, eating
disorders, and stress fractures. Female runners with a his-
tory of stress fractures are more likely to have a history
of oligomenorrhea or amenorrhea. The long-term effects
of delayed menarche are unknown. One study of female
college distance runners revealed that 50% had irregular
menstrual cycles.23 Some of the potential complications
are osteopenia, stress fractures, and scoliosis. Estrogen
deficiency, at any age, lowers bone mass. Lower fat intake
per kilogram of body weight is more likely to sustain a
stress fracture. There is still a lack of large prospective
longitudinal studies on the effect of hormone replace-
ment therapy or birth control pills on BMD in young
female athletes.
Diagnosis
A thorough history and physical, as well as a high index
of suspicion, will help make the diagnosis of a stress
fracture. The onset of pain is usually insidious, over at
least 2 to 3 weeks. At first, the athlete recalls the pain
only appearing at the end of a contest or practice, and
the pain resolves with rest. As time passes, the onset of
Figure 28-22
A, Lateral view radiograph of the proximal calf demonstrating endosteal
remodeling and cortical thickening (arrow) consistent with a stress
fracture. A faint radiolucent fracture plane is present. B, MRI of the leg
in the same patient demonstrating moderate cortical thickening and a
faint cortical fracture line (arrow). (From Sofka CM: Imaging of stress
fractures, Clin Sports Med 25(1):53-62, 2006.)
pain is earlier in the practice or game and it needs more
time to resolve. The pain finally becomes severe enough
to warrant modification of the activity. The pain is usu-
ally localized to the area of stress fracture. Physical exam
should include percussion—often tapping the bone at a
site away from the actual fracture will elicit pain.
Radiographic examination consists of x-rays, triple
phase bone scan, and MRI. Plain radiographs are normal
during the initial 2 or 3 weeks that an individual develops
symptoms. In fact, any abnormal findings may or may
not be revealed for several months. Seventy percent of
plain films are normal in patients ultimately diagnosed
with stress fractures. Abnormal findings on a plain film
are usually a thin incomplete radiolucent fracture line, a
fluffy periosteal reaction, or a thin linear area of sclero-
sis that is perpendicular to the major trabecular lines. A
positive plain radiographic finding is usually additional
cortical bone, periosteal reaction, cortical lucency, or a
fracture line. In cancellous bone, the findings are more
subtle and consist of a bandlike area of focal sclerosis
without periosteal reaction (Figure 28-22).
Triple-phase bone scans are highly sensitive but lack
specificity. They can detect increased uptake in a bone as
soon as 2 or 3 days after the onset of clinical symptoms.
Increased uptake in a stress fracture is seen in all three
phases of the bone scan: the blood flow or angiographic
phase, the blood pool or soft-tissue phase, and the delayed
phase. In contrast to stress fractures, severe tendonitis
of the tibialis posterior (“shin splints”) is positive only
in the delayed phase. Acute stress fractures reveal clear,
localized areas of increased uptake or “hot spots” on all
three phases. As healing occurs, the flow phase returns
to normal first and then the pool phase reverts to nor-
mal. Lagging behind clinical resolution, activity on the
delayed phase decreases over 3 to 18 months as the bone
remodels. For this reason, bone scans should not be used
to monitor healing and return to activity.
Magnetic resonance imaging has several advantages
over other imaging methods: greater sensitivity on par
with bone scans but much more specific, no exposure

to ionizing radiation, faster image acquisition, more
accurate anatomical location of the fracture site, and bet-
ter delineation of both the extent and orientation of the
stress fracture. MRI reveals two stress fracture patterns: a
bandlike fracture line and no clear-cut fracture line. The
bandlike fracture line, which is more common, is a low
signal on all imaging sequences and is surrounded by a
larger, more poorly defined area of bony edema. The
fracture line is continuous with the cortex and extends
into the medullary space. The fracture pattern without
the fracture line is called a stress response and represents
an earlier stage in the evolution of the stress injury. The
MRI is a sensitive test for early detection of periosteal
and marrow edema along a fracture line.
Management of Stress Fractures
Once the initial diagnosis of a stress fracture is made, a
treatment plan must be implemented as soon as possible.
The first goal of treatment is to control the athlete’s pain
using nonsteroidal anti-inflammatory drugs, ice, and
stretching. Breaking the cycle of destructive, repetitive
trauma through rest is the first step. During the period
of rest, the reparative phase dominates over the resorp-
tive phase, helping the fracture heal. At least 6 to 8
weeks are need for most stress fractures to heal, though
some may take longer. Prefabricated braces, orthoses,
and walking boots can all be used to help immobilize
stress fractures. Casts are bulky, less durable, and incon-
venient, so they are infrequently used. Surgical stabiliza-
tion should be considered for bones in which a complete
facture can lead to long-term disability (i.e., femoral
neck, tibia, navicular, fifth metatarsal). Nutritional status
must be closely examined. Intake of calcium and vita-
min D should be optimized. Eating disorders should be
identified and explored. In female athletes with abnor-
mal menstrual patterns, estrogen supplements should be
considered.
Deciding when to allow the patient to return to activ-
ity can be difficult. Several weeks of rest can be frustrat-
ing and difficult, particularly for athletes. The first step
in reconditioning should be swimming, a non-weight-
bearing activity. The next step should be bicycling and
nonimpact weight-bearing activities such as the ellipti-
cal machine or stair-climber. The duration and intensity
of each activity should be gradually increased. The final
activities allowed should be weight-bearing impact exer-
cises such as walking, progressing to jogging, and finally
running. For each impact activity, the patient should have
a pain-free progression from low intensity–short duration
to low intensity–long duration to high intensity–short
duration to high intensity–long duration. Only after this
complete, pain-free progression over at least 6 to 8 weeks
can a patient return to his or her activity.
CHAPTER 28 • Fracture Management 625
Fracture Healing
Fractures heal by either primary osteonal repair or by
secondary callus formation. Fractures treated with
absolute stability (open reduction, internal fixation with
plates and screws) heal by direct osteonal repair. No callus
formation is observed. Fractures treated with modalities
providing relative stability (i.e., intramedullary nailing or
closed reduction and immobilization with a cast or brace)
heal by callus formation around the fracture site.
Successful healing requires stability at the fracture
site as well as a viable blood supply. Most fractures
heal through a combination of intramembranous and
endochondral ossification (secondary callus formation)
(see Chapter 6). There are multiple stages of healing,
some of which take place concurrently. These include (1)
hematoma and inflammation, (2) revascularization and
cartilage formation, (3) differentiation and cartilage cal-
cification, (4) bone formation, and (5) bone remodeling.
At the time of fracture, endosteal and periosteal blood
vessels are disrupted, leading to the formation of a hema-
toma. The resulting blood clot contains important signal-
ing molecules that initiate the process of fracture healing.
Platelets release growth factors such as transforming
growth factor-beta (TGF-β) and platelet derived growth
factor (PDGF), which provides the stimulus for cell pro-
liferation and differention. By the end of the first week,
the process of cartilage and bone formation or intramem-
branous ossification has already begun. The fibrovascular
stroma overlying the fracture is infiltrated with chondro-
cytes, forming cartilage. By the second week, both hard
callus, formed by intramembranous ossification, and soft
callus, formed by endochondral ossification, are clearly
present. The cartilage is ossified in a manner similar to
the maturation of a growth plate. Chondrocyte hypertro-
phy and the surrounding matrix are calcified. Through
a process of osteoclastic and chondroclastic resorption,
the matrix is ultimately replaced with woven bone. This
is called clinical union. The woven bone (immature bone
but clinically stable) is then remodeled over the course of
several months to form the organized lamellar structure
of “normal” bone.
Varying degrees of rigid stability also alter the cascade
of bone formation. Rigid fixation tends to promote
osteoblastic differentiation without formation of a car-
tilage template (i.e., endochondral ossification). Rather,
with accurate reduction and absolute stability, osteonal
healing ensues. Osteoclastic cutting cones provide paths
across the fracture site, followed by osteoblastic lamellar
bone formation.
Respecting the level of stability around a fracture site
is important in planning a rehabilitation course. Despite
relatively rigid fixation, bracing, and casting, motion
at the fracture site in the first few weeks can lead to
nonunion. Thus, weight bearing and motion around
626 SECTION II • Principles of Practice
the fracture should be minimized when attempting to
mobilize adjacent joints.
Many variables surrounding optimal fracture healing
are under the control of the surgeon, whereas others are
not. Patient characteristics often negatively and directly
affect bone healing. Nutritional status must be optimized
to ensure adequate anabolic reserve and to limit infec-
tions. Nicotine and nonsteroidal anti-inflammatory use
have been linked to decreased bone formation.23 Local
factors during surgery can also affect bone healing. The
periosteal and muscular blood supply should be protected
by limiting physical, thermal, and chemical trauma dur-
ing surgery. Mechanical factors should also be considered.
Accurate reduction, compression, and absolutely stable
fixation constructs promote bone healing. Noncompliance
with weight-bearing and rehabilitation recommendations
can lead to excess motion at the fracture site and, ulti-
mately, nonunion. The patterns of nonunions that occur
can sometimes be related to either insufficient stability or
blood supply. Hypertrophic non-unions result from insuf-
ficient stability at the fracture site, whereas atrophic non-
unions result from insufficient blood supply to heal bone.
The cause of nonunions must be carefully identified before
attempting revision surgery.
Factors Affecting Healing
● Age of patient
● Exactness of reduction
● Type of fracture
● Blood supply
● Degree of local trauma
● Degree of bone loss
● Type of bone involved
● Type of fixation
● Presence of infection
● Presence of disease
● Presence of foreign body
● Joint involvement
● Patient’s general health
● Patient’s nutritional status
● Presence of complications (e.g., nerve or vascular injury)
Medications
●
Augmenting Healing
The orthopedic community and orthopedic patients
desire the ability to promote bony union during frac-
ture healing. Intense research has been dedicated to
developing products that can accomplish faster and
more complete fracture healing. The morbidity associ-
ated with nonunion as well as delayed union and the
economic impact measured both in health care dollars
and workplace productivity are significant.26 To date, a
number of techniques have been examined and proven
to be useful. Some of the more common means used in
practice to promote bony union are discussed in further
depth next.
Modalities Used to Augment Fracture Healing
● Ultrasound
● Pulsed electromagnetic fields
● Direct current
● Capacitive coupling
● Demineralized bone matrix
Ultrasound
Ultrasound as the name implies involves the use of sound
waves in the treatment of fractures. In 1994 the Food
and Drug Administration (FDA) approved the applica-
tion of ultrasound to the healing of fresh fractures and in
2000 approved its use in nonunions. In contrast to other
modalities, ultrasound is approved for fresh fractures.
A brief description of ultrasound will help to explain its
mechanism of action.
The sound waves utilized by ultrasound are above the
range of human hearing and are transferred to the tissues
through pressure waves. Energy transfer is dependent on
tissue density, with denser tissues absorbing more than
less dense material. In areas where two differing densi-
ties are closely opposed, much of the energy is scattered,
resulting in the production of complex energy gradi-
ents.27 In general, however, the absorption of energy
serves as a means to impart mechanical stress to the heal-
ing tissues, although to a much lesser degree than weight
bearing. This seems to allow for application of Wolff’s
law—bone is deposited when loaded and resorbed in lieu
of stress.
The intensity of the energy used depends on its
intended use. For example, ultrasonic application to frac-
tures is many magnitudes lower in energy than its use in
lithotripsy for the treatment of renal calculi. The optimal
dose for fractures is 200 µsec bursts of sinusoidal waves
at 1.5 MHz with a repetition of 1 kHz. This is delivered
with an ultrasound energy of 30 mW/cm2 for a duration
of 20 minutes per day.28
Patients who smoke are known to have decreased heal-
ing potential. This applies to the soft tissues as well as bone,
and some of the most compelling evidence for the use of
ultrasound comes from studies demonstrating its effect in
smokers. The application of a standardized ultrasound dose
in this particular patient population is shown to negate the
deleterious effect smoking has on fracture healing.29
Experimental investigations have revealed that the
use of ultrasound stimulates a local hyperemia during

application. Surprisingly, this hyperemia was found to
last for a significant amount of time after cessation of
treatment.30 Flow to the site of injury was threefold
higher at 7 days, and one-third higher at day 11. Much
of the blood supply to the external region of the callus
is derived from surrounding soft tissues and, when this
is augmented, the delivery of cells as well as nutrients
is improved. Subsequently, healing is also stimulated.
Rawool et al. found an increase in callus mass associated
with the increased flow, and the flow in the immediate
vicinity of the fracture improved.30
Many other beneficial effects of ultrasound have been
observed experimentally. For instance, it was shown
that the application of ultrasound starting at any time
in the process of healing can provide beneficial effects,
demonstrating that the process of healing is sensitive to
this stimulus at any given time.27,28 In another study, Wu
exposed chondrocyte cultures to a low-intensity ultra-
sound stimulus. The result was an increase in aggrecan
gene expression, a molecule that in combination with
others creates a proteoglycan scaffold in type II colla-
gen.31 Torsional strength had been demonstrated to be
increased with ultrasound treatment before this study,
but it had not been associated with increased aggrecan
expression.32,33
Still other effects, such as increased mineralization and
more rapid endochondral ossification,33 promotion of chon-
droitin 6-sulfate synthesis,34 increased release of PDGF,35
greater production of prostaglandin-E2 in osteoblasts,36
altered TGF-beta activity in osteoblasts,37 and altered cal-
cium utilization38 and release from chondrocytes,39 have
been discovered. These are probably only a few of the
effects of ultrasound treatment that improve healing. It
is likely more will be uncovered as the understanding of
ultrasound and fracture healing evolves.
The preceding discussion deals with some of the basic
science of ultrasound and its effect on cells and animal
models. FDA approval, however, depends on clinical tri-
als.40 Heckman et al.40 demonstrated a significant decrease
in the time to healing clinically and radiographically.
The treatment group had evidence of clinical healing at
roughly day 86 and radiographic union by day 96 com-
pared with clinical healing at 114 days and radiographic
healing at 154 days for fractures not being exposed to
ultrasound. A meta-analysis of the available literature has
shown the average decrease in healing time to be 64 days
in those groups receiving ultrasound stimulation.41
Pulsed Electromagnetic Fields
The use of pulsed electromagnetic fields (PEMF) stems
from the knowledge of electric properties of bone. The
production of piezoelectric energy in response to physical
stress placed on bone, which was described in the 1950s,
serves as a basis for the use of this modality. The dose
CHAPTER 28 • Fracture Management 627
employed is 18G pulses in trains of 20, each pulse last-
ing 220 µsec, for a duration of 4.5 msec per train. These
are repeated at 15 Hz. The production of TGF-beta has
been shown to be enhanced by exposure of osteoblast-
like cells to PEMF. The cells were also guided toward
differentiation from this exposure. Increasing levels of
alkaline phosphatase with decreasing levels of prolifera-
tion have been observed.42
The response of fractures to PEMF has been dem-
onstrated to be dose dependent. For example, patients
who were exposed for up to 10 hours per day healed 76
days sooner than those treated for shorter durations.43
PEMF use is indicated for the treatment of nonunions
as well as pseudarthrosis. It should not be used in the
presence of a devascularized fracture or segmental defect
>5 millimeters.
Direct Current
The relatively low pO2 of fracture callus is known to
create a favorable situation for the formation of bone.
Direct-current stimulation surrounding the fracture has
been observed to decrease the oxygen tension with a con-
comitant rise in the local pH in the region of the anode.
Increases in proteoglycan as well as collagen synthesis are
known to occur as well.44 The use of direct-current stim-
ulation in nonunions was approved by the FDA in 1979.
A dose of 20 µA is used with an implantable anode.
Capacitive Coupling
Capacitive coupling, also used in nonunions, uses a field
induced between two electrodes placed on the skin. The
response of bone cells is current dependent. The mecha-
nism of action appears to be the opening of calcium gated
channels with an increase in prostaglandin E2, calcium,
and calmodulin. Upregulation of TGF-beta occurs in
response to this. Utilization is for up to 25 weeks, with
discontinuation for healing or failure of progression over
a course of 12 weeks.
Demineralized Bone Matrix
Thus far we have considered physical means of augmenting
bone healing. The methods discussed involve external
stimulation. Demineralized bone matrix (DBM) is a
biological means of improving fracture healing. This
product, used at the time of open reduction internal fixa-
tion, provides both osteoinductive and osteoconductive
pathways for healing. The inductivity, though poorly
understood, appears to be secondary to proteins as well
as growth factor still present. Inductivity appears to be
affected by the technique used to process, sterilize, and
store the DBM.45 In addition, osteoinductivity varies
from donor to donor, necessitating a single donor per
628 SECTION II • Principles of Practice
batch. The physical structure of DBM provides a scaffold
for bony in-growth or its conductivity.
Fracture Management in the Skeletally
Immature
Management of fractures in skeletally immature bone poses
unique challenges. Compared to the relatively static, mature
bone of adults, the dynamic physiology and biomechanics
of immature bone make it prone to different patterns of
fracture. Healing rates, remodeling capacity, and potential
complications differ from those of mature bone and must
be considered when managing these injuries. Specifically,
injury to the growth plates, the physes, poses substantial
risk of developing angular deformities. The physes are the
site of both longitudinal and radial growth.
Fractures are more common in children than in adults,
often occurring after apparently insignificant trauma.
Injury to the physis must be identified and, similar to
fractures in adults, can be classified. Physeal fracture clas-
sification can be applied to any physis in a long bone. The
Salter-Harris classification system allows radiographic
description (see Figure 27-30). Type I fractures are non-
displaced fractures through the width of the physis and
often present as pain over the physis. Type II fractures
involve most of the physis, but the fracture exits through
metaphyseal cortex. These are the most common type of
physeal fractures. Type III fractures also involve most of
the physis but exit through epiphyseal cortex. Type IV
Figure 28-23
Ossification centers of the hand.
Radiographs of the hand and wrist
of a 4- to 5-year-old boy or 3- to
4-year-old girl (left) and of an adult
(right). C = capitate; H = hamate;
L = lunate; M = metacarpal;
P = phalanx; Pi = pisiform;
R = radius; S = scaphoid;
Td = trapezoid; Tm = trapezium;
Tq = triquetrum; U = ulna. (From
Liebgott B: The anatomical basis
of dentistry, St Louis, 1986, CV
Mosby.)
fractures traverse the epiphysis, physis, and metaphysis at
an angle. Type V fractures are crush injuries that involve
comminution and severe deformity around the epiphysis,
physis, and metaphysis.
Physeal fracture patterns vary with the maturity of bone
(i.e., the extent of ossification). Type I fractures are more
common in infants, whereas types II to IV are more com-
mon as the secondary ossification centers enlarge. The biol-
ogy of long bones contributes to the pattern of fractures
seen in the epiphysis, physis, metaphysis, and diaphysis.
The epiphysis, adjacent to the articular surface, is initially
comprised entirely of cartilage. A secondary ossification
center forms, which ultimately ossifies. These epiphyseal
ossification centers appear at varying ages, depending on
the site. For example, the distal radial epiphysis normally
appears between 0.5 and 2 years in boys and 0.4 and
1.7 years in girls, whereas the distal ulnar epiphysis nor-
mally appears around age 7 in both (Figure 28-23). The
ossification center imparts more rigidity to the epiphysis,
contributing to the fracture patterns observed.
The physis, or growth plate, is the dynamic structure
that rapidly adds longitudinal and latitudinal growth to
bone (Figure 28-24). Injuries to the physis are only seen in
skeletally immature individuals. A number of mechanisms
of injury to the physis can cause growth disturbances.
Injury to the cartilage, bone, and soft tissue surrounding
the physis can disrupt associated blood vessels leading
to ischemia. Disruption of the highly organized cellular
construct by compression, shear, or rotation can lead to
growth disturbance. Any such disruption of the physeal
 CHAPTER 28 • Fracture Management 629

Figure 28-24
Cross-sectional specimen demonstrating distal tibial and fibular
physes with secondary ossification centers. (From Beaty JH, Kasser
JR, editors: Rockwood and Wilkins’ fractures in children, ed 5, p 23,
Philadelphia, 2001, Lippincott Williams & Wilkins.)
Figure 28-25
Osgood-Schlatter disease, showing epiphysitis of the entire epiphysis
organization can lead to local slowing or cessation of (arrow), with irregularity of the epiphyseal line. Because this epiphyseal
growth. This, in turn, can lead to premature ossification cartilage is continuous with that of the upper tibia, it should not be
disturbed. If surgery is used, exposure should be superficial to the
of the physis and result in angular deformities over time.
epiphyseal cartilage. (From O’Donoghue DH: Treatment of injuries to
The metaphysis is the contoured flare at each end of the athletes, ed 4, p 574, Philadelphia, 1984, WB Saunders.)
diaphysis in a long bone (see Figure 28-7). It is character-
ized by thinning of the cortical bone and increased trabec-
ular bone in the secondary spongiosa. The metaphysis has
multiple fenestrations through which an abundant blood
supply feeds the physis and diaphysis. This is one of the
reasons many fractures frequently occur in the metaphysis.
The diaphysis grows in length via the physis and in
diameter through endosteal resorption and perios-
teal bone deposition. It has a thick cortex and a highly
vascular intramedullary component.
In children, the periosteum is a thick layer of tissue
attached to the outer surface of the diaphysis, metaph-
ysis, and physis. It is loosely attached to the diaphysis
but firmly attached to the physeal periphery (zone of
Ranvier). The periosteum is a source of osteoblasts for
radial growth as well as a major source of blood sup-
ply to the biologically active bone. It also serves as an
attachment for the majority of muscle fibers along the
metaphysis and diaphysis.
Figure 28-26
Certain attachment sites of tendon and muscle (e.g., True tibial tubercle avulsion fracture. (From Beaty JH, Kasser JR,
attachment of the patellar tendon to the tibial tuberosity) editors: Rockwood and Wilkins’ fractures in children, ed 5, p 1024,
are termed apophyses (traction epiphysis). The apophysis Philadelphia, 2001, Lippincott Williams & Wilkins.)
is composed of fibrocartilage rather than columnar car-
tilage, as in physes of long bones. Secondary ossification
centers also form initially in the distal tuberosity, inter- as well as close monitoring for premature physeal clo-
posing osseous tissue. This tissue tends to fail in tension, sure. More often than not, fractures in preadolescents
leading to avulsion injuries. Symptomatic overgrowth can be treated with closed reduction and immobiliza-
during the healing process can result, leading to chronic tion in a cast because of their vast potential to remodel.
conditions such as the Osgood-Schlatter’s lesion (Figure Unreducible physeal fractures may require open reduc-
28-25). Complete avulsion can also result at various sites tion and pinning. Fractures in adolescents near skel-
(Figure 28-26; Table 28-3). etal maturity are treated similarly to fractures in adults,
Management of injuries in the skeletally immature with a lower threshold for open reduction and internal
individual requires understanding of healing potential fixation.
630 SECTION II • Principles of Practice

Table 28-3
Management of Apophyseal Fractures
Site of Apophyseal injury Attachment Treatment

Tibial tuberosity Patellar tendon Rest, surgical reattachment

Ischial tuberosity
Anterior superior iliac spine
Calcaneus
Olecranon
Anterior inferior iliac spine
Hamstring tendons
(biceps, semitendinosus,
semimembranosus)
Sartorius
Gastroc-soleus tendon
Triceps tendon
Rectus femoris
for complete avulsions
Rest, hamstring strengthening,
rarely reattachment
Rest, quadriceps and
iliopsoas strengthening
Surgical repair
Surgical repair
Quad strengthening, rarely
reattachment

Angular deformities and displaced fractures in chil-

dren under the age of 8 have vast remodeling potential
and are often treated conservatively—casting for 3 to 6
weeks followed by bracing if necessary. Certain fractures
are more sensitive to growth disturbance (e.g., pediat-
ric distal humerus fractures) (Figures 28-27 and 28-28).
Any displacement requires reduction (sometimes open)
and percutaneous pinning. Malreduced distal humerus
fractures can result in varus or valgus deformity (cubi-
tus varus/valgus) and significant loss of range motion at
Figure 28-27
the elbow. Cubitus varus (gunstock deformity) is more a
Supracondylar fracture of humerus. (From Tachdjian MO: Pediatric
cosmetic issue; however, cubitus valgus can lead to tardy orthopedics, p 1580, Philadelphia, 1972, WB Saunders.)
ulnar nerve palsy.

Complications of Pediatric Fractures

Nonunions in children are rare. Early physeal closure
and angular or rotational deformities are more common
(Figures 28-29 and 28-30). Although usually prevent-
able, they are real and can lead to complications. These
deformities can be surgically addressed with a combina-
tion of osteotomies and lengthening procedures. Partial
physeal closures involving less than 50% of the physis can
be treated with resection of the physeal scar. Partial phy-
seal closures involving greater than 50% can be treated
with physiolysis—completion of the physeal closure to
prevent any angular deformity. The development of limb
length discrepancies in the lower extremity can pose a
formidable problem. If the child has significant growth
remaining (such as with preadolescents), limb lengthen-
ing procedures can be instituted. In adolescents, phys-
iolysis of the contralateral limb can also be performed to
maintain limb length equality.
Potential Complications
This discussion has reviewed the important concepts of
fracture management. Every fracture has its own person-
ality drawn from the mechanism of injury, the amount of
energy imparted to the patient that caused the fracture,
and the patient’s ability to heal them. Lower energy
injuries such as falls typically result in simple fractures
with little or no soft tissue consequences. Higher energy
injuries, seen in motor vehicle and industrial accidents,
are often associated with significant soft tissue injuries
that complicate fracture management. Open injuries
are associated with higher rates of infection and inju-
ries to nerves and arteries. These injuries are potentially
life or limb threatening and require careful assessment
and aggressive management. Open injuries are treated
with antibiotics at presentation and beyond, depending
on the mechanism. Uncontaminated open fractures are
 CHAPTER 28 • Fracture Management 631

Figure 28-28
Supracondylar humerus fracture treated with percutaneous pinning. A, This AP view shows percutaneous pins crossing above the olecranon fossa
to engage the opposite metaphyseal cortex. B, On the lateral view, note the equal widths of the humerus, indicating good rotational alignment.
(From Minkowitz B, Busch MT: Supracondylar humerus fractures, Orthop Clin North Am 25(4):590, 1994.)

Figure 28-29
Displaced Salter Harris II fracture of the distal femur fixed with closed
reduction and percutaneous pinning. This injury results in premature
closure of the distal femoral physis. (From Beaty JH, Kasser JR,
editors: Rockwood and Wilkins’ fractures in children, ed 5, p 122,
Philadelphia, 2001, Lippincott Williams & Wilkins.)
Figure 28-30
A 7-year-old boy sustained a fracture of the shaft of the femur and
an epiphyseal fracture-separation of the distal femoral epiphysis in a
motor vehicle accident. AP radiographs of the femur including the
knee show the initial injury, the union of the fracture of the femur,
and closure of the lateral epiphyseal plate as a result of the injury.
A varus deformity developed, which was treated by an osteotomy at
17 months, followed by a fat graft at the epiphyseal plate laterally
with no effect on the correction at 12.5 years. (From Cohen J,
Bonfiglio M, Campbell CJ: Orthopedic pathophysiology in diagnosis and
treatment, p 135, New York, 1990, Churchill Livingstone.)
632 SECTION II • Principles of Practice

typically treated with a course of cephalosporins, while Summary

contaminated fractures (e.g., industrial or farm injuries)
are treated with additional aminoglycosides and peni- This chapter has presented various aspects of fracture
cillin to prevent gangrenous infection. Severe injuries management, including fracture description, nonopera-
may involve transection of major nearby arteries. When tive techniques in fracture care, operative options, and
a fracture is limb threatening, emergent vascular repair augmentation in fracture healing. Every day we are pre-
is required. Severe soft tissue loss may require skin sented with new developments in operative technique,
grafts or even musculocutaneous flap coverage to pro- particularly in the form of fixation devices and biological
vide sufficient blood supply and a barrier to infection. augmentation. In light of these advances, corresponding
Nervous and vascular injury may leave patients with changes in the rehabilitation methods for patients with
deficient muscle groups. Rehabilitation of these types fractures will certainly follow.
of injuries must be tailored to the specific deficits and
accommodate healing of soft tissue. References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
Fracture Complications reader can view the reference source and access it on line whenever
possible. There are a total of 134 references for this chapter.
●
Nonunion
● Pseudarthrosis
● Delayed union
● Malunion
● Associated soft tissue injury
● Fat embolism
● Paralysis
● Vascular laceration or occlusion
● Early osteoarthritis (if joint involved)
● Infection
● Avascular necrosis
● Arrested epiphyseal growth
● Thromboembolic disorders
● Multisystem organ failure
● Complex regional pain syndrome (reflex sympathetic dystrophy)
● Limb shortening

F UNCTIONAL T ESTING AND R ETURN
TO A CTIVITY
Gary P. Austin
Introduction
The ultimate goal of rehabilitation of the injured patient
is the rapid, safe, complete, and permanent restoration
of function and return to activity. It is virtually impos-
sible to hasten the normal healing process following an
injury, given that there are natural limits to the speed at
which the rehabilitation process can proceed. Therefore,
to efficiently and effectively restore function and return
the patient to activity, a functional rehabilitation pro-
gram should focus on the dynamic relationship between
the application of therapeutic stresses and the ongoing
healing process. Proper understanding and application of
this relationship may minimize additional problems and
undue delays in rehabilitation and the return to activity.
Since the dose-response relationship for virtually all ther-
apeutic interventions is poorly understood, the clinician
must establish and reestablish the clinical and functional
status of the patient. Functional and clinical examination
and reexamination throughout the spectrum of rehabili-
tation, therefore, are the basis for an effective rehabilita-
tion program and, ultimately, for a successful return to
activity.
Functional Rehabilitation Program Focus
● A dynamic relationship between the application of therapeutic
stresses and the healing process
● Controlled aggressive treatment (“pushing the envelope”)
● Make the program specific to the needs of the patient
● Examination and reexamination to adjust treatment
29
C H A P T E R
Function Defined
A thorough discussion of functional testing must begin
with a definition of function. The terms function and
functional are widely used within the rehabilitation
arena, but they have not been clearly defined. A rigor-
ous account of function should be logical, theoretically
sound, and exist within the context of an accepted frame-
work; as such, it should contribute to an operational
definition of function. A universal definition would per-
mit accurate measurement of function and consistent
communication. Although the contemporary clinical
environment values function, a conventional definition
of function remains elusive. More generally, function is
defined as “the action for which a [person or] thing exists
or . . . is specially fitted or used”1 or “one of a group of
related actions contributing to a larger whole.”1 In the
context of rehabilitation, function has been defined as
“those activities identified by an individual as essential
to support physical, social, and psychological well-being
and to create a personal sense of meaningful living.”2
Defined simply, that which is functional is “used to con-
tribute to the development or maintenance of a larger
whole.”1 However, this definition offers little guidance
for determination of the presence or degree of function
with respect to injury and rehabilitation. Functional limi-
tations have been more clearly defined as the “limitation
of performance at the level of the whole organism or per-
son”2 that “are measured by testing the performance of
physical and mental behaviors at the level of the person
and should not be confused with diseases, disorders, con-
ditions, or impairments involving specific tissue, organ,
or system abnormalities that result in signs or symp-
toms.”2 Although a complete and thorough discussion
633
634 SECTION II • Principles of Practice
of function is beyond the scope of this chapter, for this
chapter function will be defined as follows: any movement
at the level of the person that is task related, goal oriented,
environmentally germane, and involves the integration of
multiple body systems and structures.
Functional Testing Versus Clinical
Testing
The examination, evaluation, and restoration of function
require the clinician to think beyond the level of impair-
ments of specific tissues and structures resulting from the
injury. Medical diagnoses address diseases, disorders, and
conditions at the cellular, tissue, or organ levels and pro-
vide information limited to the impairment level. The cli-
nician, while acknowledging the medical diagnosis and the
associated pattern of impairments, must focus on the func-
tional limitations of the patient in order to set appropriate
goals and maximize the patient’s potential. The examina-
tion should contribute to a comprehensive understanding
of the injury at the level of the whole person as a multidi-
mensional movement system and, ultimately, inform the
clinical decisions throughout rehabilitation.
Collectively, clinical testing and functional testing pro-
vide complementary information; therefore, understand-
ing the distinction between the two types of testing is
critical. Clinical testing involves the application of stress
primarily at the level of the body part and provides infor-
mation regarding the impairment and healing of specific
structures. Functional testing involves the application
of stress, via specific movements, at the level of the whole
person and provides information about the ability to
perform task-specific movements.
Functional Testing Across the
Continuum of Rehabilitation
Critical decision making at all points along the continuum
of care, in all settings, and with all patient populations is
based on established clinical and functional goals. Functional
testing, like clinical testing, should be incorporated into all
aspects of patient care, including preparticipation/employ-
ment examinations if possible, initial examination, reexami-
nations, return to activity, and follow-up.
Situations That Should Include Functional Testing
● Preparticipation examination
● Initial assessment
● Reexamination
● When returning to activity
● At follow-up
Preparticipation Examination
The clinician team may, in fact, make important decisions
about patient’s health before an injury occurs. Ideally,
comprehensive intake screening or preparticipation/pre-
employment examinations (PPE) helps to identify clients
at risk of injury,3 however, the sensitivity and positive
predictive value have been shown to be low.4 Although
many agree as to the components of the PPE, the partic-
ular tests and measures utilized show little consistency.5,6
Specifically, past personal medical history, clinical test-
ing (musculoskeletal examination), and functional test-
ing (performance assessment tests) seem most useful in
identifying risk of injury in athletes.7-9 Since those being
screened are typically injury-free or fully recovered from
previous injuries, clinical testing may only be would
be of limited value. Functional testing, however, may
reveal functional limitations in the absence of frank clini-
cal impairments. Whenever possible, the PPE or intake
screening should be modified to best address the rel-
evance to the population being tested (e.g., age, gen-
der, sport, occupation).9,10 Ideally, PPE or screening data
allow for the commencement of preventive program-
ming to address identified risk factors and, in the event
of injury, can inform clinical decision making.
Initial Examination
Although not always possible, the initial examination
may actually begin with direct observation of the mecha-
nism of injury. In effect, the injury is a failed functional
test, the mechanics of which may be useful in identifying
underlying impairments and functional limitations. The
initial examination typically begins with the systematic
collection of injury-related information. Functional test-
ing begins, in earnest, with the history, and in conjunc-
tion with available PPE data, it can help identify factors
that might have predisposed the patient to injury or may
influence recovery. For example, the history of previous
injury may suggest a preexisting functional biomechani-
cal deficit or abnormal movement pattern that may have
contributed to the initial injury and place excessive stress
on the healing structure. Based on the history, the clini-
cian can develop clinical and functional hypotheses about
possible impairments and functional limitations.
A hypothesis-oriented approach to the examination
and evaluation of the patient should necessarily include
both functional and clinical hypotheses (Table 29-1).
The primary focus of the clinical examination is to iso-
late the injured structure and determine the associated
impairments. However, clinicians should also include a
functional examination. In the absence of functional test-
ing, the clinician can only speculate as to the presence,
magnitude, and source of any functional limitations.
Testing at the level of function can reproduce symptoms
 CHAPTER 29 • Functional Testing and Return to Activity 635

Table 29-1 refine functional hypotheses; generate new functional

Clinical versus Functional Rehabilitation Goals hypotheses; introduce new functional tests; progress
the functional aspects of the rehabilitation program;
Clinical Goals Functional Goals
or compare with established long-term and discharge
Organ/tissue/structure level Person level goals. Functional tests can serve as the base movement
Impairment level Functional limitation level pattern for functional exercise and, therefore, provide
Based on tests and measures Based on tests and the clinician with opportunities to regularly reevalu-
of specific articular, mus- measures of performance ate the patient’s functional response to rehabilitation.
culotendinous, or skeletal on goal-oriented, sport- In principle, functional exercise provides the oppor-
structures specific tasks integrating tunity for functional reexamination during each treat-
multiple joints and muscles ment. Maybe most important, the results of regular
Parameters: strength, flexi- Parameters: control,
reexamination are the basis for frequent adjustments
bility, range of motion, joint coordination, strength,
mobility, swelling, pain, speed, power, agility,
to the rehabilitation program, assuring that the patient
muscular endurance balance, flexibility, mus- is progressing as rapidly and safely as possible.
cular endurance, aerobic
endurance Return to Activity
Goals relate to healing of Goals that relate to healing
isolated structures and pro- of injured structures, Based on results of functional examination and reexami-
gression of rehabilitation progression of rehabilita nation, the clinician should establish long-term goals that
program tion, return to and pro- address functional limitations. Critical decisions regard-
gression of training, and ing the ability to safely return to activity are ultimately
return to activity based on the parallel achievement of long-term goals.
The achievement of all clinical goals is in no way an indi-
cation that the patient is ready to return to activity but
rather is evidence of structural and functional changes
and also establish the threshold at which the symptoms at the tissue level. The ability of the patient to also meet
are provoked. Functional testing allows the clinician the functional goals offers additional indicators about the
to objectively measure the impact of the injured tissue ability of the patient to perform task-specific movements
on functional ability, thus better delineating the often and further informs the decision to return to the patient
unclear relationship between impairments and functional to full activity.
limitations. Specific application of stress at the levels of Functional testing determines functional thresholds
the tissue and the patient allows the clinician to test and that can be used to set short-term and long-term func-
confirm both clinical and functional hypotheses.11 Initial tional goals and determine expected outcomes for the
examination, therefore, should not be directed solely patient. Traditionally, functional goals and, therefore,
at testing and measuring symptoms and impairments. functional testing have been considered most valuable in
Functional testing, as a complement to clinical testing, the later phases of rehabilitation and in determining return
extends the scope of the initial examination to include to training/conditioning or to activity. Furthermore,
hypothesis testing about the presence and sources of functional testing has been considered appropriate only
functional limitations. for athletes. However, functional testing can and should
be performed at all points in the continuum of rehabilita-
tion and for all patient populations, not just athletes.
Reexamination
A rehabilitation program that incorporates func-
Based on results of initial functional testing, the cli- tional examination and intervention offers patients sev-
nician should establish short-term goals that address eral potential benefits. Patients in general and athletes
functional limitations. Critical decisions regarding in particular tend to be goal directed and performance
the progression of the rehabilitation program are oriented. Accordingly, the rehabilitation program should
based on the parallel and stepwise achievement of be goal and task oriented and allow the patient to par-
short-term goals. Reexamination and reevaluation ticipate in the decision-making process.12,13 In addition
involve judicious and regular clinical and functional to being objective, valid, and reliable, functional testing
testing. Indications for functional reexamination can be specific to the patient or task. Functional testing
include changes in clinical tests, lack of progress, and can clearly demonstrate and define functional limitations
new clinical or functional presentations. Continuous that may either not be commensurate with, or exist in
functional testing allows the clinician to perform the absence of, clinical limitations. As such, functional
comparisons of functional test results to prior mea- testing can be used to determine functional baselines and
surements and short-term goals; reject, confirm, or thresholds as well as to set functional goals for all patients.
636 SECTION II • Principles of Practice
Initial functional testing can be as simple as timed single-
limb stance or a 2-inch lateral step-up and can rapidly
reveal specific functional needs of the patient and the
functional demands of the task. Goals and limits identi-
fied by functional testing are typically defined in terms
the patient can easily understand and thereby capture
the patient’s attention and interest. Functionally defined
goals may also provide patients with an opportunity to
regularly evaluate their status and progress. In doing so,
the patient becomes more of a stakeholder in his or her
rehabilitation.13 Lastly, functional testing provides objec-
tive evidence that is mutually useful to the clinician and
patient and allows informed clinical decisions.
Principles of Functional Testing
Foundations for Functional Testing
Functional testing is by definition a complex and mul-
tifactorial process. Despite universal acceptance of the
importance of function, there is little agreement not
only on how best to define and measure function but
also on how to analyze function. Furthermore, the body
of evidence in this area, although growing, is still lack-
ing. Fundamentally, critical decision making related to
functional testing of the patient should, therefore, be
grounded in acknowledged principles of physiology,
biomechanics, and motor behavior. Physiological issues
relevant to functional testing include the functions of
body structures and systems, the extent of the injury, and
the patient’s healing status, energy systems, adaptation,
and overall fitness level. Relevant biomechanical consid-
erations include functional anatomy, directions/planes
of motion and stress, kinematics (time, distance, posi-
tion, displacement, velocity), and kinetics (force, torque,
mass, acceleration, inertia, momentum). Motor behavior
issues include proprioception, perception, transfer, prac-
tice, learning, control, coordination, and performance.
Decisions regarding choice and progression of functional
testing should be based on the application of sound phys-
iological, biomechanical, and motor behavior principles
to the complex interaction of individual, environmental,
and task-specific factors (Figure 29-1).
Individual Factors
The clinician would not expect patients with the same
injury or medical diagnosis either to present with identical
examination findings or to exhibit identical responses to
rehabilitation. The individual variability seen in the exam-
ination and rehabilitation process should be reflected in
the selection and progression of functional tests for the
patient. With a range of functional tests available, atten-
tion to individual factors can help the clinician in select-
ing the appropriate functional test. The most influential
Biomechanical
Physiological Motor behavior
Individual Task-specific
factors factors
FUNCTIONAL
TESTING
Environmental factors
Figure 29-1
Basis of functional testing.
individual factors include age, gender, physical capacity
(strength, power, flexibility, dexterity, agility, speed, mus-
cular endurance, cardiovascular endurance, coordination,
skill), healing status (phase of healing, weight-bearing
status, precautions/contraindications, comorbidities),
and psychological profile (motivation, fear, coping).
Despite objective indicators of healing, individual vari-
ability complicates the determination of a patient’s heal-
ing status. Indicators of healing status (healing times,
signs of inflammation, response to treatment) are helpful
but far from conclusive. Knowledge of additional factors
that might either positively or negatively affect healing
can help the clinician to determine the patient’s heal-
ing status. The clinician must, therefore, integrate these
individual indicators and factors into the clinical deci-
sion-making process. To determine the physical capac-
ity, the clinician must collect and integrate a multitude
of ongoing clinical measures (range of motion - ROM,
joint mobility, manual muscle test scores- MMT, muscle
strength scores from computerized instruments such as
isokinetic dynamometry, posture, joint/limb alignment,
pain scales, etc.) with available history and PPE/screen-
ing data. Comparing measures of physical capacity with
established clinical and functional goals can assist in the
evaluation of healing as well, thereby informing the choice
of functional test. Psychological factors can influence not
only the validity and reliability of functional testing but
 CHAPTER 29 • Functional Testing and Return to Activity
also the safety. Although more formal instruments (ques-
tionnaires and inventories) are available, observation
and documentation of affect and behaviors are typically
sufficient to assist the rehabilitation team in evaluating
common postinjury psychological factors such as mood
disturbances, depression, lowered self-esteem, anxiety,
and frustration.12,14,15 Although the available evidence
can, to a certain extent, guide the choice of a functional
test, the clinician must evaluate and integrate the many
dimensions of function on a case-by-case basis. Optimally,
functional testing allows the clinician to determine the
impact of identified impairments, healing status, and psy-
chological issues on the ability of the patient to perform
task-specific movements.
Factors to Consider in Functional Tests
● Individual
● Task specific
● Environment
Task-Specific Factors
A task-oriented approach requires that the clinician
understand the specific movement requirements of an
occupation, activity, or sport. Although tasks share many
commonalities, they differ along various dimensions,
the most useful dimensions being biomechanical, motor
behavior, and physiological. The most important aspects
of task analysis may be the biomechanical aspects of
functional testing. The clinician should assume that tasks
involve motions or stresses in all three planes; multiple
joints, segments, or limbs; contributions from uni-articu-
lar and multiarticular muscles; and the simultaneous need
for the body to move and be stable. Important specific
considerations include the common postures and move-
ment patterns, amount of motion, speed of movement,
nature and magnitude of forces/resistances, dominant
directions/planes of motion, muscular activation pat-
terns, joint specific demands, symmetry or asymmetry of
motion, and unilateral or bilateral limb demands. All of
these issues offer powerful insight in terms of how best
to organize the task-specific biomechanical dimensions
of the test, and, therefore, guide the selection or modifi-
cation of a functional test.
Motor behavior aspects of an activity may be the most
overlooked task-specific dimensions of functional testing
and among the more challenging to assess. Important
task-specific issues include the purpose or goal of all
tasks that constitute the patient’s movement repertoire,
required skill level of the patient, constraints on upper
and lower extremity dominance, learning effects, and
perceptual and sensory issues. Given that the most pow-
erful neuromuscular adaptations in the initial response to
637
training appear to be neural,16,17 motor behavior issues
are particularly relevant to decisions regarding reexami-
nation and progression of functional testing.
Physiologically, activities can de defined according
to the energetic requirements and the volume of work
required. Any volume of work requires the patient to
utilize both aerobic and anaerobic energy systems; the
clinician needs to determine which of these, if any, is the
dominant energy system. Factors to be considered include
intensity of effort (maximal, submaximal), frequency
of effort (constant, frequently, rarely, never), duration
of individual bouts, nature and magnitude of recovery
times, duration of bouts, practice/activity schedules, and
current and target fitness level.
Environmental Factors
The mutuality between the person and the environ-
ment is often so obvious as to be overlooked.18 The
effect of the environment on movement can be pow-
erful in the hands of the clinician. For example, the
clinician can constrain the patient’s movement options
by purposefully designing the environment. In doing
so, the clinician can improve the likelihood that desir-
able movements will occur and minimize the chance
that unwanted movements will occur. The environ-
mental aspects of functional testing may be the most
difficult to address. For example, in working with ice
hockey players or swimmers, the obviously different
movement media require great effort to incorpo-
rate the environmental aspects into functional test-
ing. However, they are arguably the most important
aspects of functional testing with these populations. In
addition to the biomechanical issues related to surfaces
(friction, compliance, terrain) or the medium (viscos-
ity, drag) supporting movement, the clinician should
consider the following factors as well: footgear, hand-
gear (gloves, mitts), equipment (helmets, pads, gloves,
and clothing), and tools (poles, racquets, bats, pad-
dles, clubs, balls). These issues are intimately related
to the individual preference and the physical capacity
of the patient and, therefore, the ability of the patient
to interact with the environment. Respecting the influ-
ence of the environment and the context dependence
of motion provides the clinician with additional and
substantial, if not sometimes difficult, options for
selecting and modifying functional tests.
Many of the aforementioned factors may best be
considered as continuous rather than discrete. As such,
they can assist the clinician in using the functional test
to obtain the most relevant information and thereby
best inform clinical decision making. The most suit-
able functional test comprehensively addresses and
matches the individual, task, and environmental factors.
Functional testing requires gradual, appropriate, and
638 SECTION II • Principles of Practice
patient-specific progression to tests requiring slightly
more skill, strength, power, control, and coordina-
tion. The status of the physiological, biomechanical,
and motor behavior aspects and the results of previous
functional tests help the clinician determine how to
progress functional testing. How a patient performs
on such tests may determine the readiness or ability of
that patient to progress the rehabilitation program or
return to activity.
Measurement Issues in Functional
Testing
Measurement and Standardization
Tests and measures are specific techniques and proce-
dures performed to gather data, and they can serve vari-
ous purposes during rehabilitation: determination of the
presence and extent of injury, identification of impair-
ments and functional limitations, detection of changes
in the status of impairments and functional limitations,
comparison of data to goals or standards, unambiguous
communication, and accurate prediction. Tests also per-
mit comparison of the patient to a larger group for the
purposes of differentiation, and, ultimately, prediction
based on various specified dimensions (i.e., age, gender,
occupation/activity/sport, job category/skill level).
Purpose of Functional Testing
● Determine presence or extent of injury
● Identify impairment and functional limitations
● Detect impairment changes
● Compare data to goals
● Provide clearer communication
● Allow more accurate prediction
Measurement requires that the construct of interest
be defined conceptually and be measurable. Once a con-
struct measure has been assigned a numeric value, it has
been operationally defined or given meaning according
to accepted theoretical or methodological standards. The
final step of measurement involves establishing standards
for conducting the measurement or test. Standardization
of testing should be based on acknowledged criteria, such
that the devices, procedures, and ratings are utilized appro-
priately and consistently. Conforming to established stan-
dards minimizes measurement error present in repeated
measurements taken across various settings, by various
clinicians, or at different time intervals. Rather than strict
standardization, however, functional tests require modifi-
cations for individual variability, as well as environmental
and task-specific factors. To allow for a meaningful longi-
tudinal comparison, the functional test must be repeated
using the same instrumentation, procedures, and rating
criteria as in previous tests. Accordingly, accurate docu-
mentation plays a significant role in establishing and pre-
serving the meaning and utility of functional testing.
Whereas standards for clinical tests such as manual
muscle testing and goniometry have long been estab-
lished, the standardization of functional tests is less
advanced. Ultimately, standardization of functional test-
ing improves the confidence with which the clinician can
evaluate repeated measurements, allowing for compari-
sons to larger patient populations and detecting changes
in functional status on an individual basis. A test has
two important characteristics that should ultimately be
established: reliability and validity.
Reliability and the Standard Error of Measurement
Reliability is the degree to which a test consistently and
accurately measures the construct it intends to mea-
sure.19,20 There are three major sources of error, and all are
subject to the influence of several factors. Sources of error
include the person performing the measurement (rater),
the thing used to acquire the measurement (instrument),
and the thing being measured (construct or dependent
variable).19 Random and systematic fluctuations in all of
these sources can be caused by such factors as individual
variability and the environment. Standardization of the
measurement process and well-conceived operational
definitions can minimize the impact of nonrandom and
confounding sources of error.
Reliability Tests and Functional Tests
● Inter-rater reliability
● Intra-rater reliability
● Test-retest (instrument) reliability
The reliability tests most pertinent to functional test-
ing are rater reliability and test-retest reliability. Estimates
of rater reliability determine the extent to which the rater
contributes to the consistency and accuracy of the mea-
surement, assuming that the instrument and dependent
variable are stable. Rater reliability estimates are primar-
ily concerned with two particular cases: inter-rater and
intra-rater reliability. Inter-rater reliability estimates the
extent to which two or more raters agree on the mea-
surements of the same variable. Establishing inter-rater
reliability, by showing that measurements obtained by
multiple raters demonstrate high levels of agreement,
adds to the external validity of the measurement or test.
Intra-rater reliability estimates the stability of repeated
measurements obtained by the same rater.19 Establishing
intra-rater reliability, while lacking generalizability, adds
 CHAPTER 29 • Functional Testing and Return to Activity
to the internal validity of the measurement or test. Intra-
rater or inter-rater reliability are estimated using the
intraclass correlation coefficient (ICC), based on the
relationship and agreement among the ratings.21 The
ICC is an estimate of relative, not absolute, reliability
and as such has helpful but limited clinical significance.
For example, a “high” ICC does not necessarily guar-
antee acceptable reliability, nor does a “low” ICC pre-
clude the measure as “unreliable.”20 Common uses of
the ICC involve comparison with previously established
ICCs for similar measurements, comparison to an arbi-
trary ordinal scale, and the determination of percentage
error (i.e., ICC = 0.75, indicates 25% of the variation
is caused by measurement error).20 Some authors have
cautiously proposed the following guidelines for inter-
preting reliability from ICCs: below 0.75, poor to mod-
erate; 0.75 to 0.90, good to excellent; and above 0.90,
excellent.19
A statistical complement to the ICC is the stan-
dard error of measurement (SEM).20,22 The SEM is
an index of the precision, rather than consistency, of
a measurement as demonstrated by the magnitude of
the measurement error. A reliable and clinically accurate
measure would demonstrate both a “high” ICC and a
“low” SEM. Clinicians should consider not only the
ICC but also the SEM, if reported, when selecting tests
and measures and when interpreting measurements
obtained using selected tests.
The inter-rater and intra-rater reliability of many
functional tests have been investigated. In general, the
ICCs have tended to be in the good-to-excellent range.
Unfortunately, SEMs are rarely reported, leaving the clini-
cian to speculate about the precision of the measurement.
Diagnosis, Sensitivity and Specificity
Diagnostic tests have been employed for various pur-
poses. According to Feinstein,23 diagnostic tests are used
for discovery, confirmation, and exclusion. Tests of dis-
covery and exclusion must have high sensitivity for detec-
tion, whereas confirmation tests require high specificity.
The terms sensitivity and specificity have been applied
to a variety of tests used in the identification of clinical
conditions.23 Test sensitivity indicates the ability of a test
to identify those who actually have a dysfunction (i.e.,
a true positive or a correct diagnosis based on a posi-
tive test).24 Test specificity indicates the ability of a test
to identify those who do not have a dysfunction (i.e., a
true negative or a correct diagnosis based on a negative
test).24 A functional test for discovery (e.g., PPE, screen-
ing) would be used to imply the presence of a particular
functional limitation in an apparently healthy popula-
tion. A functional test for confirmation would be used to
verify the presence of a suspected functional limitation.
A functional test for exclusion would be utilized to rule
639
out a certain functional limitation when its presence is
suspected. Although functional tests would seem promis-
ing in the area of diagnosis, few studies have reported the
specificity and sensitivity of functional tests.25 Those that
have established sensitivity and specificity have focused,
almost exclusively, on the anterior cruciate ligament
(ACL)-deficient or ACL-reconstructed knee.
Validity
Validity is closely related to reliability. Validity is the
degree to which a test or instrument actually measures
the construct it intends to measure.19,24 Validity, however,
does not ensure reliability, nor does reliability ensure
validity. It may seem that both are equally important,
since a reliably invalid test is as useless as an unreliable
valid test. Reliability, however, forms the foundation on
which validity is established. A valid measurement or
test increases the confidence the clinician can have in
the measurement and strengthens the inferences drawn
from the data for purposes such as detection, compari-
son, evaluation, and prediction. Validity can be difficult
to determine and, ideally, is established in the particu-
lar domain of inquiry (setting, population, etc.) within
which the measure will be used. This poses a particular
challenge to functional testing that, as mentioned earlier,
is highly dependent on environmental, individual, and
task-specific factors.
Types of Validity
● Face (logical)
● Content
● Criterion related
● Construct
The four types of validity are face (logical) validity,
content validity, criterion-related validity, and construct
validity. Although face validity can be helpful, it is sub-
jective and based on apparent logical relationships, allow-
ing weak inference at best. The relationships between the
more abstract parameters of function (i.e., control, coordi-
nation, agility) and the various measures that are used can
be less than obvious, complicating the face validation of
some functional tests. Content validity, also a subjective
process, often precedes face validation and is typically deter-
mined by a panel of so-called experts. Given the operational
definition of the construct and the objectives of the test,
the panel determines if the instrument or test addresses all
relevant dimensions of a particular construct and excludes
extraneous information. Criterion-related validity is a
more objective form of validation that allows stronger
inferences to be drawn. Two forms of criterion-related
validity are concurrent validity and predictive validity
640 SECTION II • Principles of Practice
(including prescriptive validity).19 In the former, the cri-
terion and target measures are acquired simultaneously,
whereas in the latter, the target measure is performed
before the criterion measure. Criterion-related validity
requires that an appropriate criterion, known as either
the criterion measure or the gold standard, be designated
for comparison with the measure being validated, some-
times called the target measure. The validity of the crite-
rion measure should have been previously determined in
terms of test-retest reliability, absence of bias and error,
and relevance to the target measure.19 Lastly, construct
validity is the most objective form of validation and best
addresses the more abstract constructs. The emphasis
here extends beyond the definition of the construct (i.e.,
content validity) to focus on the meaning or significance
of the construct. Using sophisticated analyses, construct
validation attempts to provide empirical support that the
test measures what it is intended to measure.
Functional tests often possess face validity; however,
when compared to clinical tests the multifactorial
nature of functional tests makes the relationship
between the measures and the construct of interest
(i.e., function) less than straightforward. The adoption
of a universal conceptual definition of function and,
subsequently, a sound operational definition is essential
to content validation of functional tests. Based on the
operational definition and objectives of the functional
test, content validation can be determined. Criterion-
related validation of abstract constructs, such as
function, can be difficult because of the lack of either an
available or a feasible criterion measure. For example,
although clinicians easily recognize function and agree
that function is a significant construct, defining and
measuring function remain difficult. Ultimately, once
the criterion-related and construct validity of functional
tests are established, these will serve as the basis for
strong inferences that guide clinical decision making
across the continuum of rehabilitation. To date there
has been minimal validation of the existing functional
tests, mainly for the aforementioned reasons. Future
research into functional testing should focus not only
on developing and validating new tests but on validating
existing functional tests.
Optimally, a test works as a filter, attempting to cap-
ture data of particular relevance to the clinical deci-
sion-making process from a larger set of irrelevant
data. The most useful test maximizes the meaningful
data captured and minimizes the effect of extraneous,
and potentially confounding, information. An ideal
test, which by definition does not exist, is reliable,
valid, and precise; for example, it would yield consis-
tent, accurate, meaningful, relevant, and sound infor-
mation. For this reason, clinicians must utilize both
clinical and functional tests as complements to the
examination process.
Specific Functional Tests
Balance Tests
Balance, or postural control, may be defined as the
ability to maintain the body in either static or dynamic
equilibrium with the center of gravity over the base of
support.26 Balance requires the integration of visual,
vestibular, somatosensory, and proprioceptive informa-
tion.27 In addition, Berg described balance as the abil-
ity to maintain a position, to move voluntarily, and to
react to a perturbation.28 Balance is essential to move-
ment, since patients commonly function at the limits of
their base of support.29 Although the need for balance
is readily apparent in complex activities such as gym-
nastics and ballet, activities such as walking or pitching
involve single-limb stance phases and therefore require
substantial dynamic postural control of the center of
mass.
When selecting functional balance tests, clinicians
should consider not only the reliability and validity but
also the populations studied, the instrumentation uti-
lized, the purpose, and the functional relevance of the
test. The majority of balance studies have involved sub-
jects not only with musculoskeletal disorders but also
with central nervous, vestibular, and balance disorders.30-35
Most of the studies of balance in orthopedics and sports
medicine have focused on patients with inversion ankle
sprains36-42 and anterior cruciate ligament injuries. 43-46
Laboratory-based investigations have utilized sophis-
ticated and costly equipment such as stabilometers,
force platforms, and motion analysis systems.37,45,47-49
Such analyses are not practical for clinicians35 but must
also be questioned as to the functional relevance. Much
of the information about balance has been based on
research paradigms requiring the patient to maintain a
static posture on a moving platform. Whereas this may
be a reasonable clinical test, clinicians should consider
the validity of this paradigm as a basis for functional
testing. In contrast to the moving platform paradigm,
most functional activities involve the movement of the
superincumbent body over a foot (or feet) that is fixed
to ground surfaces (notable exceptions being skating,
skiing, and swimming). By definition, a moving plat-
form test is more functionally relevant for those whose
athletic or occupational task is performed in an environ-
ment consisting of an unstable surface moving under
a fixed body (e.g., flight attendants, fishermen, sailors,
train conductors). To determine functional relevance,
the clinician must evaluate the individual, task-specific,
and environmental factors of the functional test.
The unilateral balance test is a form of static balance
assessment. This test is both simple and inexpensive to
administer. In addition, functional variations can supple-
ment the test to address specific individual, task, and
environmental factors.
 CHAPTER 29 • Functional Testing and Return to Activity
Posturography is a laboratory-based test of balance con-
sisting of six sensory organization tests (SOT); two plat-
form conditions (fixed and sway referenced) under three
visual conditions (eyes open, eyes closed, and with the
visual surround moving) combine to create the six com-
ponent tests.50 Collectively, the six component tests exam-
ine the individual’s ability to maintain balance in standing
by effectively using visual, vestibular, and proprioceptive
inputs separately and suppressing inaccurate sensory infor-
mation.51 Posturography has been used with apparently
healthy older adults52 and patients with vestibulopathy and
balance disorders.53-55 Reported test-retest reliability val-
ues (ICC) for apparently healthy older adults ranged from
poor to good for SOT 1 (r = 0.57), 2 (r = 0.57), 3 (r =
0.15), 4 (r = 0.34), 5 (r = 0.70), and 6 (r = 0.43).52 Marsh
et al. studied the relationship between static balance and
pitching performance in college pitchers using the SOT
and found low scores on tests of vestibular input to be
associated with high levels of pitching error.56
Balance Tests
● Unilateral balance
● Posturography (six sensory organization tests)
● Stork stance test
● Timed up and go (TUG)
Johnson and Nelson reported a reliability value of 0.87
for the stork stance test across sessions conducted on sepa-
rate days.57 Atwater et al. reported moderate to high test-
retest reliability coefficients when the scores for left and
right feet were combined in both eyes-open and eyes-
closed test conditions.58 Estep reported a positive relation-
ship between static equilibrium and ability in gross motor
performance.59 Subjects who rated high in motor ability in
sports also rated high in static equilibrium. Oberg et al. used
the unilateral stance as one test in a battery of functional
tests used to evaluate dysfunction of the lower extremi-
ties in patients with osteoarthritis of the hip and knee.60
A time of 40 to 60 seconds was reported in the group that
experienced no reduced function. Atwater et al. reported
a mean time of 25 seconds with the eyes-open condition
for normally developed children aged 4 through 9 years.58
Ageberg et al. found high correlations between stabilomet-
ric variables during unilateral stance and performance on
the single hop for distance test (r = 0.73-0.95).61
The only equipment required for the standing balance
test is a stopwatch or possibly a metronome. The patient
should be given several practice trials to ensure that she
or he can comfortably assume the correct test position.
Three trials are conducted, with the length of time the
patient is able to maintain balance being recorded as the
timed balance score. The mean of three trials on each
foot and under each testing condition is recorded.
641
The hands are placed on the iliac crests, and the patient
should look straight ahead and keep the eyes fixed on a tar-
get positioned at approximately eye height. The patient is
instructed to assume the specific unilateral stance position
and maintain balance as long as possible without using the
upper extremities, trunk, or contralateral lower extremity
for counterbalancing. The watch is started when the unsup-
ported foot is lifted from the floor. The watch is stopped
when either the contralateral foot touches the floor, the
hands are removed from the iliac crests, or the supporting
foot is moved from its original position.33 The same test is
repeated with the eyes closed. The subject is instructed to
close the eyes when balance has been established. Timing is
started once the eyes are closed. Timing is stopped for the
same conditions listed earlier, in addition to the patient’s
opening the eyes. However, a blindfold may be utilized to
ensure that visual input has been eliminated.
The unilateral balance test can be duplicated with a
variation in the testing surface. Surface variations, such
as foam, air bladders, mini-trampolines, or “wobble
boards,” have more to do with the effect on the informa-
tion (visual, somatosensory, vestibular) available to the
patient than with approximating the playing surface.33
The best way to assess a patient’s balance on a sport-spe-
cific surface is to perform the test (balance test or oth-
ers) on the actual surface(s) on which a patient functions
(artificial surface, natural grass, field dirt, rubber, cinder,
suspended wood, concrete, carpet, etc).
Gray has proposed unilateral balance tests that incor-
porate functionally relevant (i.e., specific to the individual,
task, and environment) variations in positions or motions.62
A pitcher throwing out of the stretch position, for example,
moves from a position of bilateral stance to unilateral stance
on the side of the throwing arm by flexing the hip and knee
opposite the throwing arm. This unilateral stance (or bal-
ance point position) is held momentarily before the delivery
toward home plate. The ability of a college pitcher to hold
this position, a functional assessment of balance, is associated
with increased throwing velocity.56 The progression of the
static unilateral balance tests might involve asking the pitcher
to maintain unilateral stance on the side of the throwing arm
while raising the leg from the side to the balance point posi-
tion without touching the ground or letting the hands sepa-
rate. This functional test can be progressed by asking a pitcher
to hold the balance point posture while slightly squatting
on the stance leg, simulating the drive toward home plate.
Both can be paced using a metronome, and either the time
or number of repetitions can be measured until the pitcher
either touches the ground or the hands separate. Unilateral
balance tests can be combined with motions or positions of
the upper extremities, head, trunk, or contralateral lower
extremity to challenge postural control in the three cardi-
nal planes. For example, contralateral hip flexion-extension,
hip abduction-adduction, and pelvic rotation can provide
sagittal, frontal, and transverse plane stresses, respectively.
642 SECTION II • Principles of Practice
The watch is started once the patient is synchronized with
the metronome. The watch is stopped for the same reasons
listed earlier in addition to a loss of synchronization with the
metronome. The length of time the patient is able to main-
tain balance is recorded. The mean of the three trials is used
for calculation. The percentage deficit of the involved limb is
calculated using the following equation:63,64
Involved limb score
Symmetry value = × 100
Uninvolved limb score
Application of these general principles allows the clinician to
introduce functional (i.e., specific to the individual, task, and
environment) stresses to the lower extremity and body.
Measuring balance at the level of functional performance
and performance has primarily been done with the Timed Up
and Go Test (TUG). This test of dynamic balance and func-
tional mobility is clinically based, can be used as a screening
tool, and was first described by Podsiadlo and Richardson.65
The TUG is similar to a shuttle run but involves walking,
rather than running. The test measures the time needed to
rise from a chair, walk 3 meters, turn, walk back to the chair,
and sit down. Both inter-rater65-67 and intra-rater65 reliabil-
ity have been shown to be high (0.98 to 0.99). Test-retest
reliability of the TUG was reported as moderate (0.56)68
to high (0.97)69 in older adults and good (ICC = 0.75) in
patients with knee or hip osteoarthritis.70 Moderate correla-
tion of the TUG with the Berg Balance Scale (r = −0.72),
walking speed (r = −0.55), and the Barthel Index of ADL
(Activities of Daily Living) (r = −0.51) suggests construct
validity.65 The sensitivity and specificity of the TUG were
found to be 87% in identifying community-dwelling elderly
persons prone to falls.67 Additionally, the TUG has been
used in patients with total knee arthroplasty,70-72 knee osteo-
arthritis,73 hip fracture,72 and total hip arthroplasty.70,72,74
The TUG has been shown to relate to gait speed in older
adults with either total knee arthroplasty (TKA), total hip
arthroplasty (THA), or hip fractures.72 Improvements in
the TUG test have been found despite persistent quadriceps
weakness and atrophy strength in patients 5 months after
THA.74 Performance on the TUG test was significantly
lower for preoperative knee osteoarthritis (OA) patients
when compared to controls, and it significantly decreased
2 months following TKA.
Balance Reach Tests
The balance reach tests for the lower extremities, first
described by Gray,62 are a natural progression of the bal-
ance tests described earlier. This goal-oriented dynamic
balance test requires the patient to maintain a unilateral stance
while reaching to touch a target with the contralateral lower
extremity or with one or both upper extremities. This test is
believed to provide an index of strength, dynamic postural
control, coordination, and proprioception. Measurements
obtained during balance reach tests can include maximal dis-
tance reached,75-78 number of reaches for a given time period
at a given distance,79 time required to complete a specified
number of reaches at a given distance, and number of reaches
at a given distance before failure.
Procedures for conducting the balance reach test are as
follows. Before beginning balance reach testing, the patient
should warm up adequately and be allowed a minimum of
6 submaximal practice attempts to ensure readiness, famil-
iarity, and reliability.75 Starting from a bilateral stance, for
a lower extremity balance reach test, the clinician asks the
patient to assume unilateral stance on the leg being tested.
The patient is then asked to reach toward the target with
the no-stance leg in the specific direction along the desig-
nated vector, as far as possible while maintaining unilateral
stance. During a successful balance reach attempt, when
trunk and upper extremity position are constrained, the
patient will not contact any surface (other than the target,
if used), change position of the stance foot, move the arms
or hands from hips or chest, or bend forward or backward.
The attempt is completed upon the immediate return of
the reach foot next to the stance leg.
Balance Reach Tests
● One plane
● Rotational
● Functional reach test (FRT)
● Balance arm rest test
Several variations in the balance reach test have been
described.62 These variations, which serve to better match
the test to the individual, environmental, or task-specific
factors, include reach direction, rotation, reach height,
body position (contralateral lower extremity, arms, trunk,
head), and surface. The direction of the reach can vary
according to a reference vector system.62 For the balance
reach tests, the direction of the reach can be described
along eight vectors referenced relative to the stance leg
(Figure 29-2). Gray initially described “nonrotational” and
rotational reaches.62 The seven nonrotational reaches are
in the following directions: anterolateral, anterior, antero-
medial, medial, posteromedial, and posterior (a true lateral
balance reach test is difficult to perform, of questionable
functional relevance, and demonstrates the lowest reliabil-
ity).76 The nonrotational tests require the patient to keep
the reach foot oriented in an anterior direction (i.e., paral-
lel to the stance foot and anterior vector and perpendicular
to the medial-lateral vector) and the pelvis oriented in the
frontal plane (Figure 29-3). Rotational balance reach tests
are intended to introduce or increase transverse plane stress
to the test.62 There are four rotational balance reach tests:
anterolateral, anteromedial, medial, and posteromedial. In
the rotational balance reach tests, the reach foot is oriented
 CHAPTER 29 • Functional Testing and Return to Activity 643

Anterior discrepant illustrations of balance reach tests, it is difficult

Anteromedial Anterolateral to determine whether the subjects in some studies per-
formed rotational or nonrotational tests.75,76,80 Rotational
balance reach tests have not been described to date.
Although previous studies have measured balance reach
tests at floor level heights, reach height may be modified
Medial R Lateral in a task-specific manner, such as with a kick in the martial
arts, by setting a target at a particular height. Body posi-
tion should in general be maintained in an upright and
erect posture. When a nonerect posture is more function-
ally relevant, posture can be modified in a manner specific
Posteromedial Posterolateral to the individual, task, or environmental factors. Some
Posterior previous studies of balance reach tests have constrained
the posture of the trunk and arms,77 whereas others have
Figure 29-2
not,75,76,80 and in other studies this was unclear.79,81 Balance
Reference vectors for balance reach tests
reach tests have been tested in all eight directions,76,80,81
four directions,75 or fewer directions.77-79 The balance
parallel to the vector along which the reach is occurring reach tests have been shown to have excellent inter-rater
(i.e., not anteriorly as in the nonrotational tests), rotating and intra-rater reliability (Table 29-2). These tests also
the pelvis in the transverse plane and out of the frontal appear useful in the screening of patients with patellofem-
plane (Figure 29-4). Based on incomplete descriptions and oral pain,79 ankle instability,81 and quadriceps strength.78

Figure 29-3 Figure 29-4

Left leg vectors for balance reach tests. Left leg medial rotational balance reach test.
644 SECTION II • Principles of Practice
Table 29-2
Reliability of Balance Reach Tests
Author(s) (Year) Subjects (n)
Hertel et al. (2000) Uninjured (16)
Loudon et al. (2002)§ Patellofemoral
pain (40)
Austin and Scibek Uninjured (18)
(2002)§
Kinsey and Armstrong Uninjured (20)
(1998)
*Intra-rater.
†
Inter-rater.
‡
Test-retest.
§
Anterior balance reach test only.
Duncan et al.82 and Gray62 have described functional
dynamic balance tests involving reaching with the upper
extremity. The Functional Reach Test (FRT)82 has been
used to study dynamic postural control in various popu-
lations. This test is a clinical measure of dynamic postural
control that requires the patient to stand and attempt a
maximal reach forward with one arm. The FRT measures
the difference between length of the arm and maximal
forward reach distance.82 Test-retest and inter-tester reli-
ability for apparently healthy adults of ages 20 to 87 years
have both been reported as high with ICC values of 0.92
and 0.98, respectively.82 FRT measures have been highly
correlated (r = 0.71) to center of pressure of excursion
measured using a force platform, and normative values
for both men and women 20 to 87 years of age have
been reported.82 The FRT has been studied in apparently
healthy individuals82 and in patients with vestibulopathy
and balance disorders.83,84 The FRT has not been able to
discriminate between patients with balance disorders and
an apparently healthy comparison group.83,84 Additionally,
predictive validity of falls using FRT has been shown to
have a sensitivity of 30% and a specificity of 92%.85 In
addition to the standard Forward Functional Reach Test,
a Backward Functional Reach Test has been described
as well with very good inter-rater reliability (>0.98) and
same-day reproducibility (0.87).86
Gray described balance arm reach tests, a variation on
the Functional Reach Test using the principles of the lower
extremity balance reach tests.62 Balance arm reach tests
require the patient to touch a target with one or both of the
upper extremities while maintaining balance. Variations in
balance arm reach tests include reach direction, rotation,
reach height, unilateral/bilateral reach, ipsilateral/contra-
lateral reach, and unilateral/bilateral stance. Although the
Functional Reach Test is performed only in bilateral stance
Standard Error of
Reliability Measurement
0.78-0.96* Not reported
0.35-0.93†
0.83* Not reported
0.96*
0.93† Not reported
0.67-0.87‡ Not reported
with unilateral forward and backward reaching at shoulder
height, the variations offer the clinician the ability to more
specifically address the individual, task, and environmen-
tal demands of the patient.62 Although the reliability and
validity of these tests have yet to be studied, the high reli-
ability of the procedurally similar Forward and Backward
Functional Reach Tests is encouraging.
Excursion Tests
Excursion tests involve movement of a specific joint
during a motion involving the extremity or trunk.62
Measurements taken during excursion tests typically
measure the amount of motion in either degrees or cen-
timeters. Some have promoted the inclusion of more
functional weight-bearing components in the physi-
cal examination to potentially enhance sensitivity and
specificity.87 Furthermore, the value of weight-bearing
ROM, in addition to passive ROM, has received sig-
nificant attention recently, with the evidence suggest-
ing significant differences between weight-bearing and
non-weight-bearing measurements of knee ROM.88-91
Weight-bearing measurements of ankle dorsiflexion have
been reported as well (Figure 29-5).92,93 Bennell et al.92
measured ankle dorsiflexion during a weight-bearing
lunge in both degrees of motion and distance of the great
toe from a wall. They reported excellent inter-rater reli-
ability for both angle (0.97) and distance (0.99), as well
as excellent intra-rater reliability (0.97 to 0.98).92 Gabbe
et al. found ankle dorsiflexion measured during weight
bearing to be associated with the risk of lower extrem-
ity injury in Australian football players.93 Weight-bearing
measurements provide information about the available
ROM but also about the ability of the patient to use this
motion in the context of a more natural environment.
 CHAPTER 29 • Functional Testing and Return to Activity
Figure 29-5
Right ankle dorsiflexion excursion tests.
Lunge Tests
A lunge is a movement that involves rapid deceleration and
acceleration of the body mass to change direction and return
to the starting position. The proper execution of a lunge
requires speed, strength, power, dynamic postural control,
flexibility, and coordination throughout the entire lower
extremity.94-97 Additionally, lunges have been shown to be
safe in terms of strain on the anterior and posterior cruciate
ligaments.98,99 Lunges have traditionally been employed to
strengthen the lower extremity; however, studies have inves-
tigated the lunge as an index of functional status.80,95,100-105
Lunge tests have been studied in healthy men and
women,96,98-100 in a healthy older population,97 during
fatigue,95 and following training.104,105 These tests have
also been studied in patients with patellofemoral pain,81
anterior cruciate injuries,101,102 and lateral ankle ligament
reconstruction.103
Lunge tests are performed in a manner similar to the
balance reach tests and have similar variations. Starting
from bilateral stance, the patient steps with the leg being
tested in the specific direction along the designated vector,
as far as possible. During a successful lunge attempt, when
the trunk and upper extremity position are constrained,
the patient will not contact any surface with the hands or
any part of the trail leg other than the foot, change posi-
tion of the trail foot, move the arms or hands from hips or
chest, or bend forward or backward. The attempt is com-
pleted upon the immediate return of the lunge foot next
to the trail leg. Measurements obtained during a lunge
test can include the maximal distance lunged,79,100,104
the number of lunges for a given time period at a given
645
distance,79,96,105 time to complete a specified number of
lunges at a given distance, and the number of lunges at a
given distance and pace before failure.95
Variations of the lunge test, which allow the clinician to
better fit the test to the individual, environmental, or task-
specific factors, include lunge direction, rotation, body posi-
tion (contralateral lower extremity, arms, trunk, head), and
surface. The direction of the lunge can be varied accord-
ing to the reference vector system.62 For the lunge tests,
the direction of the lunge is described using eight vectors
referenced relative to the lunge leg (Figure 29-6). Gray ini-
tially described nonrotational and rotational lunges.62 The
six nonrotational lunges are in the following directions:
anteromedial, anterior, anterolateral, lateral, posterolateral,
and posterior (true medial and posteromedial lunges are
difficult to perform and of questionable functional rele-
vance). The nonrotational tests require the patient to keep
the pelvis and lunge foot oriented in an anterior direction
(i.e., parallel to the stance foot and anterior vector and
perpendicular to the medial-lateral vector) and thus the
pelvis oriented anteriorly (Figure 29-7). Rotational lunge
tests are intended to introduce or increase transverse plane
stress to the test.62 There are four rotational lunge tests:
anteromedial, anterolateral, lateral, and posterolateral. In
the rotational lunge tests, the lunge foot is oriented parallel
to the vector along which the reach is occurring (i.e., not
anteriorly as in the nonrotational tests), thus rotating the
pelvis in the transverse plane and out of the frontal plane
(Figure 29-8).
The reliability for measuring maximal lunge distance
has been shown to be excellent for the anterior (0.93104
and 0.96100) and lateral lunges (0.96)100 and good for the
anteromedial lunge (0.82).79 Neither validity, specificity,
nor sensitivity has been established for lunge tests to date.
Step Tests
Ascending or descending a step requires strength, pos-
tural control, coordination, and flexibility. In stepping
up or down, the center of mass of the body must be
Anterior
Anteromedial Anterolateral
Lateral
R
Posterolateral
Posterior
Figure 29-6
Reference vectors for lunge tests.
646 SECTION II • Principles of Practice
Figure 29-7
Left leg lateral lunge.
either accelerated or decelerated with sufficient control
to transport the person without loss of stability. As with
lunges, step-up and step-down activities have been used
primarily to improve, as opposed to test for, function.
Although the step test has mainly been used to test for
maximal aerobic and anaerobic power, it can be used to
measure other important aspects of function.
The two basic forms of step tests are the step-down
test and the step-up test. Like the balance reach test, the
step-down test requires the patient to maintain unilateral
balance on the limb being tested (Figure 29-9). The step-
down test requires the patient to start from bilateral stance
on top of the step and then assume unilateral stance on the
leg being tested (Figure 29-10). The patient is then asked
to reach down toward the ground with the nonstance leg
in the specific direction along the designated vector while
maintaining unilateral stance. A successful step down is
determined in the same manner as the balance reach test,
with the nonstance leg lightly touching the ground before
returning to the top of the step. The step-up test, on the
other hand, is similar to the lunge in that it involves the
Figure 29-8
Left leg lateral rotational lunge.
loading and unloading of the limb being tested. The step-
up test requires the patient to place the test foot on top
of the step with the nontest foot on the ground 6 inches
from the step. The patient is then asked to raise the body
up onto the step using the test limb, without pushing with
the nontest limb. The test is complete when the nontest
limb is placed next to the test limb on top of the step.
The measurements taken can include the maximal height
of the step, the number of steps at a given height and pace
before failure, the time to complete a specified number of
steps at a given height, and the number of repetitions at a
specified pace and step height before failure.
Functional variations on the step tests include height of
step, direction of step, rotation, and body position.62 The
height of the step effectively determines the distance through
which the center of mass must move and thus the amount
of work performed. As with the balance reach tests and the
lunge tests, the direction of the step can be varied accord-
ing to the reference vector system. Direction is referenced
to the stance leg in the step-down test and to the step leg in
the step-up test. Similarly, there are nonrotational and rota-
tional tests for the step-down and step-up tests. For the step-
down test the six nonrotational directions are anterolateral,
anterior, anteromedial, medial, posteromedial, and posterior.
The four rotational step down tests are anterolateral, antero-
 CHAPTER 29 • Functional Testing and Return to Activity 647

Figure 29-9
A, Lateral step-down tests. Starting position. B, Stepping down. C, Lateral rotational step down. Starting position.
D, Stepping down.

Figure 29-10
Left lateral rotational step-up test.
A, Starting position. B, Stepping up.
C, Finishing position.

medial, medial, and posteromedial. The six nonrotational
step-up tests are anteromedial, anterior, anterolateral, lateral,
posterolateral, and posterior. The four rotational step-up tests
are anteromedial, anterolateral, lateral, and posterolateral.
Step-up tests have been reported in patients with lum-
bar radiculopathies106 and knee pathologies.99 Step-down
tests have been reported in patients with knee patholo-
gies,99,107 ankle instability,108 and following training.104
Various measures have been reported for the step tests.
Studies of step-down tests have measured ground reac-
tion forces104,107,108 and ACL strain.99 Measures taken
during step-up tests include ability/inability to perform
648 SECTION II • Principles of Practice
step up,106 ACL strain,99 number of repetitions in 15 sec-
onds,109 and time required to complete 50 repetitions.109
Test-retest reliability for the 15-second lateral step-up
test on a 6-inch and 8-inch step (0.90 and 0.94, respec-
tively) and the 50 repetition lateral step-up test on a 6-
inch and 8-inch step (0.91 and 0.96, respectively) has
been shown to be excellent.109 The reliability of other step
tests has not been reported. Neither validity, specificity,
nor sensitivity has been established for step tests to date.
Hop Tests
A hop, by definition, involves a single leg. Hop testing
requires the patient to propel off of and subsequently land
on the same leg. Various hop tests provide a composite
functional measure of the strength, power, agility, flex-
ibility, control, coordination, and confidence in the lower
extremity.63,110 A hop can either be vertical or horizontal
and can involve either a single or multiple hops. Vertical
hop tests are mainly interested in the height of a single
effort,111 although the frequency of continuous vertical
hopping may be of value.112-114 Single or multiple horizon-
tal hop tests can be performed in any direction or combi-
nation of directions: anterior, posterior, lateral, diagonal,
rotational, or crossover. The most commonly employed
hop tests include hop for distance, triple hop for distance,
triple crossover hop for distance, 6-meter hop for time,
6-meter crossover hop for time, 12-meter hop for time,
10-foot hop for time, 4-hop crossover, hopping course,
side–side hop test, figure-8 hop test, up and down hop
test, hexagon hop test, stair hop test, lateral hop test, verti-
cal hop test, and hop stabilization test. Measures obtained
during hop tests can include distance, time, height, and
hopping frequency. All of these values can be used to cal-
culate a limb symmetry index (LSI) as indicated previously
(see Balance Tests). Other variations in the hop test include
surface characteristics, footgear (shod or barefoot), arm
movement, and the width of the center line.
Hop Tests
● Single-leg hop for distance
● Triple hop for distance
● Triple crossover hop for distance
● 6-meter timed hop
● Hopping course
● Side-to-side hop test
● Figure-8 hop test
● Up-and-down hop test
● Hexagon hop test
● Stair hop test
● Lateral hop test
● Vertical hop test
● Hop stabilization test
Hop tests of all kinds share similar procedures and uti-
lize similar instrumentation (exceptions to these are noted
in the specific sections that follow). As with most func-
tional tests, the instrumentation needed for performing all
hop tests is rather simple and unsophisticated. A clinician
will need adequate level floor space (with the appropriate
surface), tape to mark the starting line and center lines,
gymnastic/weight lifting chalk to mark the bottom of the
shoes, a tape measure of sufficient length to measure a
particular jump, and a stopwatch. Before testing, the sub-
ject should go through an adequate warmup period. In
addition, to enhance test reliability and validity, the sub-
ject should attempt four practice hops.61,115,116 Subjects
stand on the limb to be tested behind, and as close as
possible to, the starting line. They are instructed to hop
as far as possible, propelling themselves off of and landing
on the same limb. The examiner measures the distance
between the starting line and location of the heel contact
for the hop. Subjects typically perform three successful
trials and the mean of three trials is used as the most reli-
able measure. It is difficult to ascertain from most of the
literature whether movement of the upper extremities is
permitted or constrained. The clinician needs to consider
the purpose of the test and, to ensure standardization
and reproducibility of the subsequent retests, document
thoroughly the conditions under which the test was con-
ducted. If the purpose of the test is simply to determine
the function of the lower extremity, then arm movement
should be constrained. If, however, the purpose of the test
is to assess the ability of the entire body to manage the
stresses of the test, then arm movement should be permit-
ted and, in fact, encouraged. A successful hop requires the
patient to maintain the position of the landing foot for
at least 3 seconds, not contact the floor or hop leg with
the contralateral limb, not remove arms from hips (if arm
movement is constrained), and not contact the floor with
the hands (if arm movement is permitted).
Hop Tests for Distance
Single Hop for Distance. Daniel et al. were the first
to describe the single hop test for distance.117,118 This
test measures the distance covered in one hop for use
in the evaluation of symmetry of lower extremity func-
tion (Figure 29-11). The single hop for distance may be
the most widely studied functional test, and the reliabil-
ity of this test has been established in various popula-
tions (Table 29-3). Additionally, Orishimo et al. studied
the mechanics of the single hop for distance and found
Figure 29-11
Right leg single hop for distance.
 CHAPTER 29 • Functional Testing and Return to Activity 649

Table 29-3
Reliability of Single Hop for Distance Test
Standard Error of
Author(s) (Year) Subjects (n) Reliability Measurement

Manske et al. (2003) Uninjured (28) 0.96 – 0.97† Not reported

Ross et al. (2002) Uninjured (18) 0.92† 4.61 cm
Vandermeulen et al. (2000) Uninjured (46) 0.84-0.92† 5.1-6.8 cm
Negrete and Brophy (2000) Uninjured (60) 0.85† Not reported
Brosky et al. (1999) ACL (15) 0.97* Not reported
Ageberg et al. (1998) Uninjured (75) 0.96† Not reported
Bolgla and Keskulka (1997) Uninjured (20) 0.96† Not reported
Paterno and Greenberger (1996) Uninjured (20) 0.92-0.96† Not reported
Paterno and Greenberger (1996) ACL (13) 0.89† Not reported
Bandy et al. (1994) Uninjured (18) 0.93† Not reported
Greenberger and Paterno (1994) Uninjured (20) 0.96† Not reported
Worrell et al. (1993) Uninjured (36) 0.99* Not reported
Booher et al. (1993) Uninjured (18) 0.97† Not reported
Hu et al. (1992)94 Uninjured (30) 0.96† Not reported
Kramer et al. (1992) ACL (38) 0.93† Not reported

*Intra-rater.
†
Test-retest.

peak powers to be greater at the ankle during takeoff,
greater at the knee during landing, and no different dur-
ing takeoff and landing at the hip.119 Additionally, the
knee serves as the primary shock absorber of the lower
extremity during landing, suggesting that the landing
phase may be as informative about knee function as the
distance hopped.119 The single hop for distance has been
studied in healthy populations120-123 and in patients with
ACL injuries,124-128 patellofemoral pain,129 simulated knee
effusions,116 and hamstring strain.111
Triple Hop for Distance. Noyes et al. were among
the first to report the use of the triple hop for distance.110
This test measures the distance covered in three forward
hops and is also used to assess symmetry of lower extrem-
ity function (Figure 29-12). Unique procedural aspects of
the triple hop for distance include three consecutive maxi-
mal forward hops on the same leg and measurement of the
distance between the starting line and location of the heel
contact for the third hop. The reliability of the triple hop for
distance has been studied and is reported in Table 29-4.
Noyes et al. measured both the triple hop for distance
and the crossover hop for distance and found no signifi-
cant difference between the test results for limb symmetry
scores and sensitivity ratings.110 The triple hop for distance
has been studied in healthy subjects as well as in patients
with patellofemoral pain129-130 and ACL injuries.110,127

Figure 29-12
Right leg triple hop for distance.

Table 29-4
Reliability of Triple Hop for Distance Test
Standard Error of
Author(s) (Year) Subjects (n) Reliability Measurement

Ross et al. (2002) Uninjured (18) 0.97* 11.17 cm

Bolgla and Keskulka (1997) Uninjured (20) 0.95* 17.1 cm
Bandy et al. (1994) Uninjured (18) 0.94* Not reported

*Test-retest.
650 SECTION II • Principles of Practice
Triple Crossover Hop for Distance. Like the triple
hop for distance, this test measures the distance covered in
three forward hops and is also used to assess symmetry of
lower extremity function. It differs in that the three maximal
forward hops involve crossing over the center line and land-
ing on alternating sides of a straight line (Figure 29-13). The
crossover element increases the frontal and transverse plane
stresses on the lower extremity. The triple crossover hop for
distance has been shown to be reliable (Table 29-5) and has
been studied in healthy populations as well as patients with
patellofemoral pain,129 ankle instability,127 ACL injury,131 and
simulated knee effusion.116 Sherry and Best have used a qua-
druple crossover hop for distance for testing patients with
hamstring strain.111 The quadruple jump offers the benefit
of an equal number of medial and lateral stresses applied to
the limb. In addition to the number of hops, variation in
the width of the center strip (15 cm standard) provides an
additional functional challenge.
Other Hop Tests for Distance. The previously
described hop tests for distance focus on movements
predominantly in the sagittal plane. Although the cross-
over hop for distance test does increase the frontal and
transverse plane stresses, the sagittal plane is still the
dominant plane of motion and stress. In acknowledg-
ing this apparent limitation as well as the purpose of
functional tests Vandermeulen et al. described the lat-
eral hop test for distance (Figure 29-14).132 Initially
described by Gerber et al. in a study of patients with
chronic ankle disability,133 this test is a single hop test
for distance in which the patient attempts a maximal hop
in the direction lateral to the test leg. The lateral hop
test has been shown to be highly reliable in a healthy
Figure 29-13
Right leg triple crossover hop for distance.
Table 29-5
Reliability of Triple Crossover Hop for Distance Test
Author(s) (Year) Subjects (n)
Ross et al. (2002) Uninjured (18)
Bolgla and Keskulka (1997) Uninjured (20)
Goh and Boyle (1997) Uninjured (10)
Bandy et al. (1994) Uninjured (18)
*Test-retest.
population (n = 46; ICC, 0.83–0.89; SEM 7.1–8.8 cm)
and would seem to offer the clinician an additional
test to address the individual and task specific factors
of function.132 Kea et al. introduced the medial hop
for distance (maximal hop along the medial vector),134
and they also studied the lateral hop for distance in
terms of the relation to hip adduction and abduction
strength in hockey players (Figure 29-15). Test-retest
reliability for both tests was good (ICC > 0.75); the
correlations with isokinetic strength, however, were
poor (r = −0.26–0.27), suggesting the need for both
clinical and functional testing.134
Gray provided a framework within which to address
all elements of functional hop testing for distance.62 The
direction of the hop can be varied according to the refer-
ence vector system.62 For the hop tests, the direction of
the hop is referenced relative to the hop leg (see Figure
29-2). Gray initially described nonrotational and rota-
tional hops.62 The directions of the eight nonrotational
hops are along each of the reference vectors and require
the patient to keep the hop foot oriented in an anterior
direction (i.e., parallel to the stance foot and anterior
vector and perpendicular to the medial-lateral vector)
and the pelvis oriented in the frontal plane. Rotational
hop tests are intended to increase transverse plane stress
to the test.62 Rotational hop tests can be performed in
all directions except anterior. The anteromedial, medial,
and posteromedial rotational hop tests involve ipsilateral
rotation, whereas the anterolateral, lateral, and postero-
lateral rotational hop tests involve contralateral rotation.
Posterior rotational hop tests can be performed with
rotation in either direction.
Standard Error of
Reliability Measurement
0.93* 17.74 cm
0.95* 17.1 cm
0.85* Not reported
0.94* Not reported
 CHAPTER 29 • Functional Testing and Return to Activity 651

Figure 29-14
Right leg lateral hop for distance.

Figure 29-15
Right leg medial hop for distance.

Hop Tests for Time
6-Meter Hop for Time. The 6-meter hop for time
test, like other hop tests for time, is a measure of lower
extremity strength, speed, and therefore, power. The
method for conducting the hop tests for time is similar
to the hop tests for distance except the patient is asked
to perform consecutive hops on the designated leg and
cover a 6-meter distance as fast as possible (Figure 29-16).
Using a stopwatch, the examiner should begin recording
time upon the first movement of the patient and stop tim-
ing when the patient crosses the finish line. Patients are
given three trials on each limb, with the mean of three tri-
als used as the most reliable measure.
Variations on the 6-meter hop for time test involve
covering either 10 feet135 or 12 meters,136 with each test
demonstrating excellent reliability, 0.92 and 0.96, respec-
tively. Hop for time tests (6 meter, 12 meter, and 10 feet)
have been found to be reliable (Table 29-6) and have
been studied in healthy subjects as well as patients with
patellofemoral pain,129,130 ACL injuries,127 and simulated
knee effusions.116
Crossover Hop Test for Time. This test is similar
to the crossover hop for distance test in that the three
maximal forward hops involve crossing over the center
line and landing on alternating sides of a straight line,
increasing the frontal and transverse plane stresses on the
lower extremity. Unlike the crossover hop for distance
test, the patient is asked to perform consecutive hops on
the designated leg and cover a 6-meter distance as fast as
possible (Figure 29-17). Risberg and Ekeland utilized a
crossover hop test for time as part of a battery of func-
tional tests for patients following ACL reconstruction.137

6 meters
Figure 29-16
Right leg 6-meter hop for time.

Table 29-6
Reliability of 6-Meter Hop for Time Test
Standard Error of
Author(s) (Year) Subjects (n) Reliability Measurement

Manske et al. (2003) Uninjured (28) 0.92 – 0.96† Not reported

Ross et al. (2002) Uninjured (18) 0.92† 0.06 sec
Brosky et al. (1999) ACL (15) 0.97* Not reported
Bolgla and Keskulka (1997) Uninjured (20) 0.66† 0.19 sec
Booher et al. (1993) Uninjured (18) 0.77† 0.13 sec
Worrell et al. (1993) Uninjured (36) 0.77† Not reported

*Intra-rater.
†
Test-retest.
652 SECTION II • Principles of Practice

6 meters
Figure 29-17
Right leg 6-meter crossover hop for time.

However, the center strip is wider (30 cm) than with the
standard test (15 cm). Yildiz et al. used the crossover hop
test for time in a study of patients with patellofemoral
pain.129
Stair Hop (Hopple) Test for Time. This test, ini-
tially described by Risberg and Ekeland,137 measures the
time required to ascend and descend a flight of stairs
by hopping one step at a time; it is considered more
demanding than other functional tests.136 The reliability
of this test has been demonstrated to be excellent fol-
lowing ACL reconstruction (0.96)136 and more reliable
in healthy subjects than both the figure-8 test and the
vertical jump.137 In a study of patients with ACL injury,
Risberg and Ekeland demonstrated the value of this test
as an indicator of functional strength and stability.137 In
a study of healthy female handball players, neither the
stairs hopple for time, single hop for distance, nor the
triple jump test was improved following a 5-to-7-week
ACL injury prevention program.123
Other Hop Tests for Time. Itoh et al. described a bat-
tery of functional tests referred to as the Functional Ability
Test (FAT).138 The FAT involved four timed tests: side–side
hop test, figure-8 hop test, up and down hop test, and hexa-
gon hop test. Using a limb symmetry index derived from
each of these four tests for healthy subjects and patients with
ACL deficiency, Itoh et al. assessed the validity of the compo-
nents of the FAT.138 Whereas at least 95% of healthy subjects
demonstrated symmetrical function in each of the four tests,
82% of ACL-deficient patients exhibited functional asymme-
try in at least one of the four tests. The test-retest reliability
of the four component tests of the FAT has been shown to
be adequate (Table 29-7). These findings suggest that the
FAT is a valid and reliable index of lower extremity function
in patients with ACL deficiency.
Jerosch and Bischof initially described the timed
hopping course as a measure of ankle proprioception,
stability, and function. Subjects are asked to com-
plete the course as quickly as possible.139 The course
comprises eight square panels: four are level, one is
inclined 15°, one is declined 15°, one is angled left
15°, and one is angled right 15°. Although the hop-
ping course has been used to study patients with patel-
lofemoral pain and did not reveal a correlation between
improved isokinetic strength and performance on the
hopping course, the reliability and validity have yet to
be established.129,130

Table 29-7
Reliability of Other Hop Tests for Time
Inter-rater Trial-Trial Day-Day
Test (SEM) (SEM) (SEM)

Figure-8 hop test 0.99 0.92 0.85-0.92

(0.23-0.32) (0.61-1.13) (0.82-0.91)
Up and down hop test 0.96-0.99 0.88-0.93 0.84-0.92
(0.36-0.42) (0.73-1.04) (0.81-0.96)
Side-to-side hop test 0.97-0.99 0.87-0.89 0.48-0.88
(0.27-0.41) (0.77-0.87) (0.95-1.43)
Modified hexagon hop test 0.95-0.99 0.68-0.84 0.66-0.76
(0.20-0.21) (0.44-0.70) (0.47-0.72)

From Ortiz A, Olson S, Roddey T et al: Reliability of selected physical performance tests in young adult
women, J Strength Cond Res 19(1):39-44, 2005.
 CHAPTER 29 • Functional Testing and Return to Activity
Other Hop Tests
Multiple Hop Stabilization Test. This test is an
adaptation of the Modified Bass Test140 developed by
Riemann et al.141 The purpose of this test is to assess the
postural control and muscular endurance of the lower
extremity as a patient performs a functional hop test. The
test involves sequentially hopping to 10 different, equally
spaced squares, and holding a balanced position at each
square for 5 seconds before hopping again. Performance
was scored not by recording time or distance but rather
by an error scoring system in which subjects were assessed
10 points for a landing error and 3 points for a balance
error. Inter-rater and absolute reliability of the scoring
system for this test in healthy subjects were both good to
excellent (ICC: landing 0.92, balance 0.70-0.74; SEM:
landing 0.56-0.57, balance 0.54-0.55).141 The valid-
ity of the multiple hop stabilization test has yet to be
determined.
Several investigators have reported the vertical hop
test for height, in which the patient propels themselves
vertically off of and subsequently lands on the same
leg. The vertical hop is often incorrectly referred to as
a unilateral vertical jump. By definition a jump involves
propelling or landing on two legs. In many instances
the description of the functional test is not sufficient to
conclusively determine whether subjects performed a
vertical hop or a unilateral vertical jump. The reliability
of the vertical hop test for height has been established
and is reported in Table 29-8. This test has been studied
primarily in healthy subjects, but it has also been studied in
patients with ACL injury126 and hamstring strain.111
Jump Tests
Various jump tests have been used over the years to func-
tionally measure the strength, power, coordination, and
control of the lower extremities. Jump testing requires
propulsion off of one or both legs and landing on both legs
and can be classified as either vertical or horizontal (also
Table 29-8
Reliability of Vertical Hop for Height Test
Author(s) (Year) Subjects (n)
Brosky et al. (1999) ACL (15)
Petschnig et al. (1998) Uninjured (50)
Risberg et al. (1995) Uninjured (21)
Bandy et al. (1994) Uninjured (18)
Hu et al. (1992) Uninjured (30)
*Intra-rater.
†
Test-retest.
‡
Unspecified.
653
known as a broad or long jump). Performance on vertical
or horizontal jump tests, therefore, can be measured in
terms of height or distance, respectively. Although there
is controversy in the literature as to whether the vertical
and horizontal jump tests are true measures of power,142,143
they appear to have value, particularly for power sports
requiring propulsive acts such as jumping and sprinting.
Jump Tests
● Unilateral vertical
● Bilateral vertical
● Horizontal
Vertical Jump Tests
Sargent first described the vertical jump in 1921 as “the
physical test of a man.”144 Although numerous modi-
fications have been made to the original test over the
years, the vertical jump test remains a basic measure of
anaerobic power. In addition to the standard compo-
nents, common variations in the test procedure include
the following: unilateral or bilateral, countermovement
or static squat, stationary start or run-up approach, and
free or constrained upper extremity movement.
By definition, vertical jumps can be classified as either
unilateral or bilateral jumps. A bilateral vertical jump
involves propulsion off of and landing on both feet. A uni-
lateral vertical jump, often confused with a vertical hop,
is propulsion off of one leg and landing on both legs.
Unilateral vertical jumps permit bilateral comparison and
the determination of bilateral deficits and limb symmetry.
Bilateral Vertical Jump. The vertical jumps can be
performed with or without a preceding countermove-
ment. Although some investigators employ the use of a
static squat jump (or concentric only),144,145 the use of
a quick countermovement incorporating a stretch-short-
ening cycle is recommended. Countermovement jumps
are, in most instances, much more functional than squat
Standard Error of
Reliability Measurement
0.97* Not reported
0.89† Not reported
0.95‡ Not reported
0.85† Not reported
0.96† Not reported
654 SECTION II • Principles of Practice

jumps as vertical jumps naturally involve the rapid load-
ing and unloading of the musculotendinous unit via a
countermovement. Komi and Bosco examined vertical
jump performance with different stretch loads imposed
on the leg extensor muscles.146 Results showed that the
squat jump was the least efficient condition as compared
with performance in the countermovement or drop jumps
in all groups studied. In addition, there was no significant
difference in performance between the countermovement
jump or drop jump in all groups studied. Furthermore,
Bosco et al. found that mechanical efficiency observed in
rebound (countermovement) jumps was greater than that
observed in no-rebound jumps because of the recoil of elas-
tic energy within the tissue.147 However, both the counter-
movement and squat jumps are considered the most reliable
and valid field tests of power of the lower extremities.148,149
Another common variation on the standard vertical
jump concerns the role of the upper extremities during
jumping. It has consistently been shown that the arms150-153 and
trunk154 each contribute approximately 10% to bilateral
vertical jump performance. Lower vertical jump scores
have been reported during testing with the dominant
upper extremity maintained in the elevated position.155
This method is employed to limit contribution from the
upper extremities and better isolate the lower extrem-
ity muscles. Free arm swing during the vertical jump is
more natural and may be more useful in determining the
ability of the upper extremities and trunk to coordinate
with the lower extremities and contribute to jump per-
formance.150-154 Constraining arm movement by either
holding the arms on the pelvis, chest, or in elevation,
while unnatural and awkward, may serve to better isolate
the function of the lower extremities and better indicate
lower extremity function.155
Various instruments can be used to measure vertical
jump height, varying from the inexpensive and com-
mon (measuring tape and chalk) to the expensive and
less common (force platform and motion analysis). More
moderately priced and increasingly more commonly
used devices include VerTec, Just Jump, and YardStick.
Whereas each device requires specific procedures to
ensure reliability, all require adequate floor space for safe
landing and ceiling heights sufficient to accommodate
the jumper and testing device.
Although static stretching is commonly prescribed as a
component of the warmup period, some investigators have
demonstrated negative156 or no effects157 of static stretch-
ing on vertical jump performance. Young and Behm,
however, found positive effects from a warmup period
including light running and practice jumping.156 However,
the need for practice for the purpose of familiarizing the
client with the test and enhancing the reliability of the test
may not be necessary according to Moir et al.158
There are good test-retest reliability scores for bilateral
vertical jump tests reported in the literature, with a range
of 0.85 to 0.99 (Table 29-9).140,159,160 Johnson and Nelson
reported a validity coefficient of 0.78 based on comparison
of the vertical jump to a sum of four power events in track
and field.140 In addition, they reported construct validity of
jumping ability. Ashley and Weiss found good correlations
(r = 0.53 – 0.80) between vertical jump performance and
measures of lower extremity force and power.161 Carlock
et al. found high correlations (r = 0.76 – 0.91) between
peak power measured during vertical jump performance

Table 29-9
Reliability of Bilateral Vertical Jump for Height Test
Author(s) (Year) Subjects (n) Reliability Standard Error of Measurement

Carlock et al. (2004) Uninjured (68) 0.96-0.98* Not reported

Markovic et al. (2004) Uninjured (93) 0.93-0.98† Not reported
Moir et al. (2004) Uninjured 0.91-0.93* Not reported
Manske et al. (2003) Uninjured (28) 0.98† Not reported
Stockbrugger and Haennel (2001) Uninjured (20) 0.99† Not reported
Vargas (2000) Uninjured (52) 0.97-0.99† 12.1-27.0 mm
Goodwin et al. (1999) Uninjured (15) 0.96† Not reported
Young et al. (1997) Uninjured (17) 0.93-0.94* Not reported
Thomas et al. (1996) Uninjured (19) 0.95† Not reported
Kraemer et al. (1995) Uninjured (38) 0.97† Not reported
Ashley and Weiss (1994) Uninjured (50) 0.87† Not reported
Bocchinfuso et al. (1994) Uninjured (15) 0.99 Not reported
Johnson and Nelson (1974) Uninjured (not reported) 0.93‡ Not reported
Viitasalo et al. (1982) Uninjured (18) 0.85 Not reported
Considine et al. (1973) Uninjured (30) 0.96 Not reported

*Test-retest.
†
Unspecified.
 CHAPTER 29 • Functional Testing and Return to Activity
and weightlifting ability as indicated by performance on
various lifts (clean and jerk, squat, and snatch).148 Young
et al. found low correlations (r = 0.13 – 0.30) between func-
tion of the lower extremity extensors and vertical jump per-
formance, suggesting that there may be value in including
both clinical and functional measures of lower extremity
performance.153
The peak power generated during a vertical jump can be
estimated from the obtained jump height, using body mass:
PP (W) = (60.7) × jump height (cm) + 45.3 × body mass (kg) − 2055
This equation is considered valid for two reasons: esti-
mates are accurate for both countermovement and squat
jumps and estimates are not influenced by gender.162,163
Unilateral Vertical Jump. By strict definition, a uni-
lateral vertical jump involves propulsion off of one leg and
landing on both legs. Unlike the bilateral vertical jump test,
this test allows for bilateral comparisons and the assessment
of limb symmetry. The unilateral vertical jump differs from
a single hop for distance in that the former is vertical and
only evaluates the propulsive performance of the single leg,
while the latter is horizontal and evaluates the ability of the
leg in both propulsion and shock absorption. Variations on
the unilateral vertical jump are the same as those for the
bilateral vertical jump. Importantly, reliable bilateral com-
parisons depend on procedural consistency between the
legs. Calculation of lower extremity symmetry is made by
dividing the score of the involved limb by the score of the
uninvolved limb. The result is then multiplied by 100 for
the percentage score of lower extremity symmetry (see
Balance Tests). Unilateral vertical jump performance has
been shown to be reliable (Table 29-10) and has been mea-
sured in healthy subjects,164,165 as well as in patients with
ankle instability166,167 and ACL injury.168
Horizontal Jump Tests
Horizontal jumps can be performed in any direction: ante-
rior, posterior, lateral, diagonal, or rotational. Use of the
arms during a horizontal jump may contribute to balance
and control, thus improving performance by more than
20%, as compared to without use of the arms.169 Free arm
swing during the horizontal jump may be more useful in
Table 29-10
Reliability of Unilateral Vertical Jump for Height Test
Author(s) (Year) Subjects (n)
Manske et al. (2003) Uninjured (28)
Unger and Wooden (2000) Uninjured (15)
Unger and Wooden (2000) Uninjured (15)
Negrete and Brophy (2000) Uninjured (60)
*Test-retest.
655
determining the ability of the upper extremities and trunk
to coordinate with the lower extremities and contribute to
jump performance.169 Unger and Wooden demonstrated a
significant increase in performance on the unilateral horizon-
tal jump, as well as the unilateral vertical jump, following a
resistance training program targeting the intrinsic muscula-
ture of the foot.170
By definition, horizontal jumps can be classified as
either unilateral or bilateral jumps. A unilateral horizon-
tal jump, often confused with a single hop, is propulsion
off of one leg and landing on both legs (Figure 29-18).
Unilateral horizontal jumps permit bilateral comparison
and the determination of bilateral deficits and limb sym-
metry and have been shown to be reliable (Table 29-11).
Koch et al. demonstrated no significant difference in
unilateral horizontal jump performance across warmup
routines that included high force squats, high power squats,
static stretching, and a control condition (warmup).171
Triple jumps, or repetitive horizontal jumps, have been
reported in the literature149 as well; however, there is much
confusion as to whether these are actually triple hops or
triple jumps. Horizontal jumps have also been shown to
be highly correlated (r = 0.76) with explosive power.149
Agility Tests
There is a paucity of literature concerning standardiza-
tion, reliability, and validity issues for functional tests of
agility. When the literature is analyzed, it becomes readily
apparent that investigators have utilized various tests of
agility; therefore, it is difficult to compare the studies.
Agility Tests
● Barrow zigzag run
● Line drill
● Figure-of-eight
● Shuttle run
● Slalom and hurdle
● Balance beam
● Test battery
Reliability Standard Error of Measurement
0.98* Not reported
0.95* (VerTec) Not reported
0.91* (Just Jump) Not reported
0.85* Not reported
656 SECTION II • Principles of Practice
Table 29-11
Reliability of Horizontal Jump for Distance Test
Author(s) (Year) Subjects (n)
Manske et al. (2003)* Uninjured (28)
Unger and Wooden (2000)* Uninjured (15)
Markovic et al. (2004) Uninjured (93)
Johnson and Nelson (1979) Not reported
*Unilateral.
†
Test-retest.
‡
Unspecified.
Zigzag Run Test
The Barrow zigzag run test is a measure of agility. It
assesses the patient’s ability to rapidly change direction
with cutting and turning maneuvers as well as to accel-
erate and decelerate with control. Equipment needs are
minimal and include a stopwatch to measure time to the
nearest tenth of a second, five cones, and adequate space
to accommodate the 16- by 10-foot course.57 Five cones
are set up, one in each corner and one in the center of the
course (Figure 29-19). The subject should be granted
an adequate warmup period, which includes submaximal
runs through the course for familiarization with the run-
ning pattern. The subject runs the course as rapidly as
possible without touching the standards. The stopwatch
is started when the command “go” is given and stopped
when the patient crosses the finish line.
Directional symmetry scores may be determined by
having the subject repeat the run in the opposite direc-
tion (starting on the right-hand side of the course). The
best of three trials is recorded and used for calculation of
limb symmetry or comparison with norms. Calculation of
Figure 29-18
Right leg unilateral horizontal
jump (top) and bilateral horizontal
jump (bottom).
Reliability Standard Error of Measurement
0.91† Not reported
0.91† Not reported
0.95‡ Not reported
0.96‡ Not reported
lower extremity symmetry can be made using the equa-
tion described previously (see Balance Tests).
Gentile et al. reported ICC (intraclass correlation)
values ranging from 0.90 to 0.95 for the zigzag run
test.172 Ortiz et al. reported excellent reliability (ICC
[SEM] inter-rater: 0.97 [0.18-0.21]; trial-trial: 0.93-
0.97 [0.26-0.30]; day-day: 0.92-0.94 [0.27-0.30]) in a
healthy female population (n = 50).173 In addition, reli-
ability generalized over time and session was 0.90 (p <
.05). To the best of my knowledge, there are no avail-
able measures of validity for the zigzag run test. Roetert
et al. used the zigzag run test to profile tennis players,
but reliability was not reported.174 Johnson and Nelson
presented a copy of norms for high school and junior
high school boys (Table 29-12).57
Line Drill Test
The line drill test is purported to be a measure of speed and
anaerobic capacity;175,176 however, it can be also be classified
as an agility test, since it requires rapid directional change,
cutting, pivoting, and sudden accelerations and decelera-
 CHAPTER 29 • Functional Testing and Return to Activity 657

16 ft E

10 ft

Stop Start
Figure 29-19
Barrow zigzag run test. (From Anderson MA, Foreman TL: Return
to competition: functional rehabilitation. In Zachazewski JE, Magee
DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 256,
Philadelphia, 1996, WB Saunders Co. Drawn from test description
B
in Johnson BL, Nelson JK, editors: Practical measurements for
evaluation in physical education, ed 4, New York, 1986, Macmillan
College Publishing.)

tions. There are no reported measures of reliability or valid-

ity for the line drill test in the literature.
Equipment needs are minimal. The course is designed
to be run on a basketball court, with cones marking the
correct distances (Figure 29-20). The five cones are
arranged as follows: (1) near the baseline (point A), (2)
near the free-throw line (point B), (3) at the half-court
A
Figure 29-20
Line drill test. (From Anderson MA, Foreman TL: Return to
competition: functional rehabilitation. In Zachazewski JE, Magee
DJ, Quillen WS, editors: Athletic injuries and rehabilitation, p 257,
Philadelphia, 1996, WB Saunders.)

Table 29-12
Norms for Barrow Zigzag Run Test
Grade
T-Score
7 8 9 10 11

80 20.1 down 17.8 down 20.2 down 21.6 down 21.5 down
75 21.4-20.2 19.5-17.9 21.3-20.3 22.7-21.7 22.6-21.6
70 22.7-21.5 21.2-19.6 22.4-21.4 23.8-22.8 23.7-22.7
65 24.0-22.8 22.8-21.3 23.5-22.5 24.8-23.9 24.7-23.8
60 25.2-24.1 24.5-22.9 24.6-23.6 25.8-24.9 25.8-24.8
55 26.5-25.3 26.2-24.6 25.7-24.7 26.9-25.9 26.8-25.9
50 27.8-26.6 27.8-26.3 26.8-25.8 27.9-27.0 27.8-26.9
45 29.0-27.9 29.5-27.9 27.9-26.9 28.9-28.0 28.9-27.9
40 30.3-29.1 31.2-29.6 29.9-28.0 29.9-29.0 29.9-29.0
35 31.6-30.4 32.8-31.3 30.1-29.1 31.0-30.0 31.0-30.0
30 32.8-31.7 34.5-32.9 31.2-30.2 32.1-31.1 32.0-31.1
25 34.1-32.9 36.2-34.6 32.3-31.3 33.1-32.2 33.0-32.1
20 34.2 up 36.3 up 32.4 up 33.2 up 33.1 up

From Johnson BL, Nelson JK: Practical measurements for evaluation in physical education, ed 4, Needham Heights, Mass, 1986, Allyn & Bacon.
Reprinted by permission.
658 SECTION II • Principles of Practice
line (point C), (4) at the far free-throw line (point D),
and (5) at the far baseline (point E). In addition, two
stopwatches capable of measuring to one tenth of a sec-
ond are required, one to monitor elapsed time of the run
and one to monitor the rest period. The patient should
undergo an adequate warmup before testing. The patient
should be given an explanation of the test procedure
and allowed submaximal trial runs as needed to become
familiar with the course.
The patient starts the test from the near baseline
(point A). On the command “go,” the patient makes
four continuous roundtrips: (1) from the near baseline
to the near free-throw line and return (A to B to A), (2)
from the near baseline to the half-court line and return
(A to C to A), (3) from the near baseline to the far free-
throw line and return (A to D to A), and (4) from the
near baseline to the far baseline and return (A to E to
A). The patient must touch each line with his or her foot
during the shuttle run.
The first timer stops the watch as the patient com-
pletes the course. At the same time, the second timer
starts a stopwatch to monitor the 2-minute rest period.
The original test requires the course to be repeated for a
total of four repetitions.
The original test directs that the four run times be
averaged for comparison to target times. However, addi-
tional test methods and scores can be gleaned from the
basic test. For example, the degree of fatigue can be eval-
uated by comparing the time of the first run with the
time of the fourth:
Time of last run - time of first run × 100
Percent fatigue =
Time of first run
Also, limb symmetry can be evaluated by directing the
subject to run the course pivoting only with the unin-
volved limb. After adequate rest, the test would be
repeated pivoting only from the involved limb. A mini-
mum of two trials should be granted, with the best time
of both limbs being used in the calculations of limb sym-
metry (see Balance Tests).
Figure-of-Eight Test
The figure-of-eight test of agility has been advocated
throughout the literature for use as an agility test.
However, there is no standardized figure-of-eight run in
the literature for testing purposes.
Minimal equipment is needed to conduct a figure-
of-eight test. Three accurate stopwatches measuring to
the nearest one hundredth of a second are needed if one
desires symmetry scores. Additional equipment includes
cones around which the subject can run, tape to mark
the floor, and sufficient floor space to accommodate the
desired course.
The figure-of-eight course can be set up in various
lengths and widths, depending on the degree of difficulty
desired. Tegner et al. utilized a 10-meter straight run with
narrow turns,177 whereas Reid presented various figure-of-
eight patterns that can be run on a basketball court.178
Several timers are employed. One timer measures the
overall time required to complete the figure-of-eight
run. Limb symmetry can be evaluated by placing timers
at each turn in order to measure time required to run
the turn. To evaluate limb symmetry, separate time mea-
sures are taken for turns to the left and turns to the right.
Tape marks should be placed at the start and finish of the
turns to enhance accuracy in timing. The subject should
be granted an adequate warmup period, which includes
trials of the run at a submaximal velocity.
The subject starts the test stationed at the begin-
ning of the straight run portion of the course (at the
line marking the finish of the turn). The test begins with
the command “go.” The subject runs as fast as possible
through the figure-of-eight course. Three trials should
be given, with the best time being used in symmetry cal-
culations. Each timer clocks a specified portion of the
run. Directional symmetry scores are calculated using the
equation described previously (see Balance Tests).
Anderson et al. were the only authors to present reli-
ability values for a figure-of-eight test of agility.179 They
reported a test-retest reliability score of 0.90 for the
multiple figure-of-eight course described in their study.
Anderson et al. used a multiple figure-of-eight course
to assess the relationship between various quadriceps
and hamstring forces.179 Eccentric hamstring force at 90
degrees per second was found to be the best predictor of
agility run time. Risberg et al. questioned the reliability
of the figure eight test when compared with the vertical
jump, triple jump test, and stairs tests in healthy sub-
jects.180 Risberg and Ekeland suggested that, along with
the stairs hopple test, the figure-of-eight test was a good
indicator of daily function based on factor analysis.137
To the best of my knowledge, normative data for the
figure-of-eight run are unavailable.
Shuttle Run Tests
Barber et al. evaluated the effectiveness of the shuttle run
(Figure 29-21) with and without pivot for determina-
tion of lower limb functional limitations in ACL-defi-
cient knees.181 They found that more than 90% of the
ACL-deficient population scored within the normal limb
symmetry range for both shuttle run tests. Therefore, the
researchers concluded that the shuttle run should not be
utilized to detect lower extremity functional limitations.
Giambelluca et al. used a 25-yard shuttle run and a 25-
yard figure-of-eight run in addition to the unilateral triple
jump to identify dysfunction in an ACL-deficient popula-
tion.182 Results of the study showed no significant difference
between the healthy group and the ACL-deficient group
 CHAPTER 29 • Functional Testing and Return to Activity
6 Meters
for either the shuttle run or the figure-of-eight run. Lephart
et al. conducted a study to assess the relationship between
conventional physical measures and functional performance
tests in two groups of patients with ACL-deficient knees.183
They compared the functional capacities of patients able
to return to preinjury levels of activity and those unable to
return to preinjury activities. Functional performance tests
utilized were a co-contraction semicircle maneuver, a cari-
oca run, and a shuttle run. Results of their study showed
that conventional physical measures correlated poorly with
functional test performance. In addition, they found that
patients who were able to return to preinjury levels of activ-
ity performed significantly better on the functional perfor-
mance tests than those who were unable to return. They
recommended the use of functional performance tests and
the patient’s self-assessment as the criteria for a patient’s
readiness to return to preinjury activities. Munn et al. were
unable to detect ankle instability using the shuttle run in
conjunction with the triple crossover hop for distance.131
Lemmink et al. evaluated the reliability of the interval
shuttle run test and found the test to possess high relative
reliability (0.86 – 0.99) in a healthy population (n = 17).184
Boddington et al.185 found the 5-meter shuttle run test
not only to be reliable but also to demonstrate direct and
indirect validity in field hockey players based on correlation
values (r = 0.60-0.70) between physical performance mea-
sured during activity and the 5-meter shuttle run test.186
Slalom and Hurdle Tests
Alricsson et al. described two additional tests for agility in
a population of 11 healthy children.187 In this study, high
reliability was demonstrated for both the slalom test and
the hurdle, 0.96 and 0.90, respectively.
Balance Beam Tests
These tests have been used to assess dynamic balance and
agility and have been described in both a forward and lateral
direction. They have primarily been used with children to
659
Figure 29-21
6-meter shuttle run.
study learning.188 A paucity of research is available related to
the use of these tests with other populations. Tsigilis et al.
found no significant correlation between performance on
stabilometry and performance on the Modified Bass Test,189
and forward and lateral walking for speed on a balance
beam. Punkallio found the forward balance beam walk for
speed to have high good to excellent test-retest and trial-
to-trial reliability (0.78 – 0.96) in firefighters.190
Test Battery
Tegner et al. conducted a performance test using the
single leg hop, a figure-of-eight run, a spiral staircase
run, and a slope run to evaluate dysfunction following
ACL injury.177 Separate times were recorded for the turn
running and straight running on the figure-of-eight
course. Results of the study showed that ACL-deficient
subjects were significantly slower than the uninjured sub-
jects around the turn, but no significant differences were
found in straight running. In addition, significant differ-
ences were found in stair running and slope running.
Upper Body Power Tests
The majority of functional tests designed for the upper body
assess power using throwing activities, a few of which are
described next. These tests can be broadly categorized as
seated or standing tests.
Upper Body Power Tests
● Seated shot put
● Seated backward overhead shot put throw
● Seated chest pass
● Standing backward overhead medicine ball throw
● Standing medicine ball chest pass
● Standing rotational medicine ball throw
660 SECTION II • Principles of Practice
Seated Tests
Seated Shot Put. This is one of the first and most
commonly used tests for explosive power of the upper
body. Initially proposed by McCloy,191 this test involves a
maximal put of the shot from the chest using both hands
while maintaining a seated position on the floor with
the knees slightly flexed and the feet flat on the floor.192
Performance on the seated shot put was found to be mod-
erately correlated (r = 0.66) with bench press power in
healthy subjects (n = 40). Intraclass reliability coefficients
for seated shot put ranges from 0.95 to 0.98.193,194
Seated Backward Overhead Shot Put Throw. This
test was described by Young et al. as a test of shoulder
power.153 The test requires the subject to throw a 3.6-
kg shot put backward overhead as far as possible, while
maintaining contact with the back of the chair. Neither
the reliability nor the validity of this test has been
reported.
Seated Chest Pass. Cronin et al. tested the reliability
and validity of the seated chest pass in healthy females (n
= 12).195 The test requires the subject to throw a 400-g
netball as far as possible from long-sitting on a floor while
maintaining the trunk, shoulders, or head against a wall
and the legs and pelvis on the floor. The seated chest pass
was shown to be strongly correlated with peak power,
mean power, impulse, and maximal strength in the upper
extremities (r = 0.709 – 0.810). The reliability, based on
coefficients of variation (3.50%), suggests that measure-
ments of maximal distance achieved with the seated chest
pass were stable.
Standing Tests
Standing Backward Overhead Medicine Ball Throw.
Stockbrigger and Haennel tested the reliability and validity
of the standing backward overhead medicine ball throw in
healthy volleyball players (n = 20).196 The reliability of the
test was excellent (0.996), and the correlations with verti-
cal jump power index and vertical jump height were good
(0.906 and 0.808, respectively). The backward overhead
medicine ball throw has also been shown to be positively
correlated with isokinetic peak power and work for trunk
extensors.197 This test, while emphasizing the upper body,
is related to the function of the trunk and lower body and is
thus an indicator of the ability of the individual to integrate
the lower body, trunk, and upper body in a single task.
Salonia et al. found this test to be similar to the standing
forward overhead throw and standing chest pass in measur-
ing upper body power.198
Standing Medicine Ball Chest Pass. Unlike the
seated shot put and seated chest pass with a medicine
ball,195 Salonia et al. reported the chest pass with a medi-
cine ball in standing.198 This test was studied in healthy
gymnasts (n = 60) and found to be equally effective in
measuring upper body power as the standing forward
and backward overhead medicine ball throws. Reliability
and validity were not reported.
Standing Rotational Medicine Ball Throw. Ellen-
becker and Roetert found good correlations between
forehand and backhand rotational medicine ball throw and
peak isokinetic trunk rotation torque (r = 0.779 – 0.877).199
Roetert et al. found correlations ranging from 0.62 to 0.76
between isokinetic trunk extension flexion torque and a
forehand and backhand rotational medicine ball toss.197
Other Tests
One-Arm Hop Test for Time. Falsone et al. described
a functional test of the upper extremities intended for use
in PPEs for wrestling and football.200 The test involves
the patient assuming a one-arm pushup position and
hopping onto and off of a step as quickly as possible in
5 seconds. This test was found to have high test-retest
reliability for both wrestlers and football players (0.81
and 0.78, respectively). The nondominant extremity was
4.4% slower on average than the dominant extremity,
although this difference was not found to be statistically
significant.
6-Minute Walk Test
The 6-minute walk test has been used primarily as a mea-
sure of aerobic fitness in patients with cardiac and pul-
monary pathology. This test is also useful as a functional
test in patients with fibromyalgia,201 total knee arthro-
plasty,70,202 and total knee arthroplasty.70,71 Variations on
this test include the 2-minute walk test used primarily for
patients with lower extremity amputation.
The 6-minute walk test has been shown to have high
test-retest reliability in patients with total knee or hip
arthroplasty (0.94),70 mobility impairments (0.95,203
0.93204), and fibromyalgia (0.91– 0.98).201 The 2-minute
walk test has been shown to possess high inter-rater
(0.98– 0.99) and intra-rater (0.90 – 0.96) reliability in
patients with unilateral trans-tibial amputation.205 Lastly,
the 6-minute walk test has been shown to be both valid
and responsive to change in the postoperative periods in
patients who underwent total knee or hip arthroplasty.70
Wingate Bike Test
The Wingate bike test was designed by Bar-Or to evalu-
ate muscular work with primary energy contribution
from anaerobic sources.206 This test can be used to assess
both peak anaerobic power and anaerobic capacity.
Required equipment for testing includes a bicycle
ergometer on which specific loads can be set and a stop-
watch to monitor 5-second intervals and a 30-second test
duration. The test is initiated with a 5-minute low-inten-
sity warmup period, which includes four to five intervals
of maximal sprints for a 5-second duration against the pre-
scribed load. A 2-to-5-minute recovery period should be
granted following the warmup and before initiating the
test. The load is calculated using the following equation
 CHAPTER 29 • Functional Testing and Return to Activity
and is reported to represent a task requiring approximately
85% anaerobic function:207
Force (kg) = Body weight (kg) × 0.075
The test begins with a 15-second acceleration period. The
subject cycles for 10 seconds at one third the prescribed load
and then for 5 seconds with a progressive increase in resis-
tance to the desired force setting. One technician is needed
to make the necessary adjustments in the resistance setting,
while additional technicians monitor time and revolution
counts. One technician monitors the time for each 5-second
interval and the overall 30-second test duration. Other tech-
nicians are used to count and record pedal revolutions.
The force-setting technician initiates the test with
the command “go” once the prescribed force has been
reached. The subject is instructed to pedal at maximal
capacity and remain seated on the bike throughout the
test. The technician timing the test shouts the elapsed
time every 5 seconds, while the counters record the num-
ber of pedal revolutions for each interval. Upon comple-
tion of the 30-second test, the timer shouts “stop,” the
force is reduced to a low level, and the subject pedals
comfortably for a 1-to-2-minute recovery period.
The two work measurements calculated include peak
anaerobic power and anaerobic capacity. Peak anaerobic
power is calculated by multiplying the maximal number
of revolutions achieved among the 5-second intervals by
the prescribed force setting (kg). This total is then mul-
tiplied by 6, which is the distance (in meters) the wheel
travels for each revolution.
The second calculation is for anaerobic capacity, which
is a measure of the total work accomplished during the
30-second test. Anaerobic capacity is calculated by mul-
tiplying the total number of revolutions by 6 meters to
obtain the total distance covered. The distance is then
multiplied by the prescribed force to obtain total work.
The equations for calculating both peak anaerobic power
and anaerobic capacity are as follows:
Peak anaerobic power: (kg/5 s) = Max revolutions × 6 M × force (kg)
Anaerobic capacity: (kg/30 s) = Total revolutions × 6 M × force (kg)
To convert the measures to watts, peak anaerobic power
must be multiplied by 2 and anaerobic capacity must be
divided by 3 (using the conversion factor: 6 kg/min = 1
watt). Relative power can be calculated by dividing the
power score by body weight. In addition, the fatigue index
can be determined by subtracting the lowest power score
from the peak power, divided by the peak power score:
Peak power × lowest power score
× 100
Peak power score
High rates of test-retest reliability have been reported
by Bar-Or,206 Evans and Quinney,207 and Kaczkowski
661
et al.,208 with a range of 0.95 to 0.98 for reported scores.
Additionally, Kaczkowski et al. found a significant relation-
ship between both peak anaerobic power and anaerobic
capacity when compared with fast-twitch fiber percentage
and area.208 In addition, they found a high relationship
(r = 0.91) between anaerobic capacity and time for the
50-meter dash.208 Tharp et al. found that the Wingate test
was able to differentiate between sprint and distance run-
ning ability in elite males aged 10 to 15 years when scores
were expressed relative to body weight.209 Barfield et al.
found a practice effect and suggest at least a single prac-
tice session before establishing baseline measurements.210
The Wingate test has been compared to the Bosco anaer-
obic test, and the results suggest that the two tests may
measure different facets of anaerobic power.211 Whereas
the Wingate test has been labeled a “chemo-mechanical”
conversion test,212 the Bosco test is purported to check the
elastic (i.e., stretch-shorten cycle) muscular performance.
The two tests appear to provide the clinician with the abil-
ity to best match the test to the individual and task-spe-
cific factors (i.e., the Bosco test may be more appropriate
for individuals required to jump or run).
Maud and Schultz produced a table of normative stan-
dards for peak anaerobic power and anaerobic capacity of men
and women aged 18 to 28 (Table 29-13).213 MacDougall et
al. present these norms for various sports.214
Margaria-Kalamen Power Test
The Margaria-Kalamen test was designed to measure
maximum anaerobic power or work performance.215 The
test requires a brief burst of maximal power output involv-
ing a large percentage of the body’s muscle mass, but no
particular skill or training is required of the subject.
Equipment requirements are minimal. The test uti-
lizes a staircase of 12 to 16 stairs measuring 15 to 20 cm
in height. Margaria conducted experiments to deter-
mine whether power measures could be influenced by
step height. Results of testing revealed an optimal height
value of 35 cm for stepping, which corresponds with two
steps of an ordinary staircase. However, step heights of
30 to 38 cm resulted in values that were within 5% of
the optimum. Although the use of electric switch mats
is preferable, Johnson and Nelson reported that reliable
results are obtained with an accurate stopwatch sensi-
tive to one hundredth of a second.57 An accurate scale
is needed to measure body weight of the subject at the
time of testing.
There are multiple variations of this test.215,216 The
basic test entails a brief sprint to the staircase and up
the stairs as rapidly as possible while the speed of the
climb is measured for a specified number of steps. The
subject should warm up satisfactorily before testing. The
warmup should include practice trials to allow for famil-
iarization with the test procedures. The subject stands
either 2 meters57 or 6 meters216,217 in front of the staircase.
662 SECTION II • Principles of Practice

Table 29-13
Norms for Peak Anaerobic Power and Anaerobic Capacity for the Wingate Anaerobic Test

Percentile Watts W . kgBW−1 W . kgBM−1

Rank
Male Female Male Female Male Female

95 676.6 483.0 8.63 7.52 9.30 9.43

90 661.8 469.9 8.24 7.31 9.03 9.01
85 630.5 437.0 8.09 7.08 8.88 8.88
80 617.9 419.4 8.01 6.95 8.80 8.76
75 604.3 413.5 7.96 6.93 8.70 8.68
70 600.0 409.7 7.91 6.77 8.63 8.52
65 591.7 402.2 7.70 6.65 8.5 8.32
60 576.8 391.4 7.59 6.59 8.44 8.18
55 574.5 386.0 7.46 6.51 8.24 8.13
50 564.6 381.1 7.44 6.39 8.21 7.93
45 552.8 376.9 7.26 6.20 8.14 7.86
40 547.6 366.9 7.14 6.15 8.04 7.70
35 534.6 360.5 7.08 6.13 7.95 7.57
30 529.7 353.2 7.00 6.03 7.80 7.46
25 520.6 346.8 6.79 5.94 7.64 7.32
20 496.1 336.5 6.59 5.71 7.46 7.11
15 484.6 320.3 6.39 5.56 7.28 7.03
10 470.9 306.1 5.98 5.25 6.83 6.83
5 453.2 286.2 5.56 5.07 6.49 6.70
M 562.7 380.8 7.28 6.35 8.11 7.96
SD 66.5 56.4 .88 .73 .82 .88
Minimum 441.3 235.4 4.63 4.53 5.72 5.12
Maximum 711.0 528.6 9.07 8.11 9.66 9.66

From Maud PJ, Shultz BB: Norms for the Wingate anaerobic test with comparison to another similar test, Res
Q Exerc Sports 60;144-151, 1989. Reproduced with permission from the American Alliance for Health, Physical
Education, Recreation and Dance, Reston, Va 22091.

Once ready, the subject sprints to the staircase and climbs
the stairs at a maximal velocity. In the original description
of the test, the subject was instructed to run up two steps
(17.5 cm each) at a time while the time required to cover an
even number of steps was recorded. The time was measured
from the fourth to the sixth step (70 cm height) for calculat-
ing the power measurement. Either method can be used, as
long as the sum of the steps falls in the 30- to 38-cm range.
The clock starts as the subject steps on the initially
selected step and stops as the subject reaches the last step.
Time to cover the distance between the designated steps is
recorded to the nearest one hundredth of a second by the
use of switch mats or a stopwatch. The best of three trials is
recorded for computation of power output. Power output
is computed with the product of body weight and total
vertical distance being divided by the time in seconds:
Work Force (kg) × Distance (M)
Power (kg*m)/s = =
Time Time (S)
where force is equal to body weight, distance is the vertical height
between the initial and final test steps, and time is the measure of
duration required to cover the specified distance
Margaria et al. reported a variation of 4% within the
same test session and a variability of less than 2% when
testing two subjects on multiple occasions over a 5-
week period.215 Margaria et al. also reported equivalent
anaerobic power values between treadmill running and
the stair-climb test.215 In addition, they found high
individual variability in the data, with athletes scor-
ing significantly higher than nonathletes. Johnson and
Nelson reported that sprinters have higher scores than
distance runners.57
Anaerobic Step Test
The anaerobic step test is a modification of aerobic
step tests218,219 and an anaerobic step test described by
Manahan and Gutin in 1971.220 The primary differences
between the anaerobic and aerobic step tests are that
there is no prescribed cadence, the anaerobic test is con-
ducted unilaterally, and the subject stands beside the step
rather than facing the step.
The only equipment requirements are a bench or step
with a recommended height of 40 cm (15.75 in.), a stop-
watch, and an accurate scale to measure body weight
 CHAPTER 29 • Functional Testing and Return to Activity
at the time of testing. The patient should go through
an adequate warmup, which includes practicing the
stepping technique. The stepping technique places the
majority of the work on the stepping leg. The patient
stands beside the bench (step) and places the foot of the
test leg on the top of the bench. The contralateral leg
need not touch the bench during the course of the test.
With each step, the body is raised to the level of the top
of the step as the test leg fully extends. The contralat-
eral limb dangles in an extended position throughout the
ascent but may be used for support and push off when
the foot comes in contact with the floor. The back is to
remain straight throughout the course of the test. The
upper extremities may be used for balance but are not to
be used vigorously in an attempt to assist the test limb.
There is a two-count cadence, which includes the ascent
and descent.
The subject is instructed to perform the test at maxi-
mal effort for the 60-second test. The clock is started
with the initial upward movement of the subject. A step
is counted each time the test leg fully extends and returns
to the starting position. Credit for a step is not granted if
the leg does not fully extend or if the back is flexed. The
number of completed steps is recorded at 15, 30, and 60
seconds.
The count at 15 seconds is used to calculate peak
anaerobic power (assumed to be the highest step count).
The count at 30 seconds can be used for comparison
with the Wingate bike test. The count at 60 seconds is
used to calculate anaerobic capacity. Equations for the
calculation of peak anaerobic power and anaerobic capac-
ity for the anaerobic step test are as follows:
Force × Distance × 1.33
Peak anaerobic power : (kg/s) =
Time
where force equals the weight of the subject (kg), distance equals
0.40 M × the number of completed steps in 15 seconds, time equals 15
seconds, and 1.33 is a factor used to convert positive work to total work
Force × Distance × 1.33
Anaerobic capacity : (kg/min) =
Time
where force equals body weight (kg), distance equals 0.40 M × number
of completed steps in 60 seconds, and time equals one.
Peak power is converted to watts (true power unit) by
multiplication with the conversion factor 1 kg/s = 9.81 W.
Anaerobic capacity is converted to watts by dividing with
the conversion factor 1 W = 6.12 kg/min.
Manahan and Gutin reported reliability coefficients of
0.95 for the two-count anaerobic step test.220 Manahan
and Gutin also reported that correlations between the
1-minute anaerobic step test and 600-yard run time were
fairly high (r = −0.824).220
663
Return to Unrestricted Activity
Decisions about allowing the patient to return to
unrestricted activity, ultimately, are less than straight-
forward. Although there are accepted guidelines
based on clinical measures such as isokinetic testing,
these data contribute minimally to the decision to
return to activity. Similarly, a criterion such as a Limb
Symmetry Index = 85% on a functional test is helpful,
but it has limitations as well, such as in the case of
bilateral involvement. Decisions regarding a patient’s
return to activity are by their very nature multifac-
torial and complex. As such, the decision must be
based on the integration of information from various
sources and the preponderance of the evidence. The
decision to allow a patient to return to unrestricted
activity should address several important factors from
a functional testing perspective. First, the decision-
making process should involve all members of the
rehabilitation team (patient, employer/coach, physi-
cal therapist, physician) and all available data. Each
of these individuals offers unique perspectives on the
status of the patient, which collectively provides the
best estimate of the readiness of the patient to return
to unrestricted activity. Second, all systems contribut-
ing to movement must be assessed and incorporated
into the decision-making process. Although there
is a strong focus on the musculoskeletal system, the
rehabilitation team must also consider the status and
influence of supportive systems and factors such as
cardiovascular, neurological, metabolic, immune, and
psychosocial. Third, functional testing must be pro-
gressed along a continuum that initially focuses pri-
marily on the individual factors but ultimately focuses
equally on the specific individual, task, and environ-
mental factors. Only functional testing can determine
a patient’s ability to perform “those activities iden-
tified by an individual as essential to support physi-
cal, social, and psychological well-being and to create
a personal sense of meaningful living”2 and thereby
identify the presence and magnitude of “limitation(s)
of performance at the level of the whole organism or
person.”2 A rehabilitation program with a functional
focus along the entire rehabilitation continuum from
the initial examination to discharge informs clini-
cal decision making and strengthens inferences at all
points along the continuum in all patients and practice
settings, ultimately simplifying an inherently complex
process.
Summary
Functional testing should be used primarily to inform
the clinician regarding functional limitations and dis-
ability in all patient populations and practice settings.
The testing and measuring of function requires a
664 SECTION II • Principles of Practice
universal conceptual and operational definition of func-
tion. Decisions regarding the selection of functional
tests should be based on the application of sound bio-
mechanical, physiological, and motor behavior princi-
ples to the analysis of the individual, task-specific, and
environmental factors that are the elements of function.
Similarly, variations in the administration of functional
testing are mandatory to meet the specific needs defined
by the individual, task, and environment. However,
ensuring reliability across test sessions and testers
requires standardization and accurate documentation
of all functional testing parameters. Although contin-
ued investigation of the validity of functional testing
is necessary, there is a growing body of literature that
addresses the validity and reliability of functional test-
ing. This research allows the clinician a broader selec-
tion of functional tests and permits clinicians to draw
stronger inferences from functional testing data and
therefore have greater confidence in clinical decisions.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever pos-
sible. There are a total of 220 references for this chapter.

R EHABILITATION O UTCOMES :
M EASURING C HANGE IN P ATIENTS TO
G UIDE C LINICAL D ECISION M AKING
Laura A. May and Douglas P. Gross
Introduction
This chapter explores the issue of using standardized
outcome measures as part of routine clinical practice.
Routine Use of Outcome Measures
Previous research has highlighted that the main issues facing
clinicians regarding the routine use of outcome measures are the
following:1,2
● Time constraints
● A lack of confidence in instrument selection, implementation, and
interpretation of results
● The clinician’s knowledge of available measures and their psycho-
metric properties
Publications by the Canadian Physiotherapy Asso-
ciation and others, which include compendiums of a wide
range of outcome measures commonly used in physical
rehabilitation, are now available and intended to bridge
the gap of understanding for practicing clinicians.3,4
The goal of this chapter is to illustrate the importance
of using standardized outcome measures and to facili-
tate understanding of the practical considerations when
using and interpreting their results. In addition to gain-
ing knowledge about measurements and their properties,
it is critical for clinicians to understand the concept of
effectiveness and how various outcome measures may or
30
C H A P T E R
may not contribute to the determination of treatment
effectiveness. The following case scenario provides the
context to help explain the application of the theoreti-
cal foundations, measurement concepts, and decision
principles for outcome evaluations.
Case Scenario
As a clinician, you have been asked to consult on the
rehabilitation of a 41-year-old male welder who reports a
gradual onset of right elbow pain occurring over the past
2 months. His pain has increased to the point where he
is now experiencing difficulty with the sustained upper
extremity work required at his job. He has had to reduce
the number of hours per day he spends welding and is
wondering if anything can be done to relieve the pain.
Physical examination reveals reduced active extension of
the right elbow with the wrist flexed, as well as slightly
reduced right grip strength. Grip strength is especially
reduced and painful with the elbow extended, and your
patient reports tenderness with palpation of the right
lateral epicondyle. You, as the clinician, make an ini-
tial diagnosis of lateral epicondylitis and, knowing the
research evidence for physical treatment of this condi-
tion, you consider a trial of stretching and strengthening
exercises combined with time-limited use of a counter-
force brace. Before starting treatment, you ask yourself,
“How will I know if these interventions are effective for
this patient’s condition?”
665
666 SECTION II • Principles of Practice
Clinicians are constantly faced with this critical ques-
tion. The answer that the clinician comes up with guides
future management decisions including whether to con-
tinue or withdraw treatment. Unfortunately, obtaining
a valid answer is more challenging than it appears at first
glance. Most commonly, clinicians rely on patient self-
reports of treatment success. “How does it feel today?”
and “Are your functional activities becoming easier to
perform?” are common questions. Patients’ answers,
regrettably, can be influenced by many factors. In the
hope of receiving ongoing treatment, patients may pro-
vide overly positive responses. Alternatively, patients
not seeing success may not return to the clinic, poten-
tially leading the clinician to believe that the problem
has completely resolved. Alternative methods of judg-
ing treatment success are therefore needed, including
the rigorous application and interpretation of standard-
ized outcome measures.
Theoretical Foundations
Factors Influencing Outcomes
Health care has traditionally focused on a service delivery model
that identifies how the structure (i.e., staffing, training, equipment)
and the process of care delivery (i.e., interventions used, communi-
cation) impact outcomes.5 Research now shows that outcomes are
a product of patient-specific factors as well as treatment and the
setting in which the treatment was conducted.6
Theory guides and advances practice for rehabilita-
tion professionals and fosters effective communication
between professionals and with patients. Strong theoreti-
cal foundations also direct how outcomes are evaluated.
There has been a gradual transition in views regarding
health care outcomes. The complex interaction of fac-
tors contributing to health outcomes has been captured
within the World Health Organization’s International
Classification of Functioning, Disability, and Health
(ICF),7 which can be used to classify the health status of
all persons. The ICF provides a theoretical foundation
that defines different categories of health by the compo-
nents of body functions and structures (physiological and
anatomical) and activities and participation (task and life
areas), as defined in Table 30-1.8 The classification of
health and health status domains help clinicians describe
what a person with a condition can do in a standard
environment (capacity) as well as what the person actu-
ally does in his or her usual environment (performance).
The flexibility and comprehensiveness of the ICF makes
it useful in clinical, research, and policy-development
applications.
Foundations Guiding Outcome Evaluation
● International Classification of Functioning, Disability and Health
● Health-related quality of life
● Purpose of the measurement
Table 30-1
Definitions from the International Classification
of Functioning
Body functions are physiological functions of body systems,
and body structures are anatomical parts of the body such
as organs, limbs, and their components.
Impairments are problems in body function or structure such
as a significant deviation or loss.
Activity is the execution of a task or action by an individual.
Activity limitations are difficulties individuals may have
executing an activity.
Participation is involvement in a life situation.
Participation restrictions are problems an individual may
have in involvement in life situations.
Environmental factors make up the physical, social, and
attitudinal environment in which people live and conduct
their lives.
Adapted from World Health Organization: Towards a common
language for functioning, disability and health: ICF, Geneva, 2002,
World Health Organization.
Within rehabilitation, the ICF provides a common lan-
guage and systematic way to classify patient problems and
goals and has been a useful tool to guide the measurement
of health outcomes.9-11 The ICF also encourages consid-
eration of the relationship among interventions and out-
comes. Clinically, health care professionals often assume
that intervention that affects a component of body function
will have an effect on a patient’s performance of a specific
activity. For example, with the patient in the case scenario,
clinicians may want to determine how upper extremity
muscle strengthening (body function) will influence the
patient’s ability to use his welding tools (activity). The
ICF also acknowledges the influence of contextual factors
on a patient’s abilities. Contextual factors can be external
environmental factors (physical, social, or attitudinal) or
internal personal factors, representing attributes of a person
(e.g., age, gender, education). This implies that with the
welder in the case study, the clinician definitely needs to
consider what physical and social work environment the
welder will be required to function in when facilitating the
patient’s return to work. The ICF is an integrated biopsy-
chosocial model of health12 that provides a framework to
evaluate the influence of both intrinsic and extrinsic factors
on a person’s performance in all areas of function.
 CHAPTER 30 • Rehabilitation Outcomes: Measuring Change in Patients to Guide Clinical Decision Making
Another paradigm or foundation to guide outcome eval-
uation is Health Related Quality of Life (HRQoL).13
HRQoL is a multidimensional construct representing the
subjective point of view of the patient.14 There are numer-
ous HRQoL outcome measures from which to choose;
however, the domains most often included in measure-
ments of HRQoL include physical, mental (cognitive and
emotional), social and role functioning, pain, and overall
well being.14-16 Within many areas of rehabilitation, facili-
tating the achievement of satisfactory HRQoL is the ulti-
mate goal.17,18 Generally, it is recognized that disablement
as depicted in the ICF and HRQoL are not independent of
each other. Numerous authors have proposed frameworks
in which quality of life is an overarching or underlying con-
struct such that all aspects of disablement represented in the
ICF and quality of life have a reciprocal relationship.17,19,20
Although there is a relationship between these theoreti-
cal foundations, it is still important to consider outcome
measurement within each paradigm.
Why is inclusion of a measurement of HRQoL as an
outcome important to consider? It is particularly impor-
tant in measuring the impact of chronic conditions,21
although it may have application in more acute condi-
tions as well. Although impairment-based measures
provide important information to clinicians, they have
a weak relationship with functional capacity and well-
being, issues subsumed in measures of HRQoL that are
often more important to the patient.22 Another impor-
tant reason relates to individual values and different
responses despite similar conditions or circumstances.23
For example, two patients with similar injuries as in the
case scenario presented may have very different experi-
ences regarding their role, level of function, and emo-
tional well-being, all of which could considerably impact
their successful return to work. Using a measurement
of HRQoL may provide better understanding of the
patients’ progress or lack of progress.
In addition to the theoretical foundations, outcome
measurement is guided by consideration of the broader
purpose of measurement. The purpose of the measure
not only reflects which aspect of health status is being
measured but also refers to the intended use of the instru-
ment.24 Three broad categories or indexes have been
described: discriminative, predictive, and evaluative. A
discriminative index is used to distinguish between indi-
viduals or groups on an underlying dimension based on
whether or not specific characteristics exist. There will be
common goals for treatment for patients within any given
classification. A predictive index is used to group persons
into categories based on what is expected regarding future
outcomes. The goal is to identify individuals who have,
or will develop, a specific condition or outcome. This
type of measure may help clinicians to identify treatment
667
objectives, preventative strategies, and patient education.
An evaluative index is used to measure the magnitude
of change over time or after treatment in an individual
or a group on a dimension of interest. The importance
of measuring outcomes focuses attention on evaluative
measures as they provide guidance with respect to clinical
decision making and program evaluation. Kirshner and
Guyatt advocate that measurement development and
psychometric evaluation for health status measures occur
within a framework that is specific to the purpose of the
instrument.24 The validation of a tool for one purpose
may not necessarily ensure that it can be used for the
other purposes.
Measurement Properties
The determination of which measure to choose for a
particular purpose is strongly influenced by the psycho-
metric properties of the specific measure as well as con-
sideration of different sources of bias. Determination of
the reliability, validity, and responsiveness of a measure
is crucial to guide appropriate selection and applica-
tion. These are the parameters that tell clinicians about
the quality of the measure. Many excellent resources are
available that provide detailed explanations of these mea-
surement properties.25,26 The authors’ purpose here is to
give an overview of these psychometric properties as well
as other properties related to the choice of measurement
and how they influence results and interpretability of
outcome measures.
Definitions for the psychometric properties that are
important to consider for outcome measures are pro-
vided in Table 30-2. For many clinical measures, the
approach to development and successful application is
often similar for discriminative, predictive, and evaluative
measures; however, as pointed out previously, the evalu-
ation of health status measures is guided by the consid-
eration of the purpose of the measure.24 While reliability
and validity are important for all measures, the types and
ways in which they are evaluated will differ depending
on measurement purpose. Additionally, responsiveness is
a criterion to consider only when looking at evaluative
measures as these measures focus on the magnitude of
change over time.
Reliability
When considering reliability, the issue centers on
whether on not clinicians will get similar results time
after time with minimal error.25 As such, there are
two key methods of representing reliability. The first
method focuses on the relationship of the true vari-
ability of patients’ scores to the observed variability
668 SECTION II • Principles of Practice

Table 30-2
Definitions of Key Psychometric Properties
Measurement Property Definition

Reliability The consistency of a measure

Inter-rater reliability
Test-retest reliability
Internal consistency
Validity
Face validity
Content validity
Construct validity
Criterion validity
Concurrent validity
Predictive validity
Responsiveness
The extent to which multiple raters provide consistent ratings on a
measure
The extent to which multiple applications of a measure provide
consistent results
The extent to which the items of a measure are homogeneous
The extent to which a measure assesses what it is intended to measure
The extent to which a measure appears to address the construct of
interest
The extent to which a measure provides a comprehensive
representation of the domain of interest
The extent to which a measure behaves in accordance with
hypotheses concerning how it should behave
The extent to which a measure agrees with an externally accepted
gold standard
An aspect of criterion validity that assesses the extent to which
a measure agrees with the gold standard when applied at
approximately the same point in time
An aspect of criterion validity assessing the ability of a measure to
predict a meaningful event at some future point in time
The ability of a measure to assess meaningful or clinically important
change over time

Adapted from Finch E, Brooks D, Stratford P et al: Physical rehabilitation outcome measures: a guide to
enhanced clinical decision making, ed 2, Toronto, 2002, Canadian Physiotherapy Association.

in the scores, and this is expressed as a correlation
coefficient. The value for the correlation coefficient,
which has no units associated with it, will lie between
0 and 1, with 0 representing no consistency and 1
indicating perfect agreement or consistency in the
measurement and thus excellent reliability. The most
common correlation coefficient applied to reliability
assessment is the Intraclass Correlation Coefficient
(ICC). Consideration of the error of measurement
allows interpretation of reliability with respect to
the individual scores. This is done by calculating the
Standard Error of Measurement (SEM), which is pre-
sented in the same units as the original measurement.
Interpretation of the SEM is done with respect to the
normal distribution curve. So, for example, if clini-
cians have repeatedly measured grip strength and have
determined the mean to be 25 pounds and the SEM is
4, then there is a 68% chance that the individual’s true
score lies between 21 and 29 pounds.
When measuring changes concerning the outcomes
of various rehabilitation procedures or programs, three
types of reliability are most often considered. The first
is intra-rater reliability. This type of reliability is
concerned with the variability between measurements
taken by the same rater. Is the measurement made or
taken consistently for each repeated measure? Intra-
rater reliability may often be influenced by the experi-
ence of the individual performing the measurement.
The second type of reliability is inter-rater reliability.
This type of reliability is concerned with the variability
in observations or ratings between two or more raters
who measure the same group of subjects.27 Although
measures may include operational definitions and
instructions, different raters may not always agree. It is
particularly important to establish inter-rater reliability
if intending to compare the scores of different raters.
This would be applicable in a clinical situation when
more than one clinician treats an individual patient,
and it is particularly a concern when evaluating the
results of groups of patients or programs. The third
type of reliability is test-retest reliability. This type of
reliability usually applies to measures in which a rater
is not involved as in physiological tests or quality of
life measures and is concerned with the ability of the
instrument itself to measure the variable consistently.27
A reliable test would be one in which the patients’
scores are similar for repeated measurements. One of
the difficulties in determining test-retest reliability of
 CHAPTER 30 • Rehabilitation Outcomes: Measuring Change in Patients to Guide Clinical Decision Making
an instrument is in selecting the time frame between
repeat assessments so that the patient’s condition is
likely to be stable.
Internal consistency is also a critical consideration for
outcome measures that are composed of a set of ques-
tions or performance items that are summed to a single
score. Internal consistency determines if the items are
homogeneous.27 In this case, an internally consistent
measure is one in which the items are correlated with
each other. From this measure it should be clear that
various aspects of a specific characteristic or construct are
being measured.
Validity
Validity is a property that is related not so much to the
instrument itself but rather to the meaning of the instru-
ment scores as a function of the items, the persons’
responses, and the context of measurement.28 Validity is
about the ability to make interpretations from the results
of a measurement. Does the instrument measure what
it is intended to measure? Unfortunately, investigating
and establishing validity are not as straightforward as
establishing reliability. Validity are not as absolute as reli-
ability; rather it is a property that is present in varying
degrees and may never be complete, especially for mea-
sures of abstract variables like function and quality of life.
Although validity is often categorized into different types,
these “types” should not be viewed as separate attributes
as they are all concerned with addressing the degree of
confidence clinicians have about the interpretations one
can make from the test scores.25
Face validity is a desirable feature of tests; however, it
is not validity in the technical sense. Does the test appear
to measure what it is supposed to at a superficial level?29
This is critical because this is often considered and judged
by those who take the test and those who apply the test.
Does it seem correct to them?
Content validity concerns the issue of comprehensive
representation and its impact on the inferences clinicians
make.25 In other words, does the measure include all
items that are representative of all the possible behaviors,
characteristics, or information that are associated with
the specific domain of interest. For example, if the aim of
a test is to measure upper extremity function, clinicians
would not expect to see an item related to walking. As
well, clinicians would want all items relevant to the broad
domain of upper extremity function to be included so
that their interpretation of the results is accurate.
Criterion validity is likely the most easily understood
aspect of validity. It involves determining the relationship
between the measure and some criterion that is ideally con-
sidered the gold standard.25 For example, results of range of
motion measurements using a goniometer could be com-
pared with measurement results obtained from x-ray. There
669
is a distinction made between concurrent and predictive
criterion validity.29 Concurrent validity is more relevant
to the discrimination of existing status whereas predictive
validity is most relevant when the measurement is focused
on the occurrence of a future event or outcome.
In many cases, as with the ICF levels of activity and
participation and quality of life, there are no measures
considered to be gold standards to use as criterion, thus
the most appropriate form of validity to examine is con-
struct validity. This is done by forming hypotheses based
on the theory of the construct being measured and then
determining if the measurement provides the expected
results.25 A more recent interpretation of construct valid-
ity describes it as a unifying concept subsuming the other
“types” of validity and providing the evidential basis for
score interpretation.28 As such, the importance of deter-
mining construct validity cannot be overemphasized.
One of the difficulties in establishing construct validity is
that it cannot be completed within one experiment and
is usually an ongoing process. Given its complexity, there
are many ways of establishing construct validity, and these
are adequately described elsewhere.25,26,30
For confident use of an evaluative measure, infor-
mation about the instruments’ responsiveness, or the
ability to detect clinically important change, is neces-
sary.24 Understanding the aspect of change is complex
and has been made more difficult by the inconsistency
with which it is discussed in the literature. Although the
original definition implies “change of clinical impor-
tance,” there is also the aspect related to the ability to
“detect change regardless of whether it is considered
important,” and this has been referred to as sensitivity
to change.31 Establishing the usefulness of an evalua-
tive measure requires that attention be given to both
aspects of change. Unfortunately, numerous statisti-
cal approaches have been documented, and there is
no agreed-upon method; however, several publica-
tions provide insight and guidance with respect to this
dilemma.31-35 For the practicing clinician dealing with
change in individual patients, likely the most significant
statistical approach to be aware of is the calculation the
Minimal Clinically Important Difference (MCID).4,34
MCID was first defined as “the smallest difference in
score in the domain of interest which patients perceive
as beneficial,” and although other definitions have been
proposed, the common element is the attention to the
lowest boundary of change perceived to be important.36
This coefficient is measured in the same units as the mea-
sure of interest and will provide an estimation of how
many points on the scale a person would have to change
in order to constitute clinically important change.
In most situations, attention to psychometric evalu-
ation is given at the measurement development stages.
However, ongoing psychometric evaluation is necessary
in situations in which a measure that was developed for
670 SECTION II • Principles of Practice
one population in one context is intended to be applied to
a different patient population in different situations. It is
important for clinicians to review the measurement litera-
ture to determine whether or not psychometric evaluation
has occurred with patients and within a setting that are
similar to your own patients or the patient population you
intend to use the tool on. Without knowing this, there
is a risk of misinterpreting the results. Additionally and
ideally, practicing clinicians would also undertake basic
reliability testing within their own clinical environment.
In addition to psychometric properties, other aspects
of measurement must be considered when choosing and
administering the most appropriate tool. These include
whether to use a self-report or performance-based for-
mat and whether to use a generic or disease-specific
instrument. Self-report measures rely entirely on the
patient’s perspective, whereas performance measures
allow clinicians to observe the quality of movement pat-
terns during the test. Both may have advantages or dis-
advantages depending on the unique clinical situation.
Various scoring strategies are used for self-report mea-
sures, including visual analogue scales, Likert scales, or
verbal or visual descriptors (e.g., colors or images). Self-
report measures using Likert scales or verbal descriptors
are easier to use over the phone and thus more useful if
clinicians are considering postdischarge follow-up con-
tacts. When choosing between generic or disease-specific
measures, the users must decide whether they value the
ability to compare results to other patients and popula-
tions (which is more easily done with generic measures
that can be applied to a variety of patient populations) or
value the ability to detect small changes over time (typi-
cally disease-specific measures are more responsive than
generic tools).
Ideally, a measure will not entail great amounts of
time, money, or effort on the part of the clinician or
patient, and the test items and results will be meaning-
ful. The greater the burden of a measure and the less
consequential the items, the less likely it is that the
tool will continue to be used in the clinic or by the
patient. Additionally, when a patient does not mean-
ingfully identify with an evaluation procedure (i.e.,
does not believe it relates to her or him personally),
the less likely it is that the patient will participate fully
with testing. This has implications on the validity of
both self-report and performance testing and is an
important source of bias in measurement. When con-
sidering the meaningfulness of a test, language and
cultural adaptations are also essential.37 Some of the
most common self-report measures have been trans-
lated into multiple languages.38-40 To ensure the integ-
rity of the results of translated versions, a process of
cultural validation is performed in which the measure-
ment properties of the translated measure are evalu-
ated before widespread use.
Along with differential effort on the part of patients
that may arise from a low perceived meaningfulness
of measurement, clinicians should be aware that many
other factors can influence results. Tests that utilize a
self-reporting method can be influenced by patient moti-
vations, poor memory for events, or desires to impress
the treating clinicians.4 Motivations, beliefs, and atti-
tudes can also influence performance testing,41 along
with errors in procedure made by the assessing clinician
or actual changes in ability because of daily variations
in the patient’s condition or wellness. A host of other
influential factors includes medication usage on the day
of assessment, socioeconomic factors (e.g., is the receipt
of workers’ compensation benefits depending on patient
results?), and other personal factors identified in the ICF
model. Some of these can be controlled for through stan-
dardizing test administration as much as possible, but
others are uncontrollable. After selecting a reliable, valid,
and responsive tool, during administration, the practicing
clinician must be aware of these potential confounders of
test results.
Measurement Choices
Returning to the welder in the case scenario, after con-
sidering the ICF theoretical framework and the criti-
cal importance of good measurement properties, what
would be reasonable choices of standardized outcome
measures? For this patient, the primary problems identi-
fied were reduced grip strength, difficulty with welding,
and an inability to sustain a full workday. The planned
intervention of exercise and counterforce bracing aims
to improve each of the identified problems, which cor-
respond to the three ICF domains. Suitable measures for
each will be discussed.
Factors Guiding Measurement Choices
On the most fundamental level, measurement must be linked to iden-
tified problems, set goals, and applied interventions. Ideally, multiple
measures would be used corresponding to the ICF domains of bodily
structure and function, activity, and participation (Table 30-3).
In terms of the ICF domain of bodily structure and
function, dynamometric grip strength has been found
reliable and has high face validity for the construct of
strength.42 It is also very quick and feasible to under-
take in the clinical setting. Unfortunately, what consti-
tutes a meaningful change in grip strength is difficult to
determine without considering specific upper extremity
activities (i.e., as grip increases, the patient should have
a greater ability to grasp and manipulate a welding rod).
In the domain of activity, patient-specific activities could
be tested but only at the expense of test standardiza-
 CHAPTER 30 • Rehabilitation Outcomes: Measuring Change in Patients to Guide Clinical Decision Making 671

Table 30-3
Potential Outcome Measures for Use in Injured Worker Scenario
Body Structure
and Function Activity Participation HRQoL

Measure Dynamometric grip DASH Hours at work SF-36

strength
Psychometrics Reliability: 0.90-0.99 Reliability: ICC 0.92-0.96 Reliability: untested Reliability: varies with
domain and patient
group (0.43-0.94)
Validity: excellent Validity: correlates well with Validity: high face Validity: domain
concurrent validity with ability to work (r = 0.77), validity but otherwise correlates with
known weights (r = 0.99) function (r = 0.79-0.80), not formally tested general health
and pain intensity ratings (0.43-0.69) and
(0.65-0.72) other health
measures (0.18-0.85)
Responsiveness: untested Responsiveness: Responsiveness: not Responsiveness:
MCID = 15 points formally tested MCID (2-7.8 points)
(osteoarthritis)
Feasibility Relatively quick, but <10 minutes to complete Easily tracked by 10 minutes to
costly tools patient complete, cost for
manual
Meaningfulness Forceful grip is required Includes items specific to Most relevant Covers eight domains
at work work-related ability indicator of including physical
functional and mental;
improvement compare to general
population

MCID = minimum clinically important difference.

tion, reliability, and possibly validity. For this reason,
standardized activity or functional assessment protocols
have been developed.
Both performance-based and self-report functional
assessments have been described in the literature. For the
welder in the case scenario, the self-report Disabilities
of the Arm, Shoulder, and Hand (DASH) presents an
appealing alternative.43,44 The DASH is a brief question-
naire that has been extensively tested in a variety of clin-
ical populations and settings. The DASH is a regional
outcome measure that may be used with a wide range
of disabling upper extremity conditions. More generic
measures such as the DASH may be slightly less sensi-
tive to change when compared to disease-specific mea-
sures;4 however, no well-researched outcome measure
exists that specifically addresses disability arising from
lateral elbow pain. The DASH is highly reliable and has
some ability for discriminating patients who are able to
work from those who are not able to work because of an
upper extremity disorder.45 A change of approximately
15 points on the DASH represents a meaningful clinical
improvement.45 On the first day that the clinician sees
the patient, she or he should administer a combination
of grip strength testing and the DASH questionnaire.
Subsequent testing will be performed after an inter-
val in which the clinician expects functional improve-
ment to occur, with follow-up scores being compared
to baseline in order to judge whether improvement has
occurred.
The third ICF domain is perhaps the most challeng-
ing for evaluation purposes. Few participation-level
measures have been created or tested for reliability or
validity. However, gaining improvements in the partici-
pation domain is the primary reason patients seek care
and should be the primary goal of intervention. For the
welder, the most relevant and meaningful measure of
participation would likely be an indicator of work tol-
erance. For example, the number of hours at work per
day could be monitored and is a factor that the patient
can easily track. Ideally, steady improvement on this and
all outcomes will become evident, and the patient will
ultimately be capable of returning to regular work and
home activity.
Outcome measurement options within the theoretical
foundation of HRQoL are abundant. Considering that
HRQoL is a multidimensional construct and the domains
included in any given measure will not be exactly the
same, the task of choosing a measure can be daunting.
672 SECTION II • Principles of Practice
As with other areas of measurement, there are generic
and disease-specific measures. One source of informa-
tion is the Patient-Reported Outcome and Quality of
Life Instruments Database at www.proquolid.org. For
the welder in our case scenario, there are no disease- or
pathology-specific HRQoL measures, so the most rele-
vant measure would likely be a well-known, reliable, and
valid generic instrument with general population data
for comparison. One instrument that is widely used is
the Medical Outcomes Study (MOS) 36-item Short
Form, more commonly known as the SF-36.46 It is an
eight-domain health survey encompassing both physical
and mental health. Generally good reliability, validity,
and responsiveness of the SF-36 have been demonstrated
with a number of patient groups, including those with
musculoskeletal disorders.47-50 In addition, the SF-36 has
been culturally adapted to facilitate international use.51,52
As clinicians, it is important to follow a systematic pro-
cess to decide the appropriate outcome measurement plan
for each patient. Although this discussion of suggested mea-
sures is specific to the case scenario, Table 30-4 includes a
more comprehensive list of musculoskeletal outcome mea-
sures that have been tested for their ability to detect change
over time. Additionally, there are a number of resources
with detailed information about different measures and
their psychometric properties that clinicians may use to
assist them in making appropriate choices.3,4,53 Choosing
the measure is only the first step. Clinicians must also be
aware of issues to consider when applying measures and
interpreting the results with the aim of making appropriate
clinical decisions, which is the focus of the next section.
Measurement Application,
Interpretation and Decision Making
Establishing Treatment Efficacy
Because outcomes can be influenced by many factors other than
the intervention, it is definitely necessary to establish evidence
for treatment efficacy through research, with randomized clinical
trials being the preferred design. However, established treatment
efficacy as determined by randomized controlled trials is limited in
rehabilitation.
Outcome versus Treatment Effectiveness
One of the primary benefits of using standardized out-
come measures relates to clinical reasoning and decision
making.54 Based on the findings of the specific measures
used, the clinician is able to determine both abilities and
areas needing improvement for individual patients. This
will allow the clinician to launch a systematic process to
determine treatment choices, the progression of treat-
ment, and whether or not the patient is ready for dis-
charge. In addition, standardized outcome measures can
facilitate communication between health care providers,
policy makers, third-party payers, and employers when
appropriate. Accurate tracking of outcomes may also
provide justification for funding and resource allocation
at both a patient and program level.
Clinicians usually anticipate a change in a patient’s
status as a result of clinical intervention. Outcome
measures, when used in a systematic way, provide clini-
cians with information about change that has or has not
occurred. As mentioned previously, one of the criteria
used to select measures is based on whether the tool or
measurement selected actually measures an aspect that
clinicians expect will change as a result of clinical treat-
ment. What is the implication of the change in mea-
surement with respect to treatment effectiveness? With
recent emphasis on evidence-based practice and the need
to show that what clinicians do is worthwhile, determin-
ing treatment effectiveness is a critical issue. An editorial
from the Australian Journal of Physiotherapy advocates
that outcome measures only measure outcomes, they do
not measure the effectiveness of the treatment.55 When
there is limited research, outcome measures become
more important in providing some evidence about treat-
ment effectiveness in the real world of clinical practice
and thus guide decision making. Additionally, if good
evidence for treatment efficacy exists, outcome measures
are beneficial in auditing the process of care and com-
paring clinical results with what the research literature
suggests for best practice.55 Related to this last point is
the importance for clinicians to be critical consumers of
the research evidence since interpretability and value of
research of treatment efficacy may be limited by the mea-
sures used. In particular, it has been noted that there is a
lack of attention given to the use of measures with sound
psychometric properties or the adequate documentation
of the properties.56,57
Prognosis: Treatment Intervention versus
Natural History
One major factor that has an impact on the adminis-
tration and interpretation of outcome measures is the
prognosis or natural history of the condition. Given that
many musculoskeletal conditions have a favorable prog-
nosis, clinicians are prone to attribute improvements
to provided treatment when, in reality, improvement
would likely have been seen regardless of treatment. This
is especially important in acute soft tissue disorders, in
which patients typically improve within days or weeks with
or without treatment. To determine if the applied treat-
ments are truly having a beneficial impact beyond the
 CHAPTER 30 • Rehabilitation Outcomes: Measuring Change in Patients to Guide Clinical Decision Making 673

Table 30-4
Examples of Musculoskeletal Outcome Measures with Demonstrated Ability to Detect Meaningful Change
Construct of MCID/
Name Measure Description Responsiveness Index
Generic Measures
Pain Visual Pain intensity/ 10 cm straight line anchored with “no pain” and “pain as 2.8 points
Analogue Scale severity bad as it could be”
Numerical Pain Pain intensity/ 11-point scale (0-10) anchor with “no pain” (0) and 3 points
Rating Scale severity “pain as bad as it can be” (10)
Patient Specific Functional status 11-point scale related to specific activities and their 3 points
Functional Scale associated difficulty for a particular client
Berg Balance Scale Functional 14-item performance-based instrument; each item is 6 points
balance scored on a 5-point scale
Health Utilities Health status Generic multiattribute system covering nine attributes 0.23-0.60 (effect size)
Index (emotion, cognition, self-care, pain, vision, hearing,
speech, ambulation, and dexterity)
Specific Measures
Back pain
Oswestry Disability Pain-related 10-item self-administered questionnaire; higher scores 4%-6%
Questionnaire disability represent increased disability
Roland Disability Pain-related 24-item self-report measure; scored out of 24 with 5 points or 30%
Questionnaire disability 0 indicating highest functional state and 24 represen- change
ting the lowest
Quebec Back Pain Pain-related 20-item self-administered test scored on a 5-point scale 15.3 points
Disability Scale disability with 0 signifying no disability and 100 indicating
maximum disability
Back Pain Pain-related 12-item self-report measure; scored with computational 4-5 points
Functional Scale disability aid in about 15 seconds
Neck pain
Neck Disability Pain-related 10-item self-report measure 7 points
Index disability
Upper extremity
conditions
DASH and Quick- Pain-related 30-item self-report measure 15 points
DASH disability
Upper Extremity Functional status 8-item self-report measure MDC = 9.6
Functional Scale
Lower extremity
conditions
Lower Extremity Lower extremity 20-item self-report questionnaire 9 points
Functional Scale functional status
Gait Speed Walking ability Performance measure involving a timed walk 0.12-0.17 m/s
Western Ontario Health status Self-administered questionnaire using either 100 mm VAS 9.3-10 mm
McMaster or 5-point
(WOMAC)
Osteoarthritis Index Likert scale responses

Adapted from Finch E, Brooks D, Stratford Pet al: Physical rehabilitation outcome measures: a guide to enhanced clinical decision making, ed 2,
Toronto, 2002, Canadian Physiotherapy Association.

natural history of the condition, it may be beneficial to
undertake a baseline measurement of patient status over
a period of time instead of immediately beginning treat-
ment. Following a stable baseline period of repeated
measures, clinical improvements observed after the start
of intervention can more confidently be attributed to the
intervention. For example, in patients with neck or back
pain of less than 3-week duration, it may be worthwhile
to delay specific interventions other than reassurance and
advice to stay active for a period of 1 to 2 weeks (i.e.,
674 SECTION II • Principles of Practice
watchful waiting). During this time, weekly outcome
reassessments could be performed to determine if the
patient is improving spontaneously and if not, a baseline
will be generated enhancing subsequent evaluation. In
terms of strengthening or mobility programs, generat-
ing even a brief baseline of outcome measurement allows
trends to be observed, thus incorporating a more formal
preintervention control period for comparing postinter-
vention results. This approach to evaluation incorporates
principles of single subject research design or n-of-1 tri-
als.27,58 Such rigorous evaluation procedures are uncom-
mon in clinical practice and are often difficult in acute
conditions in which patient status is often transient, but
they dramatically improve levels of certainty regarding
whether an applied intervention is having a meaningful
clinical impact.
Decision Making
The selection and administration of outcome measures
using the concepts and procedures outlined briefly in this
chapter can allow professionals to make more informed
clinical decisions. Unfortunately, the clinical application of
formal measurement seems to most frequently end at the
stage of initial assessment. To truly make informed deci-
sions, follow-up measures must be undertaken at intervals
deemed appropriate according to the nature of the patient’s
condition, the expected rate of recovery, and the levels of
detectable change of the measure used. When scores con-
firm that the patient’s rate of recovery is proceeding as
expected, clinicians are justified in continuing the thera-
peutic course they are pursuing. When outcome measures
do not confirm such improvement, clinicians are prompted
to change treatments or consider discharge. The decision
to discharge is rarely straightforward, and clinicians must
consider all information available to them. Especially when
contemplating return to sport or return to work as in the
case study at the beginning of this chapter, outcome mea-
sure scores can assist clinicians in discriminating when some
level of disability remains, evaluating when improvements
with treatment no longer are occurring, and predicting
when the patient is ready to successfully reintegrate into
regular physical activities. From the first therapeutic inter-
action when goals are agreed upon, the outcomes should
be linked to an evaluation and outcome measurement plan
that can assure both the clinician and the patient that goals
are being achieved.
Summary
This chapter has identified the theoretical, conceptual,
and practical issues that professionals must consider
when planning an outcome evaluation. A comprehensive
evaluation plan should be linked to the identified goals
of intervention and should include standardized out-
come measures with acceptable measurement properties.
Formal patient evaluation can inform clinical decisions
and provide some information on intervention suc-
cess while accounting for biases inherent to the clinical
encounter.
References
To enhance this text and add value for the reader, all references have
been incorporated into a CD-ROM that is provided with this text. The
reader can view the reference source and access it on line whenever
possible. There are a total of 58 references for this chapter.
 Index
A physical growth and physiological development during, 288f,
abdominal fat 289f, 295–300, 297t, 298t, 299t, 300f, 301f
age-related, 309 resistance training during, 441t
diabetes and, 313 sexual maturation during, 299–300, 300f, 301f
abnormal impulse-generating site, 184f, 184t, 185 skeletal and somatic maturation during, 289
accessory glide, 494 slipped capital femoral epiphysis in, 571f
acebutolol (Sectral), 442t adulthood, early (18–40), 303–304
acetaminophen (Tylenol, etc.), 256t, 267, 267t adults
acetic acids, 267t–268t bathing and dressing, 354t
Achilles tendon, 53 aerobic capacity
chronic tendinopathy of, 73, 73f age-related decline in, 308, 308f, 312
forces and stresses on, 56, 56t in elderly persons, 341–342
running affecting, 58 exercise increasing, 312
rupture of aerobic dancing, 352t
badminton associated with, 58 aerobic training. See also endurance training.
diagnostic tests for, 565t acute cardiovascular responses to, 419–421
inflammation associated with, 64–65 age-related, 423t, 424
magnetic resonance imaging of, 572f bed rest and deconditioning affecting, 423–424, 423t
tenosynovitis of, 59, 59t blood pressure changes, 420f
acromioclavicular joint in cardiac patients, 423t, 424–425
arthrokinematics of, 505t exercise intolerance, signs and symptoms of, 420t
capsular pattern of, 520t in healthy individuals, 420t
diagnostic testing of, 565t in trained athlete, 419f
joint congruency of, 502t adaptations to, 93–95
osteokinematics of, 505t using arm ergometer, 428, 429f
actin, 101, 101f using cycle ergometer, 428, 429f
action potential, 180, 181 using semirecumbent cycle ergometer, 428, 429f
active physiological movement, 503 afferent fibers
active transport, of drugs and medicines, 256–257 deep, 176t
activity, 666t. See also physical activity. in joints, 221f, 221t
activity limitations, 666t in muscle, 221t
Actonel (risedronate sodium), 273t in skin, 221t
acupuncture, 70 afferent nerve, 376f
acute pain, 217 affirmation imagery, 469, 469t
of low back, diagnostic imaging in, 588 agility tests
physical agents for, 246–247 balance beam test, 659
adalimumab (Humira), 270t, 271 figure-of-eight test, 658
adductor longus muscle, distal, 107, 108f line drill test, 656–658, 657f
adenosine, 231 shuttle run test, 658, 659f
adenosine triphosphate (ATP) molecule, 433, 433f, 434t slalom and hurdle test, 659
adenosine triphosphate-phosphocreatine (ATP-PC), 433, 433f, test battery, 659
434, 434t zigzig run test, 656, 657f, 657t
adenovirus, 44f aging, 282–304, 305–313. See also elderly persons; growth changes.
adhesive capsulitis, 68t balance and coordination affected by, 312
adjunct rotation, 491 cardiovascular system affected by
adolescence (10–16), 295–303 aerobic exercise, responses to, 423t, 424
anaerobic power during, 302 performance declines in, 312
body composition during, 296–299, 297t, 298t, 299t physical changes in, 308–309
cardiorespiratory fitness during, 301–302 drug effects changing during, 313
gender differences during flexibility affected by, 105, 334, 539–540, 540f
in anaerobic power, 302 frailty related to, 312
in body mass index, 297, 297t in individualization principle, 361–362
in cardiorespiratory fitness, 301 ligaments affected by, 34–35, 34f
in motor performance, 302–303 nervous system changes due to, 309
in muscle strength, 302 performance declines with, 105, 309–312, 310f
in musculoskeletal growth, 295 physical changes with, 305–309
in physical activity, 297–299, 298t, 299t, 303 physiological changes associated with, 332–336
in sexual maturation, 299–300 predisposition to disease related to, 312–313
motor performance during, 302–303 range of motion changes with, 538–539, 538t, 539t
muscle strength during, 302 sarcopenia related to, 312
musculoskeletal growth during, 288f, 289f, 296 sensorimotor control and, 213–214, 214f, 215f
performance development during, 301–303 skeletal and articular changes due to, 305–306
physical activity during, 297–299 skeletal muscle affected by, 105, 307–308, 309–312, 310f
insufficient, 299t AHA Risk Assessment, 418t
moderate or vigorous, 298t air cast, in fracture management, 612f
in physical education classes, 298t alendronate sodium (Fosamax), 273t

675
676 Index

alendronate sodium + cholecalciferol (Fosamax plus D), 273t arm ergometer, 428, 429f
allodynia, 65, 218, 218t arthritides
alprenolol, 442t diagnostic imaging of, 604–606
Alurate (aprobarbital), 262t osteoarthitis. See osteoarthritis (OA).
Ambien (zolpidem), 261t, 262 rheumatoid arthritis. See rheumatoid arthritis (RA).
ambulation. See also walking. arthrokinematic rolls, 492, 493, 493f
and aerobic capacity in old age, 312 arthrokinematics, 492–494
of infants and toddlers, 290–291 of glenohumeral joint, 494f
sensorimotor control of, 204f of lower limb joints, 509t–511t
amides, as local anesthetic, 279t of midline joints, 512t–513t
amphiarthrosis joints, 495, 495t of upper limb joints, 505t–508t
anabolic agents, for osteoporosis, 273t, 274–275 arthrokinematic slides (glides), 492–493
anaerobic glycosis, 434 arthrokinematic spins, 492, 493–494
anaerobic power, of children and adolescents, 302 arthrokinetics, 492
anaerobic step test, 662–663 arthrology, 494
anaerobic training, 87–93 arthroscopy, diagnostic, 566t
resistance training in, 87–92 in cartilage breakdown, 166
sprint and interval training in, 92–93 articular cartilage, 144–174, 149–153, 149f
anakinra (Kineret), 270t, 271 age-related changes to, 152–153
analgesia, 218t, 226, 229 breakdown of, 152, 164–166
analgesics, nonopioid, 267, 267t–268t chondroitin sulfate content in, 306
Anaprox (naproxen sodium), 268t in developing bone, 123f, 124f
anatomic instability, 398–399, 399f diagnostic imaging of, 587t, 598
anesthetics, local, 277–278, 279t excessive loading affecting, 171
angina medications, 280 exercise affecting, 171–173, 173f
animal care, 354t of femoral condyles, 151f (rabbit)
ankle fibrous architecture of, 149, 150f
clinical decision rules for, 582–586, 587t glycosaminoglycan (GAG) content in, 306
of infants, 283 immobilization affecting, 170–171
injury of of infants and toddlers, 282
avulsion fracture, 591f mechanical stimuli, response to, 169–173
kinematics and kinetics in, 213 mobilization affecting, 523t
plain film study of, 581f, 590f, 591f nutrition of, 161
range of motion in, 539t organization of, 150–152, 151f
ankle strategy, 202 osteoarthritis affecting, 165, 166, 306, 307f
Ansaid (flurbiprofen), 268t reduced loading affecting, 170
anterior apprehension test, 566t repair of, 166–169
anterior cruciate ligament (ACL), 24f biophysical approaches to, 168
blood supply to, 26 drug delivery in, 167
functional subunits of, 24f potential for, 166–167
injury of subchondral bone penetration in, 168
diagnostic tests for, 565t tissue transplantation therapies in, 168–169, 169f
kinematics and kinetics of, 212, 212f signaling molecules in, 147–148
magnetic resonance imaging of, 598, 599f tidemark of, 149f, 150
motor performance in children and, 303 ascending pathways, 197, 198f
scar formation following, 38 in pain perception, 223–225, 224f
in women, 442 aspirin, 267t
innervation of, 27 assembly line work, 355t
reconstruction of, kinematic evaluation of, 39–40, 40f associative stage, in stabilization training, 404
surgical reapposition of, 42 astronauts. See spaceflight.
anterior drawer test, 37, 566t atenolol (Tenormin), 442t
anterior half, 488f atlanto-axial joint, 520t
anterior pretectal nucleus, 227–228 atlanto-occipital joint, 520t
anterior tibial peturbation, 303 ATP (adenosine triphosphate) molecule, 433, 433f, 434t
antetorsion, in infants, 283 ATP-phosphocreatine (ATP-PC), 433, 433f, 434, 434t
antifibrosis agents, 116 atraumatic (translational) instability, 397–398, 396f
antigravity trunk control, 290 atrophy, age-related, 307
anti-inflammatory drugs Atrovent (ipratropium), 280–281
corticosteroids. See corticosteroids. auranofin (Ridaura), 270t
nonsteroidal. See nonsteroidal anti-inflammatory drugs (NSAIDs). Aurolate (gold sodium thiomalate), 270t, 271
antiresorptive agents, 273–274, 273t automotive work, 354t
aortic resistance, 309 autonomous stage
Apley grind test, 566t in motor skill development, 379
aprobarbital (Alurate), 262t in stabilization training, 404
aquatic exercise program, 353t axis of movement, 487–488
to burn 150 kcalories, 351t axon, 175, 176f, 177f
cardiovascular benefits of, 339–340, 425–427 axonal death, age-related, 309
Arava (leflunomide), 270t, 271 axonal transport, 180–181
arc, 490, 490f axonotmesis, 184t
archery, 353t axon sprouts, 185f
arcuate swing, 491 axoplasmic flow, biodirectional, 180, 180f
ARF (activation, resorption, formation), 135, 136t azathioprine (Imuran), 270t, 271
arm cycling machine, 352t Azulfidine (sulfasalazine), 270t, 271
 Index 677

B bioreactors, in cartilage tissue engineering, 169

backward reasoning, 324 biotransformation, 258
baclofen (Lioresal), 275–276, 276t bisphosphonates, 273–274, 273t
badminton BJHS (benign joint hypermobility syndrome). See benign joint
and Achilles tendon rupture, 58 hypermobility syndrome (BJHS).
as physical activity, 353t bleeding, in ligament injuries, 38
balance blitz program, 454
age-related change in, 312 Blocadren (timolol), 442t
of infants and toddlers, 290–291 blood glucose regulation, 263
physical activity and exercise affecting, 344–345 blood-nerve barrier, 177, 178f, 179
balance beam test, 659 blood pressure
balance reach tests, 642–644, 643f during activity, 420f
reference vectors of, 643f beta-blockers affecting. See beta-blockers.
reliability of, 644t in children, 301
balance tests, 640–642 BMI (body mass index)
balance training, 382, 383f of adolescents, 296–297
ballet, 352t of preschoolers, 294
ballroom dancing, 352t BMU (basic multicellular unit), 136
Baltimore Longitudinal Study on Aging, 310 body composition
BAPS board, 456 during adolescence, 296–299, 297t, 298t, 299t
Barbita (phenobarbital), 262t aerobic training, as adaptation to, 438t
barbiturates, 262, 262t during childhood, 296–299, 297t, 298t, 299t
bare nerve endings, 191f, 192t, 193 in fitness principle, 358–360
Barlow maneuver, 292 of infants and toddlers, 285, 286f, 287f, 288f, 289f
basement membrane, 176f during middle age and old age, 309, 309f
basic multicellular unit (BMU), 136 of preschoolers, 294
basketball, 351t, 352t resistance training, as adaptation to, 91, 438t
water, 353t body fat
wheelchair, 352t abdominal
bear-standing, 290 age-related, 309
bed rest, aerobic exercise following, 423–424, 423t diabetes and, 313
belief, in injury rehabilitation, 465 age-related changes in, 309, 309f, 335
bench press, 448f, 449 and anaerobic power of children and adolescents, 302
benign joint hypermobility syndrome (BJHS), 34–35, 37, 400 of infants and toddlers, 285
benzodiazepines, 261–262, 261t percent
beta-agonists, 280–281 detraining and, 96
beta-blockers, 422t of infants and toddlers, 285
for cardiac disease, 280 physical activity and exercise affecting, 344
exercise while on, 421 body functions, 666t
muscle affected by, 313 body mass index (BMI)
betamethasone, 263t of adolescents, 296–297
Betapace (sotalol), 442t of preschoolers, 294
Bextra (valdecoxib), 268t bone. See also skeleton.
biaxial joints, 496, 497, 498t age-related changes in, 334
biceps load test, 566t anatomy of osseous tissue, 127–130
biceps tendon, diagnostic ultrasound of, 573f cellular components, 127–128
bicycling extracellular matrix, 128–129, 128f
to burn 150 kcalories, 351t macrostructure, 129–130
level of intensity of, 352t biology and mechanics of, 122–143
for osteoarthritis, 343 blood supply of, 123f, 124f, 130–131
tendon forces and stresses during, 56t cancellous
biglycans, 147 development of, 123f, 124f
bioavailability, 257 mechanical behavior of, 134–135
bioenergetics, 433–436, 433f, 434t cortical
energy source(s) in, 434–436 development of, 123f, 124f
ATP-phosphocreatine as, 433, 433f, 434, 434t mechanical behavior of, 133–134, 133f, 135f
lactic acid as, 434 development of, 122–127, 123f, 124f, 125f, 126f, 127t, 588–590
oxygen as, 434–436 diagnostic imaging of, 587t, 588–590
recovery or replenishment of, 436, 436f, 436t edema of, 587t
and maximal effort duration, 434f fracture of. See fracture.
biomechanical ankle platform system (BAPS board), 456 immobilization affecting, 140, 541f
biomechanics, 487–495, 489t long
adaptations to instability, 402, 402t and blood supply, 124f
assessment of, 502–525, 504f development of, 123f
of fractures, 607–609 distal growth center of, 125f
kinematics in. See kinematics. fracture of, 609, 609f, 610f
kinetics in. See kinetics. growth plate (physis) of, 127t, 588f
of ligaments, 30–33 parts of, 588f
material (stress-strain) behavior, 30 mechanical behavior of, 133–135, 134f
structural (load-deformation) behavior, 30, 31–32, 31f, modeling of, 136t
32, 32f primary, 129–130
viscoelastic (relaxation and cyclic loading) behavior, 30 remodeling of, 135–137
planes of motion in, 487–488, 488f, 489t cellular events in, 135–137
678 Index

bone (Continued) mechanical behavior of, 134–135

disease-related, 141–143 cancer
disuse-related, 140–141 breast
exercise-induced, 138–140 bone scan of, 573f
modeling compared, 136t physical activity and, 348
secondary, 130 colon, 348
shaft of, 124f, 588f physical activity and, 348
subchondral, 152, 168 canoeing, 353t
zone and types of, 611f capacitive coupling, 627
bone density capillaries
loss of. See osteoporosis. blood, 158f
physical activity and exercise affecting, 342–343 lymph, 158f, 248, 248f
bone marrow (medullary cavity), 123f in synovial tissue, 158f (rabbit)
bone mass capillary membrane, 242, 242t
during adolescence, 299 capsular end feel, 518t
loss of. See osteoporosis. carbidopa, 280
bone morphogenetic protein (BMP)-2, 43 Carbocaine (mepivacaine), 279t
bone scans, 573–574, 586t, 604 cardiac disease
of breast cancer metastasis, 573f aerobic exercise in
of stress fracture, 624 acute cardiovascular responses to, 423t, 424–425
bone-tendon junction (BTJ), 48, 48f modifications to exercise program, 430–431
Boniva (ibandronate sodium), 273t medications for, 280
bony end feel, 518t physical activitiy and, 340
boosted model, of joint lubrication, 162t, 163 cardiorespiratory system
Borg Rating of Perceived Exertion (RPE), 422t of adolescents, 301–302
during aquatic exercise programs, 426 in fitness principle, 359
for cardiac patients, 425 of infants and toddlers, 284
for clients on beta-blockers, 421 of preschoolers, 294
boundary model, of joint lubrication, 162t, 163 cardiovascular exercise training, 339
boxing, 352t cardiovascular system
braces, in fracture management, 612–613, 612f–613f, 614t age-related changes of, 333
brachial plexus injury, 293 aerobic exercise, responses to, 423t, 424
brain central adiposity as, 309
age-related changes to, 335 performance declines, 312
of infants and toddlers, 284–285 physical changes, 308–309
in pain perception, 225 assessment of, 414–431
breast cancer during aerobic exercise, 419–421, 419f, 420f, 420t, 423–425, 423t
bone scan of, 573f during aquatic aerobic exercise, 425–427
physical activity and exercise and, 348 during resistance exercise, 421–423
breast development, 300f screening tools for, 415, 416t–417t, 418t
Brevibloc (esmolol), 442t diseases of
bridging matrix. See scar tissue. and age-related central adiposity, 309
bronchioles, 284 economic costs of, 331
bronchodilator drugs, 280–281 resistance training for, 444, 444t
buccal drug administration, 257t risk factors for, 331, 415
bupivacaine (Marcaine, Sensorcaine), 279t signs of clinical stability with history of, 431t
Buprenex (buprenorphine), 266t examination and evaluation, as consideration during, 319–320,
buprenorphine (Buprenex, Transtec), 266t 319f, 320f
burn injury, hyperalgesia in, 219f monitoring during exercise, 427–428
bursa, 496t physical activity and exercise affecting, 339–341
Butazolidin (phenylbutazone), 268t carisoprodol (Soma), 276t
butorphanol (Stadol), 266t carpal tunnel, 185, 186f
carpal tunnel syndrome, 565t
C carpentry, 354t
calcaneocuboid joint carpometacarpal joints
arthrokinematics of, 510t arthrokinematics of, 507t
joint congruency of, 503t capsular pattern of, 520t
osteokinematics of, 510t fifth, 501f
calcanus first, 500f, 507t, 520t
apophysis of, 588–589, 589f fourth, 501f
computed tomography of, 570f joint congruency of, 502t
fracture of, 570f osteokinematics of, 507t
plain film studies of, 570f, 589f carteolol (Cartrol), 442t
calcitonin (Miacalcin), 273t, 274 cartilage
calcium articular. See articular cartilage.
age-related muscle loss associated with, 311 composition of, 144–149
deficiency of, 306 collagen, 148, 148t, 149t
muscle, storing/releasing network within, 81, 82f elastin fibers, 148–149
calf squeeze test, 566t extracellular matrix, 145–146
calisthenics, 352t proteoglycans, 146–148, 146f
Canadian c-spine rule, 586–588, 587t in developing bone, 123f
canaliculi, 130f fibro-. See fibrocartilage.
cancellous bone immobilization affecting, 170–171, 541f
development of, 123f, 124f of infants and toddlers, 282
 Index 679

cartilage anlage, 123f chronological age, 299

cartilage tissue engineering, 169, 169f circuit training, 444, 454
cartilaginous joints, 495, 495t circuit weight training, 352t
Cartrol (carteolol), 442t Citanest (prilocaine), 279t
carvedilol (Coreg), 442t climbing, by infant, 290
cast immobilization, 612f, 613–614, 613f, 614t clinical decision rules (CDRs), 579–588, 587t
catecholamines, 259 for ankle, 582–586, 587t
cationic lipids, 44f for cervical spine, 586–588, 587t
caudal half, 488f for knee, 579–582
celecoxib (Celebrex), 268t clinical instability. See instability.
cell body, 175 clinical union, of bone fracture, 132
cellular matrix, of ligaments, 27–28, 28, 28f (rabbit), 29 Clinoril (sulindac), 268t
cellular modeling, 535 clogging, 352t
immobilization affecting, 541, 541f closed chain, 477t
remobilization and, 544, 544f closed diadochal movement, 491
cement lines, in developing bone, 130f closed-loop control, 377, 378f, 384
central nervous system closed motor skills, 379
brain close pack position, of synovial joint, 501–502, 502t, 503t
age-related changes to, 335 clubfoot, congenital, 293
of infants and toddlers, 284–285 coaching sports, 352t
in pain perception, 225 coal mining, 355t
examination and evaluation, as consideration during, 319–320, cocaine, 279t
319f, 320f codeine, 266t
pain perception via, 220–223, 222f, 223f coefficient of friction (COF), 162t, 163
peripheral nerve connecting with, 179–180 cognitive appraisal model, 459–460, 459f
perturbed homeostatic systems and, 188 cognitive stage
sensory processing in, 196–199, 197t of motor skill development, 379
spinal cord in stabilization training, 404
age-related changes to, 335 cold-induced vasodilation, 245
of infants and toddlers, 284–285 cold therapy. See also cryotherapy.
in pain perception, 223, 223f, 224f in chronic tendinopathy treatment, 70, 75
upregulation of, 188 following ligament injury, 41–42
cerebral cortex, in pain perception, 225 in muscle injury treatment, 118, 119t
cervical spine collagen, 531–533
clinical decision rules for, 586–588, 587t assembly into fibrillar structure, 51–52, 53f, 533f
halo traction for, 616 biosynthesis of, 532, 532f–533f
plain films of, 575f–576f cross-links of, 532, 533f, 534f, 542, 542f
child care, 354t defects of metabolism, 51t
childhood (6–9), 295–303 fascicles as, 20, 27, 52, 53f
anaerobic power during, 302 fibril orientation in, 533, 534f
body composition during, 296–299, 297t, 298t, 299t immobilization affecting, 541–542, 541f, 542f
cardiorespiratory fitness during, 301–302 intracellular and extracellular modifications of, 49, 50f
motor performance during, 302–303 in joint tissue, 148, 148t, 149t
muscle strength during, 302 in ligaments, 29–30, 30t
musculoskeletal growth during, 288f, 289f, 295 in muscle, 98, 119t
performance development during, 301–303 physical properties of, 103f
physical growth and physiological development during, 289f, response of
295–300, 297t, 298t, 299t, 300f, 301f immobilization affecting, 541–542, 541f
resistance training during, 441t to movement, 535–536
sexual maturation during, 299–300, 300f, 301f as suspension bridge, 531f
skeletal and somatic maturation during, 289 synthesis of, 148, 149t
children temperature affecting, 106, 106f
fracture in in tendons. See tendons.
apophyseal, 630t types of, 48–49, 531t
complications of, 630, 631f collagen barrier, to movement, 390–391
diagnostic imaging of, 590f, 592, 595f colon cancer, physical activity and, 348
management in, 628–630, 628f, 629f, 630f, 630t, 631f commitment, to injury rehabilitation, 465
playing with, 354t compensatory assistance, 325–327, 326f, 327f
resistance exercise for, 440–441 competing formulation, 321
6–9 years old, childhood (6–9) compression, therapeutic
10–16 year olds. See adolescence (10–16). cryotherapy with, 246, 246f
3–5 year olds. See preschoolers (3–5). edema and effusion minimized through, 245–246
0–3 year olds. See infants and toddlers (0–3). during inflammatory phase, 243t
Chirocaine (levobupivacaine), 279t intermittent, during reparative phase of injury, 251t
chloroprocaine (Nesacaine), 279t compressive forces
chlorphenesin (Maolate), 276t foot malignment caused by, 59, 68
chlorzoxazone (Paraflex), 276t peripheral nerve injuries caused by, 186
choline magnesium salicylate (Trilisate), 267t shoulder impingement syndrome caused by, 59, 59t
chondrocytes, 144–145 tendon injuries caused by, 59, 59t
chondroitin sulfate, 306 computed tomography, 569–570, 586t
chord, 490, 490f of calcaneal fracture, 570f
chordal swing, 491 of spine, 600
chronic heart failure, medications for, 280 of tumors, 604
chronic obstructive pulmonary disease (COPD), 281, 340–341 computed tomography arthrography, in cartilage breakdown, 166
680 Index

concave, 497 injection of, 71, 116

concavoconvex joints, 497 for rheumatoid arthritis, 270
concentric strength, 311 topical, 119–120
conditioning cortisol, 263t
evaluation/monitoring principle in, 361, 372–373 cortisone, 313
fitness principle in, 358–360, 359f, 373 cospin, 491
guidelines in, 374 costotransverse joint, 512t
homeostasis principle in, 361 costovertebral joint, 512t
individualization principle in, 361–362, 367 coupled movement, 491
interference principle in, 368–369 COX-2 inhibitors, 268t
loading/unloading principle in, 361, 367, 369, 369f, 374 coxa valga, in infants, 283
maintenance principle in, 360–361, 367, 368f cranial half, 488f
optimization principle in, 360–361, 360f, 369 creep, 102, 103f, 390
overload principle in, 362–363, 362f, 369 creeping, of infant, 290
overtraining principle in, 361, 367, 369–370, 374 cricket, 353t
performance principle in, 357–358, 358f, 360, 367, 373, 374 crimp barrier, in range of motion, 389, 389f
periodization principle in, 360, 362, 367, 369, 373–374, 373f cross-country skiing, 353t
preparation principle in, 365, 371 cross-country ski machine, 456
principles of, 357–374 crossed extensor reflex, 197f
progression principle in, 363 crossed syndromes, 396, 397f, 407t
recovery principle in, 365, 369, 370–371 crossover test, 651–652, 652f
rest principle in, 367, 369, 374 cruciate ligament
skill principle in, 363–364 anterior. See anterior cruciate ligament (ACL).
specificity principle in, 362, 363, 364–365, 364f femoral and tibial attachments of, 26f (rat)
stimulus principle in, 363, 365–367 innervation of, 26, 26f (rat)
taper principle in, 371–372, 372f posterior, 24f, 598, 599f
underload principle in, 363 cruising, 290
variety principle in, 363 crush syndromes, 187
condylar or bicondylar joints, 497, 498t, 500f crutches, using, 352t
confidence, rebuilding, 475 cryotherapy. See also cold therapy.
confirmation bias, 318 adipose thickness affecting, 239, 240f
congenital dysplasia of the hip, 291–292, 292f compression with, 246, 246f
congential muscular torticollis, 291, 292f edema and effusion minimized through, 245
congestive heart failure, physical activitiy and, 340 pain associated with, 247
congruent rotation, 491 in pain treatment, 235, 246–247
conjunct rotation, 491 during reparative phase of injury, 251t
connective tissue secondary injury, in management of, 243–244, 244f
age-related changes in, 538–539, 538t cuneocuboid joint, 511t
articular mobilization and remodeling of, 523t, 523 cuneonavicular joint
component(s) of, 530–533, 530f arthrokinematics of, 511t
cellular, 530f joint congruency of, 503t
extracellular matrix as. See extracellular matrix (ECM). osteokinematics of, 511t
immobilization affecting, 540–544, 541f curling, 353t
of muscle, 98, 98f cutaneous receptors, 195–196, 196f, 375
periarticular homeostasis of, 535–536, 536f cutback zone, 125f
of peripheral nerve, 178 cycle ergometer, 428, 429f
properties of, 536–537 cycles, in loading/unloading principle, 369
mechanical, 536, 537f cycling
physical, 536–537, 537f to burn 150 kcalories, 351t
in resistance training, 438t level of intensity of, 352t
temperature affecting, 544–546, 545f, 546f for osteoarthritis, 343
consequential movement, 491 tendon forces and stresses during, 56t
continuous skills, 378 cyclobenzaprine (Flexeril), 276, 276t
contraction cytokines, 147–148
muscle. See muscle contraction. cytoskeleton, 177f
wound, physical agents minimizing, 250
controlled mobilization D
as impairment classification, 322 daily adjustable progressive resistance exercise (DAPRE) system,
in muscle injury treatment, 118–119 453–454
contusion, cryotherapy for, 244, 244t Dalgan (dezocine), 266t
convective transport, 257 Dalmane (flurazepam), 261t
conventional radiography. See plain film studies. dancing, 351t, 352t
convex joints, 497 Dantrium (dantrolene), 276–277, 276t
coordination, age-related decline in, 312 dantrolene (Dantrium), 276–277, 276t
Coreg (carvedilol), 442t Darvocet (propoxyphene), 266t
Corgard (nadolol), 442t Darvon (propoxyphene), 266t
coronal axis, 488f, 489t Daypro (oxaprozin), 268t
coronal or frontal plane, 488f, 489t deadlift, 449
coronary artery disease, 430–431 decision-making, 314–327
cortical bone compensatory assistance, regarding, 325–327, 326f, 327f
development of, 123f, 124f direct treatment, regarding, 324
mechanical behavior of, 133–134, 133f, 135f environmental modification, regarding, 324–325
corticosteroids, 263–264, 263t evaluation, during, 321–322
inhaled, 281 evidence proportionalism in, 322–323
 Index 681

examination, during, 317 of periarticular injuries, 596–600, 598f, 599f, 600f

determining tests and measures, 317–318 plain film studies. See plain film studies.
strategies for, 318–321, 319f, 320f, 321f ultrasound. See ultrasound, diagnostic.
intervention strategies in, 323–324 diagnostic tests, 557–567
knowledge organization in, 315, 316f, 317t continuous outcome, 557
medical fallibility and, 324 discrete outcome, 557
prognostic estimate in, 323 estimates of utility of, 558
reflection on previous client outcomes in, 326–327, 327f likelihood ratios for, 564–565
regarding outcome measures, 674 predictive value of, 562–563, 562t, 563t
and theory of medical fallibility, 324 reliability of, 558–559
whole patient, recognizing, 315–316 intraclass correlation coefficient in, 558
deconditioning kappa statistic in, 558–559
acute cardiovascular responses to aerobic exercise following, sensitivity and specificity of, 559–561, 560t, 561t
423–424, 423f validity of, measures of, 559
following resistance training, 439 diaphragm, of infants and toddlers, 284
decorin antisense gene therapy, 43, 45f (rabbit), 46f (rabbit) diaphysis, 124f, 588f
decorins, 147 diarthrosis. See synovial joints.
deep heat treatment, 234–235 diathermy, 234–235, 251t
deep tissue pain, 218–219 diazepam (Valium), 276t, 277
deformation diclofenac (Voltaren), 267t
of cortical bone, 133, 133f diet, and tendon injuries, 66
force in, 546 differential diagnoses
length-tension, 483f, 484 initial, 557–558
muscle, 102–107 knowledge organization and, 315, 317t
age as factor in, 105 diflunisal (Dolobid), 267t
flexibility as factor in, 103–105 digging, 355t
temperature as factor in, 105–106, 106f, 546, 546f Dilaudid (hydromorphine), 266t
tissue properties as factor in, 102–103, 102f, 103f, 104f direct current, 627
plastic, 390, 608, 609f direct treatment, 324
tensile, of ligaments, 31f Disabilities of the Arm, Shoulder and Hand (DASH), 671
degrees of freedom, 496–497, 498t disabled persons, health promotion for, 348
delayed feedback, 384 Disalcid (salsalate), 267t
delayed-onset muscle soreness, 365 disease-modifying antirheumatic drugs (DMARDs), 270–272, 270t
DeLorme system, of resistance training, 453 biologic, 271–272
demand, and capability, 476–484 synthetic, 270–271
demand/capability relationship, 484–486 distraction, as mobilization method, 521
Demerol (merperidine), 266t disuse
demineralized bone matrix, 627–628 bone remodeling associated with, 140–141
dendrites, 175 physical agents minimizing sequelae of, 249–250, 253–254
De Quervain’s syndrome, 59t tendons affected by, 56–58, 67
descending pathways, 197, 199f diving, 353t
in pain perception, 225–228 dodgeball, 353t
facilitation of pain, 225–226 Dolobid (diflunisal), 267t
inhibition of pain, 226–228, 227f Dolophine (methadone), 266t
discrete skills, 378 dopamine agonists, 279
detraining, 95–96 Doral (quazepam), 261t
developmental dysplasia of the hip, 291–292, 292f dorsal root ganglion, 179
dexamethasone, 263t as abnormal impulse-generating site (AIGS), 185f
dezocine (Dalgan), 266t mechanical trauma to, 186–187
diabetes double crush syndrome, 187
and age-related abdominal fat, 309, 313 “double-threaded bolt and nuts” system, 482, 482f
bone remodeling associated with, 141, 141f down regulation (receptor desensitization), 261
collagen metabolism and, 49–51 drug-receptor interactions, 259
economic costs of, 332 drugs and medicines. See also specific drugs and medications, e.g.,
physical activity and, 347 infliximab (Remicade).
prevalence of, 303 absorption and transport of, 256
diadochal movement, 491 active transport in, 256–257
diagnosis, 322 facilitive diffusion in, 256
diagnostic group classifications, 322–323 passive diffusion in, 256
diagnostic imaging, 568–606, 586t vesicular transport in, 257
in acute low back pain, 588 administration of, routes of, 255–256, 257t
of arthritides, 604–606 bioavailability of, 257
clinical decision rules (CDRs) for, 579–588, 587t chemical name for, 255, 256t
for ankle, 582–586, 587t distribution of, 258
for cervical spine, 586–588, 587t elimination of, 258
for knee, 579–582 generic name for, 255, 256t
computed tomography, 569–570, 570f, 586t in management of secondary injuries, 243
of calcaneal fracture, 570f muscle affected by, 313
of spine, 600 in muscle injury treatment, 119t
of tumors, 604 topical steroidal medications, 119–120
decision making in, 578 nomenclature of, 255
of intervertebral disc injuries, 600–601, 601f, 602f potency of, 260
magnetic resonance imaging. See magnetic resonance imaging. for rheumatoid arthritis (RA), 269–272, 270t
nuclear medicine imaging, 573–574, 573f, 586t sensitivity to, 260
682 Index
drugs and medicines (Continued)
tolerance for, 260–261
trade name for, 255, 256t
Duragesic (fentanyl), 266t
Duranest (etidocaine), 279t
dynamical systems, 378
dynamic constant external resistance training, 448–449
dynamic flexibility, 105
dynamic pattern theory, on motor control, 378
dynamometer, handheld, 293
dystrophin-glycoprotein complex, 101, 101f
E endurance, 432, 433
eccentric exercise program
for chronic tendinopathy. See tendinopathy, chronic.
in frail elderly, 342
eccentric strength, 311
edema and effusion
diagnostic imaging of, 587t, 598–600, 600f
physical agents minimizing
during acute phase, 244–246
during reparative phase, 247–249, 250–251
education
physical, 298t
regarding pain management, 236–237
efferent nerve, 376f
Ehler-Danlos syndrome, 49, 51t, 52
elastic band (tubing) training, 451
elastic end feel, 518t
elastic modulus, of bones, 134f, 608, 609f
elastic zone, in range of motion, 389f, 390
elastin, 531–533
in cartilage, 148–149
in ligaments, 30, 30t
in muscle, 98
elastohydrodynamic model, of joint lubrication, 162t
elbow
capsular pattern of, 520t
fracture of
with hemarthrosis or effusion, 598–600, 600f
occult, 594f
supracondylar, in children, 595f
plain film studies of, 575f, 594f, 595f, 600f
range of motion in, 539t
elderly persons. See also aging.
exercise prescription for, 350, 430
muscle strength in
effects of exercise, 341–342
loss of muscle strength, 309–312
resistance training for, 341–342, 443
tai chi exercise program for, 338
electrical stimulation
in chronic tendinopathy treatment, 70
edema and effusion minimized through, 246
following muscle injury, 119t, 120
high voltage, 243t
interferential current as type, 233
in pain treatment, 232–233, 232f
during reparative phase of injury, 251t
transcutaneous, 232–233, 232f
electromagnetic fields
in articular cartilage repair, 168
in fracture management, 627
electromyography (EMG), 96, 566t
elevation
edema and effusion minimized through, 244–245
used during inflammatory phase, 243t
ellipsoidal joints, 497, 498t, 500f
Enbrel (etanercept), 270t, 271
end feel, 514, 517–518
of lower limb joints, 509t–511t
of midline joints, 512t–513t
types of, 518t–519t
of upper limb joints, 505t–508t
endochondral ossification, 282
endocrine system
age-related changes to, 336
physical activity and, 347
and tendon injuries, 66
endogenous analgesia systems, 226, 229
endoligament cells, 27
endomysium, 79, 80f, 98, 98f, 99f (frog)
endoneurial fluid pressure, 181, 185, 186f
endoneurium, 176f, 177, 177f, 178f
endoscopic laser speckle perfusion imaging, 39, 39f
end result imagery, 469, 469t
muscle contraction and, 106–107, 107f, 484
endurance training. See also aerobic training.
increasing kinetic chain capability, 485
minimizing age-related muscle loss, 105
resistance training compared to, 93–95, 94t, 438t
responses to, 93t
in stabilization training, 407–408
tendon dysfunction associated with prolonged, 58t
tendon loading during, 57
energy flow, 477–479, 477t, 478f, 479f
energy systems, in fitness principle, 359
ensemble processing, 191
enteral administration, 255, 257t
environmental factors, 666t
environmental modification, 324–325
enzyme activity, 438t
epiligament, 27
epimysium, 79, 80f
epineurium, external and internal, 177f, 178f
epiphyseal plate. See growth plate (physis).
epiphysis, 123f, 124, 124f, 125f, 588f
epitendon, 52, 53f
Erb’s palsy, 293
ergonomic cycle, 491
esmolol (Brevibloc), 442t
estazolam (ProSom), 261t
esters, as local anesthetic, 279t
estrogen
in adolescents, 296, 297
and age-related muscle loss, 308
ligaments influenced by, 35
for osteoporosis, 273t, 274
etanercept (Enbrel), 270t, 271
ethnicity
and BMI in adolescents, 297, 297t
and physical activity
during adolescence, 297–299, 298t, 299t
during early adulthood, 303
etidocaine (Duranest), 279t
etodolac (Lodine), 267t
evaluation
of examination findings, 321–322
impairment classifications in, 321–322
evaluation model, 315, 316f
evaluation/monitoring principle, 361, 372–373
evidence proportionalism, 322–323
Evista (raloxifene hydrochloride), 273t
examination
decision-making during, 317
premature closure of, 321
strategy(ies) during, 318–321
competing formulation as, 321
functional relationship as, 320–321, 321f
hypothetico-deductive reasoning as, 318–320, 319f, 320f
pattern recognition as, 318
updating from an anchor as, 318
tests and measures during, 317–318
excess postexercise oxygen consumption, 436, 436f, 436t
excretion, of drugs and medications, 258
excursion tests, 644, 645f
 Index 683

exercise femur
articular cartilage affected by, 171–173, 173f elastic modulus of, 134f
barriers to, 349–350 fracture of
benefits of, 337–348 and bone loss in women, 306
bone remodeling associated with, 138–140, 143 intramedullary nailing of, 622f
cardiovascular assessment prior to, 414–431 open reduction and internal fixation of, 621f
in chronic tendinopathy treatment, 72–76 of infants and toddlers, 283
duration of, 428 physeal centers of, 127t
following muscle injury, 119t proportional limit of, 134f
frequency of, 428 slipped capital femoral epiphysis, 571f
importance of, 303–304. See also health promotion, wellness, and fenamates, 268t
physical fitness. fencing, 353t
intensity of, 428–430, 429t fenoprofen (Nalfon), 268t
joint lubrication and, 163–164 fentanyl (Duragesic, Sublimaze), 266t
lack of adherence to, 349–350 fiberglass cast, 613f
ligaments affected by, 35–36, 36f fibroadipose meniscoids, 496t
mode of, 428 fibrocartilage, 153–154
monitoring cardiovascular system during, 415 intra-articular, 153–154
during old age labra as, 153–154, 496t
aerobic capacity increased, 312 menisci as, 153–154, 496t
barriers to, 349 chondrocytes in, 145
diabetes and, 313 diagnostic imaging of, 587t
maximal oxygen consumption (VO2max), decline in, 308 diagnostic tests of, 565t
osteoporosis and, 143 of knee, magnetic resonance imaging of, 598, 598f
in pain treatment, 236 fibrocartilaginous disc, 496t
preschoolers’ response to, 294 fibromodulin, 147
stress fracture associated with, 139–140 fibrosis, 114t
tendons affected by, 67 fibrous capsule, 156–157
exercise intolerance, signs and symptoms of, 420t fibrous joints, 495, 495t
exercise prescription, 350–356 fibula
components of, 428–430, 429f, 429t fracture healing in, 596f
for healthy individuals in rehabilitation, 428–430 of infants and toddlers, 283
modifications and precautions in, 430–431 physeal centers of, 127t, 629f
exhaustion set system, 454 plain film studies of, 596f
external feedback, in motor skill development, 380 Fick angle, 294
external supports, following muscle injury, 119t figure-of-eight test, 658
extraarticular lesions, 519–521 fine motor skills, during childhood and adolescence, 303
extracellular matrix (ECM) finger splints, 613f
of bone, 128–129, 128f firefighting, 355t
of cartilage, 144, 145–146 fishing, 353t
components of, 530f fitness, 329. See also health promotion, wellness, and physical fitness.
fiber(s) of, 530f components of, 359f
collagen as. See collagen. in stabilization training, 412
elastin as, 531–533 fitness principle, 358–360, 359f, 373
in cartilage, 148–149 body composition in, 359–360
in ligaments, 30, 30t cardiorespiratory system in, 359
in muscle, 98 energy systems in, 359
following muscle injury, 115f flexibility in, 360
of ligaments, 29 neuromuscular system in, 359
myofiber-, 101f FITT principle, 365
of tendons, 47–48 Flexeril (cyclobenzaprine), 276, 276t
extracorporeal shock wave therapy, 70 flexibility. See also range of motion.
age-related changes in, 105, 334, 539–540, 540f
F definition of, 527–529, 528t
facilitive diffusion, of drugs and medicines, 256 dynamic, 105, 528t
falls in fitness principle, 360
age-related, 313 immobilization associated with reduction in, 540–544, 541f,
physical activity and risk of, 345 542f
farming, 355t and injury prevention, 103, 546–550
fascia, 80f muscle, 97
fascicles, 20, 27, 52, 53f, 53f (rat), 79, 80f in hamstring injury, 117f
fasting, and tendon injuries, 66 in injury prevention, 103
fatigue and strength, 107, 107f
central (neural), 312 stretching and. See stretching.
muscle, 117f, 312 types of, 103–105
fatigue state, 362 physical activity and exercise affecting, 342
fat mass. See body fat. range-of-motion compared, 527–528
fat pad, 496t static, 103–105, 528t
Feldene (piroxicam), 116, 268t flexor hallucis tenosynovitis, 58
female triad (disordered eating-menstrual dysfunction-osteopenia), flexor reflex, 197f
299 fluoroquinolone, 66
bone loss associated with, 306 flurazepam (Dalmane), 261t
and stress fracture, 624 flurbiprofen (Ansaid), 268t
684 Index

folk dancing, 352t skeletal traction in, 614–616, 614f, 615f, 616f
follicle stimulating hormone (FSH), 299 splints and fracture braces in, 612–613, 612f–613f, 614t
foot stress fracture, 625
congenital clubfoot, 293 nonunion of, 132–133
of infants and toddlers, 283–284 occult, 591–592, 594f
malignment of, 59, 68 osteoporosis and, 142
plain film studies of, 577f patterns in, 607
football, 351t, 352t high-energy, 608f
foot progression angle, in preschoolers, 294 low-energy, 608f
forced repetition system, 454 open and closed, 608f
force relaxation response, 105–106, 106f, 545f plain film studies of
forces, types of, 477t ankle fracture, 591f
force-velocity relationship, 92, 92f calcaneal fracture, 570f
forearm elbow fracture, 594f, 595f, 600f
plain film study of, 579f fibular fracture, 596f
range of motion in, 539t hip fracture, 589f
forestry work, 354t humeral fracture, 592f
Forteo (teriparatide), 273t, 274–275 pelvic fracture, 586f, 589f
forward reasoning, 324 shoulder fracture, 593f
Fosamax (alendronate sodium), 273t wrist fracture, 594f, 597f
Fosamax plus D (alendronate sodium + cholecalciferol), 273t stable, 132f
fracture stress, 139–140, 592–594, 623–625
of ankle, 590f diagnosis of, 624–625
avulsion, 589, 589f, 591, 591f diagnosis of, classification scheme for, 140t
biomechanics of, 607–609 female athlete triad associated with, 624
of calcanus management of, 625
computed tomography of, 570f nutrition and, 624
plain film of, 570f risk factors for, 623–624
in children, 590f, 592, 595f stress reaction in, 139, 140t
classification of, 609–610, 610f unstable, 132f
diagnostic imaging of, 590–596 of vertebrae, and bone loss in women, 306
magnetic resonance imaging, 624–625, 624f frail elders, 339, 342
plain film studies, 570f, 586f, 589f, 591f, 592f, 593f, 594f, Framework of Clinical Practice, models of, 315, 316f
595f, 596f, 597f, 600f free nerve endings, 376t, 410t
displaced, 591, 592f, 593f free weights, 352t, 449, 451t, 453f
of elbow frisbee, 353t
with hemarthrosis or effusion, 598–600, 600f frontal or coronal plane, 488f, 489t
occult, 594f functional abilities, physical activity and, 338
supracondylar, in children, 595f Functional Ability Tests (FAT), 652, 652t
at growth plate (physis), 589–590, 589f, 590t functional outcome, 323
healing of, 625–626 functional relationship, 320–321, 321f
augmenting, 626–628 functional testing, 208, 208f, 209f, 633–664
fracture callus in, 132f (rabbit) 6-minute walk test, 660
imaging of, 594–595 agility tests, 655–659
inflammatory phase of, 132f anaerobic step test, 662–663
milestones of, 132f balance reach tests, 642–644, 643f, 644t
remodeling phase of, 132f balance tests, 640–642
repartative phase of, 132f clinical testing compared, 664, 665t
in stress fracture, 139–140 environmental factors in, 637–638
Hill-Sachs, 593f excursion tests, 644, 645f
of hip foundations for, 636, 636f
avulsion fracture, 589f hop tests. See hop tests.
at femoral head, bone loss in women and, 306 individual factors in, 636–637
osteoporosis and, 142 initial examination in, 664–635
physeal fracture, 589, 590f jump tests, 653–655
of humerus lunge tests, 645, 646f
classification of, 610f Margaria-Kalamen power test, 661–662
displaced fracture, 592f measurement issue(s) in, 638–640
impacted, 594f measurement and standardization as, 638
insufficiency, 592–594 reliability and error of measurement as, 638–639
of long bones, 609, 609f, 610f sensitivity and specificity as, 639
management of, 607–632 validity as, 639–640
cast immobilization in, 612f, 613–614, 613f, 614t preparticipation examination in, 664
complications of, 630–632 principles of, 636–638, 636f
external fixation in, 617, 619t, 620f reexamination in, 635
intramedullary nailing in, 619t, 622–623, 622f return to activity in, 635–636
locking plates in, 619t, 621–622, 622f return to unrestricted activity, 663
nonoperative, 611–616, 611f, 612f–613f, 614f, 614t, 615f, step tests, 645–648, 647f
616f task-specific factors in, 637
open reduction and internal fixation (ORIF) in, 617–621, upper body power tests, 659–660
619t, 621f Wingate bike test, 660–661, 662t
operative, 616–623, 618f, 619t, 620f, 621f, 622f functional training, 486
percutaneous pinning in, 617, 619t, 620f function, defined, 633–634
in skeletally immature, 628–630, 628f, 629f, 630f, 630t, 631f fusiform system, 195
 Index 685

G growth plate (physis), 123f, 124, 124f

gait of acetabulum, 126f (rabbit)
of infants and toddlers, 290–291 fracture of, 589–590, 589f, 590f, 590t
physical activity and, 345 of long bones, 127t, 588f
gamma-amino-butyric acid (GABA), 230 types of, 126f
gap sign, 566t gymnastics, 352t
gardening and yard work, 351t
gate control theory, 222–223, 222f H
gender differences habitual movement, of synovial joint, 502
during adolescence. See adolescence (10–16). Halcion (triazolam), 261t
CDC growth charts, 286f, 287f, 288f, 289f half-life, 258
of infants and toddlers, 285 of nonbarbiturate sedative-hypnotics, 261t
and ligament injuries, 37–38 hamstring injury, 117f
ligaments and, 34–35, 34f handball, 353t
and limited physical activity, during early adulthood, 303 handgrip strength, performance changes with age, 310, 310f
in sensorimotor control, 208–209, 209f hands
gene therapy ossification centers of, 628f
in ligament injury treatment, 43–46, 43f, 44f, 45f, 46f osteoarthritis of, 606f
in treatment of muscle injuries, 116 plain film study of
genetic inheritance immature hand, 579f
in individualization principle, 361 mature hand, 580f
of individual muscle mass, 310 hard interfaces, nerve injuries due to, 182
genital development, in males, 301f Haversian bone, 130f
ginglymi (hinge) joints, 497, 498t, 499f healing imagery, 469–470, 469t
glenohumeral joint health promotion, wellness, and physical fitness, 328–356
arthrokinematics of, 494f, 505t benefits of, 337–348
capsular pattern of, 520t clinician’s role in, 336, 337t, 356
joint congruency of, 502t for disabled persons, 348
osteokinematics of, 505t economic costs of lack of, 330–332, 331t
glial cells, 230 motivation in, 356
gliding, as mobilization method, 521 and physiological changes associated with aging, 332–336
glucocorticoids. See corticosteroids. in workplace, 348–349
glutamate Health Related Quality of Life (HRQoL), 667, 671–672
in chronic tendinopathy, 66 health status, in individualization principle, 362
in pain perception, 229–230 “Healthy People 2010,” 330–331
glycogen, 434 heart
glycolytic pathway, 434, 435f age-related changes to, 333
glycoproteins diseases of. See cardiac disease.
dystrophin-glycoprotein complex, 101, 101f heart rate
in ligaments, 30, 30t age-related decline in, 308
glycosaminoglycan (GAG), 532–533. See also proteoglycans. in children, 301
in cartilage, 306 heart rate reserve method, of determining exercise intensity, 429, 429t
in tendons, 49, 306 heat
glycosylated hemoglobin levels, 297 following ligament injury, 41–42
goal setting, in injury rehabilitation, 466–467 in muscle injury treatment, 119t
gold sodium thiomalate (Aurolate), 270t, 271 height
golf, 352t CDC growth charts, 286f, 287f, 288f, 289f
Golgi ligament endings, 409t changes in
Golgi-Mazzoni corpuscles, 376t, 409t during childhood and adolescence, 294–295
Golgi tendon organ-like receptors, 191f, 192t, 193, 376t, 409t in infants and toddlers, 285
Golgi tendon organs, 193–194, 193f, 376f, 376t, 408, 535, 535f phases of, 296
gomphosis joints, 495 in preschoolers, 294
gonadotrophin-releasing hormone (GnRH), 299 hemagglutinating virus of Japan liposomes, 44f
G-protein, 177f hematoma formation, following muscle injury, 119t
grafting, in articular cartilage repair, 168 hemorrhage, following muscle injury, 114t, 119t
grooming horses, 353t Hick’s law, 197
gross instability, 398–399, 399f high-speed biplanar videoradiography system, 39–40, 40f
ground substance, 532, 535 hiking, 352t
immobilization affecting, 541–542, 541f hip, 501f
proliferation of, in muscle healing, 119t arthrokinematics of, 509t
remobilization and, 544, 544f capsular pattern of, 520t
in tendons, 48 fracture of
growth changes, 282–304. See also aging. avulsion, 589f
adolescence (10–16). See adolescence (10–16). and bone loss in women, 306
adulthood, early (18–40), 303–304 osteoporosis and, 142
childhood (6–9). See childhood (6–9). physeal, 589, 590f
diagnostic imaging affected by, 588–590 of infants and toddlers, 282–283
infants and toddlers (0–3). See infants and toddlers (0–3). joint congruency of, 503t
preschoolers (3–5). See preschoolers (3–5). loading-lubricating mechanisms of, 163, 164f
growth, concept of, 295 osteokinematics of, 509t
growth factors plain film studies of, 576f, 589f
in articular cartilage, 147–148 range of motion in, 539t
in ligament injury treatment, 42–46 rotation of, in preschoolers, 295
in treatment of muscle injuries, 116 hip strategy, 202
686 Index

hockey, field or rollerblade, 352t I

homeostasis principle, 361 ibandronate sodium (Boniva), 273t
home repair, 354t ibuprofen (Motrin), 268t
hookean body, 102f ice. See cold therapy.
Hooke’s law, 133 ice sailing, 353t
hopscotch, 353t ice skating, 353t
hop tests IGF-1, 116
for distance, 648–650 iliotibial band friction syndrome, 58, 59t
lateral hop test, 650, 651f immobilization
single hop test, 648–649, 648f, 649t articular cartilage affected by, 170–171
triple crossover hop test, 650, 650f, 650t bone affected by, 140, 541f
triple hop test, 649, 649f, 649t cartilage affected by, 170–171, 541f
multiple hop stabilization test, 653, 653t casting for, 612f, 613–614, 613f, 614t
for time, 651–652 joints affected by, 35, 541f
crossover test, 651–652, 652f joint stiffness after, 35
Functional Ability Tests (FAT), 652, 652t ligaments affected by, 35–36, 36f, 40–41, 41f (rabbit), 57, 541f
six-meter test, 651, 651f, 651t muscle affected by, 96, 105, 541f
stair hop (hopple) test, 652 with early intervention, 543f
horizontal or transverse plane, 488f, 489t following injury, 116, 118–119
hormones. See also specific hormone, e.g., thyroid hormone. with muscle lengthened, 542–543
ligaments and, 34–35, 34f, 37–38 with muscle shortened, 543
physical activity and, 347 of nerves, 188–189
skeletal muscle affected by, 308 and osteoarthitis, 40
and tendon injuries, 66 range of motion and flexibility reduced due to, 540–544, 541f,
horseback riding, 353t 542f, 543f
housework, 354t tendons affected by, 57, 58t
humeroulnar joint, 499f immune system, and tendon injuries, 66
humerus Imovane (zopiclone), 261t, 262
fracture of impairments, 666t
brace as management of, 612f Imuran (azathioprine), 270t, 271
classification of, 610f incongruent rotation, 491
displaced, 592f Inderol (propranolol), 442t
open reduction and internal fixation of, 621f individualization principle, 361–362, 367
supracondylar, in children, 630f, 631f Indocin (indomethacin), 267t
mechanical axis of, 490f indomethacin (Indocin), 267t
physeal centers of, 127t infants and toddlers (0–3), 282–293
plain films of, 574f, 592f body composition of, 285, 286f, 287f, 288f, 289f
tumor of, 574f cardiorespiratory system of, 284
Humira (adalimumab), 270t, 271 musculoskeletal problem(s) of, 291–293
hunting, 353t brachial plexus injury as, 293
hunting response, 245 developmental dysplasia of the hip as, 291–292, 292f
hyaline articular cartilage. See articular cartilage. torticollis as, 291, 292f
hydrocodone (Vicodin, Lorcet, Lortab, etc.), 266t musculoskeletal system of, 282–284, 291–293, 292f
hydrodynamic model, of joint lubrication, 162t nervous system, 284–285
hydromorphine (Dilaudid), 266t performance development of, 285–291
hydrostatic model, of joint lubrication, 162t physical growth and physiological development of, 282–285, 286f,
hydroxychloroquine (Plaquenil), 270–271, 270t 287f, 288f, 289f, 292f
hyperalgesia, 218, 218t, 219f inferior geniculate artery
hyperbaric oxygen therapy, 120–121, 251t anterior cruciate ligament supplied by, 26
hypermobility, 388–389, 514, 515–517, 522 lateral, 25f
hypermobility syndrome, 34–35, 37, 400 medial, 25f
hypertension inflammation
during adolescence, 297 in ligament injuries, 38
age-related, 309 in muscle injuries, 119t
during early adulthood, 303 neurogenic, 187–188, 228
physical activity and, 340 nociceptors sensitized by, 221f, 222f
hypoalgesia, 218t physical agents minimizing
hypomobility, 388, 389, 399f, 522 during acute phase, 240, 243–247
articular, 514 during reparative phase, 247–249, 248f
capsular pattern of, 519 sequalae of, 241–243
of lower quadrant, 520t in tendon injuries, 63f, 64–65
of spine, 520t infliximab (Remicade), 270t, 271
of upper quadrant, 520t infra-patellar tendon, 573f
joint fixation as, 514–515 inhalation, in drug administration, 257t
myofascial, 514 of corticosteroids, 281
noncapsular pattern of, 519–521 injury prevention, 473–474, 473f
passive mobility testing of, 504 muscle injuries, 118
pericapsular, 514 neuromuscular training program for, 384–385
hypothetico-deductive reasoning stretching in, 103, 371, 546–556, 548t–549t, 551t, 552f, 554f
as examination strategy, 318–319 injury proneness, 473–474
with multiple subsystems, 319–320, 319f inline skating, 352t
hypothyroidism, 308 insomnia, sedative-hypnotic agents for, 261–263
hysteresis response, 102–103, 103f instability, 389, 391–396, 515–517

articular, 515, 516f
clinical adaptations to, 402–403, 403t
effects of, 402
functional/biomechanical adaptations to, 403, 403t
involuntary, 400, 401f
ligamentous, 515
neurologic/motor adaptations to, 403, 403t
predisposing factors in, 400–402
signs and symptoms of, 401, 516t
subclinical adaptations to, 403, 403t
translational (atraumatic), 397–398
traumatic, 398–399, 399f
treatment of. See stabilization training.
types of, 396–400
voluntary, 399, 400f
instability jog, 398
instability pathway, 403, 403f
instability training. See stabilization training.
instantaneous axis of motion rotation, 493, 493f
instantaneous center of rotation, 493
integrin-associated complex, 101
integrins, 101, 101f, 115f
intensity, 433
intercarpal joints, 507t
interchondral joint, 513t
intercuneiform joints, 511t
interference principle, 368–369
interferential current, 233
intermittent claudication, 340
International Classification of Functioning, 666, 666t
interphalangeal joint (finger)
arthrokinematics of, 508t
capsular pattern of, 520t
joint congruency of, 502t
osteokinematics of, 508t
interphalangeal joint (toe)
arthrokinematics of, 511t
capsular pattern of, 520t
joint congruency of, 503t
osteokinematics of, 511t
interstitial lamellae, 130f
intervention model, 315, 316f
intervention plan
clinical pathways in, 326, 326f
expectation of, 315, 317t
formulation principles for, 325–327
strategies in, 323–324
intervertebral discs, 153–156
age-related changes to, 156
anulus fibrosus of, 145, 154–155
area beneath hyaline cartilage, 155f
composition of, 155–156
diagnostic imaging of, 600–601, 601f, 602f
innervation of, 156
nucleus pulpous of, 145–146, 154, 155
nutrition of, 155f, 156
vertebral end plate of, 155, 155f
intervertebral joints
arthrokinematics of, 513t
capsular pattern of, 520t
joint congruency of, 503t
osteokinematics of, 513t
in-toeing, in preschoolers, 294–295
intraarticular drug administration, 257t
intradermal (ID) drug administration, 257t
intramuscular (IM) drug administration, 257t
intranasal drug administration, 257t
intrathecal drug administration, 257t
intravenous (IV) bolus, 257t
intravenous (IV) drug administration, 257t
intravenous (IV) infusion, 257t
involuntary instability, 400
ion channels, in pain perception, 231
Index 687
ion pair formation, 257
iontophoresis
in chronic tendinopathy treatment, 71
following muscle injury, 119t, 120
ipratropium (Atrovent), 280–281
iron deficiencies, and tendon injuries, 66
isokinetic training, 448
isometric training, 311, 448, 448f
isotonic training, 448–449
J
Jobe relocation test, 566t
jogging, 352t
joint capsule
chondroitin sulfate changes affecting, 306
glycosaminoglycan content changes affecting, 306
immobilization affecting, 541f
ligaments in, 23–24
joint fixation, 514–515
joint hypermobility syndrome, 34–35, 37, 400
joint line tenderness test, 566t
joint play
mobilization and manipulation in pain treatment, 235–236
study of. See arthrokinematics.
joint position sense, 375–376
joint receptors, 191–193, 191f (cat), 192t, 375, 376–377, 376t
joints. See also specific joint, e.g., shoulder.
afferent fibers in, 221f, 221t
aging affecting, 305–306
cartilage of. See articular cartilage.
classification of, 494–495, 495t
diagnostic imaging of
in edema and effusion, 587t, 598–600, 600f
in periarticular injuries, 596–600
edema and effusion in, 587t, 598–600, 600f
fibrous capsule of, 156–157
innervation of, 157, 410f
intra-articular pressure of, 160, 160f
intra-articular temperature of, 160
lubrication of, 161–164
exercise and, 163–164
of hip joint, 163, 164f
mechanisms of, variables in, 162t
models for, 162t
mobilization of, 521
cautions and contraindications for, 525
cellular level effects of, 523t
grading of, 521–523, 521t
passive mobilization, 521t
postulated effects of, 524t
reliability of, 523–525
techniques for, 521, 521t
nonsynovial, 495, 495t
surfaces of
range of motion limited by, 529–530, 529t
roughness of, in joint lubrication, 162t, 163
surface compliance (elasticity) in joint lubrication, 161–163, 162t
synovial. See synovial joints.
synovial lining tissues of. See synovium.
joint stiffness
after immobilization, 35
age-related changes causing, 306
sensorimotor control of, 201–202
joint tissue
collagen in, 148, 148t, 149t
mobilization affecting, 523t
judo, 352t
juggling, 353t
jujitsu, 352t
jumping
Achilles tendon, effect on, 61f
tendon forces and stresses during, 56t
on trampoline, 352t
688 Index

jumping jacks, 352t, 353t levorphanol (LevoDromoran), 266t

jumping rope, 351t, 352t, 353t lidocaine (Xylocaine), 279t
jump tests, 653–655 life span concerns. See aging.
horizontal, 655, 656f, 656t ligament creep, 33, 33f
vertical, 653–655 ligament injuries, 23–46, 37
bilateral, 653–655, 654t blood supply affected by, 27
unilateral, 655, 655t diagnosis of, 39–40
jump training, 382, 384–385, 385t, 449–450 endoscopic laser speckle perfusion imaging in, 39, 39f
juvenile rheumatoid arthritis, 606f imaging in, 587t
first-time injuries, 37
K gender-specific factors in, 37–38
karate, 352t grade I, 36, 37
kayaking, 353t grade II, 36, 37
ketoprofen (Orudis), 268t grade III, 36–37
ketorolac (Toradol), 267t grading of, 36–37
kickball, 352t innervation affected by, 27
kicking, 56t load-sharing patterns following, 32f
kinematic chain mechanisms of, 36–37
definition of, 477t phases of healing in, 38–39
kinematics, 488, 489t scar tissue formation, 38–39
arthro-. See arthrokinematics. exercise affecting, 41
osteo-. See osteokinematics. ice and heat affecting, 41–42
Kineret (anakinra), 270t, 271 immobilization affecting, 40–41, 41f (rabbit)
kinesthesia, 199–201, 375–376 surgical repair affecting, 42
kinetic chain and secondary ligament injuries, 36–37
definition of, 477t second-time injuries, 37
increasing capability, 485 treatment of
stresses and, 476–486 effects of, 40–42
kinetics, 488, 489t exercise during, 41
kinetic tests, 503–504 gene therapy in, 43–46, 43f, 44f, 45f, 46f
Klumpke’s palsy, 293 growth factors in, 42–46
knee ice and heat during, 41–42
blood supply to, 25–26, 25f immobilization as, 40–41
capsular pattern of, 520t surgical repair as, 42
clinical decision rules for, 579–582, 587t surgical replacement as, 42
joint congruency of, 503t ligaments, 23–27. See also specific ligaments e.g., anterior cruciate
kinematics and kinetics of, 212f ligament (ACL).
ligaments of, 24f, 25–26, 25f adhesions of, hypomobility due to, 519
magnetic resonance imaging of, 598, 598f aging affecting, 33–34, 34f
perturbation device for, 206f anatomy of, 23–24, 24f
plain film studies of, 577f biochemical composition of, 29–30, 30t
range of motion in, 539t biomechanical behaviors of, 30–33
kneel-sitting, 290 material (stress-strain) behavior, 30
kneel-standing, 290 structural (load-deformation) behavior, 30, 31–32, 31f, 32, 32f
kyphosis, in infants, 282, 290 viscoelastic (relaxation and cyclic loading) behavior, 30
blood supply to, 25–27, 25f, 26f (rat), 27f (rabbit)
L cellular matrix of, 28f (rabbit), 29
labetalol (Normadyne), 442t chondroitin sulfate changes affecting, 306
labrum, 153–154, 496t definition of, 23
superior labral anterior-posterior (SLAP) lesion, 565t exercise affecting, 35–36
tear of, 587t extracellular matrix of, 29
Lachman test, 37, 566t as feature of synovial joint, 496t
lacrosse, 352t functional subunits of, 23, 24f
lactic acid, 434 function(s) of, 24–25
lamellae, 130f joint stabilization as, 24
larynx, of infants and toddlers, 284 passive guidance of bone position as, 24
LASER, low power, 251t sensory, 24–25
lateral collateral ligament (LCL), 24f shared, 24
blood supply to, 27f (rabbit) glycosaminoglycan (GAG) content changes affecting, 306
femoral attachment of, 26f (rat) immobilization affecting, 35–36, 36f, 40–41, 41f (rabbit), 57,
meniscal attachment of, 26f (rat) 541f
lateral hop test, 650, 651f injuries of. See ligament injuries.
lateral superior geniculate artery, 25f innervation of, 25–27
laxity, 389 material (stress-strain) behavior of, 30
of ligaments, 41 microscopic and ultrastructural organization of, 27–36
lean body mass morphologic zones at insertion, 25f, 29, 30f
in adolescents, 296 pericellular matrix of, 28f (rabbit), 29
detraining affecting, 96 as proprioceptors, 24–25
during middle age and old age, 309, 309f shared functionality of, 24
lean leg volume, 302 structural (load-deformation) behavior of, 30, 31–32, 31f, 32, 32f
leflunomide (Arava), 270t, 271 vesicle-filled seams of, 28f (rabbit), 29
levobupivacaine (Chirocaine), 279t viscoelastic (relaxation and cyclic loading) behavior of, 30, 33, 33f
levodopa, 279–280 light-to-heavy system, 454
 Index 689

ligmento-muscular protective reflex, 376 Matles sign, 566t

line dancing, 352t matrix metalloproteinases, 147
line drill test, 656–658, 657f maturation, concept of, 295
Lioresal (baclofen), 275–276, 276t maximal oxygen consumption (VO2max)
lipohemarthrosis, 587t age-related decline in, 308, 308f, 312
load during childhood, 301–302
articular cartilage affected by, 170, 171 exercise increasing
of cortical bone, 133, 133f aerobic exercise, 93
load deformation in age-related decline in VO2max, 308
of ligaments, 30, 31–32, 31f, 32f of preschoolers, 294
and tissue stiffness, 482, 482f MCL. See medial collateral ligament (MCL).
load-deformation curve, 537–538, 537f McMurray test, 566t
of cortical bone, 133–134, 133f, 135f mean power, of children and adolescents, 302
toe region of, 32 Mebaral (mephobarbital), 262t
load deprivation. See immobilization. mechanical axis, 489, 490f
loading/unloading principle, 361, 367, 369, 369f, 374 mechanical bone competence, 136
local anesthetics, 277–278, 279t mechanical loading, 57, 58t
locked position, of synovial joint, 501–502 mechanical pain threshhold, 219f
locomotion. See ambulation. mechanoreceptors, 190–196, 375–377, 376f, 376t
Lodine (etodolac), 267t cutaneous receptors as, 195–196, 196f, 375
longitudinal or vertical axis, 488f, 489t joint receptors as, 191–193, 191f (cat), 192t, 375, 376–377, 376t
long-loop reflexes, 197, 197t, 376t of ligaments, 25, 27
loose packed position, of synovial joint, 502, 502t, 503t muscle receptors as, 193–195, 193f, 194f, 195f, 196f, 375,
Lopressor (metoprolol), 442t 376–377, 376t
Lorcet (hydrocodone), 266t “mechanostat hypothysis,” 136
Lortab (hydrocodone), 266t meclofenamate (Meclomen), 268t
loss of function, treatment of, 247 Meclomen (meclofenamate), 268t
lower extremities. See also specific structure, e.g., Femur. medial collateral ligament (MCL), 24f
and age-related muscle loss, 310–311 blood supply to, 26–27, 27f (rabbit)
plain film studies of, 578f, 596f, 624, 624f cellular matrix of, 28f (rabbit)
resistance training for, 456t decorin antisense gene therapy for, 43, 45f (rabbit), 46f (rabbit)
lunges, 456 functional subunits of, 24f
lunge tests, 645, 646f gross appearance of, 25f (rabbit)
lungs. See pulmonary system. immobilization affecting, 41, 41f (rabbit)
lutenizing hormone, 299 innervation of, 27
lymphatics surgical reapposition of, 42
microanatomy of, 248f medial superior geniculate artery, 25f
primary, 248, 248f median plane, 489t
secondary, 248–249, 248f medicine ball training, 450–451, 451t
lymph capillaries, 248, 248f mefenamic (Ponstel), 268t
lytic bone metastasis meloxicam (Mobic), 268t
CT and MRI of, 603f men. See gender differences.
plain film study of, 585f menisci, 153–154, 496t
chondrocytes in, 145
M diagnostic imaging of, 587t
macrocycle, in periodization principle, 373–374 diagnostic tests of, 565t
magnesium ion, 177f of knee, magnetic resonance imaging of, 598, 598f
magnetic resonance imaging, 570–571, 586t menopause, bone loss during, 305
of Achilles tendon tear, 572f menstrual cycle, joint and ligament laxity during, 35
in cartilage breakdown, 166 mental function
common structures on, 572t age-related changes in, 336
of intervertebral discs, 600–601, 601f, 602f physical activity and, 347
of knee, 598, 598f mental imagery, in injury rehabilitation, 468–471, 469t
of periarticular injuries, 597 mental skills and activities, in injury rehabilitation, 466–471
of shoulder, 598 goal setting in, 466–467
of slipped capital femoral epiphysis, 571f mental imagery in, 468–471, 469t
of spine, 600–601, 601f positive self-talk and attitude in, 467–468, 467t
of stress fracture, 624–625, 624f relaxation in, 468, 468t
of tumors, 604, 605f mephobarbital (Mebaral), 262t
mail carriers, 355t mepivacaine (Carbocaine, Polocaine), 279t
maintenance principle, 360–361, 367, 368f merperidine (Demerol), 266t
malingering and secondary gains, 474–475, 475t mesocycles, 369, 374, 452
manipulation, 70, 521 mesoneurium, 177f
manual therapy metabolic energy stores, 438t
joint play mobilization and manipulation as type, 235–236 metabolism
massage as, 235, 251t of drugs and medicines, 258
in pain treatment, 235 general scheme of, 433f
Maolate (chlorphenesin), 276t metabrotrophic receptor, 177f
Marcaine (bupivacaine), 279t metacarpal fracture, 584f
marching band, playing in, 353t metacarpophalangeal joint
Margaria-Kalamen power test, 661–662 arthrokinematics of, 508t
masonry work, 355t capsular pattern of, 520t
massage therapy, 235, 251t joint congruency of, 502t
690 Index

metacarpophalangeal joint (Continued) mountain climbing, 352t

osteokinematics of, 508t movement
second, 496f axis of, 489t
metaphysis, 123f, 124f, 588f barriers to, 389–390, 389f
metatarsophalangeal joint anatomic, 390
arthrokinematics of, 511t pathologic barriers, 390–391, 390f
capsular pattern of, 520t physiologic barriers, 390
joint congruency of, 503t dysfunction of, and instability, 402
metatarsus adductus, 295 planes of, 487–488, 488f, 489t
metaxalone (Skelaxin), 276t sensorimotor control of, 203, 204f
methadone (Dolophine), 266t multifaceted training, 382–384
methocarbamol (Robaxin), 276t multiple crush syndrome, 187
methotrexate (Rheumatrex), 270, 270t multiple hop stabilization test, 653, 653t
methylprednisolone, 263t multiple sclerosis, 346–347, 346f
metoprolol (Lopressor), 442t multiple-set program, 454
Miacalcin (calcitonin), 273t, 274 multi-poundage system, 454
microcycles, 369, 369f, 374, 452 muscle, 80f
micro-elastohydrodynamic model, of joint lubrication, 162t afferent fibers in, 221t
midcarpal joints, 507t age-related changes to, 333–334
middle age, 305 fatigue as, 312
body composition during, 309, 309f and muscle injuries, 311–312
older, 305 muscle loss as, 307–308
osteoarthritis associated with, 306, 307f performance declines with, 309–312
osteoporosis associated with, 305–306, 306f strength loss compared to, 311
middle geniculate artery, 25f, 26 anatomy of, 97–102
midtarsal joints, 520t connective tissue, 98f
mitochondrion, 82f, 114t contractile elements, 99–100, 534–535, 535f
mixed (fluid film and boundary) model, of joint lubrication, 162t microanatomy, 81–83, 82f, 83f, 84f
Mobic (meloxicam), 268t myotendinous junction, 48, 48f (frog), 100–102, 100f (frog), 102f
mobilization ultra-anatomy, 79–81, 80f, 81f
articular. See joints, mobilization of. calcium storing/releasing network within, 81, 82f
in chronic tendinopathy treatment, 70 contractions of. See muscle contraction.
controlled decreased use of, 95–96
as impairment classification, 322 in detraining, 95–96
in muscle injury treatment, 118–119 in immobilization. See immobilization.
distraction as method of, 521 deformation and recovery of, 102–107
gliding as method of, 521 age as factor in, 105
as impairment classification, 321–322 flexibility as factor in, 103–105
mobilizer muscles, 394–396, 395t temperature as factor in, 105–106, 106f, 546, 546f
modeling, in injury rehabilitation, 463–465 tissue properties as factor in, 102–103, 102f, 103f, 104f
moderate-to-vigorous physical activity, 303 diagnostic imaging of, 587t
modern dancing, 352t edema of, 587t
monosynaptic muscle stretch reflex, 194, 195f fatigue of
morbidity, physical activity and, 338 age-related, 312
morphine, 266t in hamstring injury, 117f
mortality, physical activity and, 338 fiber types in. See muscle fiber.
motion analysis studies, 207, 207f function of, 83–86
motion barrier to movement, 390 hormonal effects on, 308
motor and skill development increased use of, 87–93
detraining affecting, 96 in aerobic training, 93–95
of infants and toddlers, 285–290 in anaerobic training, 87–93
of preschoolers, 294 resistance training, 87–92
motor control training. See stabilization training. sprint and interval training, 92–93
motor cortex, somatotopic organization of, 199, 200f injuries of. See muscle injuries.
motor homunculus, 199, 200f loss of. See also sarcopenia.
motor nerve fibers, 191f age-related, 307–308
motor programs theory, on motor control, 378 performance declines with, 309–312
motor skills strength loss compared to, 311
classification of, 378–379 microanatomy of, 81–83, 82f, 83f, 84f
closed, 379 mobilizer, 394–396, 395t
continuous, 378 organization of, 79–81, 80f
discrete, 378 relaxants of, 275–277, 276t
development of sensorimotor control of, 84–86, 87f, 201–202, 201f, 205–207,
external feedback in, 380 206f, 211–212, 211f
factors influencing and enhancing, 379–380 stabilizer, 394–396, 395t
practice conditions affecting, 379–380 structure of, 79–83, 80f
stages of, 379 ultra-anatomy of, 79–81, 80f, 81f
fine, 303 muscle activity pattern
open, 379 assessment of, 205–207, 206f
motor units, 84–86, 87f injury affecting, 211–212, 211f
activation of, 302 muscle contraction
age-related changes to, 309 adenine nucleotides in cross-bridge cycling, role of, 84, 85f
Motrin (ibuprofen), 268t concentric, 445, 445f
 Index 691

eccentric, 445, 446f myofibrillar adenosine triphosphate (mATPase), 438–439, 439f, 440f
econcentric, 445–448, 447f myofibrils. See muscle fiber.
endurance and, 106–107, 107f, 484 myosin filaments, 82, 83f
regulation of, 84, 86f myotendinous junction, 48, 48f (frog), 100–102, 100f, 101f, 102f
sliding filament theory of, 83–84, 84f following muscle injury, 115f
in stabilization, 396 injuries near, 107–109, 108f, 109f (rabbit)
strength and, 106–107, 107f, 444, 444f myotubules, 114t
types of, 445
voluntary, tendon forces and stresses during, 56t N
muscle fiber, 79, 80f, 82f, 98, 99f (frog) nabumetone (Relafen), 268t
of adolescents, 296 nadolol (Corgard), 442t
age-related loss of, 307 nalbuphine (Nubain), 266t
detraining, effect of, 95 Nalfon (fenoprofen), 268t
hypertrophy of, 307–308 naproxen (Naprosyn), 268t
Type I (slow-twitch), 84–86, 87t, 437 naproxen sodium (Anaprox), 268t
Type II (fast-twitch), 84–86, 87t, 437 Naropin (ropivacaine), 279t
types of, 84–86, 87t, 439f narrowing the problem space, 317
muscle function, 483–484, 483f Nautilus weights, 352t
muscle injuries, 97–121 Nembutal (pentobarbital), 262t
age-related, 311–312 nerve cells, 301
clinical implications of, 117–121, 119t nerve fibers, 175–177, 176t
diagnosis, 117–118, 119t nervous system
rehabilitation and intervention, principles of, 118–121 age-related changes to, 309, 335
continuum of, 109–111, 109f (rabbit), 109t central. See central nervous system.
hyperbaric oxygen therapy for, 120–121 of infants and toddlers, 284–285
location of, 107–109 intervertebral disc supplied by, 156
mechanism of, 117, 117f mobilization affecting, 523t
of muscle belly, 107, 109f (rabbit), 111f (rabbit) neurodynamics of, 181–184
pathophysiology of, 107–109, 108f peripheral. See peripheral nerves.
rehabilitation and intervention, principles of, 118–121 Nesacaine (chloroprocaine), 279t
controlled mobility and activity vs immobility and rest, 118–119 neurapraxia, 184t
pain as guiding factor, 120 neurodynamic barrier, to movement, 39
prevention vs treatment, 118 neurodynamics, 181–184
SAID principle, 120 mechanical continuum in, 181–182
strong flexible tissue, 120 neural tissues, non-neural tissues in relation to, 182
repair and regeneration of, 109–116, 112f, 114t representation of nerve injury in, 181–182
age-related reduction in, 311–312 of sympathetic nervous system, 183–184
destruction in, 111, 113f neuroma, 185f
healing and remodeling in, 111–116 neuromuscular control. See sensorimotor control.
stages of healing, 119t neuromuscular system, 375–387
shearing, 112f, 113f in fitness principle, 359
surgical intervention for, 121 injury processed by, 377, 377f
tear, 587t mobilization affecting, 523t
threshold in, 109–111, 109f (rabbit) physical activity and exercise affecting, 344–347
muscle mass neuromuscular training program, 381–387
during adolescence, 296 evaluation in, 381
loss of. See also sarcopenia. implementation of, 384–387
age-related, 307–308, 308f, 311 for lower extremity injury prevention, 384–385
muscle strength loss compared to, 311 for rehabilitation, 385–387
muscle movement speed, 311 limiting factors in, 381
muscle reaction time, 303 for lower extremity injury prevention, 384–385
muscle receptors, 193–195, 193f, 194f, 195f, 196f, 375, methods in, 381–384
376–377, 376t balance training as, 382, 383f
muscle relaxants, 275–277, 276t multifaceted training as, 382–384
muscle spindle, 193, 193f, 194, 194f, 376f, 376t, 408, 535f perturbation training as, 382
muscle stiffness, 97–98 plyometric training as, 382, 384–385, 385t
during childhood and adolescence, 303 technique training as, 382
in passive tension, 99–100 neurons, 175
muscle strength. See strength. neuropeptides, 228–230
muscle-tendon junction, 48, 48f (frog), 100–102, 100f, 101f, 102f neurophysiology, articular, 190–196
following muscle injury, 115f mechanoreceptors in, 190–196
injuries near, 107–109, 108f, 109f (rabbit) somatosensory system in, 190, 191f
musculoskeletal system neurotmesis, 184t
of adolescence (10-16), 288f, 289f, 296 neurotransmitters
age-related changes to, 333–334 adenosine as, 231
of childhood (6-9), 288f, 289f, 295 GABA (gamma-amino-butyric acid) as, 230
examination and evaluation, as consideration during, 319–320, glial cells and, 230
319f, 320f ion channels and, 231
of infants and toddlers (0-3), 282–284, 291–293, 292f neuropeptides as, 228–230
physical activitiy and exercise, effect of, 341–344 norepinephrine as, 230–231
of preschoolers, 293 in pain perception, 228–231
myelin sheath, 176f combination therapies in, 231
myofiber-extracellular matrix (ECM), 101f glial cells and, 230–231
692 Index

neurotransmitters (Continued) optimization principle, 360–361, 360f, 369

neuropeptides in, 228–230 oral administration of drugs, 255–256, 257t
norepinephrine as, 230–231 organ of Corti, 335
in peripheral nerve fibers, 177f orphenadrine (Norflex), 276t
serotonin as, 230 orthotics, 71
neutral zone, in range of motion, 389, 389f, 514 Ortolani sign, 292
and motor control deficits, 517f Orudis (ketoprofen), 268t
with passive movement or stability testing, 518f Osgood-Schlatter disease, 629, 629f
newtonian body, 102f ossification
night pain, 566t during adolescence, 299
nitrates, 280 in infants and toddlers, 282
nociception, 219–220 primary center of, 123f
nociceptor, 218t, 221f, 224f secondary center of, 123f
node of Ranvier, 176f osteoarthritis (OA), 40
nonlinear structural behavior, 31 age-related, 306, 307f
nonopioid analgesics, 267–269, 267t–268t cartilage breakdown in, 165, 166, 306, 307f
adverse effects of, 269 diagnostic imaging of, 604–606, 606f
mechanism of action of, 267–269 ligament injuries and, 24
nonsteroidal anti-inflammatory drugs. See nonsteroidal anti- physical activity and exercise affecting, 343
inflammatory drugs (NSAIDs). sensorimotor control and, 214–216, 215f
selection of, 269 osteoarthrosis. See osteoarthritis (OA).
nonsteroidal anti-inflammatory drugs (NSAIDs), 267t–268t. See also osteogenesis imperfecta, 49, 51t
specific drugs, e.g., piroxicam (Feldene). osteokinematics, 489–492, 494
adverse effects of, 269 of lower limb joints, 509t–511t
in chronic tendinopathy treatment, 71 of midline joints, 512t–513t
following muscle injury, 116, 119, 119t of upper limb joints, 505t–508t
mechanism of action of, 267–269 osteokinematic spins, 490, 490f
for rheumatoid arthritis, 270 osteokinematic swings, 490, 490f
selection of, 269 osteoporosis, 142–143, 272
tendon dysfunction associated with, 58t age-related, 305–306, 306f, 334–335
nonsynovial joints (synarthroses), 495 economic costs of, 332
norepinephrine, 230–231 exercise and, 143
Norflex (orphenadrine), 276t loss of height with, 306
Normadyne (labetalol), 442t medications for, 272–275, 273t
Novocaine (procaine), 279t anabolic agents, 273t, 274–275
NSAIDs. See nonsteroidal anti-inflammatory drugs (NSAIDs). antiresorptive agents, 273–274, 273t
Nubain (nalbuphine), 266t otic administration of drugs, 257t
nuclear medicine imaging, 573–574, 573f, 586t Ottawa Ankle Rules, 582–586, 587t
bone scans, 573–574, 573f, 586t, 604, 624 Ottawa Knee Rules, 582, 587t
positron emission tomography, 574, 586t outcome measures, 665–674
Numorphan (oxymorphone), 266t with demonstrated ability to detect change, 67t
nutrient cavity, of developing bone, 124f measurement choices in, 670–672
nutrition, and stress fracture, 624 measurement properties in, 667–670, 668t
reliability in, 667–669, 668t
O theoretical foundations for, 666–667
OA (osteoarthritis). See osteoarthritis (OA). treatment effectiveness compared, 672
obesity validity in, 668t, 669–670
during childhood, 297 out-toeing, 294–295
during early adulthood, 303 overload principle, 362–363, 362f, 369
economic costs of, 332 overstretch weakness, 391
oblique popliteal ligament, 25f overtraining, 370
old, 305 overtraining principle, 361, 367, 369–370, 370f, 374
old age ovoid of motion, 492, 492f
body composition during, 309, 309f ovoid or spheroid joints, 497, 498t, 499f
exercise during modified or condyloid shape, 497, 498t, 501
aerobic capacity increased, 312 unmodified or ball-and-socket shape, 497, 498t, 499–501, 501f
barriers to, 349 oxaprozin (Daypro), 268t
diabetes and, 313 oxicams, 268t
maximal oxygen consumption (VO2max), decline in, 308 oxycodone (Oxycontin, Percocet, Tylox), 266t
physical changes with, 305–309 oxygen energy system, 434–436
old-old, 305, 338–339 oxymorphone (Numorphan), 266t
oligodeoxynucleotides, 43, 43f
Olympic lift, 449 P
one-arm hop test, 660 Pacinian corpuscles, 191f, 192t, 193, 376t, 409t
open chain, 477t packing boxes, 355t
open ion channels, 177, 177f paddle boating, 353t
open-loop control, 377, 378f PAG-RVM pathway in inhibition of pain, 226, 232f
open motor skills, 379 pain
ophthalmic administration, of drugs, 257t acute, 217
opioid analgesics, 229, 264–267, 266t of low back, diagnostic imaging in, 588
adverse effects of, 265 physical agents for, 246–247
agonist/antagonists, 265–267, 266t associated with tendon injuries, 64t
agonists, 265, 266t in chronic tendinopathy. See tendinopathy, chronic.
antagonists, 267 chronic, 217
mechanism of action, 264–265
 Index 693

cognitive-evaluative component of, 217 fracture of, 586f

control of. See pain control. of infants and toddlers, 282
cutaneous, 219 plain film studies of, 575f, 586f
deep tissue, 218–219 stabilizer and mobilizer muscles of, 395t
definitions of, 218t subtalar joint motion and, 482, 482f
factors involved in reporting of, 217, 218f pentazocine (Talwin), 266t
modern concepts in, 184 pentobarbital (Nembutal), 262t
motivational-affective component of, 217 peratendon, 52, 53f
muscle, 218–219 percent body fat
in muscle strain injuries, 120 detraining and, 96
from neural connective tissue, 178 of infants and toddlers, 285
neurobiology of, 220–231 percent body mass, 296
central pathways in, 222–225, 222f, 223f, 224f Percocet (oxycodone), 266t
descending pathways in, 225–228, 225–231, 226f, 227f periosteum, 123
gate control theory, 222–223, 222f performance
neurotransmitters in, 228–231 of balance and gait, 290–291
peripheral pathways in, 220–222, 221f, 221t, 222f development of
thalamus and cortex in, 225 during adolescence, 301–303
neurotransmitters and during childhood, 301–303
combination therapies in, 228–231, 231 of infants and toddlers, 285–291
glial cells and, 230–231 of preschoolers, 294
neuropeptides in, 228–230 flexibility and, 546–550
norepinephrine in, 230–231 of motor skills
at night, 566t of infants and toddlers, 285–290
in passive articular mobilization, 521t of preschoolers, 293
perception of, 217–237 resistance training compared to aerobic training, 438t
referred, 218t stress and, 473f
residual, 251–252 performance-based measures, 317–318
sensory-discriminative component of, 217 performance imagery, 469t, 470–471
treatment of. See pain control. performance principle, 357–358, 359f, 360, 367, 373, 374
pain control periaqueductal gray, 226
non-pharmacological, 231–237 perichondrial ring, 125f
in acute pain, 246–247 perimysium, 79, 80f, 98, 98f
education in, 236–237 perineurium, 177f, 178f
electrical stimulation in, 232–233, 232f periodization, of resistance training, 451–453, 452f, 452t
exercise in, 236 periodization principle, 360, 362, 367, 369, 373–374, 373f
manual therapy in, 235 periosteum, 123f, 124f, 130f
residual pain, 251–252 peripheral heart action program, 454
thermal modalities in, 234–235 peripheral nerves, 175–189
pharmacological, 264–269, 266t, 267t–268t age-related changes to, 335
nonopioid analgesics in. See nonopioid analgesics. blood supply to, 177, 178f, 179
opioid analgesics in. See opioid analgesics. connections with central nerves, 179–180
painful arc test, 566t connective tissue of, 178
pain-reducing imagery, 469t, 470 healing potential of, 188
pantendinopathy, 64t injury to, 184–185
Paraflex (chlorzoxazone), 276t categories of, 184–185, 184t
paratendinopathy, 64t healing potential of, 188
paratenonitis, 64t inflammation causing, 187
parathyroid hormone, 273t, 274–275 mechanical trauma causing, 186–187
parenteral route, of drug administration, 256, 257t at nerve branches, 182
Parkinson’s disease sequelae of, 187–188
medications for, 279–280 vulnerability of, 182–183
physical activity and exercise affecting, 345–346 multifascicular, 178, 178f
participation, 666t nerve fibers, 175–177, 176f, 176t
participation restrictions, 666t nerve trunk, 177, 177f
passive accessory intervertebral movement, 514 neurophysiology of, 180–181, 180f
passive accessory motion, 488, 504 pain perception via, 220–222, 221f, 221t, 222f
passive diffusion, of drugs and medicines, 256 structural variations in, 177–178
passive intervertebral movement, 514 vulnerability of, 182–183
passive mobility tests, 504–514, 505t–508t, 509t–511t, 512t–513t peripheral resistance, age-related increase in, 309
passive physiological intervertebral movement, 514 peripheral vascular disease, 313
passive physiological motion, 504 peritendon, 52, 53f
patellar tendon perturbation training, 382, 385–387, 386t
chronic tendinopathy of, 73 perturbed homeostatic systems, 188
forces and stresses to, 56t phagocytosis, 113f, 114t, 119t
rupture of, 60 Phalen test, 566t
patellofemoral joint, 509t pharmacodynamics, 255, 258–261
patient care, 355t mechanisms of drug action, 259–260
pattern recognition, 318 pharmacokinetics, interrelationship with, 256f
Pavlik harness, 292, 292f pharmacokinetics, 255, 256–258
peak height velocity, 296, 299 absorption as component of, 256–257
peak performers, characteristics of, 472, 472t distribution as component of, 258
peak power, 302 elimination and excretion as component of, 258
pelvis metabolism as component of, 258
694 Index

pharmacodynamics, interrelationship with, 256f of knee, 577f

pharmacology, 255–281. See also drugs and medicines. of leg, 578f, 596f, 624, 624f
definitions in, 255 of pelvis, 575f, 586f, 589f
pharmacotherapeutics, 255 of periarticular injuries, 597
phenobarbital (Barbita), 262t of shoulder, 582f, 585f, 593f
phenylbutazone (Butazolidin), 268t of spine, 575f–576f, 581f, 600
phonophoresis of thumb, 591f
in chronic tendinopathy treatment, 71 of wrist, 583f, 594f, 597f
following muscle injury, 119t, 120 planar joints, 498t, 501, 501F
physical activity plane joint, 496
during adolescence, 297–299 planes of motion, 487–488, 488f, 489t
insufficient, 299t plan of care, 323
moderate or vigorous, 298t plantaris tendon, 53
in physical education classes, 298t Plaquenil (hydroxychloroquine), 270–271, 270t
benefits of, 337–348 plastic deformation, 390, 608, 609f
to burn 150 kcalories, 351t plastic flow, 390
decreases in plastic zone, in range of motion, 389f, 390
during childhood, 297–299, 298t, 299t, 303 plyometric training, 382, 384–385, 385t, 449–450
during early adulthood, 303 polo, 353t
exercise as form of. See exercise. Polocaine (mepivacaine), 279t
level of intensity of, 352t–355t Ponsetti method, in congenital clubfoot treatment, 293
return to Ponstel (mefenamic), 268t
following stabilization training, 413 pontine nuclei, 227
during rehabilitation, 471–472 Pontocaine (tetracaine), 279t
Physical Activity Readiness Questionnaire, 416t–417t popliteal artery, 25–26, 25f
physical agents position tests, 503
acute injuries, management of, 243–247, 243t positive self-talk and attitude, in injury rehabilitation, 467–468, 467t
in acute pain management, 246–247 positive testing, 318, 321
cold therapy as type. See cold therapy. positron emission tomography (PET), 574, 586t
compression. See compression, therapeutic. posterior articular nerve, 26
cryotherapy as type. See cryotherapy. posterior cruciate ligament (PCL), 24f, 598, 599f
diathermy, 234–235, 251t posterior half, 488f
edema and effusion, minimizing, 244–246 postural muscles, age-related loss of, 311
electrical stimulation as type. See electrical stimulation. postural stability
elevation as type, 243t injury affecting, 210–211
for inflammation sensorimotor control of, 202–203, 203f, 375
acute phase, during, 239, 243–244 testing of, 205, 205f
reparative phase, during, 247–249, 248f, 250–252 potency, of drugs and medicines, 260
LASER, 251t power, 432, 433
for loss of function, 247 power lift, 449
massage therapy as, 235, 251t power tools, operating, 355t
physiological basis of, 238–254 predisposition to disease, age-related, 312–313
reparative phase, during, 247–252 prednisolone, 263t
common modalities in, 251t prednisone, 263t
disuse, minimizing sequelae of, 249–250, 253–254 pregnancy
inflammation, remnants of, 247–249, 248f diagnostic imaging during, 574
physiological problems and goals in, 247–250 exercise and resistance training during, 442–443
promoting repair and regeneration, 249, 252 ligaments influenced by, 35
secondary injury, minimizing, 243–244, 244f ligaments injuries during, 37
ultrasound as type. See ultrasound, therapeutic. premature closure, of examination, 321
physical fitness, 329. See also health promotion, wellness, preparation principle, 365, 371
and physical fitness. preschoolers (3-5), 293–295
components of, 359f body composition of, 294
in stabilization training, 412 cardiorespiratory system of, 294
physiological active motion, 488 motor and skill development of, 294
physiological passive motion (PPM), 488 musculoskeletal system of, 293
physis (growth plate). See growth plate (physis). performance development of, 294
pindolol (Visken), 442t physical growth and physiological development of, 293–294
piroxicam (Feldene), 116, 268t resistance training for, 441t
Pittsburgh Decision Rules, for knee trauma, 579, 587t pressure
pivot (trochoid) joint, 497, 498t, 499f blood
pivot shift test, 566t during activity, 420f
plain film studies, 569–570, 569f, 574–577 beta-blockers affecting. See beta-blockers.
of ankle, 581f, 591f in children, 301
of bone tumors, 585f, 604 endoneurial fluid, 181, 185, 186f
of calcanus, 570f, 589f intra-articular, 160, 160f
of cervical spine, 575f–576f pressure gradient, 185, 186f
of elbow, 575f, 594f, 595f pretest, 557–558
of foot, 577f prevention of injury, 473–474, 473f
of forearm, 579f muscle injuries, 118
of hand, 579f, 580f neuromuscular training program for, 384–385
of hip, 576f, 589f stretching in, 103, 371, 546–556, 548t–549t, 552f, 554f
of humerus, 574f, 592f PRICEMM, 66
 Index 695

prilocaine (Citanest), 279t capsular pattern of, 520t

primary injuries, 240 joint congruency of, 502t
procaine (Novocaine), 279t osteokinematics of, 506t
procedures, of clinician, 473 proximal, 499f
procollagen, 532, 532f–533f radius
prognoses, 323 fracture of, 621f
progression principle, 363 physeal centers of, 127t
progressive velocity flexibility program, 544, 544f rafting, whitewater, 353t
proliferative zone, 125f raking leaves, 351t
propionic acids, 268t raloxifene hydrochloride (Evista), 273t
proportional contribution, 320, 321f range of motion, 514. See also flexibility.
proportional limit, 133, 134f definition of, 527–529
propoxyphene (Darvon, Darvocet), 266t elastic zone in, 389f, 390
propranolol (Inderol), 442t end range of, 530t
proprioception, 199–201, 375–376. See also sensorimotor control. flexibility compared, 527–528
proprioceptive acuity hypermobile. See hypermobility.
gender differences in, 208 hypomobile. See hypomobility.
injury affecting, 210, 210f measurement of, 528
tests of, 203–205, 204f, 210f midposition, 529t
proprioceptive training, 408–411, 407t, 410f muscle training and, 485f
proprioceptors, 24–25 neutral zone in, 389, 389f, 514, 517f
ProSom (estazolam), 261t and motor control deficits, 517f
proteoglycan aggregate, 146, 146f with passive movement or stability testing, 518f
proteoglycans, 532–533. See also glycosaminoglycan (GAG). plastic zone in, 389f, 390
in cartilage, 146–148, 146f reduction of. See also hypomobility.
cell-surface, 147 age-related, 105, 538–539, 539t
in ligaments, 30, 30t barriers causing, 389–390, 389f, 390f
in tendons, 48, 49 immobilization associated with, 540–544, 541f, 542f, 543f
protocollagen, 532, 532f physical agents minimizing, 250
Protos (strontium ranelate), 275 structures causing, 529–535
provisional calcification, zone of, 125f connective tissue, 530–533, 530f, 531f, 531t, 532f–533f, 534f
psychology of injured patient, 458–475 joint surfaces, 529–530, 529t
clinicians’ skills and procedures aiding, 472–473 muscle and contractile elements, 534–535, 535f
cognitive appraisal model in, 459–460, 459f remobilization and, 544, 544f
exceptional cases of, 465–472 zones of movement in, 389–390, 389f
injury proneness and prevention in, 473–474, 473f Ratings of Perceived Exertion, 422t
malingering and secondary gain in, 474, 475t during aquatic exercise programs, 426
modeling in, 463–465 for cardiac patients, 425
patient needs during rehabilitation, 461–463 for clients on beta-blockers, 421
peak performers’ characteristics, 472 reaction time responses, 197t, 199
rebuilding confidence in, 475 reactive neuromuscular training, 382, 384–385, 385t, 449–450
scenario interaction in, 460, 460f receptor activation (agonism), 259
pubic hair development receptor down-regulation (desensitization), 261
in females, 300f receptor inhibition (antagonism), 259
in males, 301f receptor up-regulation (sensitization), 185f, 261
pulmonary disease recovery imagery, 469, 469t
medications for, 280–281 recovery principle, 365, 369, 370–371
physical activitiy and, 340–341 recruitment deficiency, 394
pulmonary system rectal administration, of drugs and medications, 257t
age-related changes to, 333 referred pain, 218, 218t, 223, 223f, 224f
examination and evaluation, as consideration during, 319–320, reflection, on previous client outcomes, 326–327, 327f
319f, 320f rehabilitation program, development of, 314–327
of infants and toddlers, 284 Relafen (nabumetone), 268t
pulsed electromagnetic fields, 627 relaxation, in injury rehabilitation, 468, 468t
push-off, Achilles tendon affected by, 61f reliability, in outcome measures, 667–669, 668t
pyknosis, 114t, 119t relocation test, 566t
pyrazoles, 268t Remicade (infliximab), 270t, 271
remobilization, 544, 544f
Q renal transplantation, 66
quadruped position, of infant, 290 repetitive loading, tendon dysfunction caused by, 58, 59
quality of life, 338 repetitive strain injuries, 58
quazepam (Doral), 261t resistance to elongation. See muscle stiffness.
resistance training, 87–92, 432–457. See also strength training.
R acute cardiovascular responses to, 421–423
racewalking, 352t in healthy individuals, 422t
racquetball, 353t bioenergetics of, 433–436, 433f, 434t
radiocarpal joint, 500f, 597f energy sources in, 434–436, 434t, 436f, 436t
radiohumeral joint and maximal effort duration, 434f
arthrokinematics of, 506t for cardiovascular patients, 444, 444t
joint congruency of, 502t for children, 440–441, 441t
osteokinematics of, 506t documentation of, 453, 453f
radioulnar joint for elderly persons, 341–342, 443
arthrokinematics of, 506t endurance exercise compared to, 93–95, 94t, 438t
696 Index

resistance training (Continued) sarcomere, 79–81, 80f

in frail elderly, 342 cytoskeletal proteins within, 83f, 84f
functional adaptations to, 92 muscle contraction, effect of, 84f
increasing kinetic chain capability, 485, 485t myotendinous junction, near, 102
individualization of, 454–457 thick filaments within, 79–81, 80f, 81f, 83f
intermittent, 58t thin filaments within, 80f, 81f, 82
minimizing age-related muscle loss, 105 sarcopenia
muscle contraction in, 445–448, 445f, 446f, 447f age-related, 312, 333–334
neural adaptations to, 87–88 economic costs of, 332
for Parkinson’s disease, 346 sarcoplasm, 80f, 113f, 114f
periodization of, 451–453 sarcoplasmic reticulum, 81, 82f, 311
during pregnancy, 442–443 sarcotubules, 82f
structural adaptation(s) to, 88–92, 437–439, 438t Sargent jump test, 302
body composition changes as, 91, 438t satellite cells, 109–111, 113f, 114f, 114t
capillary density as, 91–92 scaffolding, in cartilage tissue engineering, 169, 169f
hyperplasia as, 90 scapula
mitochondrial density as, 92 stabilizer and mobilizer muscles of, 395t
muscle fiber type transition as, 90–91, 437–439, 438t translational (atraumatic) instability of, 397f
muscle size as, 88–90 scapular rotators, weak, 68t
systems of, 453–454 scar tissue
type(s) of, 444–451, 444f in ligaments, 38–39
isokinetic training as, 448 ice and heat affecting, 41–42
isometric training as, 448, 448f post-injury exercise affecting, 41
isotonic training as, 448–449 post-injury immobilization affecting, 40–41, 41f (rabbit)
medicine ball training as, 450–451 surgical repair affecting, 42
plyometric training as, 382, 384–385, 385t, 449–450 matrix formation, 38
tubing/elastic band training as, 451 matrix remodeling, 38–39
for women, 442–443 in muscle, 114t, 115
resisted extension test, 566t schemas, 378
respiratory rate, of children, 301 Schwann cells, 176, 176f
respiratory system, of infants and toddlers, 284 sclerosis agent, 71
resting metabolic rate, 301 scuba diving, 353t
resting position, of synovial joint, 502 seated backward overhead shot put throw, 660
resting zone, 125f seated chest pass, 660
Restoril (temazepam), 261t seated shot put test, 660
rest principle, 367, 369, 374 secobarbital (Seconal), 262t
retroversion, 283 secondary injuries, 240–241, 241f, 243–244, 244f
rheumatoid arthritis (RA), 307f secretory zone, 125f
cartilage breakdown in, 164–165 Sectral (acebutolol), 442t
diagnostic imaging of, 606, 606f sedative-hypnotic agents, 261–263
juvenile, 606f barbiturate, 262, 262t
medications for, 269–272, 270t nonbarbiturate, 261–262, 261t
physical activity and exercise affecting, 343–344 selective estrogen receptor modulator, 273t, 274
Rheumatrex (methotrexate), 270, 270t selective serotonin reuptake inhibitors, 230
Ridaura (auranofin), 270t self-report measures, 317–318
risedronate sodium (Actonel), 273t sellar or saddle joint, 497–499, 498t, 499f
Robaxin (methocarbamol), 276t modified, 497, 498t, 499
roller skating, 352t unmodified, 497–499, 498t, 500f
ropivacaine (Naropin), 279t semirecumbent cycle ergometer, 428, 429f
rostral ventral medial medulla (RVM), 226, 227f sensitivity
rotation, 487 of diagnostic tests, 559–561, 560t, 561t
rotator cuff pathology, 68t to drugs and medicines, 260
diagnostic tests for, 565t of functional tests, 639
rowing, 353t Sensorcaine (bupivacaine), 279t
rowing machine, 352t sensorimotor control, 196–216
Ruffini endings, 191f, 192–193, 192t, 376t, 409t age and, 213–214, 214f, 215f
rugby, 352t following rehabilitation, 213
running, 351t, 352t, 353t following surgery, 213
Achilles tendon, effect on, 58, 61f gender differences in, 208–209, 209f
tendon forces and stresses during, 56t, 57, 58 injury and, 209–213, 210f, 211f, 212f, 215f, 377, 377f
in joint stiffness, 201–202
S kinematics and kinetics in, 212–213, 212f
sacroiliac joint methods of, 377, 378f
arthrokinematics of, 513t of movement, 203, 204f
capsular pattern of, 520t in muscle regulation, 84–86, 87f, 201–202, 201f
osteokinematics of, 513t injury affecting, 211–212, 211f
saddling a horse, 353t muscle activity pattern assessment in, 205–207, 206f
sagittal axis, 488f, 489t osteoarthritis and, 214–216, 215f
sagittal plane, 488f, 489t of postural stability, 202–203, 203f
SAID principle, 120 injury affecting, 210–211
sailing, 353t testing of, 205, 205f
salicylates, 267t proprioception and kinesthesia, 199–201, 210, 210f
salsalate (Disalcid), 267t sensory prosessing in CNS, 196–199, 197f, 197t, 198f, 200f
sarcolemma, 80f, 81, 82f, 114t
 Index 697

testing of, 203–208, 204f of clinician, 472–473

functional testing in. See functional testing. as impairment classification, 322
motion analysis studies in, 207, 207f skin, afferent fibers in, 221t
muscle activity pattern assessment in, 205–207, 206f skin-fold measurements, 297
postural stability test in, 205, 205f skipping, 353t
proprioceptive acuity test in, 203–205, 204f slalom and hurdle test, 659
theories of, 378 sledding, 353t
sensorimotor system, 375–377, 376f slipped capital femoral epiphysis, 571f
mechanoreceptors of. See mechanoreceptors. smoking, and talipes equinovarus, 293
sensory cortex, 199, 200f snorkelling, 353t
sensory homunculus, 199, 200f snowmobiling, 353t
sensory nerve fibers, 191f soccer, 352t
sensory organs, age-related changes to, 335 socioeconomic status, and limited physical activity, 303
serotonin, 230 sodium salicylate (Uracel), 267t
sex hormones softball, 352t
and age-related muscle loss, 308 soft tissue approximation, in end feel, 518t
estrogen. See estrogen. Soma (carisoprodol), 276t
testosterone, 296, 308 somatic maturation, 299
sexual maturation, 299–300 somatosensory pathways
classification of ascending, 197, 198f
breast development in females, 300f descending, 197, 199f
genital and pubic hair development in males, 301f Sonata (zaleplon), 261t, 262
pubic hair development in females, 300f sotalol (Betapace), 442t
shop put distance, 310, 310f spaceflight
shortwave diathermy, 234–235 bone remodeling associated with, 140–141
shot put tests, 660 muscle loss associated with, 311
shoulder specificity
anterior instability of, 565t of diagnostic tests, 559–561, 560t, 561t, 639
kinematics and kinetics in, 212 of exercise treatment for chronic tendinopathy, 72–73, 73f
lytic bone metastases of, 585f, 603f of functional tests, 639
magnetic resonance imaging of, 598 specificity principle, 362, 363, 364–365, 364f
plain films of, 582f, 585f, 593f specific strength, 311
range of motion in, 539t speed test, 566t
shoulder dislocation and subluxation spinal cord
with Hill-Sachs fracture, 593f age-related changes to, 335
from involuntary instability, 401f of infants and toddlers, 284–285
plain films of, 593f in pain perception, 223, 223f, 224f
traumatic instability from, 399 spinal manipulation therapy, 235–236
from voluntary instability, 400f spinal reflexes, 197, 197f, 197t, 376, 376t
shoulder impingement syndrome spine
causes of, 68, 68t cervical
compressive forces causing, 59, 59t clinical decision rules for, 586–588, 587t
shoveling snow, 351t, 354t halo traction for, 616, 616f
shuttle run test, 658, 659f plain films of, 575f–576f
side-stepping, 290 computed tomography of, 600
Sinemet (levodopa/carbidopa), 280 of infants and toddlers, 282
single hop test, 648–649, 648f, 649t intervertebral discs. See intervertebral discs.
single-leg stance test, 208 lumbar, 581f
on foam cushion, 208f magnetic resonance imaging of, 600–601, 601f, 602f
on roller board, 209f plain films of, 600
single-set program, 454 cervical, 575f–576f
sitting, 290 lumbar, 581f
sitting tolerance, decreased, 320, 321f spinomesencephalic tract, 225
6-minute walk test, 660 spinoreticular tract, 225
six-meter test, 651, 651f, 651t spinothalamic tract, 224–225, 224f
skateboarding, 353t spins
skating arthrokinematic, 492, 493–494
ice, 353t co-, 491
inline, 352t, 353t osteokinematic, 490, 490f
roller, 352t, 353t splints, 612–613, 612f–613f, 614t
Skelaxin (metaxalone), 276t spongilization, 168
skeletal age, 299 springy end feel, 518t
skeletal development, 122–127 sprint and interval training, 92–93
skeletal maturation, 34, 299, 303 square dancing, 352t
skeletal muscle. See muscle. squash, 353t
skeletal muscle relaxants, 275–277, 276t squat exercise, 449
skeletal traction. See traction. squats, 456
skeleton. See also bone. squeeze film model, of joint lubrication, 162t
aging affecting, 305–306, 306f stability
of infants, 282 component(s) of, 392–396, 392f
skiing, 353t active, 392f, 393–396
skill principle, 363–364 dysfunction of, 392, 393
skills neural, 392, 392f
698 Index

stability (Continued) periodization model of, 452, 452f, 452t

passive, 392–393, 392f for rheumatoid arthritis, 343–344
as impairment classification, 322 in stabilization training, 407–408
stabilizing systems in, 515, 516f stress(es)
stabilization training, 403–405 definition of, 477t
advanced static stabilization exercises in, 411 and kinetic chain, 476–486
dynamic stabilization exercises in, 411–412 on ligaments, 32–33
joint receptors in, 408, 409t–410t and performance, 473f
kinesthesia in, 408–411 stress demand, 476–481
observations during, 412t activity-related demands, 480–481, 481f
pitfalls to, 413 energy flow in, 477–479, 477t, 478f, 479f
principles of, 402–403 generation, transfer, and dissipation of energy, 481–484
proprioception in, 408–411, 408t, 410f individual capability in, 481–484
sequence of, 405–412, 406t structural abnormalities increasing, 479–480, 480t
stabilizer muscles, 394–396, 395t stress-relaxation properties, 102, 103f
retraining, 411 stress-strain curve, 537–538
in stabilization training, 406–407 in fracture, 608–609, 609f
Stadol (butorphanol), 266t of tendons, 52, 54f
“stage of change” model, 356 stretching
stair climber machine, 352t, 456 in eccentric exercise program, 68, 74
stair hop (hopple) test, 652 following muscle injury, 119t
stair walking, 351t in injury prevention, 103, 371, 546–556, 548t–549t, 551t,
standing backward overhead medicine ball throw, 660 552f, 554f
standing medicine ball chest pass, 660 stretch receptor, 376f
standing rotational medicine ball throw, 660 stroke, physical activitiy and, 340
standing tests, 660 strontium ranelate (Protos), 275
Starling’s law, 242, 242t subchondral bone, 152, 168
statins, 313 subcutaneous drug administration, 257t
stationary bicycling, 352t sublingual drug administration, 257t
step-count pedometers, 350 Sublimaze (fentanyl), 266t
stepping strategy, 202 subtalar joint
step tests, 645–648, 647f arthrokinematics of, 510t
sternoclavicular joint joint congruency of, 503t
arthrokinematics of, 505t kinetic chain effected by, 478f, 479f, 480t, 481f
capsular pattern of, 520t osteokinematics of, 510t
joint congruency of, 502t pelvic motion and, 482, 482f
osteokinematics of, 505t sulfasalazine (Azulfidine), 270t, 271
sternocleidomastoid fibrosis, 291 sulindac (Clinoril), 268t
sternocostal joint, 512t superficial heat, 234
steroids. See corticosteroids. superior labral anterior-posterior (SLAP) lesion, 565t
stiffness super sets, 454
joint supraspinatus tendon, 48f
after immobilization, 35 supraspinatus test, 566t
age-related changes causing, 306 surface compliance (elasticity), 161–163, 162t
sensorimotor control of, 201–202 surface roughness, in joint lubrication, 162t, 163
muscle, 97–98 surfing, 353t
during childhood and adolescence, 303 surgical treatment
in passive tension, 99–100 of chronic tendinopathy, 72
tissue, in load deformation, 482, 482f of ligament injuries, 42
stimulus principle, 363, 365–367 for muscle strain injuries, 121
strain, ligament, 33 surprise test, 566t
strength, 432, 433 suture joints, 495
with aerobic capacity/endurance training, 341 swimming, 57, 351t, 353t
in children and adolescents, 302 swings, osteokinematic, 490, 490f
contractile, 116–117 sympathetic nervous system
in elderly persons, 342 examination and evaluation, as consideration during, 319, 320f
effects of exercise, 341–342 neurodynamics of, 183–184
loss of muscle strength, 309–312 symphysis joint, 495
loss of synarthroses (nonsynovial joints), 495, 495t
age-related, 309–312 synchondrosis joint, 495
detraining, effect of, 95 syndesmosis joints, 495
loss of muscle mass compared to, 311 synotosis, 495
muscle contraction, impact on, 106–107, 107f, 444, 444f synovial fluid, 159–160
muscle injuries and gross analysis of, 159t
hamstring injury, 117f viscosity of, 162t
tensile and contractile strength following injury, 116–117 synovial joints, 494, 495, 495t
physical activitiy and exercise, effect of, 341–342 anatomical features of, 496t
in preschoolers, 293 biaxial, 496, 497, 498t
with resistance exercise training, 341, 444, 444f biomechanical assessment of, 502–525, 504f
tensile, 116–117 characteristics of, 495
strength training. See also resistance training. classification of, 495–501, 495t, 499f, 500f, 501f, 505t–508t
cardiovascular benefits of, 339 of lower limb joints, 509t–511t
following muscle injury, 119t of midline joints, 512t–513t
modes of, comparison of, 451t of upper limb joints, 505t–508t
 Index 699

complex, 496, 497f with degeneration without inflammation, 62–64, 63f

complexity of, 496 eccentric exercise program for, 72, 74–76, 74f
compound, 496, 497f assessing program efficacy, 76–77, 76f
congruency of, 501–502 incorrect diagnosis as issue in, 77
degrees of freedom of, 496–497, 498t noncompliance as issue in, 77
end feel of, 514, 517–518 outcome measures in, 76–77
of lower limb joints, 509t–511t pain during, 72, 72f, 73–74
of midline joints, 512t–513t progression of loading in, 73, 74f, 77
types of, 518t–519t reasons for success or failure of, 77
of upper limb joints, 505t–508t response to, 76, 76f
immobilization affecting, 541f exercise and disuse affecting, 67
shapes of, 497–501, 498t, 499f, 500f, 501f exercise treatment of, 72–76, 72f, 73f, 74f
simple, 496, 496f basic principles of, 72–74
triaxial, 496, 497, 498t eccentric, 72, 72f, 74–76, 74f, 76f
uniaxial, 496, 497, 498t maximal loading in, 73
synovial lining cells, 159 progression of loading in, 73–74
synovium, 157–160, 158f specificity of, 72–73, 73f
capillaries of, 158, 158f pain associated with
fluid exchange across, 158, 158f cause of, 65–66
immobilization affecting, 541f neurogenic model of, 65–66
intimal layer of, 157, 158f during treatment, 67, 69, 72, 72f, 73–74
lining cells of, 159 with possible presence of inflammation, 63f, 64–65
subintimal layer of, 158f treatment of, 67–69, 69t
exercise as, 72–76, 72f, 73f, 74f
T forms of, 70–72
table tennis, 352t pain associated with, 67, 69, 72, 72f, 73–74
tachypnea, 284 tendinosis, 56. See also tendinopathy, chronic.
tae kwon do, 352t with degeneration without inflammation, 62–64
tai chi exercise program tendinitis compared, 62, 63–64, 78
cardiovascular benefits of, 340 tendon injuries, 54–55
for elderly, 338 acute, 61
neuromuscular benefits of, 344, 345 healing of, 61
for osteoarthritis, 343 tendinitis as, 61, 63f
talipes equinovarus, 293 treatment of, 62t, 66
talocalcaneal joint, 520t chronic, 61. See also tendinopathy, chronic.
talocrual joint classification of, 61–65
arthrokinematics of, 510t diagnosis of, 61–65
capsular pattern of, 520t diagnostic imaging of, 587t
of infants, 283 disability associated with, 64t
joint congruency of, 503t forces causing, 57, 58–61, 58t
osteokinematics of, 510t compressive forces, 59, 59t
talonavicular joint eccentric muscle activation, 60f, 61
arthrokinematics of, 510t during rupture, 56t
joint congruency of, 503t sudden loading or excessive force, 59–60
osteokinematics of, 510t pain associated with, 64t
Talwin (pentazocine), 266t progression of, 63f
taper principle, 371–372, 372f terminology in, 61–65
tarsal joints, 503t treatment of, 62t, 66–76
T-ball, 353t tendon midsubstance, 48
teaching, 355t tendons, 47–56
technique training, 382 chondroitin sulfate changes affecting, 306
temazepam (Restoril), 261t collagen in, 48–49, 533f
temperature assembly into fibrillar structure, 51–52, 53f, 533f
connective tissue affected by, 544–546, 545f, 546f defects in processing and organization, 49–51, 51t
intra-articular, 160 intracellular and extracellular modifications of, 49, 50f
intramuscular, 106, 106f, 546f types of, 48–49, 54
temporary junctions, 495 composition of, 48–49, 48f
temporomandibular joint, 500f disuse affecting, 56–58, 67
arthrokinematics of, 512t exercise affecting, 56–58
capsular pattern of, 520t forces and stresses to, 55–56, 56t
osteokinematics of, 512t glycosaminoglycan (GAG) content changes affecting, 48, 306
tendinitis, 64t loading of
acute, 61, 63f physical changes during, 55
extrinsic, 59t testing and calculations of forces, 55–56, 56t
of shoulder, 68, 68t material properties of, 54–55
tendinosis compared, 62, 63–64, 78 mechanical behavior of, 52–56, 54f, 56t
tendinopathy, 62 stress-strain curve for, 52, 54f
acute, 64t structural properties of, 52–53, 54f
chronic. See tendinopathy, chronic. structure and function of, 47–52, 48f, 50f, 51t, 53f
extrinsic, 59, 68 tennis, 352t
pan-, 64t Tenormin (atenolol), 442t
para-, 64t tenosynovitis
tendinopathy, chronic, 62–64, 64t. See also tendinosis. Achilles, 59t
becoming acute, 67 compressive forces causing, 59
700 Index

tenosynovitis (Continued) training state, 362

flexor hallucis, 59 tramadol (Ultram), 266t
tenosynovium, 52 transcutaneous electrical nerve stimulation (TENS)
TENS (transcutaneous electrical nerve stimulation) acupuncture-like, 232
acupuncture-like, 232 conventional, 232
conventional, 232 in pain treatment, 232–233, 232f
in pain treatment, 232–233, 232f transdermal drug administration, 257t
tensile deformation, of ligaments, 31f translation, 487, 492, 492f
tensile load starting point, 68–69, 69t translational (atraumatic) instability, 397–398, 396f
teriparatide (Forteo), 273t, 274–275 transplantation, of articular cartilage tissue, 168–169, 169f
terminal cisternae, 81, 82f Transtec (buprenorphine), 266t
testosterone transverse friction massage, 70
in adolescents, 296 transverse or horizontal plane, 488f, 489t
and age-related muscle loss, 308 transverse tubule, 82f
tetherball, 353t traumatic instability, 398–399, 399f
tetracaine (Pontocaine), 279t treading water, 353t
thalamus, 225 treadmill, 456
thermal modalities, 234–235 treatment imagery, 469t, 470
thermotherapy. See heat. triamcinolone, 263t
thigh muscle volume, 302 triangle or pyramid program, 454
Third National Health and Nutrition Examination Survey triaxial joints, 496, 497, 498t
(NHANES), 297 triazolam (Halcion), 261t
thorax, of infants and toddlers, 284 tricyclic antidepressants, 230
three-point bending, of cortical bone, 133, 133f triggered reactions, 197–199, 197t, 376t
thumb Trilisate (choline magnesium salicylate), 267t
avulsion fracture of, 591f triple crossover hop test, 650, 650f, 650t
carpometacarpal joint of, 500f, 507t, 520t triple hop test, 649, 649f, 649t
plain film study of, 591f tri-set system, 454
thyroid hormone, 308 tropocollagen, 532, 533f
tibia truck driving, 354t
elastic modulus of, 134f tubing (elastic band) training, 451
fracture of tumors (neoplasms)
in children, 629f diagnostic imaging of, 574f, 601–604, 603f, 604f, 605f
open reduction and internal fixation of, 621f of humerus, 574f
skeletal traction for, 615f metastatic, 573f, 585f, 601–604, 603f
of infants and toddlers, 283 two-handed lift, 302
melorheostosis of, 585f Tylenol (acetaminophen), 256t, 267, 267t
physeal centers of, 127t, 629f Tylox (oxycodone), 266t
plain film studies of, 585f
proportional limit of, 134f U
torsion of, 295 ulna, physeal centers of, 127t
tibialis anterior, 108f ulnohumeral joint
tibial nerve, 26 arthrokinematics of, 506t
tibiofemoral joint, 497f, 500f joint congruency of, 502t
arthrokinematics of, 509t osteokinematics of, 506t
blood supply to, 25–26, 25f ulnohumeroradial joint, 497f
osteokinematics of, 509t ultimate tensile strength, 55
tibiofibular joint ultrasound, diagnostic, 571–572, 586t
arthrokinematics of, 509t of biceps tendon, 573f
capsular pattern of, 520t in cartilage breakdown, 166
joint congruency of, 503t of infra-patellar tendon, 573f
osteokinematics of, 509t ultrasound diathermy, 234–235
timolol (Blocadren), 442t ultrasound, therapeutic
Tinel’s sign, 566t in chronic tendinopathy treatment, 70
tissue inhibitors of matrix metalloproteinases, 147 continuous, 120
tizanidine (Zanaflex), 276t, 277 following muscle injury, 119t, 120
tobogganing, 353t in fracture management, 626–627
toddlers. See infants and toddlers (0-3). non-thermal, 251t
toe-raising exercises, 73, 73f pulsed, 120
toes, of infants and toddlers, 284 thermal, 251t
toe-walking, idiopathic, 295 underload principle, 363
tolerance, for drugs and medicines, 260–261, 265 uniaxial joints, 496, 497, 498t
tolmetin (Tolectin), 268t Universal-type weights, 352t
topical medications, 71, 257t upper extremities. See also specific structure, e.g., Shoulder.
Toradol (ketorolac), 267t and age-related muscle loss, 310–311
torticollis, 291, 292f arthrokinematics of, 505t–508t
total gym incline board, 456 capuslar pattern of, 520t
trabeculum, primary, 125f end feel of, 505t–508t
track athletes, 306 functional testing of, 659–660
traction, 614–616, 614f, 615f osteokinematics of, 505t–508t
in fracture management, 614t synovial joints, classification of, 505t–508t
halo, 616, 616f up-regulation (receptor sensitization), 261
trade names, 255, 261t Uracel (sodium salicylate), 267t
 Index 701

V water polo, 353t

valdecoxib (Bextra), 268t waterskiing, 353t
validity, in outcome measures, 668t, 669–670 weeping model, of joint lubrication, 162t, 163
Valium (diazepam), 276t, 277 weight
variety principle, 363 CDC growth charts, 286f, 287f, 288f, 289f
varus bowing, in infants, 283 changes in
vascular system during childhood and adolescence, 295
age-related changes in, 333 in infants and toddlers, 285
articular mobilization affecting, 523t phases of, 296
of bone, 123f, 124f, 130–131 in preschoolers, 294
of ligaments, 25–27, 25f, 26f (rat), 27f (rabbit) weight-bearing exercises, 456
of peripheral nerves, 177, 178f, 179 weight loss, osteoarthritis effected by, 343
of synovial tissue, 158f weight machines, 352t, 451t
of tibiofemoral joint, 25–26, 25f weight training, 352t
vaulting, of infant, 290 wellness, 329. See also health promotion, wellness, and physical fitness.
ventilation, 294 wheelchair basketball, 351t, 352t
ventricular filling, 309 wheelchair tennis, 352t
versa climber, 456 wheelchair use, 351t, 352t
vertebral fracture, 306 whitewater rafting, 353t
vertical or longitudinal axis, 488f, 489t Wingate anaerobic test, 302
vesicular transport, of drugs and medicines, 257 Wingate bike test, 660–661, 662t
Vicodin (hydrocodone), 266t Wolff’s law, 118, 119t, 122
vigorous physical activity, 303 women. See gender differences.
viscoelastic properties, of collagenous tissue, 102–103, 102f, 104f workplace, health promotion in, 348–349
Visken (pindolol), 442t work-related musculoskeletal disorders, 58, 63
vital capacity, 294 wound contraction, 250
vital signs wrestling, 352t
of infants and toddlers, 284 wrist
of preschoolers, 294 arthrokinematics of, 506t
Volkmann’s canal, 130f capsular pattern of, 520t
volleyball, 351t, 352t dislocation of, 583f
Voltaren (diclofenac), 267t fracture of
volume of training, 433 healing of, 597f
voluntary instability, 399, 400f impacted, 594f, 597f
voluntary muscle contractions, 56t joint congruency of, 502t
voluntary muscle control testing, 206–207, 206f, 211–212, 211f osteokinematics of, 506t
voluntary reactions, 376t plain films of, 583f, 594f, 597f
range of motion in, 539t
W
walking, 351t, 352t. See also ambulation. X
walking boot, 612f Xylocaine (lidocaine), 279t
walking program
neuromuscular benefits of, 344 Y
and risk of falls, 345 Yergason’s test, 566t
warm-up, 371 yoga, 352t
for athlete, 555 young-old, 305
in eccentric exercise program, 74 Youth Risk Behavioral Surveillance System (YRBS), 297, 297t
and hamstring injury, 117f
for sedentary individual or geriatric patient, 555–556 Z
washing or waxing zaleplon (Sonata), 261t, 262
cars or boats, 351t, 353t, 354t Zanaflex (tizanidine), 276t, 277
windows or floors, 351t, 354t zigzig run test, 656, 657f, 657t
water aerobics, 339–340, 351t zolpidem (Ambien), 261t, 262
water, as component of ligaments, 29, 30t zone of hypertrophy, 125f
water basketball, 353t zone of ranvier, 125f
water jogging, 352t, 353t zopiclone (Imovane), 261t, 262