PHYSICAL THERAPIES IN SPORT AND EXERCISETHERAPIES IN SPORT AND EXERCISE........... Edited by Gregory S Kolt Lynn Snyder-Mackler BSc BApeSc(Pury) GraDirED BA CexiPrysTier MS ScD GrapDirBertavHirriCare PHD Alumni Distinguished Professor and Academic Professor and Head of School, School of Director, Graduate Program in Biomechanics and Biomedical and Health Sciences, University of Movement Sciences, Department of Physical Western Sydney, Sydney, Australia; Therapy, University of Delaware, Newark, Adjunct Professor, Faculty of Health and Delaware, USA Environmental Sciences, Auckland University of Technology, Auckland, New Zealand James R Andrews mp Founding member of the Alabama Sports Medicine and Orthopaedic Center (ASMOC) and the American Sports Medicine Center (ASMI) in Birmingham, Alabama; Chairman and Medical Director of ASML Edinburgh London New York Oxford Philadelphia StLouis SydneyCHURCHILL, LIVINGSTONE, ‘An imprint of Elsevier Limited (© 2007, Flevier Limited. ll igh ceserved, [No par of this publication may be reproduced, stored in arrival system, or tansmtted in any form of by any means, electron ‘mechanical, photecopying, recording or otherwise, without the prior ‘ermision ofthe Publishers. 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You may sso complete your request on-lre via the Esevie homepage (htp:/wwreelseiercom), by selecting Support and contact’ and then ‘Copyright and Permission’ First dition 2003 ISBN: 978.0:445-10351-3 British Library Cataloguingia Publication Data ‘catalogue reoord for this book is availble from the British Library Library of Congress Cataloging ia Publication Data ‘Acatalog record fortis book is aailable from the Library of Congress [Neither the Publier nor the Editors assume any exponsibilty for any loss or injury and/or damage to persons or property arising oxt of cr ‘elated to any use ofthe material contaned inthis book. esthe| ‘esponsibility ofthe testing practioner, relying on independent cexpertise and knowledge ofthe patient, to determine th best treatment aud method of application fr the patient. The Publisher your source for books, Ea rcoetrkiredie Inthe healthicenees wwrmalsevierhealth.com pnsice Painted in ChinaSection 1 Section 2 Contributors Preface, Acknowledgments Foreword Foreword to the first edition ‘Abbreviations and acronyms About the eattors The role of the physical therapies in sport, exercise and physical activity Gregory 8, Kolt and Lymn Suyder Mackler Management principles for musculoskeletal and neural tissue in the physical therapies Muscle Per J. McNair and Andrew G. Creeneell Tendon Bill Cook Ligament Gabriel Ng Bone Pekka Kantus and Kim Bemell Nerves Rober J. Nee, David 5. Buler and Michel W. Copietrs Cartiage Stefano Zaffagisi, Mare Safran and Elizavnta Kon Concepis in managing sport and exercise injuries Motor control eal W. Hodges Pain Gregory 5: Kole Exerclse-based condltoning and rehabilitation Raja Escamilla and Robbin Wikham-Bruno Psychology of injury and rehabilitation Gregory S. Kat and Briton W Brewer ‘Screening for sport and exercise participation lisa Cason Barley and Michal. Ave ical outcomes in sport and exercise physical therapies James. Irgangand Robert G. Mare Electroptysical agents in sport and exercise injury management Laven Snyder Mackler, Lara A, Shit, Katherine Rellph and Sara Rargibar xv 26 42 59 22 400 133 149 i" 190 208 22015 Section 3 16 "7 18 19 20 21 22 23, 24 Section 4 25 26 27 28 Section 5 29 30 at Contents Prevention of injury Timothy E. Hevett, Kristin Briem and Roald Bahr Regional sport and exercise injury menagement Spine Tina Jo Mand and Anthony Delo Shoulaer Brin 1 Tovinand acon. Rise Elbow Michael. Reinold und Kevie B. Wile Wrist and hand Paul LaStayo, Susan Midilovie and Michael Lee Pelvis, hip and groin ichael T Cibulka Kr Tense L. Chelewski, Susan M. Tilman and Lymn Snyder Mockler Petellotemoral joint at Kay Crosley, Salie Cowan, Kime Bnnell and Jenny McConnell Foot, ankle and lower leg DS. Bleice Wiliams Il and lack Trnton Rehabilitation of lower im muscle and tendon injuries Thomas C. Windley, Susanne Werner, Nicola Maffli and Jack Tauaton The tole of sport and exercise physical therapies in active groups Children and adolescents Heather Southwick, Christine Pls, Lyle. Mickel, Elly Tepmian sand Lisanne Backe Barone Older exercise participants, Jeanifer B. Stevens The active female Amanda Weiss-Kelly and Martin Kiane Athletes with disability Zot Hudson and Any Brown Medical considerations for rehabilitation practitioners in sport and exercise Pharmacological agents in sport and exercise Andrew Garshane Medical imaging of injury Douglas N. Mintz Medical Issues in sport and exercise Brace Hamilton and Mark Index 236 255 283 308 338 385: 982 402 420 440 459 484 499 505, ut 558. 578 509Michael v Axe MD First State Orthopastics; Clinical Professor, Department of Physical Therapy, University of Oelanare, Newark, OE, USA, Lizanne Backe Barone NP Nurse Practitioner, Ohisien of Sports Medicine, Chidren's Hespita, Boston, MA, USA Roald Bahr MD PhO Chair, Oslo Sports Trauma Research Center, Professor ancl Char, Department of Spot Medicine, Norwegian School of Sport Scences, Oslo, Nonway Lisa Casson Barkley MO FAAFP Dean. Colege of Health and Public Policy, Head Team Physician, Delaware State Linivasity Dover, DE, USA Kim Bennell BAppSei(Physio) PHO Professor and Foundation Director of the Centre for Heath, Exercise and Sports Medicine, Facuity of Medicine, Dentistry anc Health Scierces, University of Melbourne, Victoria, Australa Britton W Brewer BA MA PhD Professor, Department of Psychology, Springfield Colegs, Springfele, MA, USA Kristin Briem BSc MHS Doctoral Student, Department of Physical Therapy. University of Delaware, Newark, DE, USA ‘Amy Brown MPT SCS Staff Pryscal Therapist, Chrstana Care PT PLUS, Smyma, DE, USA David $ Butler BPhys MAppSc GDAMT Director, Neuro Orthopedt insitute, Adelaide City West South Australia, Australia Terese L Chmielewski PhD PT SCS Assistant Professor, Department of Physcal Therapy. University of Florida, Gainesville, FL, USA Michael T Cibulka PT DPT MHS OCS Assistant Professor, Physcal Therapy Program, Maryvale Unversity, St. Louis, MO, USA, Jill Cook BAppSci PostGracDip PhD [Associate Professor, School of Exercise and Nutrition Sciences, Deakin Unversty, Victoria, Australia Michel W Coppieters PT PhO Research Fellow, School of Health end Rehabiltaion Sciences, University of Queenstnd, St Lucia, Brisbane, Australia ‘Salle Cowan Bappscl PostGradbip PnD Post Doctoral Research Flow, Cente for Health, Exercise and ‘Sports Medicine, University of Nelbourne, Victoria, Australia ‘Andrew G Cresswell BEd MSc PhO ‘Assocate Protessor, School of Human Mevement Studies, Unversty ‘of Quesnslend, Brisbane, Australia ‘Kay Grossey BAppSel PostGradDip PhD ‘Senior Lecturer, School of Physiotherapy, University of Melbourne, Vitoria, Australia ‘Anthony Delite PhD PT Protessor, Chas, Department of Physica! Therapy, School of Health ‘and Rehabitation Sciences, Universty of Pittsburgh, Pittsburgh, PA, USA Ratael F Escamilla BS MS PhO MPT CSCS. Piotessor, Department of Physical Torapy, Calfornia Stato University, Sacramento, CA, USA ‘Sara Farquhar 8S MPT Doctoral Candidate, terlscipinary Program in Biomechanics ‘and Movement Science, Department of Physical Therapy, University of Delaware, Newark, DE, USA. ‘Andrew Gernham MBBS DipRACOG FACSP ‘Sonior Lecturer, School of Exercise and Nutrition Sciences, Deakin University, Burwood, Vieoria, Australia ‘Mark Gillett BSc(Hons) MBBS FRCS(ARE) FEM FFSEM(UKAl) DipIMC RCSEé Load Physician, EIS Wast Midlands, and Clinical Director Emergency Department, Good Hope Hospital, Sutton Colcol, West Midlands, UK. Bruce Hamilton BPhEd MBChB DTMAH FACSP FFSEM(UK) Chief Maclcal Offeer, UK Athiatiee, Wost Midland, UK: ‘Timothy E Hewett PhD Dracter, Associate Professor, Cheinnatl Chicrn’s Hosplial, Sports Medicine Biodynamics Certer, Human Performance Laboratory; Univarty of Cincinnati Cologe of Madicins, Denartment of Pacatrisa ‘and Orthopaedic Surgery, Biomedical Engneerng and Fehabiation ‘Sciences, Cincnatl, OH, USA Paul W Hodges BPhty(Hons) PhD MedDr(Neurosci) Professor and NHMAG Pricipal Research Felow, NHMRC Centre of CCinicai Resoarch Excellence in Spina Pain, Injury and Health, Schoot ‘of Heath ard Rehabitation Sciences, University of Queensland, Brisbane, Australiaaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.In developing the concept and framework for Physical Therapies inSport and Exercisewe were consciousof two guiding principe the need for a book that supports its content with evidence, and the need to go beyond standard sports medicine texts and provide a resource specifically for those who work in the physical and manual therapies. We also undertook to procluce a resource that vas valuable from an international perspective, and took into account the variety of approaches to the physical therapies across the worl The appreach has been successful; the first edition was published not only in English, but also in Japanese, Spanish, Portuguese and Greek, In elation to an evidence-based text, one is reliant on the published literature that supports or refutes the wide variety of approaches that practitioners are now incorporating in their management of injury, Oniy rebtively recently has this body of evidence built to a level that affords practitioners appropriate confidence in the effectiveness of the techniques they use. ‘The form of the book is unchanged in this second edition, but wwe have added chaptersto three sections, one on cartilage to the fist section where other tissues relevant to sports rehabiltation are discuseed, a chapter on injury prevention to complement other chapters that deal with management concepts for injury and one on rchsbilitation of lower limb injuries. Other chapters have been updated with the most recent literature and available evidence, and, in several instances, completely sewritten with new authors. We hope that with a resource such as this book, practitioners will explore new approaches to managing injury ‘The breadth of topics covered in this book is testament to the everincreasing knowledge that competent practitioners are required to possess. Merely possessing this knowledge is insufficient; we must place it into an applied context with patients, athletes and the general population with which we work. The use of physical therapy in the sport and exercise environment is gaining rapid momentum ia all regions of the world. Its place in mainstream medicine and health, however, is dependent on using approaches that have demonstrated acceptability and efficacy. Not only should this book be seen asa resource for practitioners, but as a platform from which researchers draw ideas for further investigation. Take the opportunity to draw upon the extensive reference lists provided in each chapter to further your reading and knowledge. But must ofall use what is in the text to broaden the approaches you take with your patients Gregory S. Kolt, Sydney Lynn SnyderMackler, Delewareaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.FD) Foreword to the frst editon fields in sports physical therapy, Current concepts of injury ranagement and the increasingly important role the physical therapist plays in the field of sports, physical exercise and ty are described. The major advantage ofthis book is that the discussions are comprehensive and based on the scientific evidence available Thisis a high-qualty book in an increasingly important field It is my sincere opinion that this book will not only be very beneficial bt also enjoyable to read for everyone active in the field of physical cherapy, sports and physical activity. Per Renstriim, Stockholm, 2003aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.The role of the physical therapies in sport, exercise and physical activity Gregory S. Kolt and Lynn Snyder-Mackler Ruantee aanirenre Introduction Sport, exercise and physical activity pursuits are important in most societies. A result of participation in such activities, how= ever, i the risk of injury. Not only does injury occur during com petitive sport activities, but through preparation for such events, as well as during the general physical activities and exercise that an increasing number of people are becoming involved in for health benefits. ‘The field of sports medicine has developed as a result of increased participation rates in sport, exercise and physi- cal activity, and the specific medical needs of participants (Matheson & Pipe 1996). Sports medicine is a multidscipli- nary field that involves health professionals from a variety of professions. Whilst resources do not alwways allow for a large and multicisciplinary sports medicine team, the following per- sonnel are often involved in the prevention and management of sport and exercise related injuries © Family physician (primary care physician) © Sports physician © Orthopedic surgeon © Radiologist Physical thorapist/physiothorapist Massage therapist Podiatrist Distician/nutritionist © Paychologist (often sport psychologist) © Athietic tainer/sports trainer © Chiropractor and osteopath © Sport scientsts including biomechanists and exercise physiologists © Other health professionals including orthotists, nurses, dentists, occupational therapists and optometrists © Coach © Fitness coach or adviser. Although this combination of professionals is ideal, in the rmajonty of seuiings, sports medline teams will be far smaller depending on the needs and demands ofa particular sport and the availability of sports mecicine practitioners,aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.The role of the physical therapies in sport, exercise and physical activity therapy profession, Jetteet al (2003) examined the beliefs, atti- tudes, knowledge and behaviors of physical therapists towards evidence-based practice and found a positive atitude towards the inclusion of evidence-based practice within the profession. Responderts also indicated an interest in learning or improving the skills necessary to implement such practices A walk through Physical Therapies in Sport and Exercise rap Sports physical therapy does not have a unitary model, and thus ‘we have assembled a group of researchers, practitioners and educators who represent the diversity of approachesin working with sport and exercise to contribate chapters to this book. The authors come from physical therapy, psychology, sports medi- cine, athletic training, orthopedic surgery, pediatrics, radiology, biomechanics and nursing, and represent countries as diverse as the USA, Australia, New Zealand, Hong Keng, the UK, Finland, Sweden, Italy, Norway ancl Canada. As previously mentioned, the chapters of this book have, where possible, reported tech- niques and approaches to injury management thst are supported by appropriate evidence, This book is divided into five sections: Section 1: Management Principles for Musculoskeletal and ‘Neural Tissue in the Physical Therapies. This sevtion deals with five groups of body tissue: Muscle (Ch. 2), Tendon (Ch. 3), Ligament (Ch. 4), Bone (Ch 5), Nerves (Ch, 6) and Cartilage (Ch. 7). These chapters provide coverage of the basic structure and biomechanics of the tissues, the principles relating to the adaptation of the tissue to mechanical load, and the response of the tissue to injury and healing, Seetion 2: Concepts in Managing Sport and Exercise Injuries ‘The chapters in this section provide general information that fs important in the management of injures from the various regions of the body. Chapter 8, Motor Control, covers. the theory and application of motor control and motor relearaingin the management of sport and exercise related injury. Chapter 9, Prin, outlines the mechanisms and theories of pain perception, and. presents strategies to assess and manage pain from both a physical and cognitivecbehavioral perspective. Chapter 10, Exercise-based Conditioning and Rehabilitation, outlines the evidence for the use of various forms of exercise in injury pre~ vention and management, Chapter 11, Psychology of Injury and Rehabilitation, works through the psychological factorsthataffect the onset and rehabilitation of injury. Also, issues related to reha- bilitation adherence and the role of physical therapists in apply- ing basic cognitive-behavioral techniques is covered. Chapter 12, Screening for Sport and Exercise Participation, focuses on the principles and practical application of screening procedures that are used for sport and exercise partipation, Issues related to gen- eral health, and sport-specific health and fitness, are addressed Chapter 13, Clinical Outcomes in Sport and Exercise Physical ‘Therapies, covers a range of outcome measures that an be used inthe sport and exercise physical therapies. This addresses both lnical measures and conditionspecific functional measures. 4 Chapter 14, Electrophysical Agents n Sport and Exercise Injury Management, evaluates, from a scientific perspective, various clectrophysical agents commonly used by sport physical thera pists. The emphasis is on outlining the evidence to support or refute the role of such modalities in sports medicine, Chapter 15, Prevention of Injury, describes the general principles and models of iajury prevention (and associated research) in sport and exercise. Section 3: Regional Sport and Exercise Injury Management. ‘Thechaptersinthissectiondealwiththe Spine (Ch. 16), Shoulder (Ca. 17), Elbow (Ch. 18), Waist and Hand (Ch. 19), Pelvis Hip and Groin (Ch. 20), Knee (Ch. 21), Patellofemoral Joint (Ca. 22), Foot, Ankle, and Lower Leg (Ch. 23) and Rehabilitation of Lower Limb Muscle and Tendon Injuries (Ch. 24). In each of these chapters the content focuses on sport-specif applied anatomy, examination and the management of commen and less commen sport- and exercise-related injuries to the region. Section 4: The Role of Sport and Exercise Physical Therapies in Active Groups. Four groups of people are covered in this section: children and adolescents, older exercise participants, active females and athletes with disability. Chapter 25, Children and Adolescents, outlines the assessment and management of conditions specific to this age group. In particular, injuries and conditions specific to the immature musculoskeletal system are highlighted. Chapter 26, Older Exercise Participants, focuses fon the assessment and management of conditions specific to older people involved in sport, exercise and physical activity, In particular, the impact of aging on the systems of the body is addressed, as well as the benefts that can be gained from participation in sport and exercise and guidelines for exercise participation. Chapter 27, The Active Female, focuses on con- ditions specific to women involved in sport and exercise, In particular, istes related to bone health are covered, as are the anatomical and physiological considerations for women. Other areas included are the menstrual cycle and performance, the female athlete trad and exercise during pregnancy, Chapter 28, Athletes with Disability, presents information on the benefits of exercise and sport for people with disability, classification of athletes with disability and injury management and assessment, fora variety of disability groups in spor. Section §: Medicil Considerations for Rehabilitation Prac titionersin Sportand Exercise Section Shas three chaptersdeal: ing with a variety of medical considerations for physical thera pists working in sportand exercise. Chapter 29, Pharmacological Agents in Sport and Exercise, deals with therapeutic pharma cobogical agents and the impact they have on injury repair, exercise participition and physical therapies management. The chapter also covers the efiects of performance enhancing drugs onathlete health and wellbeing, and the International Olympic Committee Anti-Doping Code. Chapter 30, Medical Imaging of injury, provides those working inthe physical therapies with an understanding of the various imaging modalities used incliag- nosing sport and exercise related injuries. Chapter 31, Medical Issues in Sport and Exercise, covers common medical emergen- Ciesin sportand exercise including head injuries, cardiovascular Conditions and conditions related to environmental influences,aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Section One Management principles for musculoskeletal and neural tissue in the physical therapies 2 Muscle 3 Tendon 4 Ligament 5 Bone 6 Neves 7 CattlageMuscle Peter J. McNair and Andrew G. Cresswell Introduction ‘There are three types of muscle tissue within the body ~ skel- ctal muscle (strated voluntary), cardiac mascle (striated invol- untary) and visceral (non-striated involuntary or smooth). ‘This chapter will focus on skeletal muscle. Skeletal muscles velop force through contraction, which gives us the possi- bility of movement and interaction with our surroundings. In many pathological conditions muscle has been affected; either directly through injury or disease, or indirectly as a result of immobilization regimes. For the physical therapist to rchabili- tote patients efficaciously, an understanding of muscle func tion isimportant. This chapter provides a foundation on which effective muscle training programs might be built. Its purpose isto examine the structure af muscle, its biomechanical char- acteristics and how those characteristics influence its func- tion, This chapter will focus on the factors that influence the force generation capacity of muscle. It will also describe the ‘changes that occur when muscle isin states of injury and dis- use. Although the focusis predominantly on muscle structure we recognize the importance of neural activation in generating force. This area, however, is beyond the scope of this chapter (cee Chapter 6) Gross structure of muscle Fiber structure “To the naked eye, skeletal muscle is primorily made up of fib crs. These fibers are grouped into bundles of approximately 10 to 20 fibers, each of which is called a fascicle, Each fascicle is surrounded by connective tissue (perimysium) that separates it from its neighboring fiscicles. Muscle is built up from many such fascicles and is enclosed in a further thicker ayer of con- nective tissue, the epimysium. Collagen fibers in all the layers ‘of connective tissue are connected to the tendons at the end ‘of the muscle, In this way, every individual muscle fber is connected to the tendon and any force development from a muscle fiber will be exerted on the tendon, ‘At a microscopic level, each muscle fer contains thou- sands of smaller units (myofibrils) which are responsible for contraction of the muscle (Fig, 2.1). A myofibril has a diam- eter of approximately 1 um and is comprised of light and dark bands (striations) when viewed under light microscope (Hess °aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Muscle the Type Il to Type | fiber area. These changes are believed to result in an overall decrease in muscle force producing capac~ ity and shortening velocity (Frontera et al 2000, Klitgaard et al 1980). In contrast, exercise, training and rehabilitation are known stimuli that can lead to fiber size increase (hypertro- phy) and plastic changes in muscle fiber type. A change from ‘Type IIB to ITA appears readily possible (Pette & Staron 1997) after specific training, and in some exceptional circumstances a change from Type Ito Il can occur. Whether significant changes in the direction of fast to slow occur is not presently known, The contractile process Force is generated in a muscle fiber when actin and myosin fl rents interact. This event commences with action potentials spreading across the muscle fibers at approximately 3-Sms ‘The potentials also spread deep within the fibers by way of the ‘Trubules (Peachey 1965a, 1965), which have close contact with the terminal cisternae of the sarcoplasmic reticulum, The sap between these two structures is bndged by two proteins ~a dihydropyridine receptor (DHP) and a ryanodin receptor (RR). During rest, the ryanodin receptor channelsare closed and Ca"* Myot iad ‘etc Aber ‘bar 12 remains within the sarcoplasmic reticulum. Depolatization of the T-tubules results in activation of the dihydropyridine recep- tom which in turn causes the ryanodin receptor to open its Ca channel and rapidly release Ca'* along its concentration gradient out from the sarcoplismic reticulum, thereby increasing cyto- stolic Ca?! (Peachey 1965a, 1965b) Figure 2.4 shows the transverse tubule—sarcoplasmic reticu- Jur system, At rest, the binding sites for myosin on the actin fil ‘ment are covered; however, with the release of Ca?*, troponin undergoes a conformational change. This change lifts the topo- myosin molecule away from the actin filament and exposes sites ‘on the actin filament for myosin head attachment, and allows the Contraction to commence. Puraps in the sarcoplasmic reticulum continuously pump Ca?* back into the sarcoplasmic reticulum, ‘Atrest, this event results in the concentration of Ca?* in the sar- copll eve being ger han hatte cya, When ponin and. “qickly pumped out of the cytosol. Tropomyosin then returns to its original position on actin and prevents any further binding of myosin to actin. Since the purap has to transport Ca? against its concentration gradient, adenosine triphosphate (ATP) is required to provide the necessary energy. Figure 24 ¢ The transverse (1 tubule-sarcoplasmic reticulum system, This lustation was drasin from frog muscle, which has ane T-tubula por sercomara, locatedat the z ne. Marnmatian skeletal scl has two tubules per sarcomere, located atthe A-ijunc tion, (Reproduced from Guyton & Hall 2000 with the permission of WB Saunders) arcolemna sarcoplasmic tielum ‘tcehondtion seminal stemaeaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Muscle 1992, Nygaard et al 1983). The wide range in these values may be attributed to differences in gender and muscle architecture (Eecema & Huijing 1994). It is aio evident that the maximum force per unit area is not dependent on muscle fiber type (Bottinelli et al 1996, Herbert & Gandevia 1995). Thus, the amount of otal force prochuced by a muscle is directly related twits cross-sectional ares. Although there are differencesin the dlametersof fibers withina muscle, thelargest contributor to the different forces produced by different muscles is the absolute number of muscle fibers. Such numbers can range from approx imately 4.0 x 10* for the first dorsal interossei to 1.0 X 10° for the medial gastrocnemius (Feinstein et al 1955) ‘The physiological cross-sectional area of muscle cen be calcue lated with a knowledge of the mass and density (1.056 gem 3) of the muscle together with information related to fiber length Mass and density are determinants of the muscle’s volume, which are reflected in the different shapes of muscles in the body. The diversity in shape of each muscle often results in the line of pull of individual fibers being quite different, and this can influence their force capability. Generally speak- ing, muscles are grouped according to the orientation of their fascicul. These fasciculi are most often arranged either parsl- lel or oblique to the final direction of pull at their insertion Some muscles (¢.g. sartorius) have fibers primarily parallel co the line of pull. Others (c.g. biceps brachii) can also have a similar arrangement in the belly of a fusiform muscle and the fibers comerge to a tendon at either one or both ends of the muscle. Such muscles have longer muscle fibers and hence will have greater displacement potential, and are more effective at changing length quickly. The length of a muscle fiber is determined by the number of sarcomeres in series. There are quite large differencesin the umber of sarcomeres per fiber, with long strap muscles ike sartorius, which adklucts and flexes the leg, having approxi- mately 15.5 x 10" sarcomeres per fiber while the shorter plantar flexors, soleus and medial gastrocnemius have approxi- mately 1.4 x 10¥ and 1.5 X 10* sarcomeres per fiber, respec tively (Wickiewiez etal 1983), These numbers are often based oon the premise that individual fibers nun the full length of the ruscle. Ina number of instances, however, thisis not the case For instance, several of the longer strap muscles (e.g. rectus abdominis} have discrete compartments, defined by ibrous bands, These compartments result in significantly shorter muscle fiber lengths with sarcomere numbers in the region of 5.5 x 10* (Chleboun et al 2001, McComas 1996). Such Compartmentalization is likely to make force transmission throughout the muscle more complicated than if fibers extend the entire length of the muscle. ‘A limitation of muscles with longer muscle fibers is that they are less effective at generating force. The potential to gener- ate force will be proportional to the number of sarcomeres in parallel Fesciculi that are oblique to the line of pull are often described as being pennate (feather-like). Fennate muscles (e.g sastrocnemius) typically havea long tendon running through the muscle to which short muscle fibers are attached at angles that generally range from 5 t0 20°. The fiber organization of a pennate 16 ‘muscle ensures a relatively large physiological cross-sectional area since there can be many more fibets packed within the muscle A hirger cross-sectional area reaults in an increase in force poten tial even though the force contribution of each fiber is reduced dlue to its angle of pull. Pennate muscle fibers have significantly fewer sarcomeresin series than parallel fibered muscle. Therefore, for the same decrease in fiber length the relative shortening per sarcomere length will be greater for a short fiber (Nari 1999) ‘The muscle is therefore Jess suited to situations that demand Jong length changes or high velocity length changes Structures that influence the elasticity of muscle ‘The connective tissues of muscle can be divided into three struc- tures that are based on their position within muscle, Epimysium enrelops the entire muscle, perimysium surrounds bundles of muscle fibers and encomysium provides a cover for the base- ment membrane of individual muscle fers. Endomysium and perimysium are linked to one another, and these tissues are thought to provide « framework on which the muscle fibers attach and gin support. When muscle is stretched, it is thought that endomysium and perimysium are largely responsible for the passive tension generated in muscle at high sarcomere lengths. Purslow (1989) and Purslow & Tiotter (1994) examined the ‘morphology and mechanical properties of both endomysial and pesimysial tissues. These authors noted that at resting muscle Tengths the endomysial network was composed of wavy collagen fibrils arranged with a mean orientation to the muscle fibers of (60°. Perimysium was more organized with a cross-ply structural arrangement of crimped collagen fibers a a similarangle. A more complex arrangement has recently been described by Tarvinen etal (2002) who descrbedendemysium andl perimysiumashaving longitudinal and circularly organized ccllagen fibers. The com- plexity of this network varied across muscles, which probably reflected differencesin requirementsrelted to function. Purslow (1989) and Purshow & Trotter (1994) observed that tensile aiff ness was minimal at the resting length in both endomysial and pesimysial tissues. When the muscle fibers were stretched to high sarcomere lengths, the angle of the collagen fers to the muscle fibers in both endomysium and perimysium decreased, and the respective way and crimped appearance of these tissues was Jost. Thus at high sarcomere lengths, it has been suggested that both endomysium and perimysium may prevent overstretching of muscle (Purslow 1989, Purslow & Tiutter 1994) It is also apparent that the contractile elements have elastic properties. Short-range stiffness is a term used to describe the ati of change in force to change in length of the muscle fibers when stretched. When muscle fibers are activated, short-ange stiffnessis noted until fibers are stretched past approximately 1% of muscle length (Malamuad et al 1996). Theseafter, a yielding of the fibers is noted and resistance in the tissues decreases. It has been shown that the short-range sifness increases with muscle activation levels, and hence has been related to the number of cross bridges formed between actin and myosin at the time ofaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.D muscte of insufficient numbers to buffer the increase in oxidants that ‘ecu with inactivity. Powers et al (2005) highlight the impor- tance of oxidative stress, and suggest that hoth the ealpain- ancl proteosomal-mediated pathways can be influenced by this mechanism, There is also evidence that the supplementation of antioxidants such as vitamin E (Appell et al 1997), and the application of heat (Selsby & Dodd 2005) can decrease oxida- tive stress and seduce the amount of muscle atsophy. ‘The magnitude and the rate of change in these processes differ acrass muscles and individual animals (Booth & Seider 1979, Goldspiak 1977). Goldspink (1977) reported that over 3-day period of immebilization with the muscle in a short- ened state, the net weight of the animals’ muscles decreased by 30%. Nicks et al (1989) examined whether such changes reflected modifications to either fiber size or fiber number, These researchers observed that following immobilization for Si weeks, the fiber area of a rat's triceps brachii was decreased bby 42%, whereas fiber numbers were unchanged. The position in which a muscle is immobilized influences the magnitude of atrophy considerably. Mascles that are immobilized in a short- ened position are most affected. When muscks are immobi- lized in a lengthened state, they may increase in weight. For instance, Goldspink (1977) noted @ 10% increase in muscle weight in the extensor digitorum muscle after three days of immobilization, Rehited to these changes in muscle mass is a modification in the number of sarcomeres in series. In the early 1970s, Tabary etal (1972) reported that immobilization of a cat's soleus mus- cles in a plaster cast for four weeks in a shortened position Ted to.a 40% decrease in sarcomeres in acres. Tabary etal abo noted that when these muscles were immobilized in a length ened position, 2 0% increase in srcomeres in series occurred. Goldspink et al (174) explored whether these changes were affected by denervation of the muscle. These researchers noted that sarcomere numbers did not appear te be under neural control, and they suggested that the mechanism was a local response to altered tension in the muscle. “The ultrastructural changes that occur following immobi- lization of muscles in a shortened position involve segmental necrosis, predominantly though not exclusively at the ends of the muscle bers as compared to the mid region of the muscle. ‘The work of Baker & Matsumoto (1988) provides an excel- lent description of this process. These authors immobilized the ankle joints of rts in maximal plantarflexion for up 104 weeks. Withia 2 days of immobilization, swelling of the mitochondsia and sarcoplasmic reticulum had yecurred, and by 5 days, the structure of the sarcomeres was breaking down and in many areas appeared kinked. By 7 days, fibers had lost their striated appearance with sarcomere structure being lost completely. These changes continued for approximately 2 weeks. By 4 weeks, although still immobilized, many fibers appeared to be regenerating. Normal sarcoplasmic structure was observed and although the regenerating myofibrils were thinner than normal, they exhibited defined and Z bands, and hence a distinctive sarcomere structure. Thus, the segmental necrosis at the ends of the fibers allows the length of the fiber to be adjusted. This 20 Figire 211 ¢ The force-ength relationship in normal muscle, and ‘muscle that has been immobiized in a shortened postion, Note the shit in the postion of paak forces towards shorter muscle lengths land the decreases in frce able o be generated fn surn will affect the muscle mechanics (e.g the length-tension relationship of the muscle). A muscle after immobilization in a shortened state, when stimulated electrically at different mus cle lengths, will exhibit lesser peak force, and that force will beat a shorter muscle length compared to pre-immebil (Williams & Goldspink 1978) (Fig. 2.11). After tion, most researchers allow their animals to exercise without restriction within their cages. It is apparent that even after remobilization period similar to that of immebilization, the cross-sectional area of many muscle fibers remains significantly less than that of controls (Itai et al 2004). Where training (usu- ally treadmill running) is instituted after immobilization, the size difference between control and. previously immobilized muscle fibers is conserably less, though care in the exercise prescription is needed at the commencement of such programs as bers are easily damaged immediately after immobilization Te has been of interest whether a particular fiber type is ‘more affected by immobilization in a shortened position. The findings generally indicate that Type 1 fibers undergo greater changes than ‘Type II bers, Lieber et al (1988), however, have challenged these findings, These authors have argued that many studies have compared slow ancl fast muscles without due con- sideration for the normal activity evel of the muscles and the subsequent change in use that occurs with immobilization. As well, that these muscles are often immobilized at different lengths will influence the magnitude of atrophy. This will be ‘most apparent when muscles with different fiber lengths and fiber length to muscle length ratios are compared. Finally, the numberof joints that a muscle spans might also affect the mag- nitade of the atrophic response. In a study that controlled for these factors, Lieber et al (1988) concluded that the type of muscle to be affected most by the immobilization process was a single joint muscle containing a relatively large proportion of Type [fibers It should be noted that structural changes are not confined to just the fibers per se, they have also been observedaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Muscle Kuarisinen M, Kaariainen J, Jarvinen T otal 1998 Correlation ‘between biomechanecal and structural changes uring the regeners- tion of sholetal muscle ate laceration injury. Journal of Orthopedic Research 16:197-205, rriainen M, Jarvinen T,Jarvinen M et a1 2060. Relation between yvfibers and connective tissue during mascle injury repair, Scandinavian Journal of Nedicne and Science in Sports 10:332-337 Kanda K, Hashizume K 1932 Factors easing diference i force outpat ‘mang motor unis in the rat medal gastrocnemius muse, Journal of Physiology 448:677-695 Kandarian $C, Stevenson EJ 2002 Molecular eventsin skeletal ‘muscle dering disuse atophy. Exercse and Sport Sciences Reviews 30a 11-116 Keasembjwartana C, Menetrey J, Somogyl G et al 1998 Development oF approaches to isprove the beling following muscle costusion. Call Trarsplant 7:585-568 Kata 81939 The relations betwen force and sped in muscle contre tion. Jounal of Physiology 965-64 litgasrd H, MastoniM, Schiavo Set al 1990 Punction, orphal- ogy ad protels expression of ageing skeletal muscle: a crss-estional uy of elderly men with diferent ictining backgrounds, Acta Phystologice Scandiavice 40-11-54 ‘Nom P ¥ 1873 Measurement of the ferce-velocityrelatonship in human ‘muscle wader concentric and eccenti ations, Medine and Sport szr229 Korhosen MT, Cristes A, Alen M etal 2005 Aging, muscle fiber type fand copteactle Function io sprint-traned athletes, Journal of Applies Physiology 101:906-917 Kosuke T2008. Quadriceps maximal power ind optimal shortening ‘elecity in 333 men aged 23-88 years. European Journal of Applied Physiology 95:140-145 Kuschel R, Deiniager M, Mevermann R et al 2000 Allograft Taflammatory Factor 1 i exprosed by microphagesin injured skeletal smucle and abrogates proliferation and differentiation of stelle cel, Jouinal of Newopathology and Experimental Newrology $0:323-332 LabeitS, Gibson T Lakey A etal 1991 Evidence that nebula jprotein-rler in muscle thn Hlaments, FEBS Letters 282:313-316 cn L, Grimy G, Karlazon } 1979 Muscle strength and speed ‘of movement i relation to age and muscle morphology. Journal of Aprlied Physiology 46-451 155 Larsson L, Edstrom I, Lindegrex B etal 1891 NHC composition nd ‘enayme histochemical and physiologeal peopertios ofa evel Ist twitch motor unit ype. American Jeugnal of Paysilbgy 251:C#3-101 Lehto M; DaanceV; Restall D 1985 Collagen and loronectin in «hel: ing skeletal muscle injury. Journal of Bone and loint Surgery (0) e7E-820-028 Leivo I, Kashanen 8, Michelsson 1 E 1998 Abnormal mitochondria ard ‘sarcoplasmic changes in abbitskcltal mescle mduced by mobili ton. Act Pathologic, Microbologic, et Immanologica Scondinavics 1OGI115-1123 Lieber R, Friden I, Hargons A etal 1888 Differential espense of ‘the dog quadriceps muscle to external skeletal fixation af the knee, Muscle and Nerve 11:193-201 McComas AJ 1996 Skeletal muscle form and function. Human Kinetic, (Champaign, IL Malamud J, Godl R, Nichols R 1996 Relationship between short range stiffness ind yielding in typeidentied chemically shinned muscle ers Irom the eat tier sae muscles, Jourtal of Neurophysiology 76:2280-2289 Mauro A 1951 Sstllte cel of seleta muscle fibers. ournsl of Biophysics Biochemistry and Cytology 87.225-251 Minamoto ¥, Grazziano C, De Fatima Saleina T 1998 Effect of single ‘nd periic contusion on the rt sles miscle a different stages of egeneraton. Anatomical Record 254-281-287 NericiM 1999 Haas skeletal muscle architecture studied in vive by non-invasive imaging techniques: furctional significance and applica- ‘one lownal af Eectronyography ond Kinesiology 847-103 24 [Narict MV, Roi GS, Landon! L 1988 Force of knee extensor and HHexor musses and eros-sectonil aces determined By nucle ms- tetic resonance imaging. European Journal of Applied Physilogy snd ‘Gceupstional Physioigy 5730-44 [Navici MV, Binzoni Milthrand fetal 19% In vivo human gastoc- ‘aemias architecture with changig joint ange at rest and during faded isometric contraction, Journal of Plysiology 486:287-297 Nicks D Bencke W, Key R etal 1989 Muscle fibresize and number following immobilisation atrophy. Journal of Anatomy 163:-$ [NygaardE, Houston M, Suzali Yet al 1983 Morphology ofthe Srackl biceps muscle and elbow flexion in man. ActePhysoloska Scandinavica 117:287-292 Peaches D 19656 ‘The sarcoplasmic reticulum a transverse tubales ofthe fogs sartrius.Joumal of Cell Biology 25 (spp) 209-231 Peachey 1 1968b Travers tubules snckation-contrttion “Coupling. Federation Proceedings 24:1124-1134 Perrine 1, Edgerton V 8 1978 Maace force velocity rationships “nde soknetc loading. Nedicine and Science in Spcts and Exercise 0.ts9-168, Pete D, Saron R 1997 Maramalian skeletal mosce fber type tani- ‘dons International Review of Cytology 1702143-223, Pott D, Peukor H, Staron R § 1999 The impact of biochemical ‘methods fr single muscle bre nalyas. Acta Pbysologica Scandinavica 165261-277 Pinniger GJ, Steele JR, Thorstensson A et al 2000 Teasion regultion luring lengthening and shortening actions of the human soleus muscle European Journal of Applied Physiloy 81:375-383 Pinniger GJ, Ranetunga K W, Offer G W 2006 Crosstide and totr 1500.) fibers in longer tendons do not extend along the full length of the tendon (Benjamin & Ralphs 1995), but smaller dameter fibers may (Kirkendall & Garrett 1997) Collagen fibers are formed in tendon cells and have a specific hierarchical order. In normal tendon, this structural onder of collagen has five different levels (Robins 1988) and is described from microscopic to macroscopic structure (Fig. 3.1) Level 1 Procollagen is formed in the rough endoplasmic reticulum of tenocytes as three polypeptide chains. Each procollagen chain, consists of 1500 amino acid residues. Two of these chainsare a-1 chains and the third is an a2 chain with a different amino acid sequence. In the Golgi apparstus, procollagen forms helix and is then transported to, and excreted from, the cell membrane in vacuoles via the cellular skeletal system of microtubules and nicroflaments (O'Brien 1997). Procollagen is converted to insoluble tropocollagen in the extra-cellular matrix by cleaving the terminal extensions at both ends of the molecule Level? Five tropocollagen molecules agszegate spontaneously to form collagen fibrils. There is an ordered overlap of one quarter of cach tropocollagen molecule in fibrils which is responsible for the striated appearance of collagen on electron microscopy (Gross 1992). This overlap reinforces the collagen and leaves. no weak transverse point where stress could enuse disruption (O’Brien 1997, Robins 1988, Scott 1995), Level Fibrils, which are visible on electron microscopy, aggregate into bundles, forming fibers that sre visible on light microscopy. Lovel 4 Fibers collect into fiber bundles hexagonal in shape and up toa third of a square mm in size. Level Fibers bundles group into fascicles surrounded by endotendon (O’Brien 1997), Fascicles are the longitudinal striations een on ultrasonographic examination “There isa regular sinusoidal pattern or ‘erimp' in the extra- cellular matrix due to the tertiary structure of collagen that is ‘maintained in part by elastic bers. This crimp has a periodicity cof 100-200 am (Robins 1988). Ceimp facilitates shock absonp- tion and allowstendbon to stretch and recover fully. The so-called “toe! area on the stress/strain curve represents crimp stretch, CCrosslinks bond collagen helices. They are essential for the tensile strength of tendon and assist in maintaining tendon shape. Crosslinks between three adjacent colligen moecules occur with hydroxylysylovridinoline and lysylpyridinoline, gly- cation crosslinks with pentosidine occur increasingly in older 20 tissue (Banks et al 1999). ‘The tendon strength gained from crosslinks is reinforced by interaction between collagen and the proteoglycans in the ground substance. Ground substance Ground substance is found. between collagen fibers and con tributes to the viscoelastic properties of tendons. Although inconspicuous in normal tendon, ground substance stil plays a very important roe ia the structure of the extracellular matrix of tendon. Ground substance organizes connective tissue by orientating and ordering collagen fibrils, and thus determines the ultimate tissue and organism shape (Seatt 1995) Ground substance also has other important roles in ten- don physiology and metabolism. Ground substance attaches to, and surrounds, collagen fibrils (Vogel et al. 1984), helping collagen fibsils adhere to and slide past each other (Selvanett et al 1997). Water, which comprises 60-80% of the weight of ground substance, allows gas and nutrient diffusion (O’Brien 1997, Scott 1988) Ground substance is formed by an association between a protein core and giycosiminoglycan (amino sugat) chains. Decorin constitutes most of the protein core in tenclon assoc ated with a single ghvcosimiroglycan chain. This hydrophilic proteoglycan forms a tadpole-like ground substance that con- stitutes up 10 80% of adult tendon. The bulbous proteoglycan part binds to specific sites of the collagen fiber (the D band) and the glycosaminoglycan chain associates and holds the pro- tein parts, and hence the collagen, a specified distance apart Most proteoglycans are oriented at 90° to the collagen fiber, others are randomly arranged or lie parallel to the fiber (Scott 1988). Other small proteoglycans (biglycan, lumican and Sbro. ‘modulin) are ako found in tendon. Aggeecan and versican, large proteoglycans associated with cartilge, complete the other 201%) of protcoslycan content of mature tendon (Fig, 3.2) (Vogel & Meyers 1989) TTendons vary in compostion throughout their length, dependent on the forces placed on specific parts of the ten- don. These forces determine the levels and type of proteogly- ceans, dependent on their ading history. Terelons are subject to tensile loading and both collagen and proteoglycans resist and transmit these tensile forces (Cribb & Scott 1995). However, biclogical movement also causes compression and shearing of tissue, and tendons have weaker resistance to these forces (Selvanetei et al 1997). Tendons that consistently undergo compressive, bending or shearing forces have a higher amount of, and larger, proteoglycans (Cori et al 1993, Scott 1988). It appears that the compression of the tenocytes stimulates this proteoglycan response. Extra aggrecan protects the tendon by Increasing resistance to compression, thus protecting neurovas- cule structures and alossing collagen fiscicles to slide relative to one another (Vogel 2004), Connective tissue All bundles of collagen fibers and! fascicles are surrounded by connective tissue called endotendon, The endosendan carriesaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Tendon of collagen (e.g in the harvestingof tendon tissue for ligament reconstruction) rarely results in tendon pain. Similarly, there is poor correlation between imaging changes after tendon surgery and symptoms (Khan ct al 1999b). Both these observations suggest that collagen damage isnot a source of pai, “The concept that intact collagen surroundlingtencinopathy is overloaded and that it is the source of pain is ako partly rebut- ted by the above discussion. This model suggests that tendons with greater areas of tendinopathy should be more painful, as there is essintact tissue sustaining greater bad, Imaging studies have shown thet there is itele correlation between the amount of collagen disruption and pain, with large areas demonstrated as being asymptomatic on ultrasound, and tendons with aormal imaging having symptoms (Cook et al 198, 20003) Although collagen disruption per se may not be the source of tendon pain, the tenon reaction to collagen damage may create a Kochemical environment that stimulates nociocen- tors. Theoretically, cellular and extracellular debris, minor col- lagens andl proteoglycans have been suggested as the source of nocioceptor stimulation, Other possible mechanisms for tendon pain include irsita- tion ofthe surrounding (and usually well-inervated) structures (fat pad in the knee, subacromial bursa in the shoulder) and increased intratencinous pressure (Johnson et al 1996). These remain theories only, and further investigation is required By using methods like microdialysis, DNA-arrays and PCR, and ultrasonogaphy combined with coler Doppler, there is snow new and potentially important information about the bio- chemical and neurovascular sources of painful tendons. Tendon pathology has essociated neovascularization, and several stud ies have linked increased tendon vascularity to greater tendon pain (Cook et al 2004b, 2005). The relationship, however, is not absolute and the amount of vascularity may merely reflect increased neural ingrowth ‘Neural substances such as glutamate (Alfredson et al 1999), lactate and substance P (Gotoh et al 1998) have been shown in tendon pathology and are known to increase nocioception Receptors to substance P (Ljung ct al 1999) and NMDAR receptors have been shown associated with tendon vessels Glutamate, a wellknown neurotransmitter and very potent modulator of pain in the central nervous syste is found in high levels in painful tendons and not in normal tendons (Alfredson et al 2001). However, glutamate levels were not altered from biseline afier an exercise program that abolished pain (Alfredson & Lorentzon 2003), suggesting that glutamate does not directly contribute to pain but may act by enhancing other neuropeptides. ‘The role of these pain modulatorsin tendon pain is enhanced by the findings of a local neural ingrowth (Bjur et al 2005) Biopsies taken from an area with tencinosis with neovasculasi- zation showed nerve structures in close relation to the vessels (Bjur etal 2005), and stuclies have shown substance P nerves in the vascular wall, and CGRP nerves close to the vascular wall (Bjur et al 2005, Ljung et al 2094). Also, the neurokinin-I~ receptor, which is known to have a high affnity for substance P has been found in the vascular wall (Forsgren et al 2005). 36 The source of tendon pain is a clinically critical aspect of tendinopathy as treatment for tendinopathy is. primarily directed at decreasing pain. Further research in this area is underway, and pharmaceatical, not physical intervention may prove efficacious Physiology of tendon pathology ‘Tendoncells appear to be in a constant state of response toload, and shape their extravellular mates to suit the leading environ: ‘ment. Minor disruption of this process may lead toa cascade of change in the extracellular matrix, changing load capacity and starting a cycle of matrix damage and load sensitivity. The endstage of the pathelogy cycle is neovascularization, and the greatest stimulus for new blood vessels is hypoxia. The role of hypoxia in the development of pathology has not been clarified, but increased levels of lactate have been shown in abnormal tendons, suggesting anaerobic metabolism (Alfredson et al 2002). In addition, hypoxia simulates the production of type II collagen (Mehm et al 1988, Rempel & Abrahamsson 2001), suggesting that hypoxia could drive several changes seen in tendon pathology. In addition, rotator cuff tendinopathy has been reported to have fewer vessels than normal tendon (Biberthaler et ai 2003); however, it is unclear if this drives the hypoxia or ia result of cartilaginous metaplasia. Imaging stu ies suggest thatthe supraspinatus has compressive forces acting oni through most ranges of movement and this could resale in cartilaginous change (Bey et al 2002) In pathological tendon, change in tendon miliew has been quantified by imaging both immediately and over the long term, Afier a single bout of eccentric exercise the tendon volume and signal both increased (Shalabi et al 2004a). Eccentric exercise in the Achilles tendons over a 12-week period has been shown to decrease tendon volume and intratendinous signal, Change in pain correlated with change in signal, although the strength of the relationship was not reported (Shalabi etal 2004b). Tendon repair Soft tissue healing is usually sufficient to maintain function: however, repair of tendonsis never complete (Frank et al 1999), ‘Tencdons appear to have the capacity to repairadequately, asboth endogenous tenocytes anc extrinsic cells originally from outside the tendon can migrate to the tendon damage and contribute to the repair process. There is some debate about the relative contributions ofthe intrinsic and extrinsic cells to tendon repair, and studies have indicated that the tendon is capable of heal: ing without immigration of extrinsic cells (Kraushaar & Nirschl 199). The type anc! site of the injury may determine which repair process is initiated (Gelherman etal 1888). Repsirisinflu tenced by age, tendon vascularity, gender, nutrition, hormones, activity and disease (Hart et al 1995, Leadbetter 1992), ‘Clancy (1989) considered that the poor healing response in tendon is due in part to reparative cells failing to migrate to the site of injury. Alternatively, the poor healing responseaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Tendon Koist M, Sdn L-Jareinen M 1992 Visca changes tthe rupted ‘Actes tendon ants paatenn, Iteration Orthopaedics, 16377-382 Langherg I Bulow J, Kjaer M 1988 Blood ow a the petendizeus ‘pce ofthe human Aches teadon during excise. Acta Physiologica Steadinais 1631 49-153 Lanshera H Shorgaard D,Karamouss Metal 19994 Metaboism ‘ndillanmatery medias inthe pentendinow sce messed iy scrolls daring iterenttent sometic exercise in urns Journal of Physiology $18919.927 Langhere H Skorgaand D, Petersen J tal 19995 Tye tellgen Syathestsand degradation n prteniinus tise afer cxrclse deter ‘ined by crass in hum, Jurnl of Pysiloay$21:289-800 Langherg H. Olesen JL, Genimer Ct al 2002 Substantial elevation Piece Sconensertn orton tem eta te ‘cle following pologed exercise in humans. Joural of Physology Sa2.8s-090 Langherg H, Bowshet R,Skorgaard D tal 2003 Cyclonygense-2 ‘edited pronoglardinrlenne reguntes Sod flowin commertve {se dung mechanical oadng i hus, Journal of Physio Sse 680 LeaabeterW 1982 Call mati esponse in tendo nur. Clinisin ‘Sports Medicine 11'599-578 Leadbetter WB 1993 Tendon overs injures: diagnos and westment ins Rensvom f AFH (ee) Sports nunc, Base praciples of preven tonand care, Oxford Pres, Landon, p 440-475 Lug ForsgronS, Friden 1989 Sobstance P and cictoin gene- ‘elite peptide expresso tthe extensor care ads bev ‘uce ons mpations forthe etlog of enn elbow Jounal of Orthopaedic Research 17884-859 {jung B. Alfredson H,Forsjen $2004 Newrokiin I-eceptors and Sensory neuropeptides intend insertions a the medial sd Ler ponds ofthe humens, Studies on tennis bow and medi ep oniylalga. Journal of OthopiedieResewch 22:321-327 yma J, Wenkold P Almotindes 2004 Stan bchsvou ofthe dsl "Ahles tendos.ArericanJouma of Spars Medicize 32457-461 Meffull N. Khan KM. Puddu G 1998 Overse tendon conditions: “Time to change a cnfiing terminology. Athrscony 14:840-843, MajfulN, Econ S, Moterston Sete 2000 Teneytes rom rupted ‘srdndlnopahicAbillee tendons produce geter quanti o 72 il collagen then tevcyts fom normal Aches tendon. Atescan Touma 9 Sports Medio 28500-8083 aff N, Testa ¥; Capasso G et al 2004 Simos hisopathologeal ctr in alr wit Achilles and fatter tondnopay, Medtne aa Scice ia Sports ard Bxercie 36:1470-1473 Majin T, Yada, ToucidaT ot a1 200) Stic siding of gael lar tendos: effet on smal darter collgen fen a robbie mode Soural ef OrthpacteSenee B890-Ba1 Mehm WJ, Pimsler M Becker Rt 1988 Efecto oxygen ox in ‘iro babs cell proieration an ologen bosyrhens. oma of Hyperbaric Medicine 3:207-234 [irs P1990 Patera Tale healing tendon injury Tn: Leadbeter W B,Buchwalter] A, Gordon § (eds Spots induced elsnmatin: cca snd isc ence oncepes American Ontopedie Society for Sports Medsine, Park Rudge, IL, pores (Fries M 1992 Functional anatey an plsiloy of tendons. Cis in SprtsMedine 11308520 iris M 1997 Struct ind metablsm of terdons. Scandinavian Touma of Medicine and Seiene in Sport '58-61 Obes 1. LorenizonR, Aljredson H 2001, Neoxassirisation in ‘Achilles tendoss th pal tends but nt in normal tendons an ltrasnogrphicnvestastion. Knee Surge, Spots Taumatlos, Rrtoscopy 9233-258 Orchard J, Conk I, Mapa N 2004 Siro shickinge acne of insertind tendnopthy: the operative technique of ited adductor tenotomy supports thie theory Joural of Scterce and Medicine fn Sport 724128 40 Postlethwaite A E 1989 Failed healing responses in connective tissue and ‘ comparisn of medcal conditions. {a Leadbetter W B, Backwalter TA, Gorden § (eds) Sporteinduced inflammation: clic nd basi scence concepts. Amuncan Orthopecte Society for Sorts Medline Park Ridge IL Puddu G, Ippolito E, PostacchiniF 1976 A classifcatioa of Achilles ‘enden disease, Amencan Journ of Sports Medicine 4:145-150, Rempel D, Abrahamsson 5.0 2001 The effets of reduced oxygen ten- ‘ion en el prolferation and marx synthe in synovium snd tendon expats fom the rabbit axpal tunnel an experimental sted in vito. Jourtal of Orthopaede Research 19:143-148 Robins § P 1988 Functional properties of collagen and elastin. Baillee's Clinical Rheumatology 2:1-36 RosagerS, Aegaard P Dyhre-Poulsen Pet ai 2002 Losd-displacement oresfieref the eran artigeeereeatsonninats nel feather fers nd non-sunners Scandinavian Journal of Medicine and Selence i Sports 12:90.08 Rujai A, Ralphs JR, Besjamin M1995 Structute and hstopstholegy ofthe ineertional region of the harman Achales tendon. Journal of Orthopaecic Research 13:585-803 Sane I nhisH, Yeulon A et al 1997 Degsncratsn of the imction ‘weakens the tems strength ofthe sugaspnats tendon: acompara- {ive mechanicl ond histologic study ofthe bone-terdbn complet. Jourtal of Orthepaedie Research 15:719-726 one A G, Einhorn TA 1898 The we of bone morphogenic proteins ‘to heal fractures, articular cari defects, and ligament and tendon Injuries, Spores Medicine and Athvoscopy Review 6118-123, Sarasa-Renedo A, Chiquet M2005 Mechanical signals regulating extra- Cellule matrix gene expresion m fibroblasts. Scandinvin Journal of Medline and Science in Sports 25:273 Sehatzker J, Branemark P 1969 Intravtal observations on the micros: ‘ular anatomy’ and microcirculation ofthe tendon. Acta Orthopaedicn Seandinavis 126 (suppl) S1-523 Sclatimans 1, Beanner F, Staubli H U 1998 Effect of cyclic peccon- “toring on the tensile prepertes of humas quadricepe tendons and patel ligmenss. Knee Surgery Sports Traumatology, Arthroscopy 556-81 Scott A. Khan KM. Cook J Let al 2004 What do we mean by the term Tnflarmation? A contemporary Base scence update Tor sports edie ine. British Journal of Sperts Medicine 38372-380 Scott A, Khaw K, Heer Jet al 2008 High strain mechanical loding ap- “ally induces tendon apoptesis: a ex via rt this anterior movie British Jounal of Sports Medicine 3925 Scctt 1 1988 Proteoglycan-Sbrillr collagen interactions, Journal of Scott 1 1995 Exaacolalar mate, nepramolecular organisation snd ‘Shape. Jouinal of Anatomy 1872850"269 Seleaneiti A, Cippala M, Pudadu © 1997 Overusetenden injures: basic ‘science and clasficaton. Operative Techniques in Sparts Nedicine 5.110117 Sengar DPS, MeKendry RJ. Unthoff HK 1989 Lack of assacation [between FLA and rolatr uff rupture, Tisue Antigens 3420-205 Sengar J, MeKendy R, UnthoffH 1987 Inceessed frequency of HLA-AL ‘a cakilying tendinitis. Tissue Astigers 29:1 73-174 ShalabiA, Keistoforsen-Wiborg M, Aspalin Pet ol 20044 Immediate “Achiles tendon cesponse after stength traning evalusted by MRI Medicine and Science in Sports and Exercise 36:1841-1846 ShalabiA, Kristofierses-Wilherg Mt, Soonsson L tal, 20046 Eccentric “raining of the gstrocnemits-solews complex in chronic Achilles team em dee tenon vl ardinatenious signal a evaluated by MRI American Joural of Sports Medicine piesa ei Shirakura K. Ciarelli MJ. Armocaly JI et al 1988 Deformation ‘induced calcium signaling in enocytes in sit, Presented at Combined (Orthopaecic Research Societies Meeting, Son Diego, CA Spore IB, Roberts A 81988 Teorming pvt ctr. Malle ‘sctions and potential clinieal applications. Journal ofthe American Medical Association 262:938-941aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Ligament Gabriel YF Ng 42 Introduction The musculoskeletal system of the human body provides the morphological framework and machinery for movement. Muscles and nerves are the power generators whereas bones, cartilage, joint capsules and ligaments provide the structural strength to withstand forces imposed onto the body. Injuries from sport or exercise often involve more than one structure and type of tise. Understendiag the organization tnd function of the body tissues can enhance the design of rehabilitation programs and help athletes return to their pre- injury levels of sport performance and physical activity Development of body tissues Human life begins from the instance when a sperm fertiliaes an cag, The first 7 weeks of life is the embryonic stage, and then starting from week 8 until birth is the fetal stage (White et al 1901). At the beginning of week 4 of embryenic life, there isthe formation of neural tissue and somite, which continue to develop into muscles and mesenchyme. Mesenchyme is the precursor of connective tissues such as bones, cartilage and ligaments. Basically, the human body contains four distinct types of tissues: epithelia, nervous, muscle, and connective (Whiting & Zemnicke 1998). Ligament is classified as a form of connective tise Structure and biochemistry of ligament The word ‘lgament’ is derived from a Latin wore ligare which ‘means ‘binding’ (Dye & Dilworth Cannon 1988). As early as3000 BBC, in the Smith Papyrus, joint sprains began to be described and around 400 BC, Hippocrates described treatmenis for liga ‘ment injuries. Aithough in 100 BC, Hegator previded the first anatomical definition of ligament, the ist correct description of ligament was provided by Galen in 130 AD (Snook 1883). Prior to this stag, ligiments were generally considered to be some- thing similar to nerves but with a vague contractile function, In 1830, Schleiden and Schwann discovered cells and long fibers in dase connective tissues and then 20 years later, Rudinger and Hilton further discovered nerves in ligaments andl postulated the figument-muscle feedback system (Frank & Shrive 1994). Ligament is classifed as a form of dense regular connective tise largely consisting of collagen (Whiting & Zernicke 1998)aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.D) toement subject's age, strain rate, and loading direction. Each of these will be discussed in the following sections. Structural components ‘The strength of a ligament largely depends on the type and quantity ofits collagen fibers. An anatomical study by Ramsey (1966) revealed that clastic fibers constitate more than two- thirds of the dry weight of ligamentum flavum, A later study by Nachemson & Evans (1958) demonstrated a very distinct biomechanical behavior of this ligament, Ie is almost perfectly elastic with an unusually high strain value of 70% before failure in young subjects (Fig. 4.7) ‘The decrease in electromyographic (EMG) activities of back muscles during trunk flexion movement was considered to be associated with energy stored in ligamentumlavum thit provided ‘passive support to the upper trunk (Kippers & Parker 1984, Ng & Walter 1995, Steventon & Ng 1995), Furthermore, the elastic sment alto hasa protective function, such thatit will not buckle into the spinal canal and impinge onto the spinal cord with trunk movements (Bogiuk & Twomey 1987), Age In considering the factor of age, the processes of maturation and aging should be considered separately. Oakes & Parker (1981) reported an increase in the mean collagen fibril diameter in rat °L from birth to about 7 weeks, and then a plateau afterwards, Larson & Parker (1982) found that the ultimate tensle strength of ACL changed in a similar pattern to the collagen fibril diam- ter, demonstrating an increase from birth to maturity, and then a leveling off. Woo et al (1990) compared the biomechanical properties of medial collateral ligament (MCL) in both skeb- tally immature and mature rabbits. They found that all skeletally immature specimens failed by tibial avulsion, whereasthe mature specimens failed in the MCL substance regardless of the lading rate, These findings suggest that both the ligament substance and insertion site increaed in strenath with maturation, but the gain in strength is higherin the insertion than the ligament. Figure 4.7 + Load-defermaton characteristics of ligamentum flavum. 40 With aging, however, Noyes & Grood (1976) found that the ‘human femur-ACL-tibia complex from donors aged between 16 sind 26 yearshad highcrsltimate tensile strengthand tilfnessthan that from donorsagedbetween 48and 86yearsby afactorof2t03, ‘Similar findings have also been reported by Woo & Adams (1990) where the linear stiffness and ultimate tensile strength both decreased with aging independent ofthe direction of loading ‘The change in biomeckanical properties with age is likely to bemediated by the increase in quantity and quality of crosslinks and collagen content with maturation, and the decrease of these with aging (Viidik ct al 1982}. Strain rate Studies of the bone-ligament-bone complex have revealed that the structures responded differently at different strain rates, At strain rates of less than 100% per second, most failures occurred in the insertions with bony avulsion, whereas at strain rates of 100% or higher per second, the failures occurred in the midsubstance of the ligaments (Crowninshield & Pope 1976, Hout 1983, Noyes etal 1974a). Besides the location of failure, the ultimate tensile strength and eneray absorption capacity of the ligaments also increased with strain rate regardless of age of the subjects (Woo ct al 1980). Loading direction Ligament such as the ACL hasits longitudinal axis oriented at an angle to the bones. Previous studies have shown that with load ing applied along the longitudinal ais of the tibia, the ultimate tensile strength of the ACL decreased with knee flexion, but ‘when the loud was applied along the ACL aus, no such change occurred (Figgie et al 1986, Woo et al 1987b). ‘Woo & Adams (1590) compared the direction of loading on 14 pairs of femur-ACL-tibia specimens with one leg tested along the tibial axis and the ther tested along the ACL axis, ‘They found higher ultimate strength and stiffness, but lower ‘maximum strain to failure in the ACL when the load was applied along the ligiment axis. The mode of fuilure was also different such that midsabstance failure was produced with ‘ACL axial loading but tibial insertion failure was proclaced with tibial axial loading, It was suggested that during tibial axial load- ing the load was not evenly distributed to the collagen fiber bundles (Woo & Adams, 1990). Some fers may take up more load than others, which tends to ‘peel off” the insestion thus affecting the structural properties Ligament injury and repair ‘The mechanisms of injury can he classified into seven categoe ries (Leadbetter 1994): 41. Contact or direct trauma 2, Dynamic loading 8, Repetitive overuseaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Ligament Ina stucy of ACL-patella tendon autograftin soats(Ng 1995), it was found that most of the endogenous large collagen fibrils (Greater thin 100m diameter) in the original patellar tendon galt disappeared as early as 6 weeks ater surgery. The collagen fibril izes remained small throughout the frst year. At 3 years, there were some large fibrils repopulating and seattering inside the graft, but the packing deasity and orientations of the colla- gen fibrils were still inferior to the normal tissues (Fig 410). Naet al (1995, 1996a) studied the biomechanical strength and biochemical crosslink density of the ACL graft at different time intervals and found the rate of loac-relaxation in the graft to be significantly faster than normal at less than I year. After the fist year, however, the load-relaxation rate sloived down. ‘The ultimate strength and stiffness of the graft dropped in the initial 3 months and then gradually improved, but only achiev ing 43 and 48%, respectively, of the normal values at 3 years. [n these studies, there wasa concomitant change in hydroxypysi- inium crosslinks density in the graft, which was significantly correlated with the Young's modulus of the graft The studies of ACL graft carried out by Nx and his col- leagues (Ng et al 1995, 1996a) revealed that graft remodeling is a long and continuing process. Considering the long time (3 years} invelved in these stuctes, and the persistent lower than normal biomechanical performance of the grafts in these time periods, the implication is that the grafts may never achieve the properties of normal tissues. The findings are in agreement with other animal studies that showed the ultimate censile strength at 1 or 2 years after reconstruction was less than 50% of the normal value (Renstrom & Lysch 1998}. In contrast, a biomechanical study with a human ACL graft revealed that the graft achieved 87% of ultimate tensile strength of the control value at 8 months after surgery (Beynaon et al 1997). The dis- crepancy between this human stily and previous animal stud ies could be due to interspecies difference or success of the rehabilitation program in humans after ACL reconstruction However, the Beymnon et al study only involved one subject, and the strength of the normal ACL of that subject was 1015N, which was substantially lower than the normal value of 1730N, to 2160N reported in the literature (Noyes et sl 1984, Woo et al 1991). Therefore, caution must be exercised in interpreting the result of thit single case human study. Effects of immobilization and exercise Ligaments are sensitive to trainingand disuse. The orginal work in this area was carsied out by Noyes et al (1974b) as a part of the US Air Force experiments on the effect of long-term immo- bilization on ligaments. [¢ was demonstrated that in primates, 8 weeks of cast immobilization of the lower limb resuited in substantial loss of strength in the ACL. With a reconditioning program, it took close to 1 year for the ligament to attain 91% Ultimate tensile strength and 98% stiffiess of the normal value. From the metabolic perspective, Amiel etal (1983) analyzed the collagen tumover rate of rabbit MCL following 12 weeks se of knee immobilization. They found that the collagen mass of MCL decreased by about 30% due to degradation of the collagen. In a later study, Amiel ct al (1985) further demon stnited a close relationship between joint stiffness (as induced by immobilization) and decrease in GAGs of the joint tissues, Similar findings of ligament atrophy with immobilization were also reported by Woo et al (1987c], who demonstrated that an enforced exercise program could hasten the return of mechani- cal properties of the ligaments (Fig, 4.11) ‘The evidence in the literature clearly demonstrates that pro- longed immobilization is detrimental to ligaments. The effects of immobilization are reversible but the effects of recondition- ing took a longer time to show than that of immobilization, Exercise programs, however, can hasten the recovery following immobilization The beneficialeffects of exerciseon ligaments have beenthor- oughly investigated by several researchers (Andrews & O'Neill 1994, Cabaud et al 1980, Larsen & Parker 1982, Tipton et al 1970, 1975, Woo et al 2000). The early work of Tipton et a (1970) revealed that the MCL of dogs that had been subjected to 6 weeks of stremious exercise training were significantly stronger and stiffer than those of the conteol group. Oakes & Parker (1981) studied the collagen fibril diameters of ACL and posterior cruciate ligaments of rats after 4 weeks of treadmill running and sovimming. They found that the exercised rats had a higher numberof collagen fibrils per unit area than the control rats Interestingly, Oakes & Parker (1981) found a decrease in ‘mean fibril diameter in the exercised nats, and they explained this phenomenon as related to the change in the type of GAGs in response to leading, which mediated the collagen Rbril size, Andrews & O'Neill (1994) reported that pelvic exercise is useful in shortening the duretion and lowering the intensity of ligament pain during pregnancy. Ng & Maitland (2001) compared the anteroposterior bxity stifness, and rate of change of stiffness in the knee joints of athletes involved. basketball, running, swimming and of seden- tary control subjects during an instrumented KT-2000 anterior drawer test. It was found that swimmers had the lowest laxity and highest stiffness in their knees followed by the basketball athletes, runners and then the control subjects (Table 4.4). This could be due to the different kinetic loading of these sports to the knees and to the response of the joint structures to loading If this response also happens in ligaments uncler repair, it will have implications for the choice of rehabilitation exercises for subjects after ligament injuries Exercise may not always produce beneficial effects on lige aments. In the study by Burroughs & Dahners (1990), they examined the effect of the dosage of exercise on rats with dif ferent severity of injury to the MCL, ACL and medial joint capsule, Burroughs & Dahners (1990) measured the tensile strength of the repairing ligaments and laxity of the knee joint, and found that exercise had a beneficial effect on the healing MCL that had no associated ACL injury. For the knee joints that demonstrated severe instability with combined injuries of the MCL, ACL and the medial joint capsule, laxity in the joint deteriorated and no increase in tensile strength of the repairingaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Clinical bone conditions knowledge of their condition, there are various imaging tech- niques available. Radiography Radiogrphy has poor sensitivity bat high spe- cificity in the diagnosis of stress fractures. The classic radio- ‘graphic abnormalities seen ina stress fracture are new periosteal bone formation, a visible area of sclerais, the presence of calhis or a visible fracture line. Ifany of these radiographic signs are present, the diagnosis of stress fracture can be confirmed (Santi et al 1989), Unfortunately, in the majority of stress fractures there is no obvious radiographic abnormality. The abaormalitcs on radiog- raphy areunlikely to be seenunless symptoms have been present for at least 2-3 weeks. In certain cases, they may not become evident for up to 3 months, and in a percentage of cases, never ‘become abnormal (Meurman & Elfving 1980) Isotopic bone scan (scintigraphy) ‘The tiple phase bone scan is highly sensitive for diagnosing stress fractures (Prather et al 1977) and changes may be seen as early as 7 hours after bone injury. Astress fracture appearsas a sharply marginated oF fusiform area of increased uptake involving one cortex, or occa sionally extending the widthof the bone inthe third phase of the hone scan (Roub et al 1979) (Fig. 5.6). However, bone scintig- raphy lacks specificity because other non-traumatic lesions such as tumor (especially osteoid osteoma) can also produce localized increased uptake. It is therefore vitally important to correlate the bone scan appearance with the clinical features. ‘The sensitivity of bone scintigraphy can be further increased by the use of single photon emission computer tomography (SPECT). Bore SPECT is most helpful in complex areas of the skeleton with overlapping structures that may obscure patkol- cay such as the skull, pelvis and spine. It is particularly useful in the detection of stress fractures of the pars interarticularis in the spine. Computerized tomography Computerized tomography (CT) ‘may be usefulin differentiating those conditions with increased uptake on bone scan that may mimic stress fracture. CT scans are particularly valuable in imaging fractures where this may be important in treatment such as the navicular bone (Kiss ct al 1993). CT scanning may also be valuable in detecting fracture lines as evidence of stress fracture in long bores (eg. metatar- sal and tibia) where plain radiography is normal and isotope bone scan shows increased uptake. CT scanning will enable the clinician to differentiate between a stress fracture that will be visible on CT scan and a stress reaction. Particularly in elite athletes, this may considerably affect their rehabilitation pro- ‘sam and theic forthcoming competition progyam (Fig. 5.7). Magnetic resonance imaging. Magnetic resonance imaging (MRI, while not imaging cortical bone as well as CT scan, has certain advantages in the imaging of stress fractures. Specific MRI characteristics of stress fracture inchidle new bone forma- tion and fracture lines, and marrow and periosteal hemorrhage and edema, These changesare best seen ifthe MRI is performed within 3 weeks of symptoms (Lee & Yao 1988). Although C scan visualizes bone detail, another advantage of MR imaging in distinguishing stress fractures from a suspected bone tumor or infectious process Figure 56 + The typical bone scen appearance of a stress fracture. Fiqure 5.7 « The CT appearance of a stress factor ofthe ravicular. Treatment ‘The actual time from disgnosis ofa stress fracture to fullreturn ‘© sport or physical activity depends on a number of factors including the site of the fracture, the length of the symptoms, and the severity of the lesion (stage in the spectrum of bone stress). Most stress fractures with a relatively brief history of symptoms will heal without complication or delay and permit return to sport within the 4-8 week range, However there isa syoup of stress fractures that require additional treatment and special consideration. These are listed separately, later in the chapter ‘While there are many subtleties involved inthe treatment of stress fractures, the primary treatment is modified (mest fre ‘quently reduced) activity. During the phase of modified activ- ity, a number of important issues are attended to, including modification of risk factors, maintenance of muscular strength and fitness, pein management, investigation of bone health and prescription of orthotic devices. The treatment of stress 7aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.graduated return to, activity, Prevention of stress fractures is an additional aim of physical therapists working with athletes Identified risk factors in. women include low bore densit later than usual age of menarche, less lean mass, disordered patterns of eating and leg length discrepancy. From a physical therapy perspective, prevention of osteaporotc fracturesfocses fon regular weightbearing activity that is commenced in child- hood and continued throughout life. Management of the older individual with osteoporosis includes education, pain-relieving techniques {if appropriate) and exercises designed to improve posture, balance, range of motion and lower limb strength. Aarden EM, Burger & H, Nijwvide PJ 1994 Function of osteooytesin ‘bone. Foural of Cell Blocherstry 35:287-299 Americas College of Spor's Medicine 1998 Postion stand on eescise ‘and physical activity fr older aduls. Medicive and Seieace fer Sports snd Exercise 30:952-1008 Andvew JG, Andrew SM, Freemont A J etal 1994 Inflammatery calls ‘ignocmal human facture healing, Acta Orthepaesica Stanciravies es402-466 Atkinson K, Coutts F Hassenkamp 4 1999 Physiotherapy in onhopsod- ‘ics Chafcl Livingstone, Edinburgh Atkinson K. Coutts F Hassenkamp 4 2008 Physiatherapy in onho- ‘dies. a problem solving approach, 2nd edn. Church Livingstone, Edinbursh Bailey D A 1997 The Saskatchewan pediatic hone mineral acerzal ‘tedy: foe esinerl acquisition during the growing years fatenational JTouenal of Sports Medicine 18 (zuppl 3}8191-S1S4 Barrow GW, Saha $1988 Meretruairepilerity and strom fracuree in collegiate female distance miners. Americin Journal of Spurs Medicine 16200-216 Bass S, Pearce G, Bradney M etal 1998 Exercise before puberty may ‘confer residual benefit in bone density m adalthocd: studies m active prepubertal and rized female gymnasts lournal of Bone and Mineral Research 13:500°507 Bassey EJ, Ramesdale $ 11994 Increase ix femoral bone density inyoung wornen flowing high impact exerche, Osteoporosis Inernatonal 4:72-75, ‘bait ME, Kemp S, Keralake K 2001 Delayed union sires Tractares of ‘the anterior tba: conservative management. British Journal of Spots Medicine 35:74-77 Benarzo E Barnabei G, Ferrario A et al 1992 Stress factures in ‘yack ar field athletes. Foural of Sports Traumatology and Related Research 1451-65 Bonnell KL, Melcolm SA, Thomas SA etal 1995 Risk fctors or ‘tes fractures in female trackancs field athletes: retrospective Shilyss-Clincal louena of Sports Mediine $:229-235 Bennell KL, Meicolm $A, Thomas SA et al 1896 Risk factors for ‘ress fncturss in tick and feld athletes a 12 moath prospective study, American Journal of Sports Medicine 24:810-818 Bennell K, Khar K, MeKay 2000 The role of physiotheray inthe pre- ‘vention and teatment of osteoporosis. Mantsl Therapy 5:198-213 Blake G Mi Fogelmas 11998 Applications of bone densitometry for ‘osteoporosis: Enlecrincigy and Metabelism Clinics of Noeth America 2720-288 Roivin G,Anthoine Terrier C, Obrant KJ 1990 Teanemiaronelctron ‘microscopy of bone tissue, Acta Orhopaedica Scandinavica 61:170-180, Bonuinti D, Cranney A, levine R ot 12002 Brcrcise for preventing ‘snd testing esteoporosi in postmenopassal women. The Cochrane Database of Systematic Reviews 2<©D000333 Bradney M, Pearce G, Naughton G etal 1998 Moderate exercise ‘luring gfowth in prepuletal boys changes in booe mis, sz, References volumetric detsity, snd bone strength: contrlled prospective stud Journal of Hone and Mineral Reseatch [3:1814-1821 Bravo G, Gauthier B Roy PM etal 1996 Impact ofa 12-math exer- ‘ise program on the physical ard psychologcal health of estcopenic ‘women, ournil of tie Americin Geriatrics Society 44:755-62 Bravo G, Gruthior P Roy P etal 1997 A-weight bearing, water-tased ‘exercise program for osteopenic women: its impact on bose, fune~ tions htress, and wellsbeng, Archies of Phystal Medicine and Rebuilitation 78:1375-1380 Bosh T, Arean 1984 Toward early detection ofthe tendency to stress fractures Clinical Bomechanice :111-115 Bruker PD, Bennell KL 1997 Stress ractres. Critical Reviews in ‘Physical snd Rehabiitation Meccine 9-181 -100 Bruker P, Bensell K, Matheson G 1999 Stress fractures, Blackwell Science Ass, Melbourne Brunet M E, Cook § D, Briaker M R etal 1890 A survey ofrunsing “juries ie 1508 competitive and retreaticnal ners Fowl of Sports Medlcine and Physical Fitness 30:307-315 Baciuealter 1, Glimcher M J, Cooper R Ret al 1995. Bone biology “Journal of Bone and Join Surgery (Am) 77A1256-1273 lure D 2001 Phaemaceticltestments that may prevent or delay ‘the onset of stress factures, In: Burt D B, Milgom (ed) Musculoscletlfatgue and stress fractures. CRC Pres, Boca Raton, FL,p 258-270 Carbon R, Sambrook P N, Deakin V etal 1990 Bone densty of cite Female athletes with stress fractures: Medial Jouenal of Astral 153373375 Carter D R, Hayes WC, Seburman D1 1976, Fatigue life of com ipact bone: IT, Effects of micresteucture and density. Journal of Bromechinice :211-218) (Carter N, Rennus B Khan K M 2001 Exercise inthe prevention of falls in older people: a systematic hterture retew examine the rationale and the evidence, Sports Medicine 31:427-438 Cavanagh P R. LaFortune MA 1980 Grouad rescton feces in distance ‘Tunaing. Journal of Biomechanics 13:397-406 [Chartered Society of Paysethorapy 1999 Physictherspy guidelines for the management of osteopoross. Chartered Society of Physiotherapy, Linton (Cline 4 D, Jansen G R, Melby CI. 1998 Stes fractures in Female sem recruiter mplications oF one density, calium intake, and exer ise. Journal ofthe Amercan College of Nutrition 17128135 ‘Conroy B F Keacmer WJ, Maresh C 3 etal 1983 Bane mineral den- Sityin elite jurior olympic weight liters. Medicine and Science in Sports and Excise 25:1103-1103 Consensus Development Conference 1993 Diagnosis, popaylaxis and “resimen: ofexteoporosts. American Journal of Medicine 9446-050 Cowan DN Jones BH, Frskmas P Net al 1996 Lower lib merphol- ‘ogy and rsk of overuse imury among male infartry tatnees. Medicine and Science in Spor and Exerise 18:945-957 ‘Cummings SR, Black DM, Nevitt MC etal 1993 Bone density st varius sts for prediction of hip fractures. Lancet 341:72-75 (Carrey. D2001 Bone stength: what ae we tying to measure? ‘Calcified Tissue International €8:208-210 Carrey J D2003 How well are bones designed to ress fracture? Journal ‘of Bone and Minera Reseach 18:591-398 tutler WB, Friedmans E, Genovese Stone E 1983 Prevalence of Iyphosein a heathy sample of pre-and postemonopsveal women ‘America Journal of Physcal Medicine and Rehabitation 7221 9-225 Dalaky G BStocke K 6, Fhanei 4-4 otal 1988. Weight boating exoecic ‘raising and lumbar bone mineral content in postmenopaisal women. ‘Aaraleof Internal Medicine 108:821-828 Dickson TB, Kishline P D 1987 Functional management of sts fra: ture in Female athletes wing a pacumatic leg braces Ameriean Four of Sports Medicine 15:86-89 bvahin 8, Thompson P;Baskarate Vo al 1997 Randomized placebo: controlled til of bisk walking inthe prevention of postmenopausal fsteoporess. Age an Ageing 26.258~260 7aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Relevant functonal anatomy and physiology Relevant functional anatomy and physiology Peripheral nerves ‘Axons within peripheral nerves are arranged into bundle called fascicles. Each fascicle is surrounded by a perineurial sheath composed of 6-15 layers of connective tissue contingent upon the fascicular diameter (Lundborg 1988, Matloub & Yousif 1992, Sunderland 1990) (Fig, 6.1). Although the primary orien tation of connective tissue fbersis longitudinal, the inclination changes dlightly between successive layers of the perineuriam (Matloub & Yousif 1992). The laminated architecture ena- bles the perincurial sheath to function as a viscoelastic tube. Because of this viscoclasticity, the perineurial tube is able to change dimensions and maintain pressures in the fascicle that are within physiological limits regardless of the length of the nerve (Kwan et al 1992, Milles et al 1995, Sunderland 1990). Since the interior of a fascicle is lbeled the endoneurial space (Millesiet al 1995), thisintrafascicular pressure i refered to as endloneurial fluid pressure (Luncborg 1988). Besides preserving a constant mechanical environment for enclosed nerve fibers, the perineurium controls the biochemi- «al milieu within the fascicle. The innermost connective tissue lamellae of the perincurial sheath create a metabolically active diffusion barrier that permits only certain chemicals and ions to «come in contact with nearal tissues (Lundborg 1988, Lundborg & Dahlin 1992, Matloub & Yousif 1992, Rempel et al 1999). For example, chemicals associated with edema around a fascicle or infection around a nerve trunk do not come in contact with the intrafascicular environment (Lundberg 1988). The perineurial diffusion barrier works biditectionally. Therefore, if mechanical ‘or chemical stimuli cause endoneural inflammation followed by intrafascicularedema, the resultant increase inendoneutial fluid pressure persists because the perinearium does not allow the inflammatory exudate to escape (Lundberg 1988, Lundborg & Dahlin 1992, Lundborg et al 1983, Murphy 1977). Mechanical perturbation from surgeal dissection of nerve fascicles or from experimentally sustained compression does not alter function ‘of the perineurial diffusion barrier (Lundborg 1988) Structures within the endoncurial space rely on the opti- mal mechanical and biochemical environment regulated by ‘the perineurium. In addition to axons, the endoneurial space accommodates Schwann cells, blood vessels, interstitial fic anda connective tissue network known as the endone- rium (Matloub & Yousif 1992, Rempel et al 1999) (Fig, 6.1). Schwann cells are ghal cells that provide nutritional support for peripheral nerve fibers and contribute to satatory conduction ‘of impulses (Bear ct al 2001, Matloub & Yousif 1992). They are ako a source of proinflammatory cytokines that participate in the inflammatory response exhibited by injured neural tis- sues (Watkins & Maier 2004). A chain of Schwann cells envel- ‘ops a single axon in a myelin sheath designed for high-speed transmission of impulses. In the case of unmyelinated axons, a chain of Schwann cells surrounds several axons to insulate them from the endoneurial space (Bear et al 2001, Matloub & Yousif 1992). Endoncurial connective tissue provides a scaffold ing through which a capillary network courses to supply blood to nerve fibers and associated Schwana cells (Lundborg 1988). ‘This connective tissue scaffolding becomes specialized vo form an endoneurial tubule around each myelinated axon or group of ‘unmyelinated axons (Sunderland 1990), Integrity of enconeuial tabules phys an important role in the movement capabilities of nerve fibers. Axons follow an uundulated course within the endoneurium, and lengthening of anerve trunk causes these undulations to straighten, effectively lengthening axons with minimal to no increase in endoneurial pressure (Millesi et al 1995, Sunderland 1990). Conversely, shortening of a nerve trunk causes the undulations to increase, ‘enabling axons to adapt without being unduly compressed (Milles etal 1995). Thismechanism for accommodating change in length is lost when the endoneurial network is compromised, ‘or when the perineurium is not able to functionas a viscoelastic tube as previously discussed (Milles et al 1995), Just as axons follow an undulating path within the endoneu- rial space, each fascicle takes tortuous course within the nerve Figure 6.1 « Porgheral nerve connocive to sue sheaths, (Reproducee with permission rium ftom Butler 1991.) tema epineuriun tod veal doneurimaa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.Figure 6.10 + Normal deformation of the dura, cord and nerve mots inthe cervical canal na cadaver dueto sagittal plana movement fo! the cervical spine, A fol lamnectomy has been parformed, anc the dura opened and retracted atthough sill abe to transmit tensile ferces. In Athe cervical spne Isin exensin, the nervous system is slack, the ot sleeves have lest contact withthe pecices (ower ‘rows and the nerve roots have separated from the inner surfaces ofthe eloeves (upper arrows. In B tho conical spinehae been flexed, {and the nervous system including the dura has been stretched ‘and mavein relation to surrouraing structures. Note thatthe root ‘eeves have come in contact wth the pedicles and the nerve roots row contac the ner surface ofthe sleeves. Note aso the change in shape of blood vessels. Reproduced from Breig A 1978, with the permission of Almavist & Wiksel International, extremity, Beith et al (1995) found that combined motions of 90° hip flexion, 90° knee extension and 20° ankle dorsiflexion increased the length of the neural container for the sciatic, tibial and medial plantar nerves by 9-12cm, Nerve structures adapt to these changes in the container with a combination of strain, excursion and tensile stress (Beith et al 1995, Byl et al 2002, Coppieters et al 2006, Dilley et al 2003, McLellan & Swash 1976, Millesi et al 1995, Shacklock 1995a, Smith et al 199 Wilks & Murphy 1986, Wright et al 1996, 2001, 2005). Strain is defined as the percentage change in length of a structure relative to its original length (Rodgers 8 Cavanagh 1984), As discussed previously, axons ke an urdulatory course through all portions ofthe nervous system, fldingand unfolding as neural tissues undergo strain (Louis 1981, Millesi et al 1995, 90 Rossitti 1993, Sunderland 1990). This meckanism for adapting to length changes is dependent on the viscoelastic tubes created by the endoncurium, perineurium and dura (Millesi et al 1995, Runza et al 1999). Nerve trunks and neuroreningeal structures are also able to fold and unfold at a macroscopic level (Fig, 6.10), because intraneural connective tissues facilitate giding between fascicles (Louis 1981, Millesi et a 1995, Shacklock 1995a, Sunderland 1990, Wright etal 1996). This macroscopic folding, or ‘wrinkle effect’ (Wright et al 1995), further contrib utes to the strain behavicr of neural tissues, particularly when they nced to shorten. Examples inchide folding of the neurome: ningeal structures on the concave side ofa laterally flexed spinal column (Breig 1978), wrinkling of the median nerve at a fexed elhow (Wright etal 1996) and undulations forming in the ulnar nerve as the elbow is extended (Byi et al 2002) ‘Once neural tissues have unfolded to the point where their undulationsare eliminated, they respond to continuedlengthen- ing ofthe neural container by sling (Shacklock 19954, Topp & Boyd 2006), Excursion or sliding of neural tissues relative to interfacing structures has been documented within the spinal canal (Louis 1981, Rossitti 1993), the intervertebral foramina (Kenneally et al 1988, Smith et al 1993, Sunderland 1974) and the extremities (Coppieters et al 2006, Dilley et al 2003, MeLellan & Swash 1976, Millesi etal 1995, Wilgis & Murphy 1986, Wright et al 1996, 2001, 2005). Recalling previous sce tions on relevant neuroanatomy, this sliding is facilitated by ‘mesoneurium surrounding peripheral nerve trunks. Excursion does not only take place along the longitudinal axis of each neural structure. Neuromeningeal tissues slide in anteroposterior and literal directions daring movement of the spinal coluran (Breig 1978, Louis 1981, Rosstti 1993). Nerve root complexes move in a cephalecaudal direction within the intervertebral foramina daring spinal (Breig & Masions. 1963, Louis 1981) (Fig. 6.10) and limb movement (Kenneally et al 1988, Smith et al 1993, Sunderland 1974). Transverse slid ing has also been observed in peripheral nerves. Greening ct al (1999) demonstrated that the median nerve moves radially tnd posteriorly within the carpal tunnel during wrist flexion, and Ugholue et sl (2005) fourd that isolated meverent of the ‘metacarpophalangeal joint of the index or middle fingers caused small and irregular transverse displacement of the median nerve at the wrist. The superficial branch of the peroneal nerve exhib itsa significant amount of transverse excursion when palpated con the dorsum of the foot (Butler 2000) ‘When sliding mechanisms have been exhausted, additional strain in-nearal tissues is associated with reductions in «ross- sectional area of the nerve trunk and concomitant increases in intraneural pressure or tensile stress (Driscoll etal 2002, Kwan ct al 1992, Millest et al 1995, Shacklock 1995a) Tensile stress is defined as the Force per unit of cross-sectional area gener ated within a structure subjected to a tensile fond (Rodgers & Cavanagh 1984), The viscoelastic behavior of biological tissues is often characterized by stress-strain curves. Nerve structures in situ appear capable of unclergoing significant stain with development of relatively minimal tensile stress (Kwan et al 1992). One notable exception is the ulnar nerve at the elbow.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for viewing or reached your viewing limit for this book.aa You have either reached a page that is unavailable for 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