Exercise and Disease Management Second Edition PDF

S E C O N D E D I T I O N
EXERCISE
and
DISEASE
MANAGEMENT
Brian C. Leutholtz
Ignacio Ripoll
EXERCISE
and
DISEASE
MANAGEMENT
EXERCISE
and
DISEASE
MANAGEMENT
Brian C. Leutholtz
Ignacio Ripoll
Boca Raton London New York
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Contents
Preface...................................................................................................................... xv
Acknowledgment.....................................................................................................xxi
The Authors.......................................................................................................... xxiii
Section 1 “Postmodern” Medicine: Teaching

Patients to Be Responsible
for Their Health
Adherence to Exercise........................................................................... 2
The Exercise Prescription and Adherence............................................3
Reference...............................................................................................4
Recommended Reading........................................................................ 4
Section 2 Curing, Healing, and Maintaining Health
Chapter 1 High Blood Pressure: The Silent Killer................................................ 9

Background...........................................................................................9
Classification of Hypertension According to Cause........................... 10
Prevention of HTN......................................................................... 11
Evaluation of Individuals with High Blood Pressure.......................... 11
Complications of Hypertension........................................................... 11
Hypertensive Cardiovascular Disease............................................ 12
Hypertensive Cerebrovascular Disease.......................................... 12
Hypertensive Renal Disease........................................................... 12
Peripheral Vascular Disease and Coronary Artery Disease.......... 12
Management........................................................................................ 12
Pharmacological Therapy of Hypertension.................................... 13
Target Blood Pressure..................................................................... 16
Follow-Up of Persons with Hypertension........................................... 16
Nonpharmacological Treatment of Hypertension............................... 16
Exercise Issues.................................................................................... 17
Exercise Prescription for Patients with High Blood Pressure............. 18
Weight Training Guidelines for High Blood Pressure........................ 19
Recommended Reading......................................................................20
Exercise Prescription for High Blood Pressure................................... 21
Other Instructions........................................................................... 21
Common Questions on High Blood Pressure (a Patient’s
Perspective)......................................................................................... 22
v
© 2011 by Taylor & Francis Group, LLC
vi Contents
Chapter 2: Diabetes................................................................................................25
Background.........................................................................................25
Classification of Diabetes....................................................................25
Insulin-Dependent Diabetes Mellitus or Type 1 Diabetes.............25
Non-Insulin-Dependent Diabetes Mellitus or Type 2 Diabetes.....26
Impaired Glucose Tolerance........................................................... 27
Gestational Diabetes Mellitus........................................................ 27
Management........................................................................................28
Symptoms of Diabetes....................................................................28
Diagnosis........................................................................................28
Complications of Diabetes.............................................................28
Diabetes and Heart Disease and Strokes...................................28
Diabetes and Kidney Disease....................................................28
Diabetes and the Eye................................................................. 29
Diabetes and the Nerves............................................................ 29
Diabetes and the Mouth............................................................. 30
Diabetes and the Feet................................................................. 30
How to Prevent Complications....................................................... 30
Goals and Recommendations for the Management of
Diabetes Mellitus....................................................................... 30
Diet Therapy................................................................................... 31
Cholesterol................................................................................. 32
Pharmacological Therapy............................................................... 32
A Brief History of Treatment Strategies for Patients with Type 2
Diabetes............................................................................................... 33
Initiation of Treatment......................................................................... 36
Hypoglycemia................................................................................. 39
Sites of Administration...................................................................40
Exercise Issues....................................................................................40
Issues Regarding Exercise Prescription in Patients with Diabetes...... 41
Exercise and the Type 1 Diabetic.............................................. 42
Exercise and the Type 2 Diabetic.............................................. 42
Glucose Monitoring and Exercise............................................. 42
Summary............................................................................................. 43
Weight Training Guidelines for Diabetics..........................................44
Recommended Reading...................................................................... 45
Exercise Prescription for Diabetes......................................................46
Other Instructions...........................................................................46
Common Questions on Diabetes (a Patient’s Perspective).................. 47
Chapter 3: Kidney Disease..................................................................................... 49

Background......................................................................................... 49
Management........................................................................................ 51
Exercise Issues.................................................................................... 52

Contents vii
Benefits of Exercise............................................................................. 53
Weight Training Guidelines in Kidney Disease.................................. 53
Exercise Prescription for Kidney Disease........................................... 55
Common Questions on Kidney Disease (a Patient’s Perspective)....... 56
Chapter 4: Heart Disease....................................................................................... 59

Coronary Artery Disease: The Number One Killer............................ 59
Background..................................................................................... 59
Management................................................................................... 59
Drug Therapy............................................................................. 59
Exercise Issues................................................................................60
Weight Training Guidelines for Heart Disease................................... 62
Exercise Prescription for Heart Disease............................................. 63
Common Questions on Heart Disease (a Patient’s Perspective).........64
Congestive Heart Failure.....................................................................66
Background.....................................................................................66
Management...................................................................................66
Therapy for Patients with Systolic Dysfunction........................ 67
Therapy for Patients with Diastolic Dysfunction...................... 68
Exercise Issues................................................................................ 68
Exercise Prescription for Congestive Heart Failure............................ 70
Valvular Disease................................................................................. 70
Mitral Stenosis................................................................................ 70
Background................................................................................ 70
Management.............................................................................. 71
Mitral Regurgitation....................................................................... 71
Background................................................................................ 71
Management.............................................................................. 72
Mitral Valve Prolapse..................................................................... 72
Background................................................................................ 72
Management.............................................................................. 72
Aortic Stenosis................................................................................ 72
Background................................................................................ 72
Management.............................................................................. 73
Aortic Regurgitation....................................................................... 73
Background................................................................................ 73
Management.............................................................................. 74
Multivalvular Disease..................................................................... 74
Exercise Issues................................................................................ 74

viii Contents
Exercise Prescription for Valvular Disease......................................... 76
Hypertrophic Cardiomyopathy............................................................ 76
Background..................................................................................... 76
Management................................................................................... 77
Exercise Issues................................................................................ 77
Exercise Prescription for Hypertrophic Cardiomyopathy................... 78
Cardiac Arrhythmias and Pacemakers............................................... 79
Background..................................................................................... 79
Management................................................................................... 79
Exercise Issues................................................................................80
Patients with Cardiac Pacemakers............................................. 81
Exercise Prescription for Arrhythmias............................................... 82
Exercise Prescription for Patients with Pacemakers........................... 83
Chapter 5: Lung Disease........................................................................................ 85

Chronic Lung Disease......................................................................... 85
Background..................................................................................... 85
Management................................................................................... 85
Restrictive Disease.............................................................................. 86
COPD.................................................................................................. 87
Cystic Fibrosis..................................................................................... 89
Cor-Pulmonale....................................................................................90
Exercise Issues................................................................................ 91
Asthma................................................................................................ 93
Background..................................................................................... 93
Management...................................................................................94
Exercise Issues................................................................................ 95
Weight Training Guidelines for Lung Disease....................................96
Recommended Reading......................................................................97
Exercise Prescription for Chronic Lung Disease and Asthma............ 98
Common Questions on Lung Disease (a Patient’s Perspective)..........99
Chapter 6: Obesity................................................................................................ 103

Introduction....................................................................................... 103
Defining the Metabolic Syndrome.................................................... 105
Management................................................................................. 108
Exercise Issues.............................................................................. 113

Contents ix
Weight Training Guidelines for Obesity........................................... 114

Recommended Reading.................................................................... 115
Exercise Prescription for Obesity...................................................... 116
Other Instructions......................................................................... 117
Common Questions on Obesity (a Patient’s Perspective).................. 117
Chapter 7: Vascular Disease................................................................................ 119

Background....................................................................................... 119
Pathogenesis...................................................................................... 120
Pharmacological Treatment............................................................... 123
Diet and Exercise Management......................................................... 127
Peripheral Vascular Disease.............................................................. 128
Exercise Issues.................................................................................. 128
Weight Training Guidelines for Peripheral Vascular Disease.......... 130
Exercise Prescription for Peripheral Vascular Disease..................... 132
Common Questions on Peripheral Vascular Disease (a Patient’s
Perspective)....................................................................................... 133
Chapter 8: Osteoporosis and Arthritis............................................................... 135

Osteoporosis...................................................................................... 135
Background................................................................................... 135
Management................................................................................. 135
Exercise Issues.............................................................................. 137
Arthritis............................................................................................. 137
Weight Training Guidelines for Osteoporosis and Arthritis............. 138
Exercise Prescription for Osteoporosis and Arthritis....................... 140
Common Questions on Osteoporosis (a Patient’s Perspective)......... 140
Chapter 9: Cancer, the Immune System, and AIDS......................................... 143

Cancer............................................................................................... 143
Background................................................................................... 143
AIDS................................................................................................. 144
Background................................................................................... 144
Anxiety and Depression in Patients with Cancer and HIV
Infections........................................................................................... 145
Exercise and Cancer.......................................................................... 146
Colon Cancer................................................................................ 147
Breast Cancer............................................................................... 147
Endometrial Cancer...................................................................... 147

x Contents
Lung Cancer................................................................................. 148

Cancer Survival............................................................................ 148
Exercise and the Immune System..................................................... 148
Toll-like Receptors....................................................................... 148
Heat Shock Proteins..................................................................... 149
Cachexia............................................................................................ 150
Background................................................................................... 150
Management................................................................................. 151
Exercise Issues.............................................................................. 152
AIDS................................................................................................. 152
Management................................................................................. 152
Exercise Issues.............................................................................. 152
Cancer............................................................................................... 153
Management................................................................................. 153
Exercise Issues.............................................................................. 153
Weight Training Guidelines in Chronic Infections........................... 154
References......................................................................................... 155
Exercise Prescription for Chronic Infections: Cachexia, AIDS,
and Cancer......................................................................................... 155
Common Questions on Diseases of the Immune System
(Chronic Infections, Cachexia, and AIDS) (a Patient’s
Perspective)....................................................................................... 156
Chapter 10: The “Golden Years”........................................................................ 159

Exercise in the Healthy Elderly......................................................... 159
Background................................................................................... 159
Management................................................................................. 160
Exercise Issues.............................................................................. 160
Weight Training Guidelines during the Golden Years...................... 162
Exercise Prescription during the Golden Years................................ 164
Chapter 11: The Physically Inactive................................................................... 165

Exercise Recommendations for Healthy but Physically Inactive
Individuals......................................................................................... 165
Background................................................................................... 165
Physical Activity and Exercise: What Is the Difference?............. 165
Physical Activity and Exercise: Understanding Intensity............ 165
Weight Training Guidelines for Physically Inactive Individuals
without Disease................................................................................. 167

Contents xi
Exercise Prescription for Physically Inactive Individuals

without Disease................................................................................. 168
Chapter 12: Pregnancy......................................................................................... 171

Background....................................................................................... 171
Management...................................................................................... 172
Managing the Pregnant Athlete........................................................ 172
Exercise Issues.................................................................................. 173
Weight Training Guidelines during Pregnancy................................. 174
Exercise Prescription during Pregnancy........................................... 175
Chapter 13: Wheelchair-Dependent Patients..................................................... 177

Background....................................................................................... 177
Exercise Issues.................................................................................. 177
Weight Training Guidelines for Wheelchair-Dependent Patients..... 179
Exercise Prescription for Wheelchair Dependency
(Quadriplegia) Functional Electrical Stimulation............................. 180
Exercise Prescription for Wheelchair Dependency (Paraplegics)..... 180
Chapter 14: Prepubescent Children.................................................................... 183

Healthy Children............................................................................... 183
Background................................................................................... 183
Management................................................................................. 183
Exercise Issues.............................................................................. 184
Fitness Testing......................................................................... 184
Weight Training Guidelines for Children......................................... 184
Reference........................................................................................... 186
Exercise Prescription for Prepubescent Children............................. 186
Appendices
Appendix A: Exercise Prescriptions and “the Charts”..................................... 191
Method 1: The Age-Predicted Method............................................. 191
Method 2: Heart Rate Reserve or Karvonen Method....................... 192

xii Contents
Method 3: The Rate Pressure Product Method................................. 192

Method 4: Systolic Blood Pressure Method...................................... 193
Method 5: The Charts....................................................................... 194
How to Use the Charts.................................................................. 194
Method 6: Maximal Oxygen Consumption
(the VO2 max or Maximal Functional Capacity)............................... 196
Method 7: The Anaerobic Threshold................................................ 196
Method 8: Ventilation........................................................................ 196
Method 9: The VO2 Reserve............................................................. 197
Method 10: Weight Lifting Formula................................................. 197
Appendix B: Exercise Testing.............................................................................. 199
Medical Screening Prior to Exercise................................................. 199
Cardiac Stress Testing....................................................................... 199
Absolute Contraindications.......................................................... 199
Relative Contraindications...........................................................200
Cardiopulmonary Stress Testing.......................................................200
Aerobic Fitness............................................................................. 201
Aerobic Exercise........................................................................... 201
The VO2 max................................................................................ 201
Oxygen Economy......................................................................... 201
Anaerobic Exercise.......................................................................202
Oxygen Debt.................................................................................202
The Anaerobic Threshold.............................................................202
Heart Rate and Exercise............................................................... 203
HR, AT, and Perceived Exertion.................................................. 203
Exercise Testing for People with Common Cardiopulmonary
Problems............................................................................................204
Heart Failure.................................................................................204
Pulmonary Vascular Impairment.................................................204
Using a Cardiopulmonary Stress Test to Prescribe Exercise
for Patients with Heart Failure or Pulmonary Vascular
Impairment...................................................................................204
Restrictive Pulmonary Diseases...................................................205
Obstructive Impairment...............................................................205
References.........................................................................................207
Exercise Prescription.........................................................................207
Appendix C: Training Injuries............................................................................209
Cardiocirculatory System..................................................................209
Endocrine System..............................................................................209
Eyes...................................................................................................209
Gastrointestinal System..................................................................... 210
Hematologic System.......................................................................... 210
Muscular Pain or Injury.................................................................... 210
Musculoskeletal System.................................................................... 210
Overuse Injuries................................................................................ 211

Contents xiii
Tendinitis........................................................................................... 212
Bursitis.......................................................................................... 212
Stress Fractures............................................................................ 213
Overuse Injuries of the Arm and Hand........................................ 213
Lateral Epicondylitis (Backhand Tennis Elbow)..................... 213
Medial Epicondylitis (Forehand Tennis Elbow, Pitcher’s
Elbow)...................................................................................... 214
Little League Elbow................................................................ 214
Bicipital Tendinitis................................................................... 214
Tendinitis of the Dorsal Aspect of the Wrist........................... 214
Tendinitis of the Thumb Extensor (DeQuervain’s Tendinitis).... 214
Olecranon Bursitis................................................................... 215
Shoulder Pain........................................................................... 215
Rotator Cuff Tendinitis............................................................ 215
Overuse Injuries of the Lower Extremities.................................. 215
Shin Splints.............................................................................. 215
Stress Fractures of the Tibia.................................................... 216
Compartment Syndrome.......................................................... 216
Overuse Injuries of the Knee........................................................ 217
Chondromalacia Patella (Extensor Mechanism Injury).......... 217
Patellar Tendinitis (Jumper’s Knee)......................................... 218
Osgood–Schlatters Disease..................................................... 218
Hamstring Tendinitis............................................................... 218
Semimembranosus Tendinitis.................................................. 218
Semitendinosus Tendinitis and Pes Anserinus Bursitis........... 218
Popliteal Tendinitis.................................................................. 219
Iliotibial Band Tendinitis (IBT)............................................... 219
Overuse Injuries of the Hip and Thighs....................................... 219
Trochanteric Bursitis............................................................... 220
Back Pain................................................................................. 220
Overuse Injuries of the Foot and Ankle....................................... 222
Plantar Fasciitis....................................................................... 223
Achilles Tendinitis...................................................................224
Haglund’s Syndrome................................................................224
Metatarsal Stress Fractures.....................................................224
Navicular Stress Fractures.......................................................224
Orthotics....................................................................................... 225
Nerve Entrapment............................................................................. 225
Carpal Tunnel Syndrome.............................................................. 226
Pulmonary......................................................................................... 226
Skin................................................................................................... 226
Urinary System................................................................................. 226
Thermal Injuries................................................................................ 227

Preface
All parts of the body which have a function, if used in moderation and exercised in
labors in which each is accustomed, become thereby healthy, well-developed, and age
more slowly, but if unused and left idle they become liable to disease, defective in
growth, and age more quickly.
Hippocrates
Walk and be happy; walk and be healthy.

Charles Dickens
Take a two-mile walk every morning before breakfast. Walk as though you have some-
where to go.
President Harry Truman
We doctors can now state from our experience with people, both sick and well, and
from a growing series of scientific research, that keeping “fit” does pay richly in divi-
dends of health and longevity.
Paul Dudley White, MD
Recently, several important reports have been published that have confirmed the sen-
timents of these earlier observers. Moreover, these recent findings have far-reaching
implications for contemporary physicians and allied health professionals dedicated
to the prevention of chronic disease and disability.
In 2008, the U.S. Centers for Disease Control and Prevention (CDC) published health
recommendations for physical activity. It was concluded that adults need at least:
Two hours and 30 minutes (150 minutes) of moderate-intensity aerobic

activity (i.e., brisk walking) every week and
Muscle-strengthening activities on 2 or more days a week that work all major

muscle groups (legs, hips, back, abdomen, chest, shoulders, and arms)
One hour and 15 minutes (75 minutes) of vigorous-intensity aerobic activity

(i.e., jogging or running) every week and

xv
xvi Preface
An equivalent mix of moderate- and vigorous-intensity aerobic activity and

Recommendations for children and older adults can also be found on the CDC Web
site (http://www.cdc.gov/physicalactivity/everyone/guidelines/index.html).
The National Institutes of Health (NIH) convened a consensus development con-
ference on physical activity and cardiovascular health. Conclusions of the consensus
conference were the following:
• Physical inactivity is a major risk factor for cardiovascular disease.

• Too many Americans are sedentary.
• Moderate amounts and intensities of physical activity confer important
health benefits.
The principal recommendation from this conference was essentially identical to

that of the CDC and the American College of Sports Medicine (ACSM), with the
goal of accumulating at least 30 minutes of moderate-intensity activity each day.
Moreover, the NIH statement also called for the widespread implementation of phys-
ical activity promotion programs at the national and community levels.
In 1996, the U.S. Public Health Service published Physical Activity and Health:
A Report of the Surgeon General. This action was largely based on recommenda-
tions from professional and scientific groups concerned about the mounting evidence
linking physical inactivity and chronic disease. The CDC was asked to take the
responsibility for preparing the report, with assistance from the President’s Council
on Physical Fitness and Sports as the representative of the Surgeon General’s Office.
Among its major findings were the following:
• Physical activity is a major health problem in the United States. More than
60% of American adults are not regularly physically active. In fact, 25% of
all adults are not active at all.
• People of all ages, both male and female, benefit from regular physical
activity.
• People who are usually inactive can improve their health and well-being by
becoming even moderately active.
• Physical activity need not be strenuous to achieve health benefits.
• Greater health benefits can be achieved by increasing the amount (intensity,
frequency, or duration) of physical activity.

Preface xvii
• Physical activity reduces the risk of premature mortality, in general, and of

coronary heart disease, hypertension, colon cancer, and diabetes mellitus
in particular.
• Physical activity also improves mental health and is important for the health
of muscles, bones, and joints.
A more comprehensive review of physical activities guidelines can be found at the

following CDC Web site: http://www.cdc.gov/NCCDPHP/sgr/ataglan.htm.
The fervor of the primary care physician’s recommendation appears to be one
of the most powerful predictors of exercise participation. Accordingly, this text is
directed at proselytizing this group (and related health care professionals) regarding
the benefits of regular exercise and increased physical activity. Routine counseling
by medical and paramedical personnel may have the additional impact of favorably
modifying their patients’ lifestyles.
Although there are numerous books on exercise testing and prescription for
presumably healthy adults and cardiac patients, there remains the need for a com-
prehensive reference source that addresses the requirements of special patient popu-
lations. This virtual pharmacopoeia of exercise guidelines, geared especially toward
the primary care physician and other members of the health care team, should prove
helpful in more clearly defining the benefits and limitations of exercise testing and
training in the evaluation and management of a broad spectrum of patients, including
those with cardiovascular and/or pulmonary disease, hypertension, diabetes, kidney
disease, obesity, osteoporosis, arthritis, AIDS, and AIDS-related diseases, as well as
those who are pregnant, young (prepubescent), elderly, or confined to a wheelchair.
Exercise and Disease Management is designed to help managed care physicians
(and their allied health care professional contemporaries) integrate current exercise
guidelines into their practices. This textbook is uniquely accompanied by a series of
11 workbooks, each one for a chronic disease, designed specifically for physicians
to give to their patients. These workbooks make it convenient for physicians to pre-
scribe exercise (and physical activity) to their patients in a ready-to-use format. Each
book chapter and workbook contains a section on the background, medical manage-
ment, and exercise guidelines, accompanied with self-care instructions for patients,
encouraging them to take a proactive role in their health and disease management.
The user-friendly tables and charts in the appendices eliminate many of the tedious
calculations to quantitate fitness and establish safe and effective exercise regimens
and warrant particular commendation.
This book and the accompanying workbooks have been written by authorities in
exercise science and medicine. They provide substantial reinforcement of exercise
and increased physical activity to promote improved aerobic fitness and health, with
specific references to deficits or defects resulting from congenital deformities, injury,
or chronic disease, and needs and contraindications imposed by these conditions.
Furthermore, in the present medical environment challenged with apportioning
shrinking health care dollars, this innovative approach has the potential to help lit-
erally millions of patients help themselves—at a fraction of the cost of more tradi-
tional interventions.

xviii Preface
Lack of activity due to a sedentary lifestyle poses a major threat to the health
of individuals in the United States. It is widely accepted that inactivity results in
chronic diseases, such as cardiovascular and pulmonary diseases and diabetes, that
require repeated physician visits and hospitalizations. Health care providers have
traditionally treated their patients by prescribing medications. Emphasis on diet and
exercise has been less important. This book provides the health care professional
with the necessary tools for prescribing exercise integrated with other aspects of
disease management.
Inactivity is a powerful predictor of early mortality. A study in the Journal of
the American Medical Association (Blair et al. 1996) reported that less fit men and
women are approximately twice as likely to die during an 8-year follow-up, com-
pared to their counterparts. Currently, 25% of the population in the United States is
inactive, making this a major health issue.
On July 11, 1996, the first Surgeon General’s Report on Physical Activity and
Health was released. The health message of this 250+ page document, based in part
on the 1993 public health study conducted by the CDC, states that adults should
accumulate 30 minutes or more of moderate-intensity physical activity most, if not
all, days of the week. This report represented the first time the federal government
issued a formal statement on the importance and benefits of physical activity.
Patients who have chronic diseases routinely see their physicians for management
of their conditions. Many of these patients may require or desire exercise guidelines;
unfortunately, only 10% of visits to the physician’s office currently involve any men-
tion of exercise prescription. Exercise and Disease Management includes a medical
health care plan designed to encourage and enable patients to take an active role in
their health by incorporating exercise into their daily routines.
Exercise and Disease Management was written for physicians and medical pro-
fessionals. It consolidates the current knowledge on exercise and chronic disease
and supports the surgeon general’s recommendations on physical activity and health.
It was developed using the most current standards in exercise prescriptions. It is
designed to fit into today’s managed care system for physicians and all other medi-
cal professionals who are ever more challenged to keep their patents healthier and
more active.
THE “CONCEPT”
Exercise and Disease Management was designed to be used together with a series of
workbooks in the enclosed CD as a teaching and managing resource that emphasizes
exercise prescriptions for physicians and other medical professionals. The chap-
ters were written for the medical team with a focus on patient education and exercise
prescription. Each chapter contains a brief, concise section outlining the background
of the disease, followed by management and exercise suggestions.
Each of the disease-specific workbooks corresponds to one of the diseases out-
lined in Chapters 1–11 of this book and can be used separately by you or your
patients. Included in each workbook are sample and blank exercise prescriptions
(you may want to modify the standard exercise prescription for a particular patient),
a question and answer section about the illness, tips to assist your patients to adhere

Preface xix
to an exercise routine, and an exercise log. For the patient with multiple diseases, we
suggest prescribing the workbook that corresponds to the patient’s most significant
disease. Each workbook is designed to account for overlapping illnesses.
Chapters 1–9 deal with chronic or ambulatory sensitive conditions that can be
treated with exercise. Chapters 10–14 provide exercise guidelines for patients who
are free of disease and for wheelchair-dependent patients. Currently, very few physi-
cians and health practitioners ask their patients about their exercise habits; fewer of
them know how exercise modifies health and disease and how to prescribe exercise.
This book intends to correct that deficiency.
REFERENCE
Blair, S., J. Kampert, H. Kohl, III, C. Barlow, C. Macera, R. Paffenbarger, Jr., and L. Gibbons.
1996. Influences of cardiorespiratory fitness and other precursors on cardiovascular
disease and all-cause mortality in men and women. Journal of the American Medical
Association 276:205–210.

Acknowledgment
Dr. Ripoll would like to extend a special thank-you to his wife, Patricia Ripoll,
who generously let him use almost every weekend to research and write this book.
Without her support and encouragement, this would not have been possible.
xxi
The Authors
Brian C. Leutholtz, PhD, FACSM, received his BS in dietetics from Michigan State
University in 1985, his MS in exercise physiology from Michigan State University
in 1987, and his PhD in clinical exercise physiology from Michigan State Univer
sity in 1992. Dr. Leutholtz completed a 4-year clinical fellowship in clinical cardiol-
ogy at Butterworth Hospital in Grand Rapids, Michigan. As a fellow of the American
College of Sports Medicine (ACSM), he has earned the highest certification given
by the ACSM as a clinical program director. Dr. Leutholtz is a professor at Baylor
University in Waco, Texas. He was recruited by Baylor to improve their graduate
curriculum and begin the development of a PhD program by teaching and creating
new courses at the graduate level in sports nutrition and exercise prescription for
special populations.
Dr. Leutholtz has past experience as the director and founder of the Old Dominion
University Therapeutic Exercise Program for Chronic Disease (TEMPO) in Norfolk,
Virginia, and has served as a consultant for an aggressive managed care team provid-
ing exercise and diet evaluation/education in Virginia Beach, Virginia. He is currently
the coordinator for the exercise physiology graduate program at Baylor University.
Dr. Leutholtz has recently added a coauthored second edition book, Exercise
Prescription: A Case Study Approach to the ACSM Guidelines, to his list of book
publications. The book has been translated into Japanese, Korean, and Chinese. In
this book, the long-standing ACSM equations were enhanced and a new term, “VO2
reserve,” was adopted by the ACSM.
Ignacio Ripoll, MD, FACP, FACCP, is associate professor of internal medicine at

Eastern Virginia Medical School and medical director of the Respiratory Therapy
and School of Polysomnography Technology at Tidewater Community College. He
is also an adjunct professor of exercise physiology at Old Dominion University in
Norfolk, Virginia. He is a member of Bayview Physicians, a multidisciplinary medi-
cal group, and practices pulmonary, sleep, and bariatric medicine in Virginia Beach,
Virginia. He has a particular interest in the fields of cardiopulmonary physiology,
sleep medicine, and the evaluation and management of the metabolic syndrome.
DISCLAIMER
During the preparation of this book, Dr. Ripoll was responsible for the medical and
Dr. Leutholtz for the exercise physiology aspects of the work. The authors reviewed
sources thought to be reliable in order to provide information that is up to date.
However, there is always the possibility of human error or the possibility that the
information presented was incomplete; therefore, before acting on this information
the reader is advised to confirm the information present herein with other sources,
particularly the package information sheets present in the package of drugs to identify
possible contraindications or ill effects of those products. This is particularly impor-
tant when using medications outside the FDA accepted indications (off-label use).
xxiii
xxiv The Authors
Medical science is in a process of constant change; for example: at the time of

publication, there was considerable debate about the use of glitazones and other
antidiabetic drugs and the FDA was reviewing the pros and cons of several products
used in the therapy of obesity. Effort has been made to publish reliable information,
but the authors cannot assume responsibility for the validity of the data or the con-
sequences of its use.

Section 1
“Postmodern” Medicine:
Teaching Patients to Be
Responsible for Their Health
It is no secret that there is a growing dissatisfaction among physicians with the prac-
tice of medicine. Their autonomy restricted, they strive to safeguard their patients’
welfare, and they react to the cost-driven changes with fear and outrage.
Since the 1950s, hospital personnel per occupied bed has increased 7 times and
the cost per patient per day has increased 26 times. Since 1983, total administrative
expenditures have grown 90%—significantly higher than the 30% growth in service
departments and the 45% growth in total hospital budgets. Meanwhile, the funding
for research, which rose at a rate of 15% from 1946 to 1964, fell to less than 2%
from 1965 to 1989 (Shulkin 1993). Prior to 1950, health care costs remained stable at
3–5% of GNP; since then, they have grown to an intolerable 15% of GNP.
Nearly everyone, including physicians, business people, and politicians, agrees
that the situation has to change. The most important change has been in the attitude
of those who pay the cost of medical care. During the last few decades, in spite of
the obvious therapeutic revolution, there has been a steady decline in the confidence
of patients and payers in the ability of technology and the health care industry to
bring about improvements in health care that are, at least, proportional to the amount
of resources invested.
Individuals with chronic illnesses account for 75% of the cost of health care.
Reforming health care in such a way that it results in more effective care for patients
with chronic illnesses should be the primary goal of managed care. However, disease

2 “Postmodern” Medicine: Teaching Patients to Be Responsible for Their Health
management, which should be the focus of managed care, has not progressed beyond
the development of practice guidelines, protocols, care paths, and the concept of case
management by nurses directed by physicians. Effective care lies one step beyond
economic monitoring, incentive distribution, and case management. Effective care
is effective self-care.
Physicians and patients have different perspectives on illness. Physicians under-
stand illness within the context of diagnosis, therapy, and compliance with such
therapy. The patient and his or her family understand illness within the context of
pain; suffering; disruption to family, social, and work life; economic consequences;
and emotional impact. The gap between the physician’s and the patient’s perspective
is responsible for the separation between that which the physician prescribes and that
which the patient does.
The first step to overcome the gap between the scientific and the personal approach
to illness is to provide a service where the scientific approach to illness is modi-
fied and implemented within the context of the patient’s and the family’s psychoso-
cial and economic circumstances.
A dedicated approach to disease management is needed—one that will provide a core
of services that complements office services and results in more efficient health promo-
tion. At the same time, it will provide a strategy for disease management that combines
scientific guidelines with personal preference, resulting in improved self-care.
Effective self-care requires
knowledge of the disease and its treatment

action to promote health, including behavioral change and objective monitoring
goal setting
emotional and social support
It is not easy for the physician to change a patient’s lifestyle. There is evidence
to suggest that information obtained from the physician can motivate the patient
to change, but the effect is usually short-lived unless a system of support, reward,
and encouragement continues to reinforce the patient’s behavior until its positive
effect on the quality of life becomes obvious. Regular exercise must become a habit
because exercising can increase the desire to exercise.
Lecturing the patient on exercise or health-related issues, membership in health
clubs, and participation in cardiac or pulmonary rehabilitation programs has failed
to promote lifelong exercise habits. With current methods, 50% of patients will stop
exercising within 6 months to 1 year.
ADHERENCE TO EXERCISE
The factors known to be associated with exercise adherence include the following:
• Education: People who know about the benefits of exercise and how to
exercise are more likely to develop the habit of exercise.
• Family support: Support and encouragement from family members, espe-
cially spouses, are potent motivators to exercise.

“Postmodern” Medicine: Teaching Patients to Be Responsible for Their Health 3
• Social support: Lack of time is the most common excuse not to exercise.
Exercise should be scheduled in such a way that it is compatible with the
person’s work and preferences. Exercising with friends adds an extra layer
of reinforcement and motivation. It becomes difficult not to exercise if one
has promised friends to exercise with them.
• Medical support: Many patients, especially those who have existing med-
ical conditions, fear exercise. They fear that exercise may cause sudden
death or aggravate their cardiac or pulmonary condition. They fear that
exercise is bad for their joints, that it will cause arthritis or aggravate it, etc.
Many of these fears can be dissipated if the health care provider develops
the habit of asking the patient about exercise, formulating an appropriate
exercise prescription, and reinforcing adherence to exercise through educa-
tion, exercise logs, and personal example.
THE EXERCISE PRESCRIPTION AND ADHERENCE

To increase the probability of future long-term adherence to an exercise program,
the mode of exercise should be enjoyable and convenient. For example, walking is
an excellent modality because it requires no special or expensive equipment and
can be done just about anywhere with little or no specialized skill training. Once an
enjoyable modality has been determined, the self-confidence necessary to fulfill the
requirements of the prescription will follow, but if the exercise intensity is too great,
adherence will be compromised.
Exercise frequency and duration must fit within the patient’s schedule and become
part of his or her daily or weekly routine. Prescribing exercise is often not enough.
Patients might require a multidisciplinary team to help them acquire the skills neces-
sary to achieve a healthy lifestyle.
There are six factors that, once established, lead to success. These factors apply
to almost any activity, but are especially relevant to the successful implementation of
lifelong healthy habits, including exercise.
The Six “Aces” of Exercise Adherence

• Ability: of the physician and health care team to treat disease efficiently,
prescribe exercise properly (by providing an exercise prescription that
is specific to the patient’s social and medical condition), and monitor
the effects of therapy, adjusting it accordingly. The goal is to provide
the patient the ability to implement the therapeutic plan.
• Availability: of the environment required to effect healthy habits:
educational seminars, and group discussions facilitated by competent
caregivers, peer support, and physician and health care members when
needed to monitor and adjust therapy.
• Affability: caregivers who are likable, easy to relate with, and show a
genuine interest in the patients’ welfare.
• Associations: Friends, family, and spousal support; membership to
health clubs, support groups, etc.

4 “Postmodern” Medicine: Teaching Patients to Be Responsible for Their Health
• Antecedents: patients’ previous exercise, medical, and social history,

which determine their beliefs about, attitudes toward, fears of, and prej-
udice toward exercise and other forms of therapy.
• Attitude: this is the most important of all. Without a good attitude
toward exercise, and life in general, it would be very difficult, if not
impossible, to effect a permanent change. A good attitude is based on
a positive concept of disease. It requires that disease not be seen as
something evil that has to be conquered or defeated, but rather as part
of the human condition that needs care and compensatory methods to
overcome disease-induced limitations. A good attitude needs to be real-
istic, to accept what cannot be changed. A good attitude should enthu-
siastically change for the better those things that can be changed—to
look at life as a bridge from a preborn to a postmortem reality and
understand that, although we do not know where the final destination
might be, it is important to engage life with enthusiasm and do the best
we can to travel as well as possible.
REFERENCE
Shulkin, M. D. 1995. Reasons for increasing administrative costs in hospitals. Annals of
Internal Medicine 119:74–78.
RECOMMENDED READING
Andersen, R. E. 1997. Encouraging patients to become more physically active: The physi-
cian’s role. Annals of Internal Medicine 127:395–400.
Beeson, P. B. 1980. Changes in medical therapy during the past half century. Medicine
59:79–99.
Camacho, T. C. 1991. Physical activity and depression: Evidence from the Alameda County
study. American Journal of Epidemiology 134:220.
Dishman, R. K. 1988. Exercise adherence: Its impact on public health. Champaign, IL:
Human Kinetics.
Eisenberg, D., R. C. Kessler, C. Foster, F. E. Norlock, D. R. Calkins, and T. L. Delbanco. 1993.
Unconventional medicine in the United States. Prevalence, costs, and patterns of use.
New England Journal of Medicine 328:246–252.
Golub, E. S. 1994. The limits of medicine. New York: Time-Life Books.
Internal Medicine News. Jan. 15, 1996.
King, A. C. 1992. Determinants of physical activity and interventions in adults. Medical
Science and Sports Exercise 24:S221–S226.
Kraemer, W. J. 1989. Training responses of plasma beta-endorphin, adrenocorticotropin, and
cortisol. Medicine & Science in Sports & Exercise 21:146.
Martinsen, E. W. 1985. Effects of aerobic exercise on depression: A controlled study. British
Medical Journal 291:109.
O’Connor, P. J. 1991. Anxiety and intense running exercise in the presence and absence of
interpersonal competition. International Journal of Sports Medicine 12:423.
Rohm-Young, D. 1995. Exercise adherence: Determinants of physical activity and appli-
cation of health behavior change theories. Medicine, Exercise, Nutrition and Health
4:335–348.

“Postmodern” Medicine: Teaching Patients to Be Responsible for Their Health 5
Toufexis, A. 1995. An eccentric system of healing is staging a comeback, but many experts
still dismiss it. Time Magazine, Sept. 25, 1995.
http://www.cdc.gov/nccdphp.htm (Physical Activity and Health)
http://www.ahrq.gov/clinic/cp53dix.htm (Guide to Clinical Prevention Services)

Section 2
Curing, Healing, and
Maintaining Health

1 High Blood Pressure
The Silent Killer
BACKGROUND
The word “hypertension,” when used alone, refers to systemic arterial hypertension.
A blood pressure of 120/80 mmHg is considered normal. Hypertension is defined
as a systolic blood pressure consistently above 140 mmHg and a diastolic blood
pressure consistently above 90 mmHg. Blood pressure of 120–140/80–90 mmHg is
an intermediate state and deserves attention. Hypertension (HTN) can be classified
according to blood pressure (BP) levels as follows:
• Normal: BP ≤ 119/79 mmHg

• Pre-HTN: BP 120–139/80–89 mmHg
• Exercise HTN: BP ≥ 200/≥90 mmHg associated with exercise in patients
with normal or pre-HTN BP at rest
• Isolated systolic hypertension: BP ≥ 140/≤90 mmHg
• HTN stage 1: BP 140–159/90–99 mmHg
• HTN stage 2: BP ≥ 160/≥100 mmHg
• Resistant hypertension: failure to bring BP to appropriate levels with a
three-drug regime that includes hydrochlorothiazides
As the name suggests, pre-HTN is a precursor of HTN. During aerobic exercise,

cardiac output increases (the result of increased heart rate, stroke volume, and con-
tractility) as the systemic vascular resistance decreases (the result of vasodilatation);
consequently, the BP systolic increases and the BP diastolic remains the same or
changes very little. Exercise HTN is the result of impaired vasodilatation due to rigid
vascular walls (atherosclerosis) or failure to vasodilate due to reflex autonomic dys-
function, elevated norepinephrine levels or local paracrine factors within the arterial
walls. During isometric exercise, both the systolic and the diastolic BP increase due
to reflex vasoconstriction. Exercise-induced hypertension is more severe in subjects
with pre-existing HTN, usually due to higher norepinephrine, rennin, and aldoster-
one levels in the circulation. In patients with coronary artery disease, exercise can
induce myocardial ischemia associated with left ventricular dysfunction, reflex vaso-
constriction, and diastolic hypertension with a diastolic BP > 90 mmHg.
Patients with exercise-induced hypertension are at risk of developing HTN at
rest. The incidence of exercise HTN is 1–10% of the population, and 10–60% of
subjects with isolated exercise HTN will progress to HTN at rest. Isolated systolic
9
10 Exercise and Disease Management
hypertension is common in the elderly. Resistant hypertension is common in patients

with renal artery stenosis and in obese patients with obstructive sleep apnea.
CLASSIFICATION OF HYPERTENSION ACCORDING TO CAUSE

Hypertension is divided into two categories according to cause: primary and sec-
ondary. Of individuals with hypertension, 95% have primary or essential hyperten-
sion, which means that the cause of hypertension is not known. The remaining 5%
have secondary hypertension due to endocrine, renal, autonomic nervous system, or
sleep-related abnormalities.
Patients with essential hypertension often have one or more of the following char-
acteristics: They are sedentary, overweight or obese, suffer from insulin resistance,
drink alcohol in excess, smoke cigarettes, have a family history of hypertension, and
consume too much fructose and salt in their diets.
As in patients with obesity and diabetes, patients with hypertension have predis-
posing factors, precipitating factors, and perpetuating factors for HTN; another simi-
larity is that genetic factors are the most important predisposing factors. However, the
natural polygenic (more than one gene is implicated) predisposition to HTN requires
the nurturing of environmental factors to cause the disease and the presence of per-
petuating factors to sustain it. The pathophysiology that bridges the passage from
predisposition to disease might include inappropriate sodium handling by the kid-
neys, excessive sympathetic tone, or excessive rennin-aldosterone system activity.
Perpetuating factors include a chronic increase in blood volume, vasoconstriction, and
vascular remodeling secondary to paracrine factors such as excessive endothelin pro-
duction and abnormal prostacycline and nitric oxide production in the arterial wall.
The incidence of hypertension increases with age. It is more common in blacks
than in whites. About 45 million Americans suffer from hypertension and only 25%
of them are controlling their dangerously high pressure. Even mild hypertension
should be treated: A systolic pressure of 140–150 mmHg is associated with a 42%
increased risk of strokes and a 56% increase in heart disease. In the recent past, mild
systolic hypertension was not considered significant; today, we recognize that both
systolic and diastolic hypertension should be treated. An isolated measurement of
high blood pressure is not that important; the diagnosis of hypertension is made only
when the blood pressure has been high on three separate occasions over a period
of several months (unless the blood pressure is found to be significantly high the
first time). If the blood pressure is within 140–150 mmHg systolic or 90–99 mmHg
diastolic, it should be checked again within 2 months. However, if the systolic pres-
sure is greater than 160 mmHg and the diastolic greater than 100 mmHg, it should
be evaluated within 1 week to 1 month; if it is found to be consistently elevated, the
patient should be evaluated and treated.
Hypertension is virtually nonexistent in societies whose dietary sodium chloride
intake is very low. It appears that a sodium chloride intake in excess of that required
to stay healthy is necessary, but not sufficient for hypertension to be manifest.
Additional factors are clearly necessary in the development of hypertension because

High Blood Pressure 11
most of us can ingest a high-salt diet without developing hypertension. Genetics

and obesity play an important role. The presence of hypertension in close family
members increases the risk of hypertension. For example, children with high blood
pressure are more likely to come from families with a history of obesity and hyper-
tension. Other predisposing factors include cigarette smoking, alcohol intake (more
than three drinks per day), and certain medications such as birth control pills and
nonsteroidal anti-inflammatory medications.
Prevention of HTN
Strategies to prevent hypertension can be inferred by reading the factors that are
often associated with essential hypertension and eliminating them. Hypertension has
a strong familial association; therefore, if a person has a family history of hyperten-
sion, he or she, more than others, should
• Keep weight low. BMI (body mass index) close to 23 in males and 22 in
females is the ideal; ≤25 is recommended.
• Engage in daily aerobic exercise.
• Reduce sugar intake, especially the intake of high fructose corn syrup.
• Reduce dietary salt intake.
• Stop smoking.
• Decrease alcohol intake to one drink per day or stop altogether.
• Schedule relaxing activities such as nonstressful socializing with friends or
family, listening to music, reading, meditation, and humorous entertainment.
EVALUATION OF INDIVIDUALS WITH HIGH BLOOD PRESSURE

Following the diagnosis of hypertension, most physicians will obtain a complete
blood count; kidney function tests, including the measurement of the electrolyte
composition of the blood; and a urine analysis. An electrocardiogram is indicated in
all patients with hypertension; an echocardiogram is indicated only in patients with
suspected complications.
Other tests might be ordered if the routine tests mentioned before are abnormal,
if the physician suspects the presence of other illnesses, or if the hypertension
is difficult to control. Those tests might include tests for diseases of the endo-
crine glands or tumors associated with hypertension such as Cushing’s disease,
hyperthyroidism, hyperaldosteronism, adrenal adenomas, pituitary adenomas and
pheochromocytomas, and different x-ray and ultrasound tests of the kidneys and
renal circulation.
COMPLICATIONS OF HYPERTENSION
Hypertension is a major risk factor in the development of many other diseases. The
risk of complications doubles for each 6 mmHg increase in the diastolic blood pres-
sure. Preventing those diseases is the goal of therapy.

Hypertensive Cardiovascular Disease

The diseases of the heart and the circulation caused by hypertension are called hyper-
tensive cardiovascular disease. Heart disease can be detected with the electrocardio-
gram and the echocardiogram. When the electrocardiogram or the echocardiogram
shows evidence of thickening of the heart muscle (left ventricular hypertrophy) it
is an indication that the risk for heart disease is high. Effective antihypertensive
therapy can improve and even reverse the condition.
Hypertensive Cerebrovascular Disease

The diseases of the brain circulation caused by hypertension are called hypertensive
cerebrovascular disease. Systolic hypertension is the most important cause of stroke
and dementia caused by strokes. There is also evidence that Alzheimer’s dementia is
more common in individuals with hypertension.
Hypertensive Renal Disease

The disease of the kidney caused by hypertension is called hypertensive renal dis-
ease. It is more common in blacks. Hypertension and diabetes result in kidney disease
that, once present, will contribute to the worsening of hypertension. The progression
of this process makes it imperative that diabetics and/or persons with kidney disease
who also suffer from hypertension be evaluated and treated earlier than other per-
sons without those conditions.
Peripheral Vascular Disease and Coronary Artery Disease

Hypertension causes hardening of the arteries—a condition called atherosclerosis.
Heredity, diabetes, high cholesterol levels, and cigarette smoking also play a role in
causing atherosclerosis. Because atherosclerosis is caused by several factors, treat-
ing hypertension will not necessarily result in its prevention. However, the treatment
of hypertension will decrease the likelihood of coronary artery disease, aortic aneu-
rysm, and other diseases caused by atherosclerosis.
MANAGEMENT
The goal of antihypertensive therapy is to decrease or prevent complications such as
cardiovascular disease, coronary artery disease, peripheral vascular disease, cere-
brovascular disease, and renal failure. These goals are achieved by reducing the
blood pressure to <140 mmHg systolic and to <90 mmHg diastolic without reducing
the quality of life or causing adverse side effects. Elderly patients might not tolerate
a lowering of the systolic blood pressure to <160 mmHg without side effects.
Unfortunately, hypertension often exists as part of a larger subset of metabolic and
endocrine problems that contributes to the development of complications indepen-
dently of hypertension. These factors include elevated insulin levels, lipid or blood
fat abnormalities, and activation of the renin-angiotensin system, which can result

in the constriction of arteries. Optimal hypertensive management should reduce the

blood pressure with minimal side effects and without having the patient take too
many pills or spend too much money.
Pharmacological Therapy of Hypertension

The National Institutes of Health recommendations for choice of initial therapy and
combination of medications (June 2006) remind us that (as with patients with type 2
diabetes and obesity) lifestyle modification such as weight loss and daily aerobic
exercise is the best therapy. However, hypertension control with lifestyle modifica-
tion is seldom achieved because of poor patient adherence. It takes a long time to
obtain desired goals; therefore, it is best to begin medication to correct HTN and
encourage the patient to diet and exercise.
Monotherapy (treatment with a single drug) is sufficient to control hypertension
40–50% of the time; adding a second drug controls hypertension 80–90% of the
time. Current recommendations advocate thiazide diuretics (especially chlorthali-
done), calcium channel blockers (CCBs), or angiotensin-converting enzyme (ACE)
inhibitors for initial monotherapy. The drug of choice is not as important as the
drug’s effect on blood pressure. A drug might be effective on one patient and not on
another; interpatient variability calls for individualization of therapy.
Thiazide diuretics are inexpensive and effective; therefore, they are the best
choice for the initial therapy of HTN. Low-dose diuretics (25 mg hydrochlorothi-
azide or 25 mg chlorthalidone) lower blood pressure by decreasing plasma volume
and lowering vascular resistance without causing significant changes in blood lipids.
Thiazides and calcium channel blockers tend to work better in blacks and older indi-
viduals than ACE inhibitors or β-blockers, which work better in young whites with
hyperdynamic circulations. In women, hydrochlorothiazide offers the extra benefit
of decreasing the risk of osteoporosis, but overall each of the frontline antihyperten-
sive agents are equally effective.
The most important side effect of thiazides is hypokalemia, but this problem is
uncommon with low doses and can be prevented by eating a diet rich in fruits and
vegetables. Because low-dose diuretics alone will control hypertension in 50% of
hypertensives (other than young whites), many physicians consider diuretics the first
choice and an essential part of antihypertensive therapy.
The choice of medications depends on many factors, such as age and coexisting
disease. Persons with coronary artery disease or atrial fibrillation may obtain extra
benefits from β-blockers (non-ISA) or calcium channel blockers. Patients with dia-
betes and patients with heart failure obtain extra benefits from ACE inhibitors (see
Table 1.1).
The choice of drugs used in the therapy of hypertension is controversial.
Blood pressure is the product of cardiac output (blood flow) and total peripheral
resistance; therefore, a reduction in either or both variables will decrease the blood
pressure. Until recently, diuretics and β-blockers were the first drugs to be consid-
ered in persons with hypertension. The β-blocker reduces cardiac output, while the
diuretic decreases blood volume and lessens the total peripheral resistance. But the
common practice of a diuretic followed by a β-blocker has become less popular

TABLE 1.1
Factors in Determining Choice of Therapy
Factor Antihypertensive Therapy
No associated disease; young, white Beta-blocker, ACE inhibitor or angiotensin-II receptor blocker
Older patients or isolated systolic Thiazide, long-acting Nifedipine or Amlodipine
hypertension or African American
Diabetes ACE inhibitor
Heart failure with systolic dysfunction Thiazide, ACE inhibitor, β-blocker, diuretics
Coronary artery disease Thiazide, β-blockers without intrinsic sympathomimetic
activity (non-ISA) Nifedipine, Amlodipine
Atrial fibrillation Beta blockers, Verapamil
Athletes ACE inhibitors, Amlodipine, Nifedipine
Nonathletes with exercise-induced Beta blockers, Verapamil
hypertension
Benign prostatic hypertrophy Peripheral α-1 receptor antagonists
because of concerns about the effect that these medications have on blood lipids
(increased blood fats and cholesterol) and insulin (resistance to insulin and increased
insulin blood levels). Two important exceptions are the β-blockers labetalol and ace-
butolol; these agents are lipid neutral.
If one drug is not enough, combining Chlorthalidone with an ACE inhibitor or a
calcium channel blocker is a good second step. If that is not sufficient, but the target
goal is close, discontinuing the thiazide and combining a calcium channel blocker
with an ACE inhibitor might be sufficient; if not, triple therapy is necessary.
Sometimes it is advisable to begin with two drugs rather than with one drug.
Patients with blood pressures that are greater than 20/10 above target blood pressures
are unlikely to be well controlled with one medication alone. If triple drug therapy
(thiazide + ACE + CCB) is still insufficient, consider adding another diuretic such as
spironolactone, a β-blocker, or an α-blocker and rule out conditions linked to resis-
tant hypertension such as renal artery stenosis and obstructive sleep apnea.
If a β-blocker is necessary (to address other comorbid conditions such as heart
failure or for other reasons), consider that β-blockers decrease renin production and
therefore angiotensin levels, making ACE inhibitors somewhat irrelevant and less
effective. When combining β-blockers with a calcium channel blocker, be aware that
Verapamil and Diltiazem can potentiate myocardial depression, worsen bradycardia,
and induce heart block.
All β-blockers block β-receptors; however, some β-blockers also block α-1
receptors, which provide additional vasodilator capacity; the most popular ones are
labetalol and carvedilol. Other β-blockers show antagonism of certain β-receptors and
agonism of others; they are designated β-blockers with intrinsic sympathomimetic
activity (ISA). Beta-blockers with ISA are not used following myocardial infarction
(lack of proven benefit) and are less effective in the therapy of supraventricular tachy
arrythmias. They are used in patients that do not tolerate other β-blockers because of
excessive bradycardia; the most popular ones are pindolol and acebutolol.

ACE inhibitors (angiotensin receptor antagonists) are a class of medications that

decrease levels, or antagonize the receptors of circulating angiotensin II (an adren-
aline-like substance) and result in an increase in aldosterone (a hormone that causes
water and sodium retention by the kidneys). They do not adversely affect serum lipids
and their use is becoming increasingly popular. They are a reasonable first choice
in the therapy of hypertension. Moreover, ACE inhibitors or angiotensin receptor
antagonists may be the drug of choice for athletic competitors concerned about the
reduction in maximal oxygen consumption (or exercise capacity) that may result when
a β-blocker is prescribed. Since all ACE inhibitors are equally effective and have the
same side-effect profile, it is advisable to choose the least expensive. If ACE inhibitors
are not effective in athletes with exercise-induced hypertension, consider the calcium
channel blockers amlodipine or nifedipine and use β-blockers as last resort.
The drugs of choice for nonathletes with normal cardiac function but with exer-
cise-induced hypertension are β-blockers without intrinsic sympathetic activity
and Verapamil.
Calcium channel blockers decrease blood pressure by disrupting the traffic of
calcium within calcium channels and thus reducing arterial smooth muscle con-
tractility and promoting vasodilatation, but they can also decrease the strength of
cardiac contraction (have a negative inotropic effect) and decrease cardiac electric
conduction reducing the heart rate. They should be used with caution in patients
with cardiomyopathy and conduction defects; however, they are particularly use-
ful in patients with atrial fibrillation and in patients who would benefit from their
negative ionotropic actions, such as those with coronary artery disease and exercise-
induced hypertension.
Calcium channel blockers are divided into the following clinical groups:
1. Dihydropyridine CCBs reduces systemic vascular resistance and arterial

pressure but are not indicated in the treatment of angina because they can
induce a hypotension-mediated reflex tachycardia. This include all CCBs
that end in dipine except amlodipine and nifedipine.
2. Nondihydropyridines:
• Phenylalkylamines are selective for myocardium; they decrease myocar-
dial contractility and are weak vasodilators; therefore, they are mainly
used to treat angina and supraventricular tachycardia. The best known
is Verapamil.
• Benzothiazepines are a class halfway between the other two. They com-
bine negative inotropic effects with vasodilating effects; the best known
in the group is Diltiazem.
Hydralazine lowers blood pressure by altering cellular calcium metabolism and

relaxing vascular smooth muscle. Unfortunately, this induces vasodilatation. It
causes a reflex sympathetic discharge with increased rennin production and overpro-
duction of angiotensin II and aldosterone, leading to a hyperdinamic circulation and
increased myocardial oxygen demands. Therefore, hydralazine should be avoided in
patients with coronary artery disease.

Clonidine occupies α-receptors in the brainstem (central α-blocker), resulting in

a reduction in the sympathetic outflow and reduced systemic vascular resistance and
reduced plasma rennin and aldosterone, without adversely affecting renal blood flow
and glomerular filtration. The heart rate at rest decreases but the heart rate adaptation
to exercise remains within normal limits. Problems associated with clonidine include
clonidine withdrawal symptoms of nervousness, hypertensive crisis associated with
abrupt interruptions of therapy, and tolerance to its antihypertensive effects.
Peripheral α-blockers such as doxazosin, terazosin, and prazosin antagonize α-1
adrenergic receptors in the periphery; they are useful in patients that suffer from hyper-
tension plus benign prostatic hypertrophy (BPH) in the dose recommended for BPH.
Patients with diabetes and patients with heart failure obtain extra benefits from
ACE inhibitors (see Table 1.1).
Target Blood Pressure

The blood pressure should be reduced to less than 130/80 in diabetics, patients
with renal disease associated with proteinuria, patients with known atherosclerotic
cardiovascular disease, and patients with isolated systolic hypertension. However,
the diastolic blood pressure should remain above 65 mmHg, especially in the elderly,
to minimize the risk of thrombotic events such as strokes and myocardial infarction.
In all other patients, the target blood pressure is less than 140/90 mmHg.
FOLLOW-UP OF PERSONS WITH HYPERTENSION

During the initial stage of blood pressure control, patients need to see their physician
often. If the blood pressure is less than 180/100 mmHg, follow-up visit should be
scheduled every 1 or 2 months to allow the antihypertensive medication to manifest
its full potential. Patients with higher blood pressures need to see their physicians
more often. Once the blood pressure has been controlled, the number of visits can be
reduced to once yearly.
Patients with high blood pressure should learn how to measure their own blood
pressure and should measure it often (once a month). If the blood pressure is
found to be consistently high, the patient should return to his physician. Follow-up
laboratory testing would be dictated by the specific needs of individual cases.
Blood lipids should be checked yearly especially in patients taking β-blockers.
Electrocardiograms should be repeated every 2–4 years depending on the presence
of other cardiac risk factors.
NONPHARMACOLOGICAL TREATMENT OF HYPERTENSION

Mild hypertension can be treated without medication. The treatment of hypertension
includes weight reduction, exercise, a diet containing foods high in potassium and
magnesium, and avoidance of alcohol, salty foods, and cigarettes. Potassium may
help to help vasodilate vasodilatation or open arteries, thereby lowering blood pres-
sure. Bananas are high in potassium; a banana a day could keep the doctor away!

Exercise lowers blood pressure; it also has a positive effect on preventing weight
gain and maintaining weight loss. Exercise and diet have an additive effect. When
exercise is combined with diet, weight loss and blood pressure reduction increase
significantly. The effect of exercise on blood pressure is proportional to the intensity
and duration of exercise; light exercise such as calisthenics lowers blood pressure but
the higher the exercise intensity and the longer the duration of exercise, the greater
the blood pressure reduction will be. Because hypertension increases the risk of
cardiovascular disease, an added benefit of exercise, especially when combined with
a hypocaloric diet low in salt and saturated fat, is the additive effects those inter-
ventions have on cardiovascular disease risk factors. Exercise, independent of diet,
lowers systolic blood pressure, lowers fasting blood sugar and insulin resistance,
increases high-density lipoprotein, and decreases triglycerides. However, the effect
of exercise on end points such as mortality and myocardial infarction is not known
for the simple reason that there are no long-term studies dealing with that subject.
In general, physicians have not been very good at following through with exer-
cise recommendations for patients. Data from the National Health Interview Survey
reveal that only 48% of hypertensive subjects are counseled to exercise by their phy-
sicians and only 46% are advised to lose weight. It is a well-known fact that moderate
exercise has an antihypertensive effect and can correct hypertension in individu-
als who are mildly hypertensive (i.e., resting pressures no greater than 145/90). For
every two pounds of weight loss, there is a 2 mmHg decrease in blood pressure. This
reduction may be even more marked in individuals with secondary hypertension due
to renal dysfunction. Decreasing the intake of dietary sodium and avoiding alcohol
would decrease blood pressure further, especially in individuals who are “sodium
sensitive” and thus susceptible to increases in blood pressure when salty meals are
consumed. If lifestyle measures are not sufficient, then one or more drugs from dif-
ferent drug classes might be added.
EXERCISE ISSUES
There is evidence that exercise reduces the incidence and severity of cardiovascular
risk factors, including hypertension, allowing a possible reduction in the dosage of
antihypertensive medication and thus attenuating the risk for early mortality. The
decision to treat or not to treat the patient with mild hypertension can be deferred
pending evaluation of the results of a program of exercise therapy. Recent evidence
suggests that high levels of physical fitness are associated with a lower resting sys-
tolic blood pressure. Weight loss and avoidance of tobacco and alcohol will decrease
blood pressure further.
A review of the literature reveals that blood pressure reduction can be achieved
with moderate exercise intensities, but not with light physical activities such as walk-
ing or gardening except in elderly subjects who have a totally sedentary lifestyle. For
example, training at a moderate intensity equal to about 50% of the VO2 max (see
Appendix A, Method 6), or maximum fitness level, almost completely blunted the
morning blood pressure rise, an effect unique to physical training. Lowering the blood
pressure in the morning is particularly important because this is the time of greater

risk for cardiovascular morbidity and mortality because of the shift from parasym-
pathetic to sympathetic control.
The frequency, modality, duration, and intensity recommendations do not sig-
nificantly differ from those for healthy individuals. However, prescribing exercise
at 40–70% of the maximum fitness level, or a rating of perceived exertion (RPE)
of between 11 and 13 (see Appendix A, Methods 5 and 6), seems to have a greater
effect on lowering blood pressure when compared to exercise at higher intensi-
ties. Decreases in blood pressure that result from exercise usually occur within 4
or 5 weeks and are maintained for as long as the exercise program is continued.
Individuals with markedly high resting blood pressures (i.e., 180–209 systolic
and 110–119 diastolic) should not exercise until pharmacological therapy has
been initiated. Remember that if your patients are taking vasodilators, they may
require longer cool-downs to prevent venous pooling of blood following abrupt
cessation of exercise. A special note: In the past, the American College of Sports
Medicine has cautioned against continuing exercise when systolic blood pressure
drops during exercise by 10–15 mmHg. However, many times, acute blood pressure
responses to exercise in hypertensive individuals result in vasodilation, which may
decrease systolic blood pressure. This decrease is normal and is not the result of a
reduction in stroke volume.
EXERCISE PRESCRIPTION FOR PATIENTS

WITH HIGH BLOOD PRESSURE
By performing aerobic exercise, patients at risk for high blood pressure will dem-
onstrate a reduction in hypertension over time, thereby justifying exercise as a
nonpharmacological method. If there are marked elevations in blood pressure,
aerobic exercise is to be the treatment regimen only following pharmacological
therapy. Exercise may reduce the blood pressure further, allowing a reduction in
medications and attenuating the risk for premature mortality. The mechanisms
by which exercise lowers blood pressure are complicated. Possibilities include
the following:
• A decrease in plasma norepinephrine levels

• Increase in circulating vasodilator substances
• Amelioration of hyperinsulinemia
• Alteration in renal function
If antihypertensive therapy in conjunction with hygienic measures (i.e., weight reduc-

tion, salt restriction) is successful, then an exercise stress test and training program
are appropriate (see Appendix B).
The blood pressure response during exercise may provide additional caveats ear-
marking individuals at risk for high blood pressure. For example, blood pressures
greater than 180/90 at 50% of maximum exercise capacity and greater than 225/90
at peak exercise can be warning signs for mild primary hypertension. Moreover,
individuals who are hypertensive before and early in the exercise session and then
normalize their resting and peak blood pressures during and immediately following

the exercise session may also be at risk. Individuals on β-blocking drugs to reduce
hypertension will experience a reduction in HR and maximal exercise capacity. If
a β-blocker is used, prescribing exercise by heart rate would be inaccurate. This
may result in an exercise intensity or target heart rate that is too high for the patient.
Exercise prescription intensity should be prescribed by the Borg index of RPE for
these individuals (see Appendix A, Method 5).
Elevated diastolic blood pressure can be aggravated by strength training or any
other form of exercise that has a strong isometric component (e.g., shoveling snow).
High anaerobic work also elicits a hypertensive response. Weight training is gener-
ally not recommended as the primary form of exercise therapy for hypertension,
with the exception of high repetitions and low weight. Weight training has not been
proven to lower resting blood pressure consistently.
Weight training should be concomitant with special precautions to avoid holding
the breath during lifting (Valsalva’s maneuver). For more detailed information, see
weight training guidelines in the next section.
Aerobic exercise duration can range from 20 to 60 minutes with a minimum of
3 days per week. Aerobic intensity can be prescribed using the RPE or by target heart
rate, provided the heart rate is below the predetermined systolic blood pressure level.
See Appendix A, Method 4, for a detailed explanation on how to use a method that
involves prescribing exercise intensity based on systolic blood pressure. Typically, a
systolic and diastolic pressure > 250/115 mmHg or an RPE greater than “somewhat
hard” during training should not be exceeded. Furthermore, an exercise should not be
performed when resting systolic or diastolic blood pressure exceeds 200/110 mmHg.
Based on the high number of exercise-related health benefits, it is appropriate
to recommend exercise as part of the initial treatment strategy for mild to moder-
ate hypertension.
WEIGHT TRAINING GUIDELINES FOR HIGH BLOOD PRESSURE

When people with hypertension are undergoing weight training, resting and peak
blood pressures are of the utmost concern. Patients with uncontrolled hypertension
(systolic > 160 mmHg or diastolic > 100 mmHg) should avoid weight training. Other
contraindications to weight training include:
• Congestive heart failure

• Uncontrolled arrhythmias
• Severe valvular disease
• Aerobic capacity of less than 5 METs (metabolic equivalents)
When weight lifting takes place, circuit training using moderate weights with
frequent repetitions is recommended. Circuit training involves moving from exercise
to exercise at a consistent pace. This will develop muscle endurance and strength.
To control blood pressure and prevent the elevation of after-loads on the heart, iso-
metric or static components should be minimized when the weight-lifting exercise
is performed by breathing on exertion and using a weight that can be lifted without
stopping halfway through the motion.

The type of weight-lifting equipment used depends on the patient’s preference

and abilities. Weight machines and free weights can be used once the patient is able
to join a gym or fitness center. Exercises that can be performed at home and guide-
lines for patients are presented in the high blood pressure workbook CD.
When selecting the proper intensity, it is important that the amount of weight
lifted be based on the ability of the individual rather than on an arbitrary weight. We
recommend two methods to determine the intensity. All exercise or repetition sets
may be performed one or two times or in one or two sets—for example:
• Method 1: Choose a weight that can be lifted comfortably 10–15 times.

When 15 repetitions can be comfortably performed, the weight may be
increased to an amount that can be lifted at least 10 times.
• Method 2: Determine one repetition maximum (1RM). The 1RM can be
calculated from the following formula:
[100 – (# reps × 2.5)] = % 1RM
A load of 30–50% of the 1RM is recommended for beginners, progressing to 60–80%

of the 1RM. An example using this equation to determine the 1RM can be found in
Appendix A, Method 10.
The preceding methods for prescribing intensity can be used for any weight-lifting
equipment: free weights (barbells and dumbbells), weight machines, or hand weights
and stretch elastic bands. The RPE of 11–13 prescribed for aerobic work should not
be exceeded when weight lifting is undertaken.
RECOMMENDED READING
Adams, G. M. 2008. Exercise physiology laboratory manual, 5th ed., chaps. 16, 17. New York:
McGraw–Hill Co.
American Association of Cardiovascular and Pulmonary Rehabilitation. 1991. Guidelines for
cardiac rehabilitation programs, 2nd ed., chap. 3. Champaign, IL: Human Kinetics.
ACSM’s guidelines for exercise testing and prescription, 8th ed. 2010. New York: Wolters
Kluwer/Lippincott Williams & Wilkins.
Centers for Disease Control and Prevention. 1994. Adults taking action to control their blood pres-
sure (interview conducted by CDC). Morbidity and Mortality Weekly Report 43:509–517.
Durstine, J. H. et al. 2009. ACSM’s exercise management for persons with chronic diseases
and disabilities, 3rd ed., chap. 14. Champaign, IL: Human Kinetics.
Hagberg, J. M. 1990. Exercise, fitness and hypertension. In Exercise, fitness, and health, ed.
C. Bouchard, R. J. Shephard, J. R. Sutton, et al. Champaign, IL: Human Kinetics.
Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure.
1993. The fifth report of the Joint National Committee. Archives of Internal Medicine
153:154–183.
Marceau, M. 1993. Effects of different training intensities on 24-hour blood pressure in hyper-
tensive subjects. Circulation 88:2803–2811.
Palatini, P. 1994. Relation between physical training and ambulatory blood pressure in stage I
hypertensive subjects. Results of the HARVEST Trial. Circulation 90:2870–2876.
Reaven, P. D. 1991. Relation between leisure time physical activity and blood pressure in older
women. Circulation 83:559–565.

EXERCISE PRESCRIPTION FOR HIGH BLOOD PRESSURE
Frequency
Exercise a minimum of three times per week, preferably all days. Try to
alternate the exercise days to allow plenty of time for recuperation.
Modality
Activities that have low isometric or strenuous static components and work
the large muscles are recommended. Walking is an excellent modality
and it does not require any special equipment. Stationary or active bike
riding and swimming are also acceptable aerobic modalities. You may
even want to combine different modalities during the exercise session.
However, a rigorous weight-training program may be harmful, while a
moderately fast-paced weight-training program using light weights may
be beneficial.
Duration
If the patient has not been exercising regularly, begin with a time that is
comfortable for him or her—about 10 minutes initially. Gradually
increase the aerobic exercise time by 2–4 minutes each week until
30–60 minutes is achieved without stopping. Be sure to include weight
training in the workout.
Intensity
The aerobic intensity can be prescribed using the RPE chart in Appendix A,
Method 5, or 40 to <60% of the VO2 reserve, Method 9, also in Appen
dix A. The perceived exertion rating between light and somewhat hard,
an RPE of 11–13/20, is recommended. The weight-training intensity
should not exceed an RPE of 13. When weight training is undertaken,
use a light weight for 10–15 repetitions and do one to two sets for each
muscle group. Work upper and lower muscle groups. See the weight-
training section in this chapter and in the workbook CD for more
detailed instructions.
Other Instructions
• Any weight gain, shortness of breath, or chest pain should be reported
immediately.
• Encourage progress follow-up in the workbook exercise logs for the next
follow-up visit.
• Instruct the patient to stop exercising immediately if faintness, dizziness, or
heart palpitations occur.
• Warm up and cool down prior to exercising for at least 10 minutes at a
comfortable intensity.

COMMON QUESTIONS ON HIGH BLOOD PRESSURE

(A PATIENT’S PERSPECTIVE)
Question: What is hypertension?
Answer: Hypertension is also called high blood pressure. You may have
hypertension if, when at rest, the systolic (top) number is 140 or above and
the diastolic blood pressure (bottom) number is 90 or above. The diagnosis
of hypertension is made following three consecutive elevated readings on
separate occasions.
Question: Does everyone have the same level of high blood pressure?
Answer: No. Once a diagnosis has been made, your medical professional will
rate your blood pressure. Currently, there is a standardized classification
of hypertension. Ask your medical professional what your stage is. The
categories include high normal, stage I, stage II, stage III, and stage IV.
Previously, stages I through IV were referred to as mild, moderate, severe,
and very severe, respectively.
Question: How did I get hypertension?
Answer: Essential or primary hypertension may have no known cause.
However, certain things put you at risk to develop high blood pressure:
excessive salt in the diet, obesity, lack of exercise, high consumption of
alcohol, and a family history. Secondary hypertension is another form of
high blood pressure. This type is generally a result of kidney or central ner-
vous system problems. Your medical professional will determine whether
you have primary or secondary hypertension.
Question: How do I know if I have hypertension?
Answer: Typically, you are symptom free. However, you may experience
headaches, dizziness, visual problems, chest pain, shortness of breath, and
nosebleeds.
Question: What happens if high blood pressure is not treated?
Answer: Untreated hypertension can lead to kidney damage, heart disease
(heart attacks, congestive heart failure), stroke, and eye damage.
Question: What is the treatment for hypertension?
Answer: Lifestyle modifications are generally the first step in the treatment of
hypertension. Positive lifestyle modifications include lowering salt intake,
decreasing caloric intake, weight loss, smoking cessation, and exercise. This
therapy is tried for several months and if it fails, medications are the next step.
If you have severe hypertension, the first step may involve medications.
Question: Once I start on medication, do I have to continue for life?
Answer: That depends on the reason you have hypertension. Medication may
be prescribed, but if you lose weight and watch what you eat, your blood
pressure may decrease to the point where you will not need medication.
With close follow-up and continuous monitoring, your medical professional
will determine your individual needs.
Question: How much exercise is required?
Answer: Exercise at least three times a week. Before beginning any exercise
program, consult your medical professional. If you have not exercised in a

long time, start slowly and gradually increase to at least 30–60 minutes,
three to four times a week. For more detailed information, see the exercise
section in the workbook.
Question: What type of exercise is best?
Answer: The most important factor in choosing an exercise program is finding
one that you will stick with. Exercise that is repetitive, rhythmic, and works
the heart and large muscle groups is recommended. See the guidelines on
exercise in your workbook for more information.
Question: What dietary changes should I make?
Answer: Start by lowering your caloric intake. Fat and salt reduction is a key
element in the management of hypertension. Your medical professional will
help you to determine how many calories and how much fat should be con-
sumed daily. Lower your salt intake to 2400–3000 mg a day. Do not add
salt when cooking, buy reduced-salt foods, and avoid foods high in sodium
such as pickles, olives, soups, and canned vegetables. Choose foods low in
cholesterol and fat. Attempt to eat less than 300 mg of cholesterol a day.
Your medical professional may ask you to consult a dietitian.

2 Diabetes
BACKGROUND
Diabetes is one of the oldest known diseases. Earliest records of diabetes can be
traced to 400 BC. Ancient physicians noted that the urine of diabetic individuals
had a sweet taste. “Mellitus” is the Latin word for honey and refers to the sweet-
ness of the urine, which provided a test for this disease. Diabetes mellitus is often
present with other diseases such as heart disease or hypertension. According to the
latest data from the American Diabetes Association (ADA; http://www.diabetes.org/
diabetes-basics), diabetes affects 23.6 million people, nearly 7.8% of all adults and
children in the United States. Diabetes is 50% more common in females, and the
prevalence is greater in blacks than whites; however, males appear to have a greater
likelihood for developing type 1 diabetes. The overall economic impact of this dis-
ease is in the billions of dollars each year. The latest ADA cost analysis reports that
the economic cost of diabetes in 2007 exceeded $174 billion. The health care cost
for persons with diabetes is 2.3 times more than for those without diabetes. For
more information regarding the cost of diabetes by state, visit the ADA Web site
(http://www.diabetesarchive.net/advocacy-and-legalresources/cost-of-diabetes.jsp).
Diabetes is a metabolic disorder characterized by a lack of the hormone insulin,
insulin resistance, or both, resulting in hyperglycemia (high blood sugar) and other
metabolic disturbances. Individuals diagnosed with diabetes are at risk for having
neurological, cardiovascular, ocular, renal, and other complications.
Genetic factors contribute to the development of diabetes, while nongenetic fac-
tors are necessary for its expression. For example, a woman might be genetically
predisposed to diabetes, but express the disease only when she is pregnant. The
hyperglycemia associated with the type of diabetes (type 2) caused by resistance to
insulin may be reversed by weight loss. Therefore, patients who are overweight and
have type 2 diabetes may be able to reduce or discontinue taking medications once
obesity is eliminated.
CLASSIFICATION OF DIABETES
Insulin-Dependent Diabetes Mellitus or Type 1 Diabetes
Type 1 is also known as juvenile-onset and insulin-dependent diabetes mellitus
(IDDM). It is usually diagnosed in early childhood, but can occur at any age. It is char-
acterized by inadequate insulin production by the β-cells in the islets of Langerhans in
25
the pancreas. Predisposing factors for the development of type 1 diabetes are heredity
and viral infections. The exact cause of type 1 diabetes remains unclear.
Type 1 diabetes can occur at any age, but it usually appears abruptly before 30 years
of age. As many as 10–20% people are diagnosed with diabetes after 35 years of age.
Many type 1 diabetics are not overweight; insufficient insulin secretion is the cause
of their IDDM. Only 10% of all patients with diabetes are insulin deficient. Islet cell
antibodies that attack the insulin-secreting cells in the pancreas are found in 90% of
these patients. Viral infections (coxsackie and mump viruses) in genetically predis-
posed individuals are the most likely cause of this condition.
Non-Insulin-Dependent Diabetes Mellitus or Type 2 Diabetes

Type 2 diabetes is also referred to as maturity-onset or non-insulin-dependent diabetes
mellitus (NIDDM). Approximately 80% of reported diabetic cases are type 2. The term
NIDDM is confusing because many patients with this condition may, during the course
of their disease, require insulin. This disease is characterized by insulin resistance
caused by genetic factors (90% concordance in identical twins) and several acquired
factors, such as obesity and inactivity. The majority of patients with type 2 diabetes do
not require insulin initially and are not prone to ketosis (a metabolic complication com-
mon in type 1 diabetics caused by the burning of fats for energy) except under extreme
stress. However, patients with type 2 diabetes may require insulin for correction of
symptoms that are not remedied by exercise, diet, weight loss, or oral agents.
Symptoms of type 2 diabetes usually begin after 45 years of age and progress
slowly. This condition is found in 10.7% of all people age 20 or older and increases
to 23.1% of people age 60 or older. Most patients with type 2 diabetes are over-
weight or obese (see http://www.diabetes.org/diabetes-basics/diabetes-statistics/).
The increase in the incidence of NIDDM has been attributed to an increase in the
prevalence of obesity, decreased physical activity, and increased insulin resistance
associated with aging.
Insulin resistance and hepatic overproduction of glucose are the characteristic
features of type 2 diabetes. Initially, pancreatic β-cells compensate for the resistance
to insulin by secreting more insulin. NIDDM becomes clinically apparent when the
amount of insulin produced by the pancreas becomes insufficient to overcome the resis-
tance to insulin. The hepatic overproduction of glucose is responsible for the hyper
glycemia present during fasting.
Insulin resistance and hyperinsulinemia are commonly associated with abnor-
malities in the metabolism of fats and cholesterol. These patients have higher VLDLs
(very low-density lipoproteins), higher plasma triglycerides (TGs), lower HDLs
(high-density lipoproteins), and more atherogenic or artery blocking low-density
lipoprotein (LDL) particles. They also have a tendency to hyperuricemia, a condi-
tion associated with gout.
The obesity associated with type 2 diabetes is characterized by an excessive
amount of fat deposition inside the abdomen (intra-abdominal or visceral obesity)
and is often associated with high blood pressure. Obesity and high blood pressure
increase the risk of vascular or blood vessel disease. Hypercaloric diets and physi-
cal inactivity are the most important environmental factors responsible for

Diabetes 27
insulin resistance and hyperinsulinemia. It is likely that the same genetic fac-
tor responsible for the metabolic abnormality that causes insulin resistance is also
responsible for the metabolic abnormality that causes obesity. An elevated blood
sugar is a manifestation but not the cause of type 2 diabetes.
Type 2 diabetes is the result of a progressive resistance to the physiologic effects
of insulin. The location of the abnormality causing resistance to insulin can be at
the level of the insulin receptor or within the cell itself. The result is reduced glu-
cose uptake and changes in the way glucose is processed by the cell, which in turn
increases the concentration of blood glucose and a compensatory increase in insulin
levels, driving glucose into an impaired cell and leading to fatty liver, increased
central adiposity, and other pathologic manifestations.
As insulin resistance progresses, the body requires higher and higher doses of
insulin to maintain the blood glucose within normal limits until the β-cells fatigue
and cannot produce as much insulin as required and the blood glucose level rises
unopposed. Insulin resistance is not only the cause of diabetes, but also the cause
of many of the problems that plague the diabetic, such as atherosclerosis, the seed of
vascular disease in the coronary arteries. Cerebral and peripheral vascular beds are
often well advanced by the time the diagnosis of type 2 diabetes is made.
Once hyperglycemia develops, the elevated blood glucose begins to cause addi-
tional problems. It attaches to protein (protein glycation) and forms advanced gly-
cation end products (AGEs). Along with the formation of reactive oxygen species
(ROS) and other products resulting from the abnormal metabolism of fuels, AGEs
further impair cell function, increasing the possibility of vasculopathy, gromerul-
opathy, retinopathy, and neuropathy. Diabetes mellitus can occur in association with
certain conditions:
• Drugs and diseases of the endocrine glands, such as diuretics, β-blockers,

oral contraceptives, glucocorticoid therapy, Cushing’s syndrome, acromeg-
aly, glucagonoma, and pheochromocytoma
• Insulin receptor diseases, such as acanthosis nigricans
• Pancreatic diseases, such as pancreatitis and hemochromatosis
• Certain genetic disorders, such as myotonic dystrophy and lipodystrophy
Impaired Glucose Tolerance

There are persons who have elevated glucose levels after a glucose load, but do not
have diabetes. This condition might be present for many years prior to the development
of NIDDM. Patients with impaired glucose tolerance (IGT) are known to have insulin
resistance and the other metabolic factors that increase the risk of atherosclerosis and
coronary artery disease. The conversion rate of IGT to NIDDM is 7% per year.
Gestational Diabetes Mellitus

This type of diabetes results from contra-insulin effects present during pregnancy and
is more likely to develop during the second or third trimester. Gestational diabetes
mellitus (GDM) is more likely to occur in persons with a family history of diabetes,

previous delivery of a large-birth-weight baby, and obesity. Gestational diabetes

resolves postpartum; however, approximately 50% of women who develop gestational
diabetes will develop type 2 diabetes later in life. It occurs in 3% of all pregnancies.
MANAGEMENT
Symptoms of Diabetes
Common symptoms of diabetes include thirst, increased urination, weight loss, and
fatigue. If the disease is not recognized and treated, these symptoms progress to
rapid heartbeat, shortness of breath, nausea, vomiting, confusion, and, in extreme
cases, coma, shock, and death.
Diagnosis
The diagnosis of diabetes is based on a determination of a blood sugar of 125 mg/dL
or higher after fasting overnight, at least two times, or a random blood glucose value
of 200 mg/dL or greater during an oral glucose tolerance test (OGTT). Laboratory
tests, such as the detection of C-peptide, hemoglobin A1c and ketone levels are often
needed for the appropriate diagnosis and management of diabetes. Hemoglobin A1c
reflects the blood glucose level over a prolonged period of 60–90 days. The diag-
nosis of prediabetes is based on the presence of an impaired fasting glucose (IFG)
of 100–125 mg/dL or an IGT with blood glucose of 140–199 mg/dL 2 hours after a
meal of 75 g of glucose.
Complications of Diabetes
Diabetes causes hardening of the arteries and increases the blood pressure. In turn,
this contributes to the development of heart disease, kidney disease, stroke, and other
conditions listed in the following sections.
Diabetes and Heart Disease and Strokes

Diabetes can cause weakening of the heart muscle and contributes to coronary artery
disease. Patients with diabetes are more prone to having “silent ischemia,” or a heart
attack without chest pain. High blood pressure, smoking, abnormalities in blood lip-
ids, and a history of coronary artery disease before age 50 in first-degree family
members increases the risk of heart attacks. Adults with diabetes have an incidence of
heart disease that is two to four times higher than in people without diabetes. In 2004,
heart disease was mentioned in 68% of death certificates of people age 65 and over.
The risk for strokes is also two to four times higher in people with diabetes than in
people without it. Strokes were mentioned in 16% of death certificates of people age
65 or older (see http://www.diabetes.org/diabetes-basics/diabetes-statistics/).
Diabetes and Kidney Disease

Diabetes is responsible for 44% of all new cases of renal failure. Patients report-
ing having type 1 diabetes for 20 years or more have a 30–40% greater chance for
significant kidney disease. Patients with type 2 diabetes are 15–20% more likely

Diabetes 29
to develop significant kidney disease in their lifetime. The first and earliest sign
of kidney disease is the appearance of protein in an overnight urine collection A
spot urine albumin/creatinine of <30 μg/mg is normal. High blood pressure and
high LDL cholesterol increase the amount of protein in the urine. Correcting these
two diseases decreases the amount of protein in the urine. Angiotensin-converting
enzyme (ACE) inhibitors have a protective effect on the kidney above and beyond
their effect on lowering the blood pressure. Patients with diabetes should have their
kidneys checked at least every year.
Diabetes and the Eye

Patients with diabetes are predisposed to cataracts, retinopathy, and glaucoma.
Diabetes is the leading cause of blindness in the United States. Dilated eye exams
should be done at least yearly in all patients with diabetes.
Cataracts: Premature cataracts in diabetics are caused by the binding of glu-

cose to protein in the lens. This condition, like cataracts in elderly nondia-
betic individuals, can be corrected with surgery.
Retinopathy: This is damage to the small blood vessels of the retina located
on the inside and back of the eye. In the earliest stage, the blood vessels
develop balloon-like deformities (aneurysms) and slowly developing hem-
orrhages and swelling. Later, small infarcts that look like “cotton-wool”
spots are formed. Following this, the formation of new, abnormal blood
vessels that bleed easily results in scar tissue formation. This scar tissue in
the retina can lead to retinal detachment. Finally, a stage called proliferative
retinopathy can result; this can be treated with laser treatments.
Glaucoma: This is a disease characterized by an increase in pressure of the
fluid inside the eye. It occurs in 6% of diabetic patients and can be treated
with eye drops.
Diabetes and the Nerves

Diabetes can affect the nerves responsible for muscle function and sensation
(i.e., peripheral neuropathies) and the nerves responsible for organ function (i.e.,
autonomic neuropathies). About 60–70% of all people with diabetes have some form
of neuropathy.
Peripheral Neuropathies
One or more nerves can be affected, with the most common form of peripheral neu-
ropathy involving the hands and feet. Generally, both sides are involved at the same
time. A decreased perception of pain, temperature, and vibration along with tingling
or burning, which is usually the most severe at night, are common. Amitriptyline,
taken at night, or capsaicin cream rubbed into the affected skin two to four times a
day may be effective in treating the pain.
Autonomic Neuropathies
The nerves affected are generally the sympathetic fibers associated with the heart
and the parasympathetic fibers that innervate the gastrointestinal system. The

parasympathetic system is usually affected first. This may result in tachycardia (early)
or chronotropic incompetence (late) or the inability to increase the heart rate with
exertion, along with other symptoms of sympathetic dysautonomia such as postural
hypotension or inappropriate blood pressure response to exercise. Patients with this
condition may not experience pain when they are having a myocardial infarction.
Other nerves, such as those in the stomach, may also be affected, resulting in a
delay or slowing of its ability to empty. This condition, called gastroparesis, is the
result of parasympathetic dysfunction; it tends to occur early in the disease pro-
gression of dysautonomia and is associated with nausea and heartburn. When the
nerves of the bowel are affected (enteropathy), bouts of diarrhea or constipation
occur. Treatment may involve high-fiber meals and/or medications to treat diarrhea
and constipation and avoidance of medications that could further compromise the
dysautonomia. When the nerves innervating the bladder are affected, frequent blad-
der infections and incontinence may result. Impotence can result when the nerves of
the penis are affected. Atonic bladders and impotence can be treated with surgical
procedures and medications.
A urologist should be consulted when these conditions are present.
Diabetes and the Mouth

Patients with diabetes are more prone to problems associated with the teeth and
gums. Inflamed gums that become swollen and tender may result in gingivitis. Teeth
may decay, becoming loose and rotten. Diabetics should be reminded of the impor-
tance of a regular daily program of brushing and flossing.
Diabetes and the Feet

Nerve and artery damage to the feet may result in multiple problems. Diabetics are
20 times more likely to develop infections and gangrene leading to amputation of
toes or the lower leg. Any redness, swelling, or skin lesions can quickly become
infected and action should be taken immediately to prevent skin ulcers. New shoes
should be comfortable, properly sized, and slowly broken in to reduce the likelihood
for infections. Furthermore, instruct patients to report “athlete’s foot” immediately,
to treat dry skin on the feet with vegetable oil, and to practice good toenail hygiene
by cutting the nails straight across.
How to Prevent Complications

Goals and Recommendations for the Management of Diabetes Mellitus
• Weight: <120% of ideal body weight
• Glucose levels: 80–120 mg/dL before meals, 180 mg/dL 1½ to 2 hours
postprandial, and 100–140 mg/dL at bedtime
• Hemoglobin A1c: <7% or <2% above the upper limit of normal; individual-
ize for patient. Measure every 3 months in IDDM and PRN (pro re nata)
in NIDDM. Elderly patients who are at greater risk of complications from
hypoglycemia should aim at blood glucose levels less than 200 mg/dL
before meals and a HgA1c < 3% above the upper limit of normal. Repeat

Diabetes 31
every 3 months until goals are reached, then every 6 months. The closer to
normal the better: 1% reduction in HbA1c is associated with a 37% reduction
in microvascular complications.
• Blood pressure: <130/85 measured annually or more often if abnormal
(see Chapter 1). A blood pressure < 120/80 is optimal.
• Lipid profile: annually if abnormal:
LDL of <100 mg/dL and <70 mg/dL for patients with coronary artery
disease
HDL of >40 mg/dL in males and >50 mg/dL in females
Total cholesterol < 200 mg/dL
TG < 150 mg/dL
• ECG: baseline and PRN in adults
• Visual examination: dilated eye exam annually
• Urinalysis: annually
• Urine micro-/albumin: annually
• Creatinine/creatinine clearance: annually
• Exercise: 20–60 minutes daily or at least 4–5 days a week. Avoid not exer-
cising for 2 days in a row.
• No smoking
• Family counseling
• Patient education
Diet Therapy
Patients with diabetes should consume an amount of calories consistent with the
maintenance of ideal body weight, usually around 2,000–2,500 calories per day.
A good rule of thumb for daily energy intake requirements is ideal body weight in
kilograms × 30. Many type 2 diabetics who are obese should not reduce their daily
caloric intake to less than 1,200 without medical supervision. Hypoglycemia, loss of
muscle mass, and vitamin and mineral deficiencies may result.
An example of a diet that achieves caloric dietary targets while avoiding hunger
is an egg-white vegetable omelet and a glass of skim milk for breakfast, a fruit snack
at midmorning, a salad with low-fat salad dressing for lunch, another fruit for the
midafternoon snack, and a dinner plate filled half with vegetables; one fourth with
fish, poultry, or meat; and the other one fourth with a carbohydrate such as rice,
bread, potatoes, etc. This diet provides approximately 1,500 calories per day, leav-
ing room for a postdinner snack. We usually tell our patients to become vegetarians
during the day and have a normal meal at night. Diet and medications alone are not
enough to treat diabetes; exercise must be added to the regimen.
A diet that controls fluctuations in blood glucose and emphasizes unrefined car-
bohydrates such as vegetables, legumes, and starches and the simple carbohydrates
present in fruits is recommended. Other simple carbohydrates, like candy and cook-
ies, should be avoided because they can cause rapid rises in blood glucose. Diets high
in fat and protein are no longer prescribed. Diets that contain 10–20% of their calo-
ries from protein, 50–60% from carbohydrates, and less than 30% from fat (no more

than 10% of these from saturated fat) are optimal. A referral to a clinical dietitian
may be necessary for education.
Cholesterol
Patients with diabetes are prone to developing abnormally high cholesterol levels.
Limiting foods high in fat and limiting cholesterol to less than 300 mg per day are impor-
tant to maintaining a healthy blood cholesterol level. Butter and egg substitutes may
prove to be a beneficial replacement to lower the intake of animal fat and cholesterol.
Pharmacological Therapy
Individuals who cannot adequately control their diabetes with diet and exercise
require medications. There are three general types of medications available to con-
trol diabetes: insulin, incretins, and oral agents. Insulin is required to prevent ketosis
in type 1 patients and to control the metabolic abnormalities associated with uncon-
trolled hyperglycemia in type 1 and 2 patients. Insulin secretion by the patient’s
β-cells is required for the oral hypoglycemic medications to be effective. The use of
insulin secretagogues is contraindicated in patients with type 1 diabetes or patients
prone to ketoacidosis.
Insulin is indicated in patients with type 1 diabetes, type 2 diabetes that cannot
be controlled with diet or other medications, in women with gestational diabetes who
cannot be controlled with diet, and in patients with cystic-fibrosis-related diabetes.
Regular, daily blood sugar checks at 7 a.m., 12 p.m., 5 p.m., and 9 p.m. are recom-
mended, usually before each meal and at bedtime. A daily schedule may begin with
a combination of intermediate or long-acting insulin with lispro or regular insulin
before breakfast. Lispro or regular insulin may be injected before lunch, followed
with a combination of intermediate or long-acting insulin with lispro or regular insu-
lin before dinner. Another option is to inject lispro or regular insulin before dinner
and intermediate or long-acting insulin at bedtime. Measuring blood glucose levels
gives an account of the effectiveness of the insulin as follows:
7 a.m. Fasting glucose levels reflect the effectiveness of the intermediate or

long-acting insulin taken before dinner (5 p.m.) or at bedtime (9 p.m.).
Therapy usually begins with 0.2 units per kilogram of ideal body weight
(or 10 units) increasing the dose by two units every 3 days until the fasting
blood sugar levels are between 70 and 130 mg/dL.
12 p.m. Once the fasting blood sugar is under control, the glucose levels
before lunch reflect the effectiveness of the lispro or regular insulin taken
before breakfast.
5 p.m. Glucose levels before dinner reflect the effectiveness of the lispro or
regular insulin taken before lunch.
9 p.m. Glucose levels before going to bed reflect the effectiveness of the lispro
or regular insulin taken before dinner.
Blood sugars taken 2 hours after a meal are useful to adjust how much lispro or reg-
ular insulin to take before a meal. Patients should count the number of carbohydrates

Diabetes 33
eaten to determine the optimal insulin/carbohydrate ratio. A postprandial blood

sugar of 110–180 mg/dL is optimal. Once this number is known, the postprandial
blood sugar should be checked periodically. An elevated glucose level before lunch
and dinner is an indication that the insulin/carbohydrate ratio should be changed.
An insulin pump greatly improves the quality of life of patients with diabetes and
allows a much tighter control of blood glucose levels. The subcutaneous plastic can-
nula of the pump is usually changed once weekly, minimizing the number of injec-
tions. The pump is programmed to deliver a constant infusion of fast-acting insulin
(which can be adjusted according to the time of day or night) and to deliver insulin
boluses as needed according to the insulin/carbohydrate ratio of the meal or snack.
The amount of insulin should be adjusted to obtain a blood glucose level between
80 and 140 mg/dL and a hemoglobin A1c of <7% or <2% above the upper limits of
normal. (If the laboratory eReports normal values between 4 and 6%, the hemoglo-
bin A1c should be <6–8%). Elderly patients, who are at greater risk for complica-
tions from hypoglycemia, should aim for blood glucose levels of <200 mg/dL before
meals and a hemoglobin A1c of 2–3% above the upper limit of normal.
A BRIEF HISTORY OF TREATMENT STRATEGIES

FOR PATIENTS WITH TYPE 2 DIABETES
Before 1960, regular, nonhuman insulin was the only medication available for the
therapy of diabetes. During the 1960s, oral hypoglycemics (biguanides and clorpro-
pamide) became available for the treatment of patients with mild diabetes, but there
were concerns that hyperstimulation of β-cell function would accelerate the progres-
sion of diabetes.
Regular human insulin and intermediate human insulin (regular and NPH insu-
lins) were approved by the FDA in 1982 and their combination was approved in
1989. Better sulfonylurea medications such as glipizide, glyburide, and glimipiride
were approved in 1984, 1984, and 1995, respectively. Before 1995, the treatment
of diabetes did nothing to decrease insulin resistance (the driving force behind the
metabolic impairment in type 2 diabetes) and did not protect the β-cells. Biguanides
(metformin), approved in 1995, were the first medication type that improved diabetes
by decreasing insulin resistance; this was also the first medication that did not cause
hypoglycemia and was associated with weight loss.
Recommendation for the therapy of type 2 diabetes included diet and exercise
for all patients. If a medication was needed, metformin (used as a single agent in
patients who did not require insulin at the time of diagnosis) was the drug of choice.
The ADA recommended that patients who could not be controlled with metformin
alone be treated with a combination of metformin and insulin or metformin and
a sulfonylurea.
Between 1995 and 2000, three new classes of medications were introduced.
Alpha-glucosidase inhibitors were approved in 1995 (acarbose) and in 1996 (migli-
tol). Thiazolidinediones (TZDs) received FDA approval in 1999. The glinides were
approved in 1997 (repaglinide) and 2000 (nateglinide).
Alpha-glucosidase inhibitors are given before meals; they reduce the absorption
of carbohydrates, reduce postprandial hyperglycemia, and are weight neutral. TZDs

increase insulin sensitivity in muscle fat and liver; they do not cause hypoglyce-
mia, but they are associated with increased weight and fluid retention and there are
concerns over the possibility of increased cardiovascular risk. Glinides are insulin
secretagogues but, unlike sulfonylureas, they result in rapid and short-lived insu-
lin responses. Therefore, they are usually administered t.i.d. (ter in de) before each
meal; unfortunately; like sulfonylureas, they can be associated with weight gain
and hypoglycemia.
Better insulin forms were introduced between 1996 and 2005, including rapid-
acting insulin analogues such as lispro (1996), aspart (2000), and glulisine (2004) and
long-acting basal insulin analogues such as glargine (2000) and detemir (2005).
Orally administered glucose provides a stronger release of insulin by the pancreas
than intravenous glucose does. The effect of nutrient intake on glucoregulation is
called the incretin effect and is responsible for 50–70% of insulin secretion following
oral glucose ingestion. The introduction of incretin-based therapies is probably the
most important contribution to the therapy of diabetes over the last 10 years.
The incretin effect is mediated by two gastrointestinal hormones: glucose-depen-
dent insulinotropic polypeptide (GIP), produced by intestinal K cells in the duode-
num and jejunum, and glucagon-like-peptide-1 (GLP-1), produced by the intestinal
L-cells in the distal small bowel and colon. Defective action of incretin hormones
GIP and GLP-1 plays a significant role in the pathophysiology of obesity-related dia-
betes mellitus. GIP and GLP-1 bind β-cell receptors in the pancreas. In addition to
binding β-cell receptors, GLP-1 (but not GIP) binds receptors in glucagon-producing
α- and δ-cells and in central nervous system cells.
• GIP actions:
• Increases insulin production and β-cells replication in the pancreas
• Decreases gastric acid secretion in the stomach
• Increases fat synthesis in fat cells
• GLP-1 actions:
• Decreases the release of glucagon and increases the amount of β-cell
replication and insulin gene expression in response to glucose in the
pancreas
• Decreases gastric acid secretion and gastric emptying in the stomach
• Increases satiety in the brain
• Promotes insulin sensitivity and lowers triglycerides and fatty acid lev-
els in muscle and fat
Both GIP and GLP-1 are rapidly degraded by the enzyme dipeptidyl peptidase-4
(DPP-4). Independently of each other, elevated glucose levels and obesity decrease
the incretin effect, leading to a vicious cycle of obesity ® reduced incretin effect +
diabetes + ® more obesity. Weight loss improves the incretin effect.
Exenatide is the only FDA-approved GLP-1 receptor agonist (approved in 2005); it
is administered by subcutaneous injection BID. It not only improves glucose control
and reduces weight, but also improves β-cell function. Unfortunately, exenatide has
frequent gastrointestinal side effects and a 2008 FDA warning regarding the (remote)
possibility of pancreatitis and renal problems associated with it has limited its use.

Diabetes 35
The DPP-4 inhibitors sitagliptin and saxagliptin were approved in 2006 and
2009, respectively, and in 2007 a single pill combination of sitagliptin and met-
formin was also approved. DPP-4 inhibitors are less effective than GLP-1 recep-
tor agonists but have rare to no gastrointestinal side effects and offer significant
advantages to patients who will not use injectables or have significant side effects
with exenatide.
Amylin agonists (pramlintide) approved by the FDA in 2005 are used only in
combination with insulin to decrease postprandial glucose elevations. Amylin is
another β-cell hormone that decreases glucagon production in a glucose-dependent
fashion. Unfortunately, it decreases gastric emptying and causes nausea in 30% of
patients who use it; however, this side effect decreases over time. It is associated with
weight loss.
Newer and better treatments for the therapy of type 2 diabetes have resulted in a
considerable change in treatment practices. The use of sulfonylureas has decreased
precipitously from 67% of all patients in 1994 to 34% in 2007, and it should continue
to decline. It is difficult to justify the use of these drugs in the current therapeutic
environment. The use of metformin has increased—as it should have, considering
its therapeutic profile; unfortunately, it is contraindicated in patients with significant
renal impairment. In 2007 TZDs were used in 28% of diabetics, but a steady stream
of bad news regarding potential cardiovascular problems has decreased its use. The
use of insulin has decreased from 38% in 1994 to 28% in 2007. There is no informa-
tion regarding the current use of glinides and incretins; however, a 2009 report from
Eli Lilly estimated exenatide market penetration at around 5.5% (a decrease of 1.5%
when compared with January 2008 and a 6% growth from 2008 to 2009).
Metabolic control may not be achieved with a single agent. Over the course of
15 years, patients are likely to progress from diet and exercise alone to lifestyle changes
plus monotherapy (one medicine), combinations of oral therapies, and, finally, insulin
therapy. Newer sulfonylureas have the same action as the first-generation agents but are
more potent. Chlorpropamide has a prolonged half-life and is eliminated by kidneys,
thus increasing the risk of hypoglycemia in the elderly and patients with renal disease.
Glipizide, glyburide, and glimepiride are metabolized in the liver and are most useful
in patients with renal disease. Glyburide has the longer duration of action and the
greater potential for hypoglycemia. Glipizide and glimepiride are the sulfonylurea of
choice in the elderly because of the lower incidence of hypoglycemia. Maximal doses
of oral agents should be used before a second or third agent is added.
The combination of insulin and sulfonylurea is controversial because even though
sulfonylurea medications often improve glucose levels, they do not improve β-cell
function and they may accelerate their loss. However, if insulin is to be added to a
sulfonylurea, consider the following recommendations:
• If insulin is added to a sulfonylurea, use a long-acting insulin preparation

at bedtime.
• If patients require insulin twice a day, discontinue the sulfonylurea.
• If the patient has severe hyperglycemia and/or other signs of insulin deficiency
such as ketosis and weight loss, insulin therapy must be initiated immediately.

Oral agents are indicated in patients with mild type 2 diabetes whose hemoglobin
A1c is not too far from the target range. The efficacy and risks of different therapies
are presented in Tables 2.1 and 2.2.
INITIATION OF TREATMENT
Patients who have a hemoglobin A1c of <8.5% at the time of diagnosis usually do
well on diet/exercise plus monotherapy. Patients with higher hemoglobin A1c will
probably need combination therapy. Patients who have very high hemoglobin A1c or
show signs of ketosis are best managed with insulin, at least initially; this medication
can later be lowered or removed according to the effects obtained with oral agents.
Monitoring of fasting blood glucose levels is necessary to prevent hypoglycemia in
patients receiving insulin or oral insulin secretagogues.
Monitoring of fasting, preprandial, and postprandial glucose and hemoglobin A1c
is used to adjust therapy. The goals of therapy are fasting and preprandial blood
glucose of 70–130 mg/dL, 2-hour postprandial blood glucose of <180 mg/dL, and
hemoglobin A1c of <7%.
The ADA recommends that all patients be treated with lifestyle interventions and,
if this is not enough, that metformin be added. Patients with insulin resistance who
are not diabetics should be treated with diet and exercise; metformin can be added as
an adjuvant to diet and exercise until the target weight loss has been achieved and the
insulin resistance has been corrected.
Metformin can be titrated over 1–2 months beginning with 500 mg PO (per os)
once or twice daily (or 850 mg daily). The dose should be increased weekly until
significant side effects appear or a daily dose of 2000 mg is achieved.
Hemoglobin A1c levels are monitored every 3 months. If it is very close to target and
there are no side effects, the dose can be increased to a maximum of 2500 mg daily.
If the target hemoglobin A1c is not achieved with diet and exercise and metformin
alone, or if the patient cannot tolerate metformin, another medication can be intro-
duced to replace metformin or add to it. The ADA consensus is to add insulin or
a sulfonylurea because these are well-validated interventions in regard to glucose
homeostasis; however, neither insulin nor sulfonylurea will correct insulin resistance
and the latter could accelerate the progression of β-cell functional decline. Therefore,
if the hemoglobin A1c is close to the target range, an agent other than sulfonylureas
makes more clinical sense. The choice of the second agent varies according to the
patient risk profile and hemoglobin A1c (see Tables 2.1 and 2.2). If the patient is
obese, the second agent should probably be something other than thiazolidinediones.
Adding a third oral agent rather than switching to insulin makes sense only if the
hemoglobin A1c target is easily within reach.
The ADA recommends that, when insulin is added to the therapy, all insulin
secretagogues should be discontinued or tapered off and then discontinued.
The treatment of persons with NIDDM is different in obese and nonobese per-
sons. Tables 2.3 and 2.4 outline our opinion for the therapy of patients according to
the severity of their disease.

Diabetes 37
TABLE 2.1
Benefits and Risks of Oral Agents
Medication Benefit Risks
Sulfonylurea Potentiates insulin secretion Hypoglycemia
Inexpensive Weight gain
Has no effect on insulin resistance
May accelerate the loss of β-cell
function; hypoglycemic effect
decrease over time
Biguanides Reduce hepatic glucose production Lactic acidosis (0.03 per 1,000 patient
(metformin) Improves fasting hyperglycemia years) in patient with renal or liver
Increase insulin sensitivity disease. Avoid use if glomerular
Improves lipid profile filtration is <30 mL/min.
Combine with sulfonylurea to treat Discontinue before radiological
early-morning hyperglycemia procedures that involve i.v. contrast
Low risk of hypoglycemia Do not use in alcoholics
No weight gain Diarrhea in 30% of patients
Can be used safely in the therapy of
insulin resistance without diabetes
Α-glucosidase Delays the hydrolysis of complex Flatulence
inhibitor carbohydrates, slowing their
(acarbose) absorption and thus reducing
postprandial hyperglycemia
Thiazolidinediones Reduce insulin resistance Severe liver disease has been reported
Lower insulin levels in 1/80,000 cases
Correct or improve IGT Mild abnormalities in liver function test
Decrease hepatic glucose output occur in 2% of cases. Liver function
Reduce plasma triglyceride tests should be measured at the start of
Increase HDL therapy, every month for 6 months,
Prevent NIDDM? every other month for the next 6
Very few side effects months, and periodically thereafter.
May slow the rate of β-cell failure; Might increase the risk of MI;
whereas rosiglitazone may increase rosiglitazone may have a 30–40%
the risk of myocardial infarction increased risk for MI and should be
(MI), pioglitazone has been avoided.
associated with a 16% reduction in All may cause weight gain and
death and MI peripheral edema
All increase the risk of congestive heart
failure
All increase the risk of bone fracture
Insulin Like sulfonylureas, stimulate insulin Risk of hypoglycemia is less but risk of
secretagogues secretion but bind to a different weight gain is the same as for
(glinides) sulfonylurea receptor and their sulfonylureas
half-life is shorter; therefore, they
are dosed more frequently
(continued on next page)

TABLE 2.1 (continued)
Benefits and Risks of Oral Agents
Medication Benefit Risks
Incretin-based Increase insulin secretion Decrease gastric emptying
drugs injectable Improve β-cell function Frequent gastrointestinal side effects
GLP-1 receptor Reduce glucagon secretion due to its inhibitory effect on gastric
agonist Decrease appetite motility. There have been reports of
(exenatide) Induce satiety pancreatitis associated with its use.
Induce weight loss Between April 2005 and October 2008
Decrease blood glucose, mainly by the FDA received 75 reports of kidney
lowering postprandial glucose problems associated with Byetta
Not associated with hypoglycemia (exenatide)
Exenatide should be avoided in patients
with renal impairment, patients with a
history of pancreatitis, and patients
who abuse alcohol
Amylin agonists Decrease postprandial glucose Approved only as adjunctive therapy
(pramlintide) Induce weight loss combined with insulin
Decrease gastric emptying
Gastrointestinal side effects
TABLE 2.2
Effectiveness of Diabetes Therapies
Medication Effect on hemoglobin A1c
Diet plus exercise Varies according to the magnitude of weight loss, but improvement in
glucose homeostasis often begins as soon as the patient begins to lose
weight
Metformin Lower Hg A1c by 1.5%
Sulfonylureas Lower Hg A1c 1.5%
Glinides Lower Hg A1c by 1.5%
Alpha-glucosidase inhibitors Lower Hg A1c by 0.5–08%
Exenatide Lower Hg A1c by 0.5–1%
DPP-4 inhibitors Lower Hg A1c by 0.6–0.9%
Pramlintide Lower Hg A1c by 0.5–0.7%
Thiazolidinediones Lower Hg A1c by 0.5–1.4%
Insulin Lower Hg A1c % proportional to dose
Combination therapy If the starting hemoglobin A1c is >8.5%, combination therapy might be
indicated
Notes: The American Diabetes Association recommends a target hemoglobin A1c of <7%. The International
Diabetic Federation recommends a target hemoglobin A1c of <6.5%. The normal upper limit is
5% ± 2%.

Diabetes 39
TABLE 2.3
NIDDM Therapy in Obese Patients according to Disease Severity
Evidence of insulin resistance without Diet and exercise
hyperglycemia or IGT or GDM or OR
mild hyperglycemia Diet and exercise + metformin
Hyperglycemia Diet and exercise + metformin
If goals of therapy are not achieved and Diet and exercise + metformin + incretinsa or acarbose
hemoglobin A1c is close to target range
If goals of therapy are not achieved and Diet and exercise + metformin + incretinsa + acarbose
If goals of therapy are not achieved and Diet and exercise + metformin + incretinsa + acarbose +
hemoglobin A1c is close to target range glinides
OR
Diet and exercise + metformin + incretinsa and/or acarbose +
insulin
OR
Diet and exercise + metformin + insulin
a If incretins are not tolerated or are contraindicated, replace with thiazolidinediones.
TABLE 2.4
NIDDM Therapy in Nonobese Patients according to Disease Severity
IGT or GDM or mild hyperglycemia Diet (eliminate candy, cookies, and other non-nutrient
sugars, especially those containing sucrose, and decrease
animal fat) and exercise
OR
Diet and exercise + metformin or thiazolidinedionesa
Diet and exercise fail to correct the Diet and exercise + metformin + thiazolidinedionesa
signs and symptoms of diabetes, and
If goals of therapy are not achieved and Diet and exercise + metformin and/or thiazolidinediones +
hemoglobin A1c is close to target range insulin
a Thiazolidinediones can be replaced with incretins if they are not tolerated or there are contraindications
to their use.
Hypoglycemia
Hypoglycemia or low blood sugar is a common complication of diabetic therapy with
insulin and/or insulin secretagogue agents. Early symptoms of hypoglycemia include
hunger, anxiety, tremors, tachycardia, sweating, tingling of the lips or tongue, dizzi-
ness, and/or headache. Advanced cases of hypoglycemia can cause confusion, loss
of consciousness, and seizures. Some patients with diabetes do not develop early

symptoms of hypoglycemia. Diabetics should carry packets of sugar or candy to

use at the first signs of hypoglycemia and a bracelet or necklace alerting others of
the presence of diabetes. Family and friends should be instructed on how to inject
glucagon, a medication that can restore consciousness within 15 minutes in victims
of hypoglycemia, allowing patients to ingest sugar and to seek medical help. Beta-
blocker medications used in patients with heart disease, hypertension, and other dis-
eases may mask the early warning signs of hypoglycemia and should be avoided, if
possible, in diabetic patients.
Sites of Administration
The usual sites for injection of insulin are the subcutaneous tissue, quadriceps, del-
toids, abdominals, and the gluteal muscles. Caution is advised when injecting insu-
lin into a muscle that will be involved in physical activity. This may accelerate the
absorption of insulin into the blood, resulting in a more rapid onset of insulin and
hypoglycemia. Exercise or activity has a hypoglycemic effect; therefore, insulin dos-
age may need to be adjusted when a regular exercise program is begun.
It is important to have a treatment plan to control blood sugar. Such a plan should
be flexible and developed with the active participation of the patient. Education,
involvement, and commitment are essential to the success of any treatment plan.
Tight glycemic control is important to prevent complications in IDDM and
NIDDM patients. When three or four daily injections of insulin fail to provide eugly-
cemia (normal blood sugar levels), consider using a subcutaneous insulin pump. The
use of such a pump is associated with less variation of glucose levels, fewer hypo-
glycemic events, less weight gain, and higher quality of life. It is often the method of
choice for insulin delivery in IDDM and a select subgroup of patients with NIDDM
in which oral agents and frequent doses of insulin have failed to control the disease.
EXERCISE ISSUES
Exercise is an important part of the therapy of all diabetics, but especially for the
type 2 diabetic. The health benefits of exercise include:
• Improved physical fitness

• Prevention and/or reduction of obesity
• Improved lipid profile and metabolic control of blood sugar
• Increase in number of muscle mitochondria
• Increase in the number of oxidative enzymes in the muscle
• Increased capillary density in muscle
• Reduction in the risk for coronary heart disease
• Psychosocial benefits
• Reduction of stress
• Possible reduction or elimination of diabetic medications for the type
2 diabetic

Diabetes 41
Cardiopulmonary exercise testing prior to beginning an exercise program is rec-

ommended due to the high association of diabetes and coronary artery disease (see
Appendix B). A multidisciplinary approach is recommended for the management of
diabetes. Careless exercise may result in exacerbation of the following conditions:
• Further deterioration of the metabolic state

• Hypoglycemia
• Retinopathies
• Musculoskeletal and soft-tissue injuries
• Foot injury complications
• Myocardial infarction and/or sudden death
When the blood sugar level is greater than 300 mg/dL, exercise may worsen the
metabolic state and is contraindicated. Optimal blood glucose levels prior to exercise
should be in the range of 100–150 mg/dL. Since exercise has an insulin-like effect,
the following precautions may be used to reduce the likelihood for the development
of hypoglycemia:
• Monitor blood glucose before, during, and after exercise.

• Reduce insulin by one to two units prior to exercise and/or increase carbo-
hydrate intake by 10–15 g 30 minutes prior to exercise.
• Inject insulin subcutaneously or in a muscle that will not be vigorously
active during exercise.
• Bring and eat carbohydrate snacks during prolonged exercise.
• Exercise with a partner who is knowledgeable about the treatment, signs,
and symptoms of hypoglycemia.
Other precautions are to avoid exercise during peak insulin times, avoid exercis-
ing in the heat, and practice good foot hygiene.
Issues Regarding Exercise Prescription in Patients with Diabetes

In some patients, autonomic neuropathies may prevent the accurate calculation of
a predicted maximum heart rate. Therefore, exercise intensity prescribed by tar-
get heart rate may be inaccurate. For these patients, we recommend instructing the
patient on using the perceived exertion rating (RPE) chart found in Appendix A,
Method 5. An intensity corresponding to 40–85% of maximum exercise capacity
(see Appendix A, Method 6)—an RPE of 10–16—is recommended. The patient
should exercise on a daily basis to maximize caloric expenditure and stabilize blood
sugar levels.
Successful management depends on the patient’s ability to monitor blood sugar
levels and administer insulin accurately. Exercise should not be prescribed until
adequate diet, metabolic control, and blood sugar levels are achieved. Exercise
does not improve glycemic control in IDDM; however, the benefits of exercise exceed

the risk by lowering the risk for cardiovascular disease, improving the quality of life,
and reducing or eliminating weight gain. Exercise is an indispensable form of treat-
ment for patients with type 2 diabetes. Low-intensity exercise, such as walking,
which can be safely performed and incorporated into the routine of daily life, is as
effective as high-intensity exercise for improving insulin sensitivity in patients with
type 2 diabetes.
Exercise and the Type 1 Diabetic

Juvenile diabetics or insulin-dependent type 1 diabetics do not benefit from exer-
cise in the same way as an insulin-resistant or type 2 diabetic. Exercise for the type
1 diabetic will help the patient prevent the risk of cardiac complications (e.g., macro
angiopathies), but will not correct the glucose intolerance. Furthermore, exer-
cise might be detrimental in uncontrolled diabetes with blood glucose levels of
>250–300 mg/dL. It is very important to time meals with exercise. Eating a snack
containing 5–10 g of carbohydrates every 20–30 minutes during exercise is often nec-
essary. A particularly good time to exercise is about 1–2 hours after a light meal or
carbohydrate snack because the postprandial blood glucose level peaks at this time.
Exercise and the Type 2 Diabetic

Aerobic exercise training has long been recognized as a form of therapy for individu-
als with adult-onset type 2, non-insulin-dependent diabetes mellitus. Recent studies
have reported near normalization of blood glucose levels and insulin metabolism
resulting from diet and exercise programs. A program of exercise reduces glucose-
stimulated hyperinsulinemia. Some of these results have even occurred without a
reduction in weight. Exercise must be maintained or the benefits are lost within
10 days of its cessation. The effect of exercise on glucose and insulin metabolism
depends on the degree of muscle glycogen depletion that occurs during exercise.
The beneficial effects of exercise are related to the exercise done the day before.
If exercise is to play a significant role in the management of diabetes, it must be done
frequently, ideally daily for at least 30 minutes and at least 4–5 days per week, avoid-
ing two consecutive days without exercise. The type 2 diabetic, unlike the type 1
diabetic, may have elevated levels of insulin; a cellular resistance to the metabolic
effects of insulin prevents a concomitant uptake of glucose by the cells. Recent
research has determined that this decreased sensitivity to insulin is improved with
exercise and weight loss. Similar hypoglycemic and exercise guidelines apply as
outlined for the type 1 diabetic in patients with type 2 diabetes on insulin therapy or
insulin secretagogues.
Glucose Monitoring and Exercise

The following guidelines should be followed when monitoring blood glucose levels
during exercise: for at least the first five exercise sessions, measure finger-stick blood
glucose before and after exercise. If these measurements yield values in the safe
range (Table 2.5) and are stable from day to day, then measure only once per week
(unless signs or symptoms warrant on-the-spot measurements). (Note: this is a mini-
mum guideline. It is best if the patient monitors his or her own levels several times a

Diabetes 43
TABLE 2.5
Interpretation of Preexercise Blood Glucose Values
>250 mg/dL or more No exercise that day; refer to physician for better control.
150–249 mg/dL Exercise with caution; remeasure after 10 minutes of exercise; if the value is
rising, stop exercise and refer to physician for better control. Goals of therapy
are not met, but it is safe to begin exercise sessions.
100–149 mg/dL Exercise with caution; watch for signs and symptoms of hypoglycemia;
remeasure as needed; give light snack (candy) or juice of 10–15 g of
carbohydrates as needed.
80–90 mg/dL Exercise with caution; instruct patient to eat a carbohydrate snack; 1 hour of
exercise requires an additional 15 g of carbohydrates before exercise. An
additional 15–30 g of carbohydrates may be needed every hour when exercise
is vigorous (e.g., 70–85% of maximal capacity) or of long duration (more than
1 hour). Remeasure after 15 minutes; if above 100, exercise may continue
with caution; discuss pre-exercise habits of medication and food consumption
with patient.
<80 mg/dL Do not exercise until blood sugar levels improve.
Note: These ranges are only guidelines. Frequent monitoring at the beginning of the program allows you
and the patient to understand the blood glucose responses.
day, including before and after all exercise sessions. If blood glucose values are not
stable, monitoring before and after every exercise session is required.)
SUMMARY
Several general factors should be considered in developing an exercise prescription
for the diabetic. An exercise program is not recommended for uncontrolled diabe-
tes. Two potential problems may occur in exercising insulin-dependent diabetics.
The first, a lack of sufficient insulin, may cause a hyperglycemic effect in the blood
because cellular absorption of glucose is restricted. The second is the hypoglycemic
effect, which occurs due to an increased mobilization of depot insulin, particularly if
the injection site was in the exercising muscle. Since physical activity has an insulin-
like effect, the exercise program requires an insulin-dependent diabetic to reduce
insulin intake or to increase carbohydrate intake.
It is important to instruct the diabetic exerciser that, during prolonged activi-
ties, adequate nourishment must be available in the form of sugar, fruit juice,
and/or readily digestible carbohydrates. Special attention should be given to
patients taking β-blockers because hypoglycemic symptoms may be masked by
the β-blockers. Since exercise may precipitate a hypoglycemic event in diabet-
ics (particularly type 1), it is recommended that exercise be done with a partner
and the patient be knowledgeable of the signs and symptoms of hypoglyce-
mia. Always remind the patient to carry a carbohydrate source during exercise.
Generally, diabetics can avoid hypoglycemic events by injecting insulin in an
area, such as the abdomen, that will not be active during exercise and avoiding

exercise during periods of peak insulin activity, in addition to the dietary precau-
tions mentioned before.
Long-term elevation of blood glucose may lead to microangiopathy and neuropathy.
Patients with severe neuropathies may not be as sensitive to angina or chest pain and
may require additional monitoring of blood pressure and HR. Furthermore, predict-
ing exercise target HR by using the formula 220–AGE (see Appendix A, Method 1)
may not be appropriate for patients with neuropathies. In these patients, exercise may
be prescribed using perceived exertion as outlined earlier. A cardiopulmonary stress
test yields accurate HR information. Because of impairment of peripheral circulation
and anhydrosis (decreased ability to sweat), diabetic exercisers should take particu-
lar care in selecting footwear, practice careful foot hygiene, and be particularly cau-
tious when exercising in conditions of heat stress.
WEIGHT TRAINING GUIDELINES FOR DIABETICS

When weight training is conducted for people with diabetes, resting and exercise
blood sugars are of the utmost concern. Patients with uncontrolled or brittle diabetes
(blood sugars > 300 mg/dL) should avoid weight training. Other contraindications to
weight training include:

• Aerobic capacity of less than 5 MET (metabolic equivalents)
frequent repetitions is recommended to reduce the likelihood of microvascular com-
plications from elevated blood pressures. Circuit training involves moving from
exercise to exercise at a consistent pace. This will develop muscle endurance and
strength. To control blood pressure and prevent the elevation of after-loads on the
heart, isometric or static components should be minimized when the weight-lifting
exercise is performed by breathing on exertion and using a weight that can be lifted
without stopping halfway through the motion.
and abilities. Weight machines and free weights can be used when the patient is
able to join a gym or fitness center. Weight-lifting exercises that can be done at home
are illustrated in the diabetes workbook CD.
When the proper intensity is being selected, it is important that the amount of
weight (pounds) lifted is based on the ability of the individual rather than being
an arbitrary weight. We recommend two methods to determine the intensity. All
exercise or repetition sets may be performed one or two times or in one or two
sets—for example:


Diabetes 45

[100 – (# reps × 2.5)] = % 1RM
A load of 30–50% of the 1RM is recommended for beginners, progressing to

60–80% of the 1RM. An example using this equation to determine the 1RM can be
found in Appendix A, Method 10.
The preceding method for prescribing intensity can be used for any weight-lifting
be exceeded when weight lifting is undertaken.
RECOMMENDED READING
American Association of Cardiovascular and Pulmonary Rehabilitation. 1991. Guidelines
for cardiac rehabilitation programs, 2nd ed., chap. 3. Champaign, IL: Human Kinetics.
ACSM’s guidelines for exercise testing and prescription, 8th ed. 2010. New York: Wolters
American Diabetes Association. 1996. Clinical practice recommendations 1996. Diabetes Care
19:S1–S118.
Bergman, R. N. 1996. Toward an integrated phenotype in pre-NIDDM. Diabetic Medicine
(Suppl. 13) 6:S67–S77.
Braun, B. 1995. Effects of exercise intensity on insulin sensitivity in women with non-insulin-
dependent diabetes mellitus, Journal of Applied Physiology 78:300–306.
———. 1996. Relationships between glucose metabolism and thermogenesis with and
without prior exercise in obese woman with non-insulin-dependent diabetes mellitus.
Metabolism 45:747–752.
Davidson, M. B. 1995. Clinical implications of insulin resistance syndromes. American
Journal of Medicine 99:420–426.
Durstine, J. L. et al. 2009. ACSM’s exercise management for persons with chronic diseases and
disabilities, 3rd ed., chap. 24. Champaign, IL: Human Kinetics.
Eriksson, K. F. 1996. Poor physical fitness, and impaired early insulin response but late hyper-
insulinaemia, as predictors of NIDDM in middle-aged Swedish men. Diabetologia
39:573–579.
Felber, J. P. 1995. Regulation of nutrient metabolism and energy expenditure. Metabolism 44
(Suppl. 2): 49.
Fielding, R. A. 1995. The role of progressive resistance training and nutrition in the preser-
vation of lean body mass in the elderly. Journal of the American College of Nutrition
14:587–594.
Kennedy, L., ed. 2009. The role of incretin-based therapies in treating patients with type 2 dia-
betes mellitus. Cleveland Clinic Journal of Medicine 76 (Suppl. 5): December 2009.
Leon, A. S. 1989. Patients with diabetes mellitus. In Exercise in modern medicine, ed. B. A.
Franklin, S. Gordon, and G. C. Timmis. Baltimore, MD: Williams & Wilkins.
Nathan D. M. et al. 2009. Medical management of hyperglycemia in type 2 diabetes: A con-
sensus algorithm for the initiation and adjustment of therapy. A consensus statement
of the American Diabetes Association and the European Association for the Study of
Diabetes. Diabetes Care 32:193–203.
Nolan, J. J. 1994. Improvement in glucose tolerance and insulin resistance in obese subjects
treated with troglitazone. New England Journal of Medicine 331:1188–1193.

Pract, S. F. E. 2009. Exercise therapy in type 2 diabetes. Acta Diabetologica 46:263–278.

Ryan, A. S. 1996. Resistive training increases insulin action in postmenopausal woman.
Journals of Gerontology A: Biological Sciences and Medical Sciences 51:199–205.
Saudek, C. D. 1996. Implantable insulin pump vs. multiple-dose insulin for non-insulin-depen-
dent diabetes mellitus. A randomized clinical trial. Journal of the American Medical
Association 276:1322–1327.
Slovid, D. M. 1997. Diabetes and rehab. REHAB Management February/March 116:46–53.
Yamanouchi, K. 1995. Daily walking combined with diet therapy is a useful means for obese
NIDDM patients not only to reduce body weight but also to improve insulin sensitivity.
Diabetes Care 18:775–778.
EXERCISE PRESCRIPTION FOR DIABETES

Frequency
Exercise a minimum of 3 days per week, preferably daily, to maximize
caloric expenditure and to control blood glucose and insulin patterns.
Modality
Walking is an easy, preferred method because it does not require any special
equipment; however, stationary or active bike riding and swimming are
also acceptable aerobic exercises. You may even want to recommend
different modalities during the exercise session. A resistance or weight-
training program should be included.
Duration
Begin with an exercise time that is comfortable—initially, perhaps 10 min-
utes. Gradually increase the aerobic exercise time by 2–4 minutes each
week, until 20–60 minutes of exercise is achieved without stopping. Be
sure to include weight training in the workout.
Intensity
The aerobic and weight-training intensity should be prescribed using an
RPE chart like the one in Appendix A, Method 5. A perceived exer-
tion rating between very light and hard, with an RPE of 10–16, is
recommended. When weight training, use a light weight for 10–15
repetitions and prescribe one to two sets for each muscle group. Work
the upper and lower muscle groups. Do not exceed the aerobic pre-
scribed RPE of 16 when weight training. See the section on weight
training in this chapter and in the diabetes workbook CD for more
detailed instructions.
Other Instructions
• The patient should avoid exercise during the hottest part of the day.
• Instruct the patient to report any weight gain, shortness of breath, or chest
pain immediately.
• Encourage progress follow-up in the workbook exercise log for the next
follow-up visit.

Diabetes 47
• Instruct the patient to stop exercising immediately if he or she feels faint or

dizzy or has heart palpitations.
• The patient should warm up and cool down prior to exercising for at least
5–10 minutes at a comfortable intensity.
• When a patient begins an exercise program, check blood sugar levels before,
during, and after exercise.
• Blood sugar should be less than 250 mg/dL prior to exercise. If it is greater
than that or less than 100, the patient should not exercise.
• Instruct the patient to recognize the signs of low blood sugar and to carry
hard candy in case the blood sugar drops.
• Be sure the patient has shoes that fit properly and takes special precautions
to prevent foot sores.
COMMON QUESTIONS ON DIABETES (A PATIENT’S PERSPECTIVE)

Question: What is diabetes?
Answer: Diabetes is a chronic disease affecting the pancreas. The pancreas
secretes insulin, which takes glucose (sugar) into the cells. Without glucose,
your cells would starve. When you have diabetes, there is a problem with
insulin: Your pancreas is not producing insulin, your cells are resistant to
insulin, or a combination of the two is occurring.
Question: How do people get diabetes?
Answer: Diabetes is not a disease that you “catch” from someone. You get it
when your pancreas stops making insulin or you have become resistant to
it. Genetics, obesity, and lack of exercise all play a role in type 2 diabetes.
Genetics also plays a role in type 1 diabetes, as do viral infections. Type 2
diabetes has a stronger genetic association and a stronger environmental
influence. Patients with the type 2 diabetes gene seldom express it unless
they become overweight or obese.
Question: How many types of diabetes are there?
Answer: There are two types of diabetes:
Type 1 diabetes is called juvenile-onset or insulin-dependent diabetes. This
type occurs when the pancreas produces little insulin and it usually
begins at birth or at a very young age. Without these cells, your body
cannot produce insulin. A virus may have attacked your pancreas kill-
ing these cells. In type 1 diabetes, insulin needs to be injected.
The second type of diabetes is type 2, which is also called adult-onset or
non-insulin-dependent diabetes. However, insulin injections are often
required. Type 2 diabetes occurs when the cells become resistant to the
insulin produced in the pancreas.
Question: How would I know if I have diabetes?
Answer: Several warning signs are present when your blood sugar is not nor-
mal. Fatigue, visual changes, thirst, hunger, frequent urination, poor wound
healing, and tingling in legs and arms are all symptoms associated with
high blood sugars. If you experience these symptoms, report them to your
medical professional. A blood glucose level may be drawn at random and,

if that is high, you may be asked to repeat the lab work. Based on the results
of these blood tests, diabetes is diagnosed.
Question: Can diabetes cause other problems?
Answer: Yes. Poor control of blood sugar will eventually damage your kidneys,
nerves, and eyes. In addition, heart disease and blood vessel diseases are
common in diabetics who have poor management of their blood sugars.
Question: What should I eat?
Answer: Your medical professional or dietitian will help you determine how
many calories you should take in daily based on your ideal body weight.
These calories will be appropriately balanced in proteins, fats, and carbo-
hydrates to deliver a well-balanced diet.
Question: Does eating too many sweets cause diabetes?
Answer: No. However, a hypercaloric diet high in carbohydrates, especially
sucrose, can lead to oxidation injury—the most common proximal cause of
diabetes. Eating too many sweets can worsen diabetes and result in obesity,
which is a risk factor for type 2 diabetes.
Question: Do I have to take insulin shots?
Answer: This may depend on the type of diabetes you have and how serious
it is. Type 1 diabetes requires insulin shots. Type 2 diabetes may require
insulin shots, but can usually be managed through diet, exercise, and pills.
If blood sugars are not controlled with pills, insulin shots may be needed
later on.
Question: What can I do to prevent other complications caused by diabetes?
Answer: Manage and control your blood sugar. Tight control of blood sugar
has proven to be effective in controlling and preventing long-term com-
plications of diabetes. If you are overweight, lose the extra pounds; if you
do not exercise, start. If your diet is not balanced, talk with a dietitian and
develop an eating plan that is appropriate for your lifestyle.
Question: How does exercise affect blood sugar control?
Answer: Exercise improves blood glucose control by increasing insulin sen-
sitivity. That means it helps insulin work so that glucose or sugar can get
into your cells more easily and be processed more efficiently. In addition, it
assists in weight loss.
Question: How much should I exercise?
Answer: This is individualized based on your needs. At least three times
a week is suggested but daily exercise is preferred. Start out slowly and
advance to at least 20 minutes. Both aerobic exercise and weight training
are recommended. For more information, see the exercise sections in the
diabetes workbook.
Question: Will I have to take medicine the rest of my life?
Answer: If you are a type 1 diabetic, you will be on insulin shots the rest of your
life. If you are a type 2 diabetic and obesity is a major factor in your diabetes,
you may be able to stop taking medication if you lose weight and exercise.

3 Kidney Disease
BACKGROUND
Renal insufficiency or renal or kidney failure is a clinical condition caused by several
pathologic entities that cause a deterioration of renal function, adaptation, and eventu-
ally uncompensated renal failure. The disease can be classified qualitatively into three
groups according to the severity of the functional impairment: (1) decreased renal
reserve, (2) renal insufficiency, and (3) uremia. The disease can be classified quantita-
tively according to the estimated glomerular filtration rate (eGFR) as follows:
• Stage 1: evidence of kidney damage but normal eGFR: ≥90

• Stage 2: mildly decreased eGFR: 60–89
• Stage 3: moderately decreased eGFR: 30–59
• Stage 4: severely decreased eGFR: 15–29
• Stage 5: kidney failure eGFR: <15
Early evidence of kidney damage, before the eGFR decreases, includes micro-
scopic hematuria and/or proteinuria. The albumin-to-creatinine ratio in a spot urine
sample is a useful test to screen for early kidney damage in patients at risk of kidney
disease such as those with diabetes or hypertension. The normal albumin/creatinine
ratio is <30 μg/mg; values of 30–299 indicate microalbuminuria and values of ≥300
indicate macroalbuminuria.
As renal function deteriorates, a variety of compensatory mechanisms adapt to
preserve homeostasis. Further deterioration causes azotemia (elevation of plasma
urea and creatinine). When the glomerular filtration approaches 6 mL/min/m2, the
azotemia is severe and fluid and electrolyte balance are considerably impaired, with
a characteristic metabolic acidosis, anemia, hypocalcemia, hyperphosphatemia, and
hyperkalemia. Urinary osmolality is usually fixed and close to the plasma. Urinary
volume is also fixed (does not vary proportionally to fluid intake) somewhere between
1 and 4 L per day.
There are multiple causes of renal failure. Congenital glomerulonephritis and
nephrotoxins are more common in the young. Renal failure in the elderly is more
commonly caused by chronic glomerulonephritis, obstruction, hypertension, and dia-
betes. The most important consideration at the time of diagnosis is to rule out treat-
able diseases such as hypercalcemia, renal artery obstruction, nephrotoxic agents, and
prerenal causes of azotemia, such as heart failure and dehydration.
49
Higher blood pressure and socioeconomic status are thought to be responsible for
the relatively high risk of end-stage renal disease (ESRD) in African Americans. The
incidence of ESRD is 13.9 per 100,000 person-years in Caucasian men and 44.22
per 100,000 person-years in African American men. Patients in renal failure have
increased protein degradation, but are not hypermetabolic. Energy expenditures in
patients at rest and for a given physical activity in nondialyzed and in maintenance
hemodialysis are not different from normal.
Hypertension can cause renal failure and/or favor the progression of renal fail-
ure. The appearance of renal impairment is thought to be secondary to abnormalities
in the factors that regulate the vasomotor tone of the afferent–efferent arterioles,
and/or the development of periglomerular fibrosis and reduction of the lumen of the
vessel by intimal proliferation and hyaline deposits. Other factors responsible for
renal failure in hypertension include the depositing of atherosclerotic plaque in the
wall of renal arteries and/or cholesterol microembolization.
Blood pressure control has reduced the incidence of stroke, coronary artery dis-
ease, and renal failure. Renal disease secondary to hypertension has increased by
16–26% during the last decade. Angiotensin-converting enzyme (ACE) inhibitors
and calcium antagonists (Verapamil, Diltiazem) are able to provide some protection
in patients with mild to moderate hypertensive renal disease. The combination of
these two drugs might have additive protective effects. ACE inhibitors are a double-
edged sword because the renal mechanisms underlying the adverse effects of ACE
inhibitors—intrarenal efferent vasodilatation with a consequent fall in filtration
pressure—are held to be involved in their renal-protective effects as well.
In conditions in which glomerular filtration is critically dependent on angiotensin
II-mediated efferent vascular tone (such as a poststenotic kidney or patients with
heart failure and severe depletion of circulating volume), ACE inhibition can induce
acute renal failure; this is reversible upon withdrawal of the drug. Those at greatest
risks for adverse renal effects—patients with heart failure, diabetes mellitus, and/or
chronic renal failure—can also expect the greatest benefit. ACE inhibitors should
therefore not be withheld in these patients, but dosages should be carefully titrated,
with monitoring of renal function and serum potassium levels.
Calcium antagonists slow the progression of renal disease. They are natriuretic
and may benefit salt-sensitive hypertensives. They have been shown to block vaso-
constriction of the afferent arteriole in the presence of constrictors such as endothe-
lin, thromboxane, norepinephrine, and angiotensin II.
Renal artery stenosis may be caused by either atherosclerosis or fibromuscular
dysplasia and is often responsible for hypertension or renal failure. Screening of
hypertensive patients with relatively high prevalence for the disease, such as severe
hypertension resistant to therapy or associated with progressive renal insufficiency,
is recommended. Noninvasive tests with a high predictive value include Doppler
ultrasonography, intravenous angiography, spiral CT angiography, and captopril
renography. Arteriography remains the “gold standard” for detecting and quantify-
ing renal artery stenosis.
Diabetic nephropathy is caused by a combination of an abnormal regulation of
the vasomotor tone of the afferent–efferent arterioles and the effect of hyperglycemia

Kidney Disease 51
and other toxins in the glomerulus. The afferent arterioles are vasodilated by means
of prostaglandins, bradykinins, and other mediators. The efferent arterioles are
vasoconstricted by thromboxane A2, resulting in a state of hyperfiltration that,
coupled with high levels of glucose and other by-products produced under condi-
tions of insulin resistance, causes thickening of the basal membrane, resulting in
glomerulosclerosis.
Diabetes mellitus is the most common cause of renal failure, accounting for one
third of all cases of end-stage renal disease. Of all patients in dialysis, 60% have
non-insulin-dependent diabetes mellitus (NIDDM) and 40% have insulin-dependent
diabetes mellitus (IDDM). Diabetic patients entering dialysis have a 50% greater
risk of death than other patients.
The first clinical sign of renal impairment is albuminuria. Microalbuminuria
(30–300 mg/24 h) can occur in the presence of a normal glomerular filtration rate.
Hypertension usually follows microalbuminuria by 2–5 years. When microalbumin-
uria occurs, it is a sign that renal damage will progress unless the patient receives
appropriate therapy.
Hypertension without albuminuria suggests that an etiology other than diabetes is
responsible for the elevated blood pressure. Hypertension increases the rate of pro-
gression of renal disease in the diabetic; a blood pressure of 130/85 should be treated
unless the lowering of the blood pressure compromises the perfusion of selected
vascular beds. ACE inhibitors can reduce proteinuria and probably slow the develop-
ment of renal disease. Calcium channel blockers (Verapamil, Diltiazem) can reduce
proteinuria and might also reduce the progression of renal disease.
The presence of hematuria (blood in the urine) or pyuria indicates a cause
other than diabetes. Macroalbuminuria (300 mg/24 h) indicates renal disease that
would progress to renal failure within 7–10 years. Approximately 9% of patients
with microalbuminuria progress to macroalbuminuria each year. Screening for
microalbuminuria should be done yearly. The standard dipstick test detects only
macroalbuminuria.
MANAGEMENT
The treatment of chronic renal failure includes the following:
• Diet: Protein ≤0.8–1.0 g/kg ideal body weight daily for patients with
mild renal disease and 0.8 g/kg for patients with more advanced dis-
ease, 3–5 g Na, and at least 35 calories/kilogram/day ideal body weight
to reduce protein degradation and muscle breakdown. A renal diet is
recommended when the serum creatinine is between 1.5 and 2.5 mg/dL.
Benefits from protein restriction can only be achieved if energy intake is
greater than 35 kcal/kg/day.
• Calcium carbonate 500 mg PO (per os) t.i.d. (ter in de) before meals to
reduce hyperphosphatemia and improve hypocalcemia.
• Calcium and vitamin D preparations for hypocalcemia and secondary
hyperparathyroidism, which leads to bone demineralization.

• Sodium bicarbonate 600 mg PO t.i.d. adjusted until the serum bicarbonate

level is close to 20 mEq/L to reduce muscle degradation and other problems
of metabolic acidosis.
• Epoetin-α is indicated when the hematocrit falls below 30%.
• Dialysis.
• Renal transplantation.
• Exercise: renal failure patients (RFPs) have muscle weakness, which is
worse in the proximal muscle groups—especially in the lower extremities.
Muscular strength of RFPs is 50–70% of normal and quadriceps strength is
80% of predicted. Exercise training improves muscular function in RFPs.
Patients with chronic renal failure are also insulin resistant. Studies per-
formed on uremic rats have shown that regular exercise training reduces
muscle protein catabolism and improves insulin sensitivity.
EXERCISE ISSUES
Exercise training ameliorates the enhanced muscle protein degradation associated
with chronic renal failure. Heart disease is a major concern for patients with renal
disease. Many of these patients have multiple medical problems, including hyperten-
sion, elevated triglycerides, elevated cholesterol, and reduced high-density lipopro-
tein (HDL) levels.
With numerous medical problems associated with ESRD, the major concern prior
to initiating an exercise program is stability. Exercise might cause a potassium efflux
from exercising muscles and may elevate blood levels, increasing the possibility of
cardiac arrhythmias. However, the possibility of exercise-induced hyperkalemia is
small. Patients should be able to perform moderately intense physical exercise with-
out developing significant hyperkalemia.
Serum potassium levels must be controlled prior to exercise and should not be
greater than 5 mEq/L of blood. Blood pressure should be monitored in the arm
opposite the arteriovenous shunt prior to exercise. If blood pressure is greater
than 200/110 at rest, exercise should not be undertaken. Another consideration
involves the appropriate time for exercise. Exercise can be performed before, during,
or after dialysis. When exercise is prescribed following dialysis, blood chemistry
levels will be at their optimum, although fatigue may be a factor. Exercising during
dialysis may be an option for some; however, maximum exercise capacity has been
reported to be 20% lower then. Exercise during dialysis improves the efficiency of
dialysis, probably because of better mobilization of dependent fluids and better filtra-
tion pressure. There is no significant difference in exercise ability if exercise is done
before or during peritoneal dialysis. Having the peritoneal cavity full of dialysate
does not decrease the aerobic capacity.
We recommend exercise training during dialysis and the day after dialysis. The
day before dialysis might not be the best day because there may be a higher likelihood
of instability. The best time for an exercise test is the day after dialysis (see Appendix
B). Patients on dialysis may have a low exercise capacity, which could be as low as
half that of healthy individuals matched to age and gender. This corresponds to a

Kidney Disease 53
VO2 max (maximum exercise capacity) of 15–20 mL/kg/min or about 3–5 METs

(metabolic equivalents; activities of daily living require 1.5–5 METs); 1 MET is
equal to the energy expenditure at rest.
Walking is an excellent form of exercise. If exercise is performed on a cycle
ergometer, maximum power outputs of 75–100 W are typical. This modality is rec-
ommended, especially in the initial stages of training, because work levels can be
accurately set and monitored on a cycle.
Autonomic dysfunction and peripheral neuropathies may prevent the linear or
normal relationship between heart rate and VO2 typically seen in healthy individu-
als and limit maximal age-predicted heart rates by as much as 20–40 beats/min.
Therefore, when prescribing exercise intensity, we recommend using the perceived
exertion rating (RPE) chart (see Appendix A, Method 5).
BENEFITS OF EXERCISE
ESRD patients routinely increase their exercise capacity by 20–42%. Other improve-
ments resulting from exercise include
• Increase in hematocrit of 16–35%

• Increase in hemoglobin of 27–37%
• Increased reticulocyte counts
• Reductions in blood pressure of up to 31 mmHg systolic and 19 mmHg
diastolic
• Decrease in plasma triglyceride levels of 29–41%
• Increase in HDL cholesterol levels of 16–23%
• Improvement in plasma insulin levels by 20–40%
• Near-normalized insulin and glucose tolerance in type 2 diabetics
• Psychological profile improvements
Training with free weights can reduce muscle wasting and increase strength and
flexibility. You should prescribe light hand weights that allow 15–20 repetitions, as
illustrated in the kidney disease workbook CD. One-repetition maximum lifts are
not recommended to prescribe lifting intensity. Intensity should not exceed the aero-
bic RPE level of 10–16. See the following weight training guidelines.
WEIGHT TRAINING GUIDELINES IN KIDNEY DISEASE

When weight training patients with renal disease, resting and exercise blood pres-
sures (>200/110 mmHg) and potassium levels (>5 mEq/L) are of the utmost concern.
Patients with uncontrolled blood chemistries should avoid weight training. Other
contraindications to weight training include the following:

• Aerobic capacity of less than 5 METs

and ability. Weight machines and free weights can be used when the patient is able to
join a gym or fitness center. Weight-lifting exercises that can be performed at home
are illustrated in the kidney disease workbook CD.
lifted be based on the ability of the individual rather than on an arbitrary weight.
We recommend the following method to prescribe the intensity: All exercise or rep-
etition sets may be performed one or two times or in one or two sets. For example,
choose a weight that can be lifted comfortably 10–15 times. When 15 repetitions can
be comfortably performed, the weight may be increased to an amount that can be
lifted at least 10 times. Most patients have a very low 5-MET capacity. Therefore,
weight training should be supervised when possible and consist of low weight and
high repetitions as described before.
be exceeded when weight lifting is undertaken. However, most patients will be too
weak to use free weights. The RPE of 10–16 prescribed for aerobic work should
not be exceeded when weight lifting is undertaken.
RECOMMENDED READING
ACSM’s guidelines for exercise testing and prescription, 8th ed. 2010. Baltimore, MD: Wolters
Beasley, C. R. 1986. Exercise capacity in chronic renal failure patients managed by continuous
ambulatory peritoneal dialysis. Australian & New Zealand Journal of Medicine 16:510.
Castaneda, C. 1998. Potential benefits of resistance exercise training on nutritional status in
renal failure. Journal of Renal Nutrition 8:2–10.
Davis, T. A. 1985. Muscle protein turnover: Effects of exercise training and renal insufficiency.
American Journal of Physiology 248:E337–E345.
disabilities, 3rd ed., chap. 24. Champaign, IL: Human Kinetics.
Elkohen, M. 1996. Screening of renal artery stenosis: Which patients, by what methods? Revue
du Praticien-Medcine Generale 46:1091–1095.
Hagberg, J. M. 1989. Patients with end-stage renal disease. In Exercise in modern medicine,
ed. B. A. Franklin, S. Gordon, and G. C. Timmis. Baltimore, MD: Williams & Wilkins.
Heiwe, S. 2001. Twelve weeks of exercise training increases muscle function and walking
capacity in elderly predialysis patients and healthy subjects. Nephron 88:48–56.
Jacobson, H. S. 2009. Exercise training for adults with chronic renal disease (protocol).
Cochrane Library Issue 3.

Kidney Disease 55
Klag, M. J. 1997. End-stage renal disease in African American and white men: 16-year MRFIT
findings. Journal of the American Medical Association 277:1293–1238.
Lens, X. M., J. A. Oliva, P. Codinach, R. Pascual, J. Carrio, and J. M. Mallafre. 1989. Physical exer-
cise and serum potassium in renal insufficiency. Revista Clinica Espanola 184:285–288.
Monteon, F. J. 1986. Energy expenditure in patients with chronic renal failure. Kidney Inter
national 30:741–747.
Navis, G. 1996. ACE inhibitors and the kidney. A risk-benefit assessment. Drug Safety
15:200–211.
Painter, P. L. 1997. Renal failure. In ACSM’s exercise management for persons with chronic
diseases and disabilities, ed. J. L. Durstine, L. E. Bloomquist, S. F. Figoni, et al.
Champaign, IL: Human Kinetics.
Pearce, C. J. 1996. Calcium antagonists and the kidney. New Horizons 4:123–128.
Rodicio, J. L. 1996. Does antihypertensive therapy protect the kidney in essential hyperten-
sion? Journal of Hypertension 14 (Suppl.): S69–S75.
Shalom, R. 1984. Feasibility and benefits of exercise training in patients on maintenance dialy-
sis. Kidney International 25:958–963.
Steinman, T. I. 1996. Kidney protection: How to prevent or delay chronic renal failure.
Geriatrics 51 (8): 28–35.
Wardle, E. N. 1996. How does hyperglycemia predispose to diabetic nephropathy? Quarterly
Journal of Medicine 12:943–951.
EXERCISE PRESCRIPTION FOR KIDNEY DISEASE

Frequency
Exercise a minimum of 3 days per week. If the patient is on dialysis, exer-
cise the day of and following dialysis. Try to avoid exercising the day
before dialysis.
Modality
Walking is an easy, preferred method because it does not require any
special equipment. Stationary or active bike riding is also an accept-
able aerobic modality and is recommended in the initial stages of
training to monitor workloads more accurately. Try combining dif-
ferent modalities during the aerobic exercise session to maximize
the training effect. A weight-training program should be included
when possible.
Duration
Begin with a time that is comfortable—initially, about 10 minutes.
Gradually increase the aerobic exercise time by 2–4 minutes each week
until 20–60 minutes is achieved without stopping.
Intensity
The aerobic and weight-training intensity can be prescribed using the RPE
chart in Appendix A, Method 5. A perceived exertion rating between
light and hard, an RPE of 10–16, is recommended. Prescribe a weight
light enough to do 10–15 repetitions and do one to two sets for each

muscle group. Do not exceed an aerobic intensity RPE of 16. See the
weight training section in the kidney disease workbook CD for specific
instructions.
Other Instructions
• The patient should avoid exercising during the hottest part of the day.
pain immediately.
follow-up visit.
• Before starting an exercise program, the patient should be sure potassium
levels are normalized.
COMMON QUESTIONS ON KIDNEY DISEASE

Question: What is kidney or renal disease?
Answer: Renal disease is a condition in which the kidneys cease to func-
tion normally. This causes the kidneys to stop eliminating waste products
and toxins in your blood stream. This can lead to high blood pressure,
abnormal electrolytes (sodium, potassium, calcium, and magnesium, to
name a few), and fatigue resulting from anemia (low stores of iron in
your blood).
Question: What causes renal disease?
Answer: There are several conditions that cause renal disease. In young chil-
dren, the most common causes are heredity, congenital anomalies (birth
defects), glomerulonephritis (inflammation in the kidney), and nephrotox-
ins (substances that may destroy the filtering process in the kidneys). In the
elderly, hypertension, diabetes, chronic glomerulonephritis, and obstruction
(blockages) are the culprits leading to renal disease.
Question: How fast does renal disease progress?
Answer: This depends on the reason(s) why you have kidney problems. The
body has built-in mechanisms that try to compensate for the failing kidneys.
Once these have been exhausted, the ability of the kidneys to function will
begin to decline. It is important that you seek medical attention because
other diseases can aggravate kidney problems. For example, if you have
hypertension (high blood pressure) and you take your medication regularly,
well-controlled blood pressure can actually slow the disease process. The
same goes for diabetes: The more controlled your diabetes is, the slower is
the progression of kidney failure.

Kidney Disease 57
Question: How will I feel?

Answer: In the beginning, you may experience fatigue, weariness, lack of
appetite, and a general feeling of discomfort. Increased thirst, frequent
urination, and getting up at night to use the bathroom are also common
symptoms. As the disease progresses, you may have nausea and vomiting,
itching, irritability, muscle cramps, and shortness of breath.
Question: How often should I see the doctor?
Answer: You and your doctor will discuss this. The severity of your disease
will determine the frequency of visits.
Question: What types of things will the doctor be looking for?
Answer: The first thing the doctor notes is how you look and feel. How you
feel will decide the direction of the exam. Laboratory values (a blood test)
are also very important because they reveal how your disease is progress-
ing. You may hear the terms potassium, sodium, BUN, creatinine, cal-
cium, phosphate, hemoglobin, and hematocrit. These are all very specific
labs from a blood test that are frequently monitored and tracked for dis-
ease progression.
Question: How will I know if my disease is getting worse?
Answer: As mentioned earlier, you may start feeling physically worse. You
may start itching all over and be short of breath. Swelling in your legs and
hands may occur. You may also become irritable and unable to concentrate.
You might not feel any of these symptoms now, but your doctor will be able
to tell whether your disease is getting worse by running a blood test.
Question: What causes the swelling associated with renal disease?
Answer: Your kidneys are not excreting sodium (salt) as well as they should.
As the sodium or salt builds up in your body, this can lead to edema or
swelling of your hands and ankles.
Question: Should I change my diet?
Answer: When you are first diagnosed with renal disease, your medical pro-
fessional may tell you to lower your caloric intake and proteins, and to
limit sodium (salt), potassium, magnesium, and phosphorus. The amount
of fluid that you take in also may need to be controlled. You may be asked
to consult with a registered dietitian, who will help you make these changes
in your diet.
Question: Are there any medications I can take to cure me or prevent my dis-
ease from getting worse?
Answer: Angiotensin-converting enzyme inhibitors (better known as ACE
inhibitors) help reduce the pressure in the kidneys. They may help to slow
the disease progression. Medications that contain vitamins such as calcium
and vitamin D help to correct the low calcium levels and other minerals that
may be abnormal with kidney disease.
Question: Why do I feel tired?
Answer: The kidneys assist in the production of red blood cells. When they are
not functioning properly, the red blood cells in your blood may decrease.
This decrease results in anemia and may make you feel tired. If your anemia

gets bad enough, your doctor may give you injections of a drug called ery-
thopoetin to increase your red blood cells. Iron supplements are also used
if iron levels in your blood get low. It is important to avoid drugs such as
aspirin and nonsteroidal anti-inflammatory agents such as ibuprofen.
Question: Will I have to go on dialysis?
Answer: When medications no longer help your kidneys to filter the blood and
make urine, it may be necessary for you to go on dialysis. If you do not go
on some type of dialysis, the potassium levels in your blood may get so high
that your heart might stop beating. Before this happens, your doctor will
decide the appropriate type of dialysis treatment for you.
Question: What about a kidney transplant?
Answer: Some patients treated with dialysis could benefit from kidney
transplantation.
Question: What about exercise?
Answer: Exercise has many positive benefits, including increasing your red
blood cells and improving other risk factors associated with kidney dis-
ease, such as improving insulin levels and lowering your blood pressure.
Collaborating with your medical professional in designing an exercise pro-
gram that is ideal for you should be your first step in exercise maintenance.
See the aerobic and weight-training guidelines in this chapter for more spe-
cific information.

4 Heart Disease
CORONARY ARTERY DISEASE: THE NUMBER ONE KILLER
Background
During exercise, coronary blood flow can increase as much as five times above the
resting value. A patient with coronary artery disease might not be able to increase
coronary flow to the affected coronary beds, causing an imbalance between the
myocardial oxygen demand and the myocardial oxygen supply. Myocardial oxygen
demand increases proportionally to the product of heart rate and systolic blood pres-
sure called the double product (DP) or rate pressure product (RPP). Angina (chest
pain) at peak exercise intensity requires greater than 50–70% obstruction of a coro-
nary artery. At rest, angina requires 90% obstruction. Factors such as coronary vaso-
constriction and platelet fibrin deposition will further decrease the coronary blood
flow. Moderate exercise decreases and high-intensity exercise increases platelet
adhesiveness. Angina at rest, triggered by emotions and silent ischemia (electrocar-
diographic evidence of ischemia without chest pain), is thought to have a significant
vasoconstrictor component.
The response to exercise includes vasodilatation of the vasculature of the exercis-
ing muscles caused by local metabolic factors and vasoconstriction of the nonexer
cising vascular beds caused by cortical influences and activation of mechanoreceptors
in skeletal muscle. The vasoconstrictor effect on the coronary vascular beds is atten-
uated by a neurogenic vasodilatation caused by the activation of baroreceptors and
probably other receptors located in the myocardium. The overall effect of the vaso-
constrictor and vasodilating influences is a considerable increase in blood flow to
the exercising muscle, a mild increase in the blood pressure, and a decrease in the
systemic vascular resistance. For patients with coronary artery disease, increasing
the double product results in vasoconstriction of the diseased coronary arteries.
Management
Drug Therapy
The goal of therapy is to decrease the myocardial oxygen demand or to increase the
coronary blood flow to the ischemic myocardium.
Beta-blockers reduce myocardial oxygen demand by decreasing heart

rate, myocardial contractility, and blood pressure. The reduction in the
double product allows patients receiving β-blockers to achieve a higher
59
submaximal exercise capacity without symptoms of myocardial ischemia.

Patients should be cautioned not to discontinue β-blockers abruptly because
this might cause unstable angina.
Calcium channel blockers may result in a negative inotropic effect. Their
peripheral vasodilating effect reduces myocardial oxygen consumption.
The coronary vasodilating effect increases coronary blood flow and pre-
vents coronary vasoconstriction. This results in a decrease in the double
product during any given level of exercise, significantly prolonging the
onset of ischemia. Verapamil and Diltiazem slow the sinus and atrioven-
tricular (AV) nodes and cause a reduction in heart rate, Nifedipine might
cause reflex tachycardia. Nifedipine is the drug of choice in patients receiv-
ing β-blockers. The combination of nitrates with calcium channel blockers
could produce postural hypotension.
Nitrates reduce oxygen demand by reducing the preload (venous dilating
effect) and increasing the coronary blood flow by producing nitric oxide,
which is an arteriolar dilator. In addition, nitrates decrease platelet aggre
gation. The most important drawback of nitrates is the development of
tolerance; this problem can be minimized by using the medication for a few
hours each day or on alternating days.
Angioplasty or a coronary bypass is indicated when symptoms are not well
controlled with drug therapy or when there is considerable functional impair-
ment (i.e., in patients with triple coronary artery disease or impaired ven-
tricular function and in patients with left main coronary artery disease).
Exercise Issues
A recent review of the literature reported that patients who participate in cardiac
rehabilitation programs drop their rates of rehospitalizations from 21 to 14%.
Furthermore, health care costs during a 21-month period following heart attacks
were reduced. Rehabilitation programs for cardiac patients have traditionally been
divided into phases:
Phase I is inpatient rehabilitation and occurs immediately after the intervention

while the patient is still receiving care in the hospital. This phase involves
mainly physical therapy and risk factor counseling.
Phase II is termed outpatient rehabilitation. Here, the patient is exercised in a
hospital under the direct supervision of a nurse and/or exercise physiologist.
Phases III and IV are usually combined into what is termed maintenance or
ongoing rehabilitation. This form of rehabilitation requires a fairly autono-
mous patient who has the ability to exercise safely with little or no ECG
monitoring and limited supervision.
These rehabilitation programs are typically structured away from the hospital at
a university, a YMCA, or other health care facility that contains CPR-certified staff
or graduate students in exercise science. The exercise prescriptions contained in

Heart Disease 61
this chapter and the associated patient heart disease workbook on the CD are
intended for patients who have completed or are currently involved in an inpa-
tient phase II rehabilitation program and/or are asymptomatic. It is strongly
recommended that before patients are provided with the exercise recommenda-
tions contained in this book, patients with coronary artery disease be referred
to a phase II rehabilitation program for instructions or be stable.
Benefits of exercise include increasing the functional capacity accompanied with
physiological changes mainly in the peripheral exercising muscles and a reduction in
ischemia at rest and during activity. However, there are risks associated with exer-
cise. Exercise hypotension in patients with coronary artery disease (CAD) has been
considered to be secondary to a sudden decrease in cardiac output during exercise.
Recent observations suggest that abnormally severe vasodilatation of the nonexer-
cising vascular beds associated with an increased cardiac output caused by acti-
vation of ventricular receptors by ischemia is the dominant mechanism. The same
pathophysiology has been observed in exercise-induced hypotension associated with
aortic stenosis and hypertrophic cardiomyopathy and in patients with normal hearts
and a positive tilt-table test.
Exercise hypotension in patients with CAD, valvular disease, or cardiomyopathy
is associated with a poor prognosis, while exercise hypotension in patients with nor-
mal hearts is benign. Exercise-induced ventricular arrhythmias do not represent an
independent risk factor for subsequent mortality or coronary events. The risk of death
is lower in patients who exercise when compared to risks for sedentary groups.
The risk of sudden death associated with exercise is related to the severity of
disease and exercise intensity and is minimal. For patients with cardiac disease, an
event rate of one per 112,000 patient-hours, a myocardial infarction rate of one per
300,000 patient-hours, and a mortality rate of one per 790,000 patient-hours has
been reported. Exercise-based cardiac rehabilitation programs minimize the func-
tional disability that follows a myocardial infarction or coronary bypass surgery.
Exercise is safe in patients with coronary artery disease who
are free of ischemia at an exercise intensity below 6 METs (metabolic

equivalents)
have no history of exercise-induced ventricular tachycardia, exercise-induced
hypotension, or exercise-induced cardiac arrhythmia
have ejection fractions greater than 50%
have reported uncomplicated MI, CABG, angioplasty, or arthrectomy
If the patient does not meet these criteria, he or she may be at a higher risk of
morbidity and mortality during exercise and should participate in exercise programs
prescribed by qualified medical personnel, such as an exercise physiologist. If the
patient has unstable ischemia or uncontrolled arrhythmias, exercise should not
be attempted without seeing a physician. See Appendix A for an explanation of the
different methods that can be used to prescribe exercise intensity for patients with
heart disease.

Weight lifting expands the health and fitness program. Benefits include improve-
ments in blood pressure control in hypertensive patients, increased self-efficacy and
glucose tolerance, and, finally, improvements in insulin sensitivity, lipids, and lipo-
protein levels. See the section on weight lifting for more complete information.
WEIGHT TRAINING GUIDELINES FOR HEART DISEASE

The safety of resistance training in patients with a history of heart disease has
been well documented. Many patients report a reduced likelihood of ST depres-
sion, angina, and arrhythmias regardless of the intensity. The rate pressure product
(heart rate × systolic blood pressure) or myocardial oxygen consumption (MVO2) is
reduced during maximal isometric exercise, mostly due to lower peak heart rates.
Furthermore, myocardial perfusion during elevated diastolic pressures may improve,
resulting in lower ischemic responses when compared to the same MVO2 that elicited
ischemia during aerobic or dynamic exercise.
Weight training for patients with heart disease has resulted in moderate increases
in submaximal aerobic capacity while reducing hypertension at absolute work loads
by attenuation of the pressor response to static exertion. Other benefits include
improved self-esteem, increased glucose tolerance, and better insulin sensitivity, lip-
ids, and lipoproteins.
When individuals with heart disease undergo weight training, the following con-
traindications should be avoided:
• Uncontrolled hypertension, (systolic ≥ 160 mmHg or diastolic ≥ 100 mmHg)

• Aerobic capacity of less than 5 METs
and abilities. Weight machines and free weights can be used when the patient is able
lines for patients are presented in the heart disease workbook CD.

Heart Disease 63

[100 – (# reps × 2.5)] = % 1RM

and stretch elastic bands. The perceived exertion rating (RPE) of 12–14 prescribed
for aerobic work should not be exceeded when weight lifting is undertaken.
RECOMMENDED READING
Ades, P. A. 1993. Exercise conditioning in older coronary patients. Circulation 88:572–577.
disabilities, 3rd ed., chaps. 6–12. Champaign, IL: Human Kinetics.
Fletcher, G. F. 1990. Exercise standards: A statement for health professionals from the
American Heart Association. Circulation 82:2286–2322.
Goldberg, A. P. 1989. Aerobic and resistive exercise modify risk factors for coronary heart
disease. Medicine and Science in Sports and Exercise 21:669–674.
Goldberg, L., D. L. Elliot, R. W. Schutz, and F. E. Kloster. 1984. Changes in lipid and lipoprotein
levels after weight training. Journal of the American Medical Association 252:504–506.
Hurley, B. F. 1988. Resistive training can reduce coronary risk factors without altering VO2 max
or percent body fat. Medicine and Science in Sports and Exercise 20:150–154.
Lele, S. S. 1994. Mechanism of exercise hypotension in patients with ischemic heart disease.
Circulation 90:2701–2709.
Wang, J. 1994. Different effects of strenuous exercise and moderate exercise on platelet func-
tion in men. Circulation 90:2877–2885.
EXERCISE PRESCRIPTION FOR HEART DISEASE

Frequency
Exercise a minimum of 3 days per week. Alternate days to allow for maxi-
mum recuperation.
Modality
Walking is an easy, preferred method because it does not require any spe-
cial equipment. Stationary or active bike riding and swimming are also
acceptable aerobic activities. Combining different modalities during the

exercise session may enhance compliance and improve overall training

effects. A resistance or weight-training program should be included.
Duration
For sedentary or nonexercisers, begin with a time that is comfortable—about
10 minutes. Gradually increase the aerobic training exercise time by 2–4
minutes each week until 20–60 minutes is achieved without stopping.
Intensity
light and hard (heavy), an RPE of 12–14, is recommended for both.
When weight lifting is undertaken, use a weight light enough to do
10–15 repetitions and do one to two sets for each muscle group. Work
upper and lower muscle groups. See the weight-training section in the
heart disease workbook CD for specific instructions.
Other Instructions
pain immediately.
follow-up visit.
COMMON QUESTIONS ON HEART DISEASE

Question: What is coronary artery disease?
Answer: This is a disease of the blood vessels that supply blood to your heart.
These heart vessels or arteries become clogged with plaque and limit the
blood flow to your heart.
Question: How do the heart vessels become clogged?
Answer: Plaque builds up and narrows the vessels in your heart. There are
several things that may contribute to this, including a high-fat and high-
cholesterol diet, smoking, and family history of heart disease.
Question: What causes chest pain?
Answer: When the arteries become narrowed, blood has a difficult time flowing
through the heart. This leads to poor oxygen supply, resulting in chest pain.
Question: How do I keep from getting chest pain or angina?

Heart Disease 65
Answer: Several things can be done. If you already have poor blood flow due
to plaque, you may need medications to help open your arteries. In addition,
changing certain behaviors will also help. If you smoke—stop. Change your
diet and eat healthy by lowering fat, cholesterol, and calories. If you have
high blood pressure or diabetes, make sure it is under control.
Question: How do I know if the chest pain I am having is serious?
Answer: Any chest pain is a concern. If you are not certain whether your
pain is related to the heart or stomach (i.e., indigestion), go the emer-
gency room immediately—waiting can result in damage that may not
be repairable.
Question: Why does exercising cause chest pain?
Answer: When you exercise, your body uses more oxygen and the blood ves-
sels become narrower; this results in decreased blood flow and decreased
oxygen to the heart, thereby precipitating chest pain.
Question: What else can cause chest pain?
Answer: Stress. When you become anxious or upset, your body releases
chemicals that can constrict the vessels in your heart.
Question: What is a stress test?
Answer: A stress test monitors how well your heart works while you exercise.
You may be asked to walk on a treadmill or ride a stationary cycle. During
this time, your heart rate, breathing, blood pressure, and electrocardiogram
(EKG) are monitored by a physician or exercise physiologist. This test is
usually stopped when you reach your maximum heart rate. Remember,
you will not be asked to exercise at that intensity on a regular basis. Some
people cannot exercise on a treadmill or cycle and may require a drug that
is injected into a vein that takes the place of exercise.
Question: What is a heart catheterization?
Answer: If your stress test is positive or if you have chest pain while at rest,
you might need a cardiac catheterization. This procedure is performed by
a cardiologist under local anesthesia. A blood vessel in your leg is used to
thread a thin catheter up to your heart. Dye is then injected into the heart so
that the blood flowing through all the arteries in your heart can be viewed.
Question: Will I need surgery?
Answer: Surgery may be required depending on where the blockage is and
how severe it is. A procedure called an angioplasty may be the first choice
to open the blocked artery. An angioplasty is performed in the same way in
which a catheterization is done, except there is a tiny balloon at the tip of
the catheterization wire. When the clogged vessel is reached, the balloon is
inflated, thereby opening the vessel.
Question: What kind of exercise should I do?
Answer: Cardiac rehabilitation should be initiated as soon as your physician
says that it is safe. Generally, supervised exercise is the first step. Your med-
ical professional will direct you to the appropriate facility for this super-
vised regimen. Exercise and lifestyle changes are the keys to preventing
further disease and destruction.

CONGESTIVE HEART FAILURE

Background
Congestive heart failure (CHF) is a pathophysiologic state characterized by conges-
tion in the pulmonary or systemic circulation caused by a progressive decline in
the ability of the heart to pump an adequate amount of blood to meet the metabolic
demands of the body. A hallmark symptom may be a rapid gain in body weight.
CHF is usually classified according to left ventricular function as systolic dysfunc-
tion or diastolic dysfunction. A history of myocardial infarction, valvular insuffi-
ciency, Q waves in the ECG, an S3 gallop, or an enlarged heart are usually associated
with systolic dysfunction. A history of hypertension, infiltrative or hypertrophic car-
diomyopathy, findings of left ventricular hypertrophy in the electrocardiograph, an
S4 gallop, and a small heart are associated with diastolic dysfunction. A diagno-
sis of hypertrophic cardiomyopathy contraindicates any intense (>60% of the
VO2 max) structured exercise program because of the risk for sudden death.
All patients with heart failure should be evaluated with echocardiography or
radionuclide angiography (MUGA scan). Those with a normal ejection fraction who
demonstrate symptoms and signs of heart failure are considered to have diastolic
dysfunction, provided that diseases that cause a reduction in left ventricular filling
(pulmonary and valvular diseases, constrictive pericarditis, etc.) are ruled out. Other
echocardiographic evidence of diastolic dysfunction includes increased relaxation
time (measured from aortic valve closure to mitral valve opening) and reduced veloc-
ity of left ventricular filling, increased left ventricular wall thickness, and a normal
or small left ventricular cavity.
Regardless of the cause, the consequences of poor left ventricular function are the
same: an increased concentration of catecholamines caused by the activation of the
sympathetic nervous system. This causes an initial improvement in left ventricular
performance but, eventually, arteriolar constriction increases the systemic vascular
resistance, decreases cardiac output, decreases renal perfusion, and increases sodium
and water retention. As time progresses, the elevated left ventricular filling pressure
leads to pulmonary congestion, right ventricular failure, and peripheral edema.
Approximately 50% of patients die within 5 years of onset of CHF; however, the
prognosis varies according to the type of impairment and the functional capacity.
Heart failure due to systolic dysfunction and coronary artery disease is associated
with a poorer prognosis. Patients with New York Heart Association class IV CHF
have a 1-year mortality rate of approximately 50%.
Management
The therapy of heart failure varies considerably according to the type of impairment
and the severity of the disease. General interventions include the following:
• Correction of diseases that cause the decline in left ventricular function

• Weight reduction for overweight patients
• Correction of anemia

Heart Disease 67
• Low-sodium diet
• Diuretics
Therapy for Patients with Systolic Dysfunction

Digitalis improves cardiac performance and exercise capacity by improv-
ing contractility. It is particularly useful in patients with atrial fibrillation
and in patients with moderate and severe heart failure. Controversy exists
over its usefulness in patients with mild heart failure and the possibility of
increased risk of death following myocardial infarction.
Diuretics reduce plasma volume, thus reducing congestion and thereby
improving dyspnea, edema, and exercise capacity. Combined with vasodi-
lators, they are the therapy of choice in patients with mild to moderate CHF.
Overuse predisposes to dehydration, activation of the renin-angiotensin-
aldosterone (RAA) system with increased vascular resistance, electrolyte
imbalance, and cardiac arrhythmias.
Isosorbide dinitrate (venous vasodilator) decreases right- and left-filling pres-
sures. Tolerance can be avoided or decreased by using it only during the
day. Combined with β-blockers, it could be beneficial in patients with myo-
cardial ischemia. When used alone, its effect on exercise capacity is negli-
gible, but left ventricular performance and exercise capacity are improved
when nitrates are used in combination with arteriolar vasodilators such as
hydralazine and angiotensin-converting enzyme (ACE) inhibitors. The use
of vasodilators other than ACE inhibitors is limited by side effects, tachy-
phylaxis, and questionable improvement in exercise capacity.
ACE inhibitors are probably the most important medications in the therapy for
patients with systolic dysfunction. Inhibition of the RAA system decreases
ventricular-filling pressures and increases cardiac output without increas-
ing heart rate. Improvement in exercise tolerance and functional class are
greater than with digoxin. They interfere with the deleterious myocardial
effects of catecholamines, prevent or decrease the ventricular dilation that
often follows myocardial infarction, and may prevent fatal arrhythmias.
They also improve survival in patients with severe CHF and can replace
digoxin in the therapy of patients with mild to moderate heart failure. There
is a growing consensus that ACE inhibitors should be prescribed to all
patients with CHF, even if they are asymptomatic, unless contraindicated.
Hydralazine: the use of vasodilators other than ACE inhibitors is limited
by side effects, tachyphylaxis, and questionable improvement in exercise
capacity. However, if therapy with ACE inhibitors is contraindicated (angio
neurotic edema, renal impairment, hyperkalemia, hypotension), hydrala-
zine, in combination with isosorbide dinitrate and digoxin, has been proven
to prolong life and improve ventricular function and exercise capacity.
Amlodipine (5–10 mg/day), unlike other calcium channel blockers, does
not worsen congestive heart failure in patients with nonischemic systolic
dysfunction. Rather, it decreases the risk for death by an impressive 46%.

Heart failure patients most likely to benefit from this drug are patients with
angina, hypertension, and/or atrial fibrillation.
Carvedilol is a unique, nonselective β-receptor antagonist that also blocks α-1
receptors, significantly improves survival, and lowers hospitalization rates.
The benefits of this drug cannot be extrapolated to other β-blockers, how-
ever, because β-blockers can aggravate heart failure. Patients most likely
to benefit from this medication are those with ischemic cardiomyopathy.
Start with a small dose and slowly titrate upward (increase dose weekly) to
a target dose of 25–50 mg twice daily.
Therapy for Patients with Diastolic Dysfunction

Diuretics are used to correct excessive blood volume, improve ventricular relaxation,
and control heart rate. Digitalis compounds and vasodilators are of little benefit and
could be detrimental. Patients with diastolic dysfunction are highly dependent on
preload; therefore, diuretics should be used with caution. Prescribe just enough to
remove excessive blood volume and improve pressure–volume relationships.
Rapid heart rates decrease the time available for ventricular filling and are poorly
tolerated. Heart rate control in atrial fibrillation is very important because these
patients might not be able to maintain an adequate cardiac output.
• Calcium channel blockers and β-blockers control hypertension, decrease

heart rate, and reduce myocardial oxygen demand. They are the drugs of
choice for patients with diastolic dysfunction.
• ACE inhibitors may improve diastolic function by reducing blood pressure,
decreasing the activity of the RAA system, and preventing or decreasing
the formation of myocardial fibrosis. However, the vasodilatation caused by
ACE inhibitors might be poorly tolerated.
The syndrome of pulmonary edema in coronary artery disease and preserved sys-
tolic function can be treated with nitrates, β-blockers, or calcium-channel blockers.
Medical therapy is often ineffective. Angioplasty or bypass surgery is the therapy
of choice.
Exercise Issues
There is no strong correlation between exercise capacity and objective measures of
ventricular performance or strength. The principal difference between exertional
dyspnea in patients who exercise regularly and those who do not is the degree of
activity necessary to cause the symptom. Improving musculoskeletal fitness clearly
improves the exercise capacity in patients with heart failure by enhancing peripheral
skeletal mechanisms (i.e., mitochondria and capillarization).
The ideal aerobic exercise intensity corresponds to the heart rate at the anaerobic
threshold; this can be obtained from a cardiopulmonary exercise test that measures
expired gases (see Appendix B). Intensities greater than the anaerobic threshold can
cause a greater incidence of exercise-induced hypotension, which predisposes the

Heart Disease 69
patient to cardiac arrhythmias. Stable patients benefit from low- to moderate-intensity

exercise (i.e., 40–60% of maximum VO2; see Appendix A, Method 6) or an
intensity well within the individual’s current capacity that can be comfortably sus-
tained for a prolonged period of time of 15–60 minutes. This exercise should have
gradual initiation and progression and be noncompetitive. Patients with uncompen-
sated heart failure can develop exercise-induced pulmonary edema. Exercise
is not advisable if the condition is not stable; patients should be advised not to
exercise if they are not feeling well or have developed new signs or symptoms.
For patients taking nitrates, adequate cool downs of at least 10 minutes are
recommended to attenuate any venous pooling that might result if activity is
abruptly stopped. Unless a maximal cardiopulmonary stress test is performed,
target heart rates predicted from age cannot be accurately prescribed by generic
training formulas. Using these methods will be particularly inaccurate in patients
with diabetes and in patients medicated with β-blockers. Therefore, an RPE of
11–16 or 3–6 on the dyspnea chart is recommended as a safe intensity level for
prescribing exercise in these patients (see Appendix A, Method 5). Anaerobic
exercise, including weight training, is contraindicated for patients with con-
gestive heart failure.
Benefits of exercise in patients with heart failure caused by left ventricular dys-
function have been reported. Improvements in exercise tolerance measured by
increases in VO2, duration, and power output resulted partly from an increase in
peak heart rate.
RECOMMENDED READING
Aronow, W. S. 1990. Prognosis of congestive heart failure in elderly patients with normal ver-
sus abnormal left ventricular systolic function associated with coronary artery disease.
American Journal of Cardiology 66:1257–1259.
Dougherty, A. H. 1984. Congestive heart failure with normal systolic function. American
Journal of Cardiology 54:778–782.
Geltman, E. M. 1989. Mild heart failure: Diagnosis and treatment. American Heart Journal
118:1277–1291.
Keteyian, S. J. 1996. Exercise training in patients with heart failure: A randomized, controlled
trial. Annals of Internal Medicine 124 (12): 1051–1057.
McKelvie, R. S. 1995. Effects of exercise training in patients with congestive heart failure: A
critical review. Journal of American College of Cardiology 25:789–796.
Packer, M. 1996. Effect of amlodipine on morbidity and mortality in severe chronic heart
failure. Prospective Randomized Amlodipine Survival Evaluation Study Group. New
England Journal of Medicine 335:1107–1114.
———. 1996. The effect of carvedilol on morbidity and mortality in patients with chronic
heart failure. U.S. Carvedilol Heart Failure Study Group. New England Journal of
Medicine 334:1349–1355.
Szlachcic, J. 1985. Correlates and prognostic implications of exercise capacity in chronic con-
gestive heart failure. American Journal of Cardiology 55:1037–1042.

EXERCISE PRESCRIPTION FOR CONGESTIVE HEART FAILURE

Frequency
mum recuperation.
Modality
Walking is an easy, preferred method because it does not require any special
equipment. Stationary or active bike riding and swimming are also accept-
able aerobic activities. Try combining different modalities during the exer-
cise session to maximize the training effect. Avoid weight training.
Duration
For sedentary individuals or nonexercisers, begin with a time that is
comfortable—about 10 minutes. Gradually increase the aerobic train-
ing exercise time by 2–4 minutes each week until 20–60 minutes is
achieved without stopping.
Intensity
The aerobic exercise can be prescribed using the RPE or dyspnea chart in
Appendix A, Method 5. A perceived exertion rating between light and
hard, an RPE of 11–16, is recommended. If the dyspnea chart is used, a
level between moderate and severe of 3–6 is recommended. Encourage
the patient to swing the arms to work the upper body muscles as much
as possible during the aerobic exercise.
Other Instructions
pain immediately.
follow-up visit.
VALVULAR DISEASE
Mitral Stenosis
Background
The most common cause of mitral stenosis (MS) is rheumatic fever. When the cross-
sectional area of the valve is reduced to 2 cm2, the patient has mild stenosis; if the
cross-sectional area is 1 cm2, the stenosis is severe and the atrial pressure required

Heart Disease 71
to maintain a normal cardiac output at rest is close to 25 mmHg. When the obstruc-
tion is severe, minor activities that increase the blood flow through the valve further
increase the atrial pressure. Dyspnea on exertion correlates with the magnitude of
atrial pressure during exercise. An atrial pressure of 25 mmHg increases pulmonary
venous pressure, causing dyspnea. A doubling of the blood flow across the valve
quadruples the atrial pressure; because atrial pressures greater than 25 mmHg result
in dyspnea, the exercise intensity associated with dyspnea is a good indicator of
the severity of the stenosis. This is the early warning sign of MS. Doppler echocar-
diography allows diagnosis, determination of the valvular area, and measurement of
pulmonary arterial pressures.
Atrial fibrillation is often associated with severe dyspnea and acute pulmonary
edema. The absence of atrial contraction decreases the transmitral gradient by 30%
and the tachycardia associated with it considerably decreases the diastolic time. That
combination greatly impairs ventricular filling.
Patients with mitral stenosis report very mild symptoms, if any at all, and these
symptoms may remain unchanged for many years (the asymptomatic period might
last 25 years). Once symptoms begin, however, the disease progresses rapidly and
within 5 years patients develop severe disabilities.
Management
Medical management of patients with mitral stenosis consists of removing or con-
trolling all causes of tachycardia, such as anemia, atrial fibrillation, etc.
• Beta-blockers improve exercise capacity by decreasing heart rate and myo-

cardial oxygen consumption.
• Diuretics decrease dyspnea by decreasing venous congestion.
• Digitalis helps only those patients with atrial fibrillation. The dose of digi-
talis and β-blockers should be titrated to achieve a resting heart rate of
60–65 beats per minute.
• Patients with rapidly progressing symptoms require surgery.
Mitral Regurgitation
Background
Mitral regurgitation (MR) can result from abnormalities of any of the components
of the mitral valve apparatus: the annulus, leaflets, chordae tendineae, and papillary
muscle. Diseases that cause dilatation of the left ventricle cause MR by dilating the
mitral annulus. Severe calcification of the annulus common in hypertension, aor-
tic stenosis, and diabetes can also cause MR. Abnormalities of the chordae can be
encountered as a result of endocarditis or rheumatic fever. Papillary muscles are per-
fused by terminal vessels and are commonly damaged by ischemia; therefore, MR is
a common finding in patients with coronary artery disease.
The severity of MR depends on the size of the regurgitant orifice, the pressure
gradient between the ventricle and the atrium, and the resistance to aortic flow.
Usually half of the regurgitant volume is regurgitated into the left atrium before

the aortic valve opens. The left ventricle compensates by emptying more rapidly
and more completely, but eventually the diastolic volume increases. As the ventricle
dilates, the severity of MR increases. During the compensated state, myocardial con-
tractility and ejection fraction are increased above normal levels. Echocardiographic
indices that reflect myocardial contractility such as ejection fraction underestimate
the severity of the disease. An ejection fraction of 40–50% indicates severe, not
moderate, impairment. Measurement of end systolic volume is a good overall index
of myocardial function in patients with MR.
Patients with MR lack the early warning signs of mitral stenosis. Typically,
MR patients remain asymptomatic until severe and often irreversible left ven-
tricular dysfunction occurs. Doppler echocardiography helps to establish diagnosis
and measure the severity of disease.
Management
Medical therapy is indicated when surgical treatment is not possible. It consists of
after-load reduction with ACE inhibitors or hydralazine, and reduction of ventricular
dilatation with digitalis and diuretics. Digitalis is particularly useful in patients with
atrial fibrillation. Because of the lack of correlation between symptoms and severity
of ventricular dysfunction, patients should be evaluated for surgery as soon as they
develop dyspnea on exertion.
Mitral Valve Prolapse

Background
Mitral valve prolapse (MVP) is commonly seen in patients with coronary artery
disease and in otherwise normal patients as a congenital condition transmitted
in an autosomal dominant way. Patients usually complain of palpitations. MR
is uncommon in patients with mitral valve prolapse, occurring in 15% of these
patients. The risk of endocarditis is low, but the risk of cerebral microemboli
resulting from platelet aggregation is high. Doppler echocardiography establishes
the diagnosis and often detects mild MR that could be missed in M-mode or two-
dimensional echocardiograms.
Management
Asymptomatic patients do not require therapy, but should be followed with Doppler
echocardiography every 4 years. Endocarditis prophylaxis is debatable, but advis-
able. Patients with a history of palpitations should undergo 24-hour electrocardio-
graphic monitoring and stress testing. Beta-blockers are the drug of choice, except in
patients with a prolonged Q-T interval, who would benefit from phenytoin.
Aortic Stenosis
Background
Isolated aortic stenosis (AS) in the young is most likely a congenital problem.
Degenerative stenosis (heavily calcified valves) is the most common cause of aortic

Heart Disease 73
valve replacement in adults. Diabetes and elevated cholesterol levels are predispos-
ing factors.
Aortic stenosis associated with mitral valve disease is often caused by rheumatic
fever, whereas the most common cause of isolated AS is a congenital malformation
of the valve. Congenitally bicuspid valves become stenotic, resulting in damage to
the leaflets caused by turbulent blood flow. Tricuspid stenotic valves might be con-
genital (abnormal leaflets), rheumatic, or degenerative (senile calcifications), which
is more common in diabetics and patients with elevated cholesterol levels. When the
cause for degenerative calcification of the aortic valve is the normal “wear-and-tear”
of the valve, calcification of the mitral valve annulus is often present. Rheumatic
aortic stenosis is often associated with aortic regurgitation and mitral valve disease.
AS causes severe left ventricular hypertrophy. Considerable pressure gradients
across the aortic valve can be sustained with few or no symptoms. A normal aortic
valve is 3 cm2 (>2 cm2). If the valve area is 1.6–2 cm2, the stenosis is mild; if it is
between 0.7 and 1.6 cm2, it is severe and an orifice size of less than 0.7 cm2 is criti-
cal. As the valve area decreases, the pressure gradient between the ventricle and the
aorta increases. A normal valve has no pressure gradient. If the pressure gradient is
<25 mmHg, the obstruction is mild; if it is between 25 and 50 mmHg, it is moderate
and >50 mmHg is severe. The marked hypertrophy of the ventricle causes compli-
ance to decrease, diastolic pressure to increase, and ventricular filling to deteriorate.
The loss of atrial contraction and the tachycardia that accompanies atrial fibrillation
are very poorly tolerated.
Patients with AS remain asymptomatic for a long time, but when symptoms begin,
patients deteriorate rapidly and are likely to die during the next 5 years. The most com-
mon symptoms are dyspnea (CHF), syncope, and chest pain (angina). Sudden death is
rare in asymptomatic patients. Doppler echocardiography allows diagnosis and calcu-
lation of the pressure gradient across the valve. Echocardiographic follow-up should
be repeated every 2 years with more frequent monitoring as the gradients approach
critical levels. Cardiac catheterization (to evaluate the site and severity of the obstruc-
tion and to assess the coronary arteries) is indicated as soon as symptoms develop.
Management
Medical therapy is of little help. Digitalis is useful only very late in the disease when
there is evidence of ventricular dilatation and systolic dysfunction. Diuretics should
be used with great caution to treat excessive edema. Beta-blockers can precipitate
left ventricular failure. Valvular commisurotomy or balloon valvuloplasty results in
considerable improvement, has a very low mortality rate, and should be considered in
asymptomatic patients with critical valvular obstruction. The valve should be replaced
in patients with calcified stenosis who are symptomatic, patients with severe obstruc-
tion, and asymptomatic patients with progressive left ventricular dysfunction.
Aortic Regurgitation
Background
Rheumatic fever is the most common cause of aortic regurgitation (AR) and it is often
associated with mitral valve disease. Diseases of the connective tissue and dilatation

of the aortic arch are uncommon causes of AR. Aortic regurgitation causes consid-
erable dilatation of the left ventricle and secondary mitral insufficiency. During the
early stages of the disease, the heart compensates for the increase in the left ventricu-
lar diastolic volume by eccentric hypertrophy. These patients have enlarged hearts,
good ejection fractions, high diastolic volumes, and normal diastolic pressures.
As the ventricle continues to dilate, left ventricular systolic function begins to
deteriorate. The development of mitral regurgitation leads to left atrial dilatation and
increased left atrial and pulmonary pressures. Since coronary artery flow is directly
proportional to the diastolic blood pressure, coronary blood flow is reduced, which
could cause myocardial ischemia. Symptoms of myocardial ischemia occur late in the
disease and are usually associated with exercise or bradycardia (nocturnal angina).
Doppler echocardiography provides diagnosis and evaluation of the severity of AR.
Measurement of end systolic volume is a good overall index of myocardial function.
Management
Digitalis is the drug of choice and should be used in all patients with dilated ven-
tricles. Vasodilators and diuretics are indicated in patients with left ventricular dys-
function. Patients with good left ventricular function should be reassessed with a
cardiopulmonary stress test and Doppler echocardiography at least every 6 months.
Surgical therapy is indicated in patients with progressive deterioration in exer-
cise capacity even before the development of impaired left ventricular function.
Furthermore, patients with severe left ventricular dysfunction often deteriorate and
have high postoperative mortality.
Multivalvular Disease
More than one valvular involvement is common in patients with rheumatic valvular
disease and in patients who develop valvular regurgitation as a result of ventricu-
lar dilatation. Usually, symptoms and clinical courses are determined by the pre-
dominant illness. However, when two valves are affected equally, symptoms are
determined by the most proximally located valve. The combination of AR with MR
is the most common and the combination of mitral valve disease (either MR or MS)
with AS is the most problematic.
Exercise Issues
Exercise testing for most patients with valvular disease is of limited value. For exam-
ple, there is a poor correlation between the degree of mitral stenosis and the dura-
tion of symptom-limited treadmill exercise. However, exercise echocardiography
performed on a stationary cycle can be a valuable means for determining left ven-
tricular function in patients during exercise. Patients should be evaluated (including
radiography, electrocardiography, and echocardiography) based on symptoms.
In general, exercise outcomes differ between aortic, mitral, and mitral/aortic
valve surgery. Functional capacity is substantially increased following aortic valve

Heart Disease 75
surgery, but is limited for patients who have undergone mitral and mitral/aortic sur-
gery. This seems to be due to differences in oxygen-uptake kinetics associated with
heart rate and atrial venous oxygen difference. For patients with mitral disease such
as mitral stenosis, exercise may be useful because it provides an early warning sys-
tem. The onset of dyspnea with strenuous exercise marks the beginning of clinical
deterioration. Worsening dyspnea during exercise is an indication for surgery.
Patients with mitral regurgitation lack the early warning signs of mitral steno-
sis. These patients should be evaluated for surgery as soon as the onset of dyspnea of
severe exertion develops. The most common cause of mitral regurgitation is mitral
valve prolapse. In this condition, stress testing concomitant with thallium is indi-
cated to evaluate the possibility of ST-segment abnormalities and other changes, such
as exercise-induced arrhythmias, electrocardiographic abnormalities such as chest
pain, palpitations, and auscultatory systolic clicks. These changes may, however, be
false-positive with respect to coronary artery disease. Aerobic exercise training may
be useful in these patients, especially those without functionally significant mitral
regurgitation; however, studies are limited in number and scope.
In patients with aortic stenosis, the risks during exercise stress testing do not
outweigh any additional information that might be obtained from the stress test;
therefore, candidates for aortic valve replacement should be evaluated on the basis of
functional status and other noninvasive clinical assessments. However, there are no
exercise restrictions in asymptomatic patients with mild stenosis. Patients are asked
to report the symptoms of dyspnea, syncope, near syncope, and chest pain. When
these symptoms develop, patients should be advised to avoid high-intensity exer-
cise greater than 60% of the VO2 max until they are reevaluated (see Appendix A,
Method 6). Patients with critical obstruction should avoid even moderate forms
of exercise.
In aortic regurgitation, there are no exercise restrictions until the patient has
developed signs of left ventricular dysfunction. At this time, patients should avoid
high-intensity exercise greater than 60% of VO2 max (see Appendix A, Method 6).
Angina is a sign of either severe regurgitation or coexisting coronary artery disease
(see the section on exercise issues for patients with heart disease).
In summary, aerobic exercise can be prescribed for most patients with mild val-
vular functional disease. Because many patients who have prosthetic valves are on
anticoagulants, mechanical hemolysis during exercise-induced tachycardia may
result—especially in patients with limited valve orifice sizes. Caution is therefore
recommended when prescribing exercise for valvular diseased patients. An RPE
not greater than 14 or dyspnea level greater than 6 is recommended. See Appendix A,
Method 5, for more information on using the RPE and dyspnea charts.
RECOMMENDED READING
Braunwald, E. 1992. Valvular heart disease. In Heart disease. A textbook of cardiovascular
medicine, 4th ed., ed. E. Braunwald. Philadelphia, PA: Saunders.

EXERCISE PRESCRIPTION FOR VALVULAR DISEASE

Frequency
mum recuperation.
Modality
acceptable aerobic activities. Try combining different modalities dur-
ing the exercise session. Avoid weight training if the patient is symp-
tomatic with shortness of breath or chest pain.
Duration
Begin with a time that is comfortable—about 10 minutes initially. Gradually
increase the aerobic training exercise time by 2–4 minutes each week
Intensity
The aerobic and weight-lifting exercises should be prescribed using the RPE
or dyspnea chart in Appendix A, Method 5. A perceived exertion rating
between light and somewhat hard, an RPE of 11–14, is recommended.
If the dyspnea chart is used, a level between moderate and severe of
3–6 is recommended. Remind the patient to swing the arms to work the
upper body muscles as much as possible during the aerobic exercise.
Other Instructions
pain immediately.
follow-up visit.
HYPERTROPHIC CARDIOMYOPATHY
Background
Hypertrophic cardiomyopathy is a disorder characterized by asymmetric hypertro-
phy of the left ventricle, with predominant involvement of the septum, which is out
of proportion to the hemodynamic load of the ventricle. It can occur spontaneously,
although half of the patients with this disease inherited it in an autosomal dominant

Heart Disease 77
way. This condition is rare, occurring in less than 0.2% of the population, but it is the
most common cause of sudden death in young patients.
In addition to the expected diastolic dysfunction (see the section on congestive
heart failure), patients with this condition suffer from a narrowing of the outflow
tract located between a hypertrophic septum anteriorly and the anterior leaflet of
the mitral valve posteriorly. It is possible that the jet of blood passing through such a
narrow space could cause a Venturi effect, pulling the valve against the septum and
obstructing the flow during systole. The combination of an elevated diastolic pres-
sure and increased myocardial O2 demand (of a hypertrophic ventricle) contributes to
the development of subendocardial ischemia, which is a common problem.
Patients with this condition are usually asymptomatic; often the presenting
symptom is syncope and sudden death during competitive sports. The disease is
most often diagnosed in patients 30–40 years old during the evaluation of exercise-
induced dyspnea, chest pain, syncope, or presyncope. A history of syncope carries a
much greater risk of sudden death in a child or adolescent than in adults.
Echocardiography reveals a septum at least 15 mm thick (normally, 11 mm), which
is at least 1.3 to 1.5 times the thickness of the posterior wall in diastole, before atrial
systole. Other findings include a mitral valve abnormally close to the septum, systolic
anterior motion of the mitral valve, mitral regurgitation (Doppler echocardiography),
and evidence of diastolic dysfunction (see the section on congestive heart failure).
Management
Beta-blockers and calcium-channel blockers (verapamil) are the drugs of choice.
Beta-blockers decrease heart rate (increasing diastolic filling), decrease myocar-
dial oxygen consumption, and have an antiarrhythmic effect. Unlike Verapamil,
β-blockers do not improve functional capacity. Verapamil is the most widely used
calcium-channel blocker in the treatment of this condition. Since patients with hyper-
trophic cardiomyopathy are suspected of suffering from an intracellular calcium
overload, the use of calcium-channel blockers makes common sense. Verapamil
improves diastolic filling and improves myocardial relaxation. Approximately two
thirds of patients treated with Verapamil report improvement in symptoms, includ-
ing exercise capacity. Surgery is indicated in patients who are symptomatic in spite
of medical therapy.
Exercise Issues
In patients treated with Verapamil, an improvement in exercise capacity is reported as
a result of the decrease in left ventricular outflow tract obstruction. Propranolol may
enhance exercise capacity in a similar fashion; however, it has been associated with a
deterioration of functional capacity in some patients. In treadmill tests, improvements
in cardiac output and left ventricular function have been shown to improve following
myotomy and myectomy in patients with obstructive hypertrophic cardiomyopathy.
Strenuous exercise should be avoided because of the risk of sudden death.
Although many individuals with subclinical hypertrophic cardiomyopathy exercise

regularly, high-intensity exercise (>60% of the VO2 max) and competitive sports are
to be avoided and are contraindicated in patients with one of the following:
• A family history of sudden death

• Severe ventricular hypertrophy
• Outflow gradient of 40 mmHg at rest
• Exercise-induced syncope (in young patients)
An RPE no greater than 11 is recommended (see Appendix A, Method 5).
RECOMMENDED READING
Hanroth, P. 1983. Influence of Verapamil therapy on left ventricular performance at rest and
during exercise in hypertrophic cardiomyopathy. American Journal of Cardiology
52:544–548.
Redwood, D. 1979. Exercise performance after septal myotomy and myectomy in patients
with obstructive hypertrophic cardiomyopathy. American Journal of Cardiology
44:215–220.
Wynne, J., and E. Braunwald. 1992. The cardiomyopathies and myocarditides: Toxic, chemi-
cal, and physical damage to the heart. In Heart disease. A textbook of cardiovascular
medicine, 4th ed. Philadelphia, PA: Saunders.
EXERCISE PRESCRIPTION FOR HYPERTROPHIC CARDIOMYOPATHY

Frequency
mum recuperation.
Modality
acceptable aerobic activities. Try combining different modalities dur-
ing the exercise session. Avoid weight training if the patient is symp-
tomatic with shortness of breath or chest pain.
Duration
Intensity
Aerobic exercise can be prescribed using the RPE chart in Appendix A,
Method 5. A perceived exertion rating between extremely light and
light, an RPE of 7–11, is recommended. Remind the patient to swing
the arms as much as possible to work the upper body muscles during the
aerobic exercise.

Heart Disease 79
Other Instructions
pain immediately.
follow-up visit.
CARDIAC ARRHYTHMIAS AND PACEMAKERS

Background
The most common types of cardiac arrhythmias in patients without heart disease
are ventricular arrhythmias. Supraventricular arrhythmias and conduction defects
can cause challenging clinical problems. The prevalence of premature ventricular
beats (VPBs) occurs in 40–70% of normal persons and can be detected by continu-
ous ambulatory electrocardiography. Long-term follow-up studies for patients with
asymptomatic complex ectopy (i.e., frequent premature beats, multiforms, and brief
runs of tachycardia) have revealed a prognosis similar to that for patients without
arrhythmias. In patients with coronary artery disease, the occurrence of VPBs is
associated with an increased risk of sudden cardiac death.
The most important intervention in the prevention of sudden cardiac death is
the prescription of antiarrhythmic drugs; however, although these medications will
decrease the risk, they will not prevent fatalities and could be the source of problems,
especially if they are prescribed routinely in nonsymptomatic patients who are
not at high risk for sudden death. Documentation of efficacy might require repeat
Holter monitoring and repeat stress testing. If an exercise test is performed, patients
should be tested while on their medications. All antiarrhythmias may cause arryth-
mias (5–15%); the risk of arrhythmia is greater in the presence of hypokalemia or
hypomagnesia. All antiarrythmias are negative isotropes and should be used with
caution in patients with systolic impairment.
Management
The best therapy for cardiac arrhythmias is to treat the cardiac or metabolic con-
dition responsible for the arrhythmia. Unfortunately, this is often impossible and
therefore medications are needed. Beta-blockers are commonly used in ventricular
and supraventricular arrhythmias.
Beta-blockers lower the heart rate and the blood pressure response to any given
physical activity. When used in patients with abnormal left ventricular function, they
can precipitate cardiac failure and severely limit the exercise capacity. The use of
β-blockers increases the possibility of exercise-associated hypotension, especially

during high-intensity exercise. Patients on antiarrhythmic drugs are at a higher risk

of developing an arrhythmia during exercise.
One should always keep in mind that many of the agents used to prevent arrhythmias
can induce arrhythmias or exacerbate the arrhythmia that they are intended to treat.
Exercise Issues
Exercise can cause cardiac arrhythmias in patients receiving digitalis and diuretics.
Exercise testing can be used as a method to predict the likelihood of cardiac arrhyth-
mias as well as to evaluate the results of antiarrhythmic therapy. The greatest risk
of exercise is the development of sudden death caused by ventricular arrhythmias or
sudden ventricular failure. The risk of sudden death is highest in patients with one
or more of the following characteristics:
• Severe hypertrophic cardiomyopathy

• Severe aortic stenosis
• Severe left ventricular systolic dysfunction
• Exercise-induced complex ventricular arrhythmia
• Exercise-induced hypotension (more than 20 mmHg systolic)
• Exercise-induced angina
• Previous history of ventricular fibrillation
• Experiencing ventricular arrhythmias when angina is experienced
• Prolonged Q-T intervals and a history of syncope
Patients who suffer from a severe form of any one of these conditions should be
advised not to exercise. However, patients with mild to moderate conditions can
benefit from exercise if it is done in moderation after a supervised exercise test.
Exercise-induced syncope is common in patients with pulmonary hyperten-
sion, aortic stenosis, hypertrophic cardiomyopathy, and coronary artery disease.
Ventricular arrhythmias are a possible cause of syncope and sudden death in patients
with hypertrophic cardiomyopathy. Other possible mechanisms of exercise-induced
syncope include left ventricular failure and neurocardiogenic vasodilatation. When
possible, the abnormality responsible for exercise-induced arrhythmias should be
corrected prior to the beginning of an exercise program. When that is not pos-
sible, exercise should be prescribed at an exercise intensity 10 beats below the
heart rate found to be associated with symptoms. Patients unable to estimate
exercise intensity should exercise with a heart rate monitor. Special emphasis should
be placed on the appropriate warm-up and cool-down activities.
Even though the heart rate response to exercise is blunted in patients taking
β-blockers, heart rate can still be used as a parameter to prescribe the intensity of
training. These patients can exercise at a heart rate that corresponds to the anaerobic
threshold. If a cardiopulmonary stress test is not available, exercise should be pre-
scribed at an RPE that corresponds to a level no greater than 16 (see Appendix A,
Method 5).
Exercise testing is not a sensitive method to evaluate the possibility of exercise-
induced symptoms, but it is the only tool we have. Abnormal results at high work

Heart Disease 81
loads are not as predictive of exercise-related risks as abnormal results at low work
loads. Ventricular arrhythmias not present at rest can be provoked by exercise, but
arrhythmic risk correlates better with the severity of ventricular abnormalities than
with electrocardiographic findings observed during exercise testing. Ventricular
tachycardia is commonly seen during high-intensity exercise because such exercise
is most likely to be associated with myocardial ischemia and high-circulating levels
of catecholamines. Ventricular tachycardia is also commonly seen immediately after
exercise because of a relative excess of norepinephrine and lactic acid-induced vaso-
dilatation, which occurs during this period.
Supraventricular tachycardias are infrequently triggered by exercise, but when
they do occur, it is usually in patients with pulmonary disease, with Wolff–Parkinson–
White syndrome, or who abuse alcohol and/or caffeine. Exercise-induced atrial
flutter/fibrillation occurs more frequently in patients with valvular disease, hyper-
thyroidism, and cardiomyopathy. Exercise can cause right- or left-bundle branch
blocks as a result of myocardial ischemia (in which case it usually happens at a heart
rate of 125 beats per minute) or as a rate-related phenomenon.
Patients with Cardiac Pacemakers

Pacemakers were first implanted about 50 years ago and were used to prevent recur-
rent syncope and death. Today, pacemakers are standard therapy—not only for
manifest syncope, but also for controlling near syncope, exercise intolerance, and
chronotropic incompetence. Indications for permanent pacing and clinically signifi-
cant bradycardia include the following:
• Complete AVB
• High-grade, second-degree AVB
• Mobitz type 2, second-degree AVB
• Sinus pauses
• Sinus or atrial arrest
• Trifascicular block—BBB and L. ant. and L. post. fascicular block
Considerations that may influence the clinical decision to implant a pacing sys-
tem include:
• Absence of other life-threatening disease

• Associated cardiac condition aggravated by bradycardia
• Motor vehicle operator
• Remote or inaccessible medical attention
• Medications that depress conductivity or automaticity
• Slowness of basic escape rhythm
• Cerebrovascular disease aggravated by bradycardia
• Desires of patient and family
Patients with pacemakers should undergo a supervised exercise test prior to the
beginning of an exercise program. Patients who have a fixed cardiac rate depend
on the increase in stroke volume associated with venous return as a result of the

exercising muscles acting as pumps to increase the cardiac output. Many patients
treated with these devices cannot increase the heart rate in response to exercise (e.g.,
asynchronous pacemakers). In patients with A-V node conduction blockades, the
ventricular rate remains constant at the preset pacemaker rate even if the atrial rate
increases with exercise.
Patients who have sick sinus syndrome, intermittent AV block, and those treated
with a dual-chamber pacemaker can increase the heart rate with exercise. Patients
with synchronous pacemakers who are able to increase their ventricular rate with
exercise can be prescribed exercise by target heart rate (see Appendix A, Methods 1
and 2).
However, even though some pacemakers can increase the cardiac rate with exer-
cise (e.g., synchronous pacemakers) or DDD pacing, it may be best to prescribe
exercise by methods other than heart rate. For example, exercise may be prescribed
by substituting the resting and maximum systolic blood pressure substituted into the
Karvonen or heart rate reserve equation (see Appendix A, Method 4). The systolic
blood pressure can then be monitored during exercise in place of the heart rate.
Prescribing exercise at a perceived exertion intensity no greater than hard, an RPE
of 16 (see Appendix A, Method 5), is the recommended option.
If the heart rate is not ruled by the pacemaker, the intensity of exercise can be pre-
scribed at the AT or just slightly below (see Appendix A, Method 7). High-intensity
exercise—greater than 60% of the VO2 max—is not recommended. Exercises that
are associated with excessive arm and upper body motions are to be discouraged
because of the possibility of displacing the ventricular pacing wire.
RECOMMENDED READING
Fletcher, G. F. 1990. Exercise standards: A statement for health professionals from the
American Heart Association. Circulation 82:2286–2322.
Kennedy, H. 1985. Long-term follow-up of asymptomatic healthy subjects with frequent and
complex ventricular ectopy. New England Journal of Medicine 312:193–197.
Lown, B. 1992. Cardiovascular collapse and sudden cardiac death. In Heart disease. A text-
book of cardiovascular medicine, 4th ed. Philadelphia, PA: Saunders.
EXERCISE PRESCRIPTION FOR ARRHYTHMIAS

Frequency
mum recuperation.
Modality
cial equipment. Stationary or active bike riding and swimming are
also acceptable aerobic activities. Try combining different modalities
during the exercise session. A resistance or weight-training program
should be included.

Heart Disease 83
Duration
Begin with a time that is comfortable—perhaps 10 minutes. Gradually
Intensity
chart in Appendix A, Method 5. A perceived exertion intensity between
very light and hard/hard (heavy), or RPE of 10–16, is recommended.
When weight training is undertaken, use a weight light enough to do
10–15 repetitions and do one to two sets for each muscle group. See
the weight-training section in the heart disease workbook CD for spe-
cific instructions.
Other Instructions
pain immediately.
follow-up visit.
EXERCISE PRESCRIPTION FOR PATIENTS WITH PACEMAKERS

Frequency
mum recuperation.
Modality
cial equipment. Stationary or active bike riding and swimming are
also acceptable aerobic activities. Try combining different modalities
during the exercise session. A resistance or weight-training program
should be included.
Duration
Begin with a time that is comfortable—initially, about 10 minutes. Gradually

Intensity
light and hard/hard (heavy), an RPE of 11–16, is recommended.
When weight training is undertaken, use a weight light enough to do
10–15 repetitions and do one to two sets for each muscle group. See
the weight-training section in the heart disease workbook CD for spe-
cific instructions.
Other Instructions
pain immediately.
follow-up visit.

5 Lung Disease
CHRONIC LUNG DISEASE
Background
Individuals who present with chronic lung disease (CLD) have a gradual downhill
prognosis. As the disease worsens, so does the dyspnea. The quality of dyspnea will
vary from patient to patient, but there is a relationship between the intensity of activ-
ity and the intensity of discomfort. The therapeutic value of pulmonary rehabilitation
for patients with chronic lung disease has come under question based on the lack of
improvement in pulmonary function testing in patients completing an exercise-based
pulmonary rehabilitation program.
However, a plethora of recent research has documented the value of this modality
using end-points other than pulmonary function testing. Rather than concentrating
on reversing the disease process, exercise-based rehabilitation aims to reduce the
functional impairment caused by chronic lung disease. Most of the literature about
pulmonary rehabilitation focuses on patients with chronic obstructive pulmonary dis-
ease (COPD), but it also benefits patients with restrictive diseases, cystic fibrosis, and
other chronic pulmonary conditions that affect the airways, parenchyma, thoracic
cage, or combinations of them. Currently, there is ample evidence to support the
fact that patients with chronic lung disease who exercise improve their endur-
ance, decrease dyspnea, and improve their emotional well-being. Furthermore,
evidence shows a modest decrease in hospitalization rates.
Management
General measures that apply to all patients with chronic lung disease include
• Proper nutrition
• Pneumococcal vaccine every 6 years
• Influenza vaccine each fall
• Stress reduction and relaxation
• Bronchial hygiene (postural drainage and chest physiotherapy) in patients
with excessive mucous production
• Breathing retraining to improve synchrony between the diaphragmatic and
thoracic respiratory muscles, improving the pattern of respiration
• Regular exercise
85
• Oxygen therapy for patients with resting, nocturnal, or exercise-induced

hypoxemia
• Patient and family education
• Treatment of congestive heart failure
• Psychosocial therapy including vocational rehabilitation
Breathing training involves diaphragmatic and pursed-lip breathing and should

be regularly practiced. Techniques of ventilatory muscle training have been taught
based on the premise that exercise capacity in patients with symptomatic COPD is
limited by impaired ventilatory mechanics. Two methods are used for training ven-
tilatory muscles: resistive and hyperpneic methods. The resistive method requires
the patient to inspire against a resistance to generate a greater than normal mouth
pressure for each breath. Improvements in exercise tolerance are equivocal using
this method. In the hyperpneic method, a specially constructed rebreathing system
is used. This method has been reported to improve the maximum sustained ventila-
tion (MSV), which is the maximum ventilation that can be sustained for 15 minutes
under isocapnic conditions. It also improves the overall exercise capacity. These
changes may result from improved aerobic enzyme concentrations of the diaphragm
and inspiratory muscles.
We do not share the enthusiasm of others regarding ventilatory muscle training.
Furthermore, we believe that the most effective method for maintaining fitness in
patients with CLD includes a combination of good nutrition and exercise.
RESTRICTIVE DISEASE
Diseases that restrict lung function can be classified in two large groups: diseases
located outside the lung parenchyma, such as obesity, muscular or skeletal diseases,
and diseases of the pleura, and diseases that involve the lung parenchyma, such as
sarcoidosis, diffuse pulmonary fibrosis, and other forms of diffuse interstitial lung
disease (ILD). Both groups of patients have decreased lung volumes and normal
exhalation flows. Those whose restriction is located outside the lung parenchyma
have a normal diffusion capacity and seldom require oxygen therapy. Those with
restrictive disease located within the lung parenchyma usually have low diffusion
capacity and often require oxygen supplementation first during activities; later, as the
disease progresses, during sleep; and, finally, at rest, in that order.
Restrictive lung disease usually remains stable or progresses slowly in patients
whose disease is located outside the lung parenchyma. However, this is not the case
in patients with ILD, especially patients with idiopathic and autoimmune forms of
ILD, which can progress rapidly.
There are no reported studies of negative effects of exercise training in patients
with restrictive lung disease. Unfortunately, the amount of work regarding the effect
of exercise in this patient population is small; however, the data indicate that exercise
training improves exercise capacity, decreases functional limitations, and improves
dyspnea and quality of life even in patients with ILD.

Lung Disease 87
COPD
COPD is a disease state characterized by chronic airflow limitation with or without
airway hyper-reactivity. Chronic airway obstruction must be documented before a
diagnosis of COPD is made. The obstruction can be caused by chronic bronchitis or
by emphysema. On forced exhalation, a patient with COPD does not empty the lungs
to normal levels. As a result, the functional residual capacity (FRC) and the resid-
ual volume (RV) are increased. Exercise-induced tachypnea can then increase the
amount of air trapped—a phenomenon called dynamic hyperinflation.
The severity of exercise-induced dyspnea correlates well with the degree of hyper-
inflation. As the lungs become more and more inflated, the diaphragm is displaced
downward, increasing the amount of pressure required to move air and decreasing
the capacity of the diaphragm to generate pressure. Treatment of COPD consists of
bronchodilators, antibiotics, airway clearance, and nutritional therapy.
COPD is divided into different stages, according to the severity of impairment, as
follows (gold classification):
• Stage I (mild COPD)

• FEV1/FVC < 0.7
• FEV1 ≥ 80% predicted
• Stage II (moderate)
• FEV1/FVC < 0.7
• FEV1 > 50% and < 80% predicted
• Stage III (severe)
• FEV1/FVC < 0.7
• FEV1: 30–50% predicted
• Stage IV (very severe)
• FEV1/FVC < 0.7
• FEV1 < 30% predicted or < 50% with PCO2 retention (chronic respira-
tory failure)
The treatment of COPD varies according to disease state. All patients benefit
from reduction of risk factors such as cigarette smoking and exposure to airborne
pollutants, as well as vaccination against influenza and short-acting bronchodilators.
Patients with moderate or greater severity benefit from long-acting bronchodilators
such as salmeterol (or a similar β-adrenergic agent), tiotropium, or (probably better)
both of them. Patients with severe or very severe disease benefit from the addition of
an inhaled corticosteroid; however, there is great individual variation. Patients with
mild or moderate disease with an asthmatic component will benefit from a combina-
tion of a long-acting bronchodilator and inhaled corticosteroids even if the disease
is of moderate severity.
Ipratropium bromide is a short-acting anticholinergic; in patients without a reac-
tive component, it is the most effective bronchodilator in the therapy of patients
with COPD and should be used regularly (rather than PRN [pro re nata]). The use
of ipratropium has declined due to the availability of the long-acting anticholinergic

tiotropium. Ipratropium is dosed every 6 hours, whereas tiotropium allows single

daily dosing and facilitates the patient’s therapeutic adherence.
Patients with reversible bronchospasm benefit from an inhaled β2-agonist as
needed. The administration of 12-hour release theophylline at bedtime results in
therapeutic serum theophylline levels at 2–4 a.m., when the airflow obstruction usu-
ally worsens.
Prednisone is not as effective as previously regarded. Oral prednisone (40 mg
for 2 weeks) improves FEV1 in only 10% of patients and is associated with serious
side effects. Consider a trial of prednisone therapy (40 mg for 2 weeks) in those
patients who do not improve with maximal doses of bronchodilators and monitor any
changes in FEV1. Patients who benefit from prednisone (greater than 15% improve-
ment over the baseline FEV1) might benefit from inhaled corticosteroids at a daily
dose of 1 mg. This dose can be achieved with 20 puffs per day of beclomethasone,
10 puffs per day of triamcinolone, or 4 puffs per day of flunisolide. Consider chronic
prednisone therapy only for those patients who clearly benefit from it and cannot
maintain the improvement with inhaled corticosteroids.
The role of antibiotics during an exacerbation of COPD is controversial. Current
practice calls for avoidance of antibiotics when the patient is stable but liberal
use during an exacerbation. Patients are usually advised to begin therapy with
trimethoprim-sulfamethoxazole or doxycycline at the first sign of an exacerbation.
Macrolide antibiotics such as Azithromycin have significant anti-inflammatory prop-
erties and have become part of the standards of care for patients with cystic fibrosis
who have the worst possible form of chronic bronchitis. Patients with severe bron-
chitic symptoms who fail to improve with inhaled therapy might benefit from azithro-
mycin 500 mg PO (per os) Mondays, Wednesdays, and Fridays—as patients with
cystic fibrosis do.
Chest physiotherapy is particularly important in patients with abundant secre-
tions, especially those patients with bronchiectasis.
In the terminal stages of the disease, patients with COPD become cachectic—a
condition characterized by higher than normal resting energy expenditure and the
burning of muscle and visceral protein. Proper nutritional support and exercise,
including weight training, are essential to prevent or decrease weight loss and main-
tain the level of fitness.
Pulmonary rehabilitation for chronic obstructive pulmonary disease has been inves-
tigated extensively and nearly all studies have documented improvement in quality of
life, exercise capacity, and ability to function. Pulmonary rehabilitation should be
part of the management of patients with COPD when they are stable and following
severe exacerbations.
Pulmonary rehabilitation following exacerbations reduces subsequent hospital
admissions and mortality compared with usual community care (no rehabilitation)
and improves the quality of life, exercise capacity, and the ability to function in
patients who have had a severe exacerbation. Pulmonary rehabilitation is a highly
effective and safe intervention in COPD patients after they suffer an exacerbation.

Lung Disease 89
CYSTIC FIBROSIS
Cystic fibrosis (CF) is the most common life-threatening genetic disease in the United
States. Not long ago, patients affected by this disease seldom lived into adulthood.
At the present time, 34% of all patients with CF are adults. Patients with CF have an
abnormality in the long arm of chromosome 7, which causes a defect in the manu-
facture or traffic of a protein called the cystic fibrosis transmembrane conductance
regulator (CFTR). CFTR protein is manufactured within the endoplasmic reticulum
(ER) of epithelial cells and transported through the Golgi apparatus to the apical sur-
face of the cell, where it regulates sodium and other chloride channels. Of patients
with CF, 70% lack an amino acid (phenylalanine) at position 508. Patients with this
mutation (∆F–508) manufacture CFTR but transport through the ER is defective.
Cystic fibrosis affects organs throughout the body, including sinuses, pancreas,
liver, sweat ducts, and fallopian tubes; 95% of males with CF suffer from bilat-
eral absence of the vas deferens and cannot have children. However, the most
important problem affecting patients with CF is the progressive lung disease it
causes. The defect in the electrolyte transport causes the airway mucous to be
salty. The abnormal electrolyte concentration impairs the function of normal bac-
tericidal factors present in the airways (defenses) and hampers the clearance of
microorganisms, predisposing the patient to colonization with pseudomonas and
staphylococcus. Neutrophils migrate to the site of infection in great numbers,
releasing toxins that induce mucus production and damage the tissues of the air-
way. DNA released by degenerating neutrophils further increases the viscosity of
the mucus.
Treatment of CF consists of a coordinated approach to treat infections, evacu-
ate airway mucous, decrease bronchial inflammation, and improve nutrition and
functional capacity. This requires a mixture of antibiotics, bronchodilators, medica-
tions, and techniques to improve airway clearance, anti-inflammatory agents, and
nutritional therapy. Timely use of short-term (usually 15 days) oral or intravenous
antibiotic combinations and lifelong (every other month) inhalations of tobramycin,
aztreonam, or colistin help keep the infections under control.
Inhaled and oral bronchodilators benefit mostly those patients who suffer from
airway hyperreactivity; they are used as with patients with COPD. Airway clear-
ance with daily inhalations of dornase alfa (Pulmozyme© 2.5 mg) plus inhalations of
7% hypertonic saline (4 cc b.i.d. [bis in de—twice daily] or t.i.d. [ter in de—thrice
daily]), frequent chest physiotherapy, and frequent use of mucoevacuants devices
such as Accapella© and the Vest© are extremely important in patients with abundant
airway secretions and in patients with bronchiectasis. Measures to decrease inflam-
mation include inhaled corticosteroids and azithromycin 500 mg PO Mondays,
Wednesdays, and Fridays for life.
The use of oral corticosteroids is usually limited to patients with a severe asthmatic
component who cannot be controlled otherwise, such as patients with active allergic
bronchopulmonary aspergillosis (15% of all CF patients). The use of nonsteroidal
anti-inflammatory medications is uncommon in adults because of concerns over

its gastrointestinal and renal side effects. Patients with CF have a tendency to lose
weight secondary to two different mechanisms: (1) the cachectic condition caused by
chronic respiratory infections, and (2) malabsorption caused by exocrine pancreatic
insufficiency. These patients require a high-calorie diet, vitamin supplementation,
and administration of pancreatic enzymes at high enough doses to obtain desired
goals, such as normalization of blood levels of vitamins A, D, E, and K; elimination
of gastrointestinal symptoms; and normalization of pancreatic function tests.
Among the pancreatic function tests, the measurement of pancreatic elastase-1
in a stool sample is the most commonly used because it is not affected by oral pan-
creatic enzymes and has excellent correlation with invasive forms of testing (which
require the placement of a double lumen duodenal tube and stimulation of the pan-
creas with secretin); it is 93% specific and has 100% sensitivity in severe disease.
Unfortunately, however, it is 77–100% sensitive for moderate disease and <77% sen-
sitive for mild pancreatic impairment. Patients with advanced pancreatic dysfunction
develop insulin-dependent diabetes, which adds another level of complexity to the
care of those patients.
The sweat of patients with cystic fibrosis contains more salt than the sweat of
subjects without this disease, and they may lose a considerably larger amount of salt
during exercise than other people (the mainstay for the diagnosis of CF is a sweat
chloride concentration > 60 mmol/L). This is seldom a problem, however, because
patients will crave salt and the amount lost will be replenished over a period of hours.
Replacing lost fluid during and immediately after exercise is more important.
Lack of regular exercise leads to more severe impairment because it decreases
strength, endurance, and the capacity to perform activities of everyday life. Problems
associated with exercise include overheating, dehydration, and damage to bone and
muscles in patients with osteoporosis—a common condition in patients with CF.
Exercise therapy is part of the CF care guidelines published by the Cystic Fibrosis
Foundation and there are several papers documenting the benefits of exercise in the
CF population. Obviously, the benefits vary according to the type of exercise pro-
gram, but there are no studies comparing aerobic training with anaerobic training
and resistance training or a combination of them.
COR-PULMONALE
The development of right ventricular failure is a sign of poor prognosis in patients
with chronic lung disease. The best treatment for cor-pulmonale is to treat the pul-
monary condition that caused it. Diuretics are indicated in patients with significant
edema. Furosemide is the agent of choice if the patient is hyponatremic, a condition
common in patients with chronic lung disease secondary to the common occurrence
of an increased production of antidiuretic hormone. A combination of furosemide
with a thiazide diuretic is synergistic and will help decrease the amount of calcium
loss associated with the use of furosemide.
Digitalis is not indicated in patients with cor-pulmonale. It does not improve right
ventricular function. It is an arteriolar vasoconstrictor and could increase the pulmo-
nary vascular resistance. It may also increase the risk of cardiac arrhythmias. Patients

Lung Disease 91
with chronic lung disease often suffer from multifocal atria tachycardia and atrial
fibrillation. Quinidine or lidocaine types of medications are ineffective. The drugs
of choice to treat these arrhythmias are verapamil or amiodarone. Diltiazem or nife-
dipine might be useful in patients with pulmonary hypertension with a documented
reversible component. To document improvement, it might be necessary to perform
right-side cardiac catheterization followed by the infusion of increasing doses of dil-
tiazem. Those patients who demonstrate improvement can be treated with an oral
dose proportional to the intravenous dose required to obtain the desired effect.
The majority of patients with pulmonary hypertension secondary to chronic lung
disease have mild pulmonary hypertension that will not improve with calcium-
channel blockers or any other pulmonary vasculature dilator, with the exception of
oxygen in those patients suffering from hypoxia and β2-agonists in patients with
reversible airway disease. If a patient with COPD is found to have severe pulmonary
arterial hypertension, another condition is likely to be present in association with
COPD; on the other hand, patients with ILD (particularly scleroderma) often have
severe pulmonary hypertension and would benefit from the administration of oral
endothelin receptor antagonists, oral phosphodiesterase inhibitor nitrates or inhaled,
SC, or IV prostanoids either alone or in combination.
Exercise training does not improve the hemodynamic abnormalities of patients
with cor-pulmonale and/or pulmonary arterial hypertension. However, it does increase
the patients’ quality of life and functional capacity by improving muscle function.
Exercise Issues
Studies evaluating the effects of exercise training programs for patients with COPD
have revealed an improvement in exercise tolerance. A considerable benefit has been
reported after just 3–4 weeks of exercise. Further improvement has been reported if
exercise is continued beyond this time. The percentage of improvement in exercise
tolerance is very individualistic and depends on many factors, such as disease sever-
ity. A comprehensive pulmonary rehabilitation program includes an educational pro-
gram (to teach patients and significant others the facts about lung disease, its therapy,
and coping strategies) and an exercise program. Of all the components of a pulmo-
nary rehabilitation program, the exercise training component is the most important.
Benefits for patients with all types of lung disease include
• Improvement in skeletal muscular endurance and strength

• A reduction in minute ventilation by 6%
• Dyspnea levels reduced by 30%
• Lactic acid levels decrease by 17% for any given exercise workload
• Increased motivation
• An improvement in ventilatory muscle function
• Improved technique of performance
These benefits have been documented in patients with mild, moderate, and severe
lung disease. The magnitude of the improvement is not influenced by the severity

of the pulmonary impairment. Exercise training can be performed at home and

directed by nonspecialists. The only issue that remains controversial is the cost
effectiveness of formal, medically supervised pulmonary rehabilitation programs.
Many patients with chronic lung disease are afraid of exercise. They associate
the dyspnea caused by exercise with their disease and avoid all forms of exercise.
Supervised exercise could alleviate those fears and help the patient overcome the
psychological barriers to exercise.
In our experience, once the benefit of exercise becomes obvious, any resistance
to this mode of therapy is greatly reduced. We strongly recommend that all patients
with chronic lung disease undergo a symptom-limited cardiopulmonary stress test
prior to the initiation of an exercise program (see Appendix B). If gas-exchange
monitoring equipment is not available, a cardiopulmonary stress test can be replaced
by a cardiac stress test with O2 saturation monitoring and spirometry before and after
the test.
Indications for cardiopulmonary exercise testing include the following:
• Rule out exercise-induced hypoxia.

• Rule out exercise-induced bronchospasm.
• Rule out exercise-induced cardiac arrhythmias and other cardiovascular
problems.
• Prescribe exercise intensity using the anaerobic threshold in Method 7, pre-
sented in Appendix A.
• Determine the need for supplemental oxygen.
Patients who will require oxygen during exercise (usually patients with an FEV1 less
than 50% of predicted) are those who desaturate to a level less than a PaO2 of 55 mmHg or
a saturation (SaO2) of less than 88% during exercise. Patients with severe CLD will attain
their maximal power output at a ventilatory level close to their maximum voluntary ven-
tilation (MVV), while their cardiac stress is relatively low. The opposite is true in normal
individuals. In addition, the patient with CLD suffers from an abnormally elevated ven-
tilatory requirement for the work rate. In other words, the volume of air required for any
given amount of work is higher in patients with CLD than in normal individuals. This is
due to a decreased efficiency of gas exchange evidenced by an increase in the physiologi-
cal dead space to tidal volume ratio (VD/VT) and the ventilatory equivalents (VE/VCO2
and VE/VO2), as observed during cardiopulmonary stress testing.
Prescribing exercise intensity for patients with pulmonary disease can be
improved using the data obtained during a cardiopulmonary stress test. There is not
a universally agreed upon exercise intensity; however, at least four approaches are
recommended when a cardiopulmonary test is available:
1. If data from a cardiopulmonary stress test are available, prescribe exercise

at a heart rate corresponding to 40–50% of the VO2 max. (See Appendix A,
Method 6, for detailed information.) This is the minimal intensity recom-
mended for healthy adults and will reduce the risk for injury and achieve
reconditioning. However, there are patients with severe lung disease whose
decreased MVV would prevent them from exercising at this intensity.

Lung Disease 93
2. An exercise intensity corresponding to a heart rate at the anaerobic threshold

can be prescribed provided that the minute ventilation is less than 80% of
the maximal ventilation. Many patients with severe COPD may not achieve
an anaerobic threshold during a cardiopulmonary stress test; however, in
those who do, we recommend prescribing exercise at the heart rate associ-
ated with the anaerobic threshold or 80% of the maximal ventilation, which-
ever is less. (See Appendix A, Methods 7 and 8, for detailed information.)
3. If the patient has severe lung disease, prescribe exercise at a heart rate equal
to 80% of the maximal work (see Appendix A, Method 8, and Appendix B).
Patients with moderate to severe lung disease can sustain this percentage
of their MVV, but patients with mild lung disease who are limited by their
cardiovascular systems cannot. Such an intensity will place them above the
anaerobic threshold. At this intensity, these patients would not be able to
sustain exercise.
4. If the patient has mild lung disease and cardiopulmonary stress test data are
not available, use the dyspnea chart in Appendix A, Method 5. A dyspnea
rating of 3–6 in normal subjects corresponds to 50–85% of the VO2 max.
This method guarantees a moderate exercise intensity; however, the subjec-
tive nature of this method becomes a problem for patients who have severe
disease and are afraid of exercise. These patients report dyspnea at inap-
propriately low exercise intensities.
Exercise modalities should involve large muscle groups. Upper body aerobic
and weight-lifting activities are not contraindicated even if the cost of ventilation
may be greater compared to a similar workload using larger lower-body muscles.
Frequency and intensity may need to be adjusted based on individual conditioning
levels. All patients should be encouraged to practice pursed-lip breathing to decrease
the frequency of respiration, increase tidal volume and oxygenation, and provide a
sense of control over breathing.
ASTHMA
Background
An expert panel report, “Guidelines for the Diagnosis and Management of Asthma,”
was released in 1991 and has been updated several times, most recently in 2007.
The definition of asthma has evolved to reflect advances in the pathophysiology of
the disease. The most recent definition is the following:
Asthma is a chronic inflammatory disorder of the airways in which many cells and cel-
lular elements play a role, in particular, mast cells, eosinophils, T-lymphocytes, macro
phages, neutrophils and epithelial cells. In susceptible individuals this inflammation
causes recurrent episodes of wheezing, breathlessness, chest tightness and coughing,
particularly at night or in the early morning. These episodes are associated with wide-
spread, but variable, airflow obstruction that is often reversible either spontaneously
or with treatment. This inflammation also causes an associated increase in existing
bronchial hyper-responsiveness to a variety of stimuli.

Management
The therapeutic goals are to
1. Prevent chronic and troublesome symptoms.

2. Maintain nearly “normal” pulmonary function.
3. Maintain normal activity levels (including exercise and other physical
activities).
4. Prevent recurrent exacerbation of asthma and minimize the need for emer-
gency department visits and hospitalizations.
5. Provide optimal pharmacotherapy with minimal or no adverse effects.
6. Meet patient and family expectations for satisfaction of asthma care.
The following activities are important to meet these goals:
1. Environmental control including control of allergens and other factors that

cause asthmatic attacks, such as exposure to occupational factors and non-
specific airway irritants
2. Monitoring of the severity of asthma with symptom scores and peak flow
measurements mornings and evenings
3. Control of five comorbidity states that often aggravate asthma: rhinitis/
sinusitis, gastroesophageal reflux, sensitivity to aspirin/other nonsteroidal
anti-inflammatory drugs/sulfates, adverse effects from corticosteroids, and
viral infections
Patients with asthma who are exposed to perennial inhalant allergens should have
either skin or in vitro testing to assess the presence of allergic triggers. Many patients
with asthma may experience allergies to foods. Patients allergic to certain foods
might experience asthmatic episodes hours after ingestion and might not be aware of
the relationship. Table 5.1 describes the therapies used in asthma cases.
The role of antileukotrienes is unclear. However, they appear to be useful in
aspirin-sensitive asthmatics and have the potential to decrease the dose of corti-
costeroids. Many patients with exercise-induced asthma (EIA) are sensitive to cold
and/or dry air. In fact, hyperventilation can even evoke asthma in some individuals.
It appears that cold-induced asthma is related to respiratory heat loss.
The dry air we breathe is humidified with water from the respiratory tract. It is
warmed before entering the lungs and we exhale warm water and air. In the field,
asthma can be detected by using an inexpensive portable peak-flow meter. A 12.5%
decrease in peak flow during or following exercise is an indication of EIA.
Numerous studies have demonstrated the efficacy of salmeterol in the prevention
of EIA; however, the use of this medication might not be enough to control EIA.
The strategy for treating EIA includes exercising in warm- and moist-air environ-
ments, if possible, and avoiding allergens. The goal of therapy should be to allow the
patient to participate in exercise without symptoms. The best medications to prevent

Lung Disease 95
TABLE 5.1
Pharmacological Therapy of Asthma According to Severity
Step 1: mild; Long-term control: none
intermittent Quick relief: short-acting
inhaled β2-agonist
Step 2: mild; Long-term control: all patients Leukotriene blockers, oral theophylline and
persistent over the age of 5, inhaled cromoglycates are alternative agents, but
corticosteroids results are not as good as those obtained with
Quick relief: short-acting inhaled corticosteroids; among them, we prefer
inhaled β2-agonist the leukotriene blockers
Step 3: moderate; Long-term control: inhaled Double the dose of inhaled corticosteroids
persistent corticosteroids; long-acting Consult pulmonary specialist
inhaled β2-agonist Theophylline is an alternative long-term
Quick relief: short-acting bronchodilator, but long-acting β-blockers
inhaled β2-agonist such as salmeterol are more effective
Leukotriene blockers might help
Step 4: severe; Long-term control: high-dose Add prednisone
persistent inhaled corticosteroids; Consult pulmonary specialist
long-acting inhaled Consider theophylline in addition to long-acting
β2-agonist β-blockers such as salmeterol
Quick relief: short-acting Leukotriene blockers and anti-IgE therapy with
inhaled β2-agonist omalizumab might help
EIA are salmeterol and the short-acting inhaled β2-agonists. Other agents, such as
ipratropium bromide, cromolyn, nedocromil, and even calcium channel blockers,
have some utility in the prevention of EIA, but are usually ineffective.
Exercise Issues
Exercise-induced asthma can cause symptoms such as coughing, dyspnea, and chest
tightness during or immediately after exercise; it limits exercise performance and
prevents people from engaging in exercise. Two approaches can be taken to prevent
exercise-induced asthma when prescribing exercise. The first involves prescribing
the exercise at an intensity that avoids EIA. This will probably result in an intensity
that may limit activities; therefore, the individual will not be able to participate in
certain sports. Activities less likely to induce bronchospasm include swimming in a
warm, humid environment and intermittent work of short duration, such as weight
lifting or baseball. Running outdoors on a cold day is likely to cause EIA.
A warm-up period of 10–15 minutes at a relatively low intensity (i.e., a heart
rate corresponding to 40–50% of the VO2 max or a dyspnea rating of less than 2)
may reduce EIA (see Appendix A, Methods 5 and 6). The intensity of the warm-up
period should be low enough to allow the patient to breathe comfortably through the
nostrils. If exercise is performed in the cold outdoors, a mask or bandanna tied over
the mouth will help to warm the air before it reaches the lungs.

The second approach to prevention of EIA involves medicating the subject. Three
types of medications are available to prevent or minimize exercise-induced asthma:
nedocromil, sodium cromoglycate, and β-adrenergic agents. Nedocromil sodium and
sodium cromoglycate are similarly effective in preventing exercise-induced asthma
for both children and adults but are seldom sufficient when used alone. Most physi-
cians will use them in conjunction with β-adrenergic agents.
The use of a long-acting bronchodilator such as salmeterol alone (two puffs twice
daily) might be sufficient to prevent EIA. If further help is needed, albuterol or a
similar short-acting β-adrenergic can be prescribed using two to six puffs 15 minutes
before exercise. This may allow the patient to participate in activities that require
moderate to high intensities of exercise. If β-agonists are prescribed immediately
prior to exercise, it might result in an increase in the resting heart rate, which could
make exercise prescription by heart rate unreliable. This is seldom the case, but in
some cases exercise intensity should be prescribed and monitored using the dyspnea
scale in Appendix A, Method 5.
Patients with severe EIA can engage in vigorous physical activity if their condi-
tion is properly treated. However, until adequate control of the disease is achieved,
activities that may provoke EIA should be avoided.
Exercise training has no effect on the resting lung function of asthmatic subjects
or the severity of their disease. However, exercise training of the asthmatic popula-
tion improves cardiopulmonary and muscular fitness.
WEIGHT TRAINING GUIDELINES FOR LUNG DISEASE

When patients with pulmonary disease undergo weight training, oxygen saturation
levels are of the utmost importance. Patients who desaturate while exercising (usually
patients with an FEV1 less than 50% of predicted) are those who desaturate to a level
less than a PaO2 of 55 mmHg or a saturation (SaO2) of less than 88% during the pre-
scribed exercise intensity. These individuals should avoid weight training unless they
are using supplemental oxygen. Other contraindications to weight training include

and abilities. Weight machines and free weights can be used when the patient is able

Lung Disease 97
lines for patients are illustrated in the lung disease workbook CD.

[100 – (# reps × 2.5)] = % 1RM

The preceding methods for prescribing intensity can be used for any weight-
lifting equipment: free weights (barbells and dumbbells), weight machines, or hand
weights and stretch elastic bands. The prescribed dyspnea rating of 3–6 for aerobic
work should not be exceeded when weight lifting is undertaken.
RECOMMENDED READING
Belman, M. J. 1989. Exercise in chronic obstructive pulmonary disease. In Exercise in modern
medicine, ed. B. A. Franklin, S. Gordon, and G. C. Timmis. Baltimore, MD: Williams
& Wilkins.
Bradley, J. M., and F. Moran. 2008. Physical training for cystic fibrosis. Cochrane Database of
Systematic Reviews Issue 1. Art. no. CD002768. DOI: 10.1002/14651858.CD002768.pub2
Celli, B. R. 1997. Is pulmonary rehabilitation an effective treatment for chronic obstructive lung
disease? American Journal of Respiratory and Critical Care Medicine 155:781–783.
disabilities, 3rd ed., chaps. 6–12. Champaign, IL: Human Kinetics.
Holland, A. E., and C. Hill. 2008. Physical training for interstitial lung disease. Cochrane
Database of Systematic Reviews Issue 4. Art. no. CD006322. DOI: 10.1002/14651858.
CD006322.pub2
Jones, N. L., and K. J. Killian. 1990. Exercise in chronic airway obstruction. In Exercise, fit-
ness, and health: A consensus of current knowledge, ed. C. Bouchard, R. J. Shephard,
T. Stephens, et al. Champaign, IL: Human Kinetics.
Kelly, K. D., C. Spooner, and B. H. Rowe. 2000. Nedocromil sodium versus sodium cro-
moglycate for preventing exercise-induced bronchoconstriction. Cochrane Database of
Systematic Reviews Issue 3. Art. no.: CD002731. DOI: 10.1002/14651858.CD002731
Lacasse, Y., R. Goldstein, T. J. Lasserson, and S. Martin. 2006. Pulmonary rehabilitation for
chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews
Issue 4. Art. no. CD003793. DOI: 10.1002/14651858.CD003793.pub2

Moorcroft, A. J. 1997. Long-term change in exercise capacity, body mass, and pulmonary
function in adults with cystic fibrosis. Chest 111:338–343.
National Asthma Education Program. Expert Panel Report. 1991. Guidelines for the diagnosis
and management of asthma. U.S. Department of Health and Human Services. Public
Health Service. National Institutes of Health. Publication no. 91-3042.
———. Expert Panel Report II. 1997. Guidelines for the diagnosis and management of asthma.
U.S. Department of Health and Human Services. Public Health Service. National
Institutes of Health.
———. Expert Panel Report III. 2007. Guidelines for the diagnosis and management of
asthma. U.S. Department of Health and Human Services. Public Health Service.
National Institutes of Health. National Heart and Lung Institute.
Nickerson, B. G. 1989. Asthmatic patients and those with exercise-induced bronchospasm.
In Exercise in modern medicine, ed. B. A. Franklin, S. Gordon, and G. C. Timmis.
Baltimore, MD: Williams & Wilkins.
Orenstein, D. M., and P. A. Nixon. 1989. Patients with cystic fibrosis. In Exercise in modern
medicine, ed. B. A. Franklin, S. Gordon, and G. C. Timmis. Baltimore, MD: Williams
& Wilkins.
Puhan, M., M. Scharplatz, T. Troosters, E. H. Walters, and J. Steurer. 2009. Pulmonary
rehabilitation following exacerbations of chronic obstructive pulmonary dis-
ease. Cochrane Database of Systematic Reviews Issue 1. Art. no. CD005305. DOI:
10.1002/14651858.CD005305.pub2
Ram, F. S. F., S. Robinson, P. N. Black, and J. Picot. 2005. Physical training for asthma.
Cochrane Database of Systematic Reviews Issue 4. Art. no.: CD001116. DOI:
10.1002/14651858.CD001116.pub2
Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease.
1997. American Journal of Respiratory Critical Care Medicine 18:128–138.
Whipp, B. J. 1990. Discussion: Exercise and chronic airway obstruction. In Exercise, fit-
ness, and health: A consensus of current knowledge, ed. C. Bouchard, R. J. Shephard,
EXERCISE PRESCRIPTION FOR CHRONIC LUNG DISEASE

AND ASTHMA
Frequency
mum recuperation.
Modality
acceptable aerobic activities. Swimming in a warm, moist environment
may be especially beneficial if the patient has exercise-induced asthma.
A resistance or weight-training program should be included.
Duration
20–60 minutes is achieved without stopping.

Lung Disease 99
Intensity
The aerobic and weight-training intensity can be prescribed using the dys-
pnea chart in Appendix A, Method 5. A dyspnea rating of moderate
to severe, a rate of perceived exertion (RPE) of 3–6, is recommended.
When weight training is undertaken, use a light weight for 10–15 rep-
etitions and do one to two sets for each muscle group. See the attached
section on weight training and the illustrations in the lung disease work-
book CD for specific instructions.
Other Instructions
• Patients, especially those who have cystic fibrosis, should avoid exercising
during the hottest part of the day.
pain immediately.
follow-up visit.
COMMON QUESTIONS ON LUNG DISEASE

Question: What is asthma?
Answer: Asthma is a chronic disease of the lungs. It involves reversible airway
closure and inflammation.
Question: What are the symptoms of asthma?
Answer: Wheezing, shortness of breath, tightness in the chest, cough and/or a
combination of these symptoms.
Question: How often can I have asthma attacks?
Answer: This depends on how well controlled your asthma is. The goal is to
have as few flare-ups as possible. You can achieve this goal by taking medi-
cation and controlling triggers that may cause an asthma attack.
Question: What causes an asthma attack?
Answer: When you have asthma, your lungs are very sensitive to certain
things. When you come in contact with these things (triggers), your asthma
may get worse. These triggers may cause your airways to become inflamed
and narrowed, making it hard to breathe. There are several triggers asso-
ciated with asthma: viral infections such as upper respiratory infections;
allergens like dust mites, animal dander, fungus, and pollens; chemicals
such as pesticides or lawn sprays; aspirin; cigarette smoke; and vigorous
exercise in a cold environment.

Question: Can I cure my asthma?

Answer: No. There is no cure for asthma; however, your symptoms can be
controlled.
Question: What is the treatment?
Answer: The first step is to identify what triggers your asthma and then avoid
this trigger. The severity of your symptoms will determine the medical
treatment. There are various medications that are used in a step-wise fash-
ion to aid in the treatment of asthma. They include inhaled bronchodilators,
inhaled anti-inflammatory agents, and oral steroids.
Question: Are there different levels of asthma? How do I know which one
I have?
Answer: Yes. The levels range from mild to moderate and severe. You have
mild asthma if you have less than two asthma attacks a week. It is rare for
you to have symptoms at night and you have normal peak flow readings
between asthma attacks. Moderate asthma includes more than one or two
asthma attacks a week lasting longer than 24 hours, frequent symptoms at
night, and a peak flow of 60–80% of normal. Severe symptoms involve con-
tinuous asthma attacks that require you to take a large amount of inhaled
bronchodilators, frequent emergency room visits and hospitalizations, poor
exercise capacity, and peak flow less than 60% of normal. Your medical
professional will help you determine which category applies to you.
Question: Can I exercise if I have asthma?
Answer: Yes. Your medical professional can discuss and prescribe appropriate
treatment and exercise regimens that are best for you. For a detailed pro-
gram, refer to the exercise section in the lung disease workbook.
Question: How can I prevent having an asthma attack?
Answer: The best way to prevent an asthma attack is to work closely with your
medical professional to develop a suitable medical plan that will keep you
from having asthma attacks. In addition, determining what your triggers
are and then avoiding these triggers will also be very important in control-
ling the number of asthma attacks you will have.
Question: What is a peak flow meter?
Answer: A peak flow meter is a device that evaluates how well you are breath-
ing by measuring how fast you can exhale air in one breath.
Question: What does “personal best” mean?
Answer: This is the best number or the highest peak flow you achieve. To
determine your personal best, you should check your peak flow when
you are asymptomatic (your asthma is under good control) every day for
2 weeks. It is a good idea to check your peak flow twice daily, before and
after you take your inhaled bronchodilators and chart the results. The best
number is your personal best.
Question: How often should I use my peak flow meter?
Answer: The key is to know on a daily basis how well your asthma is con-
trolled. If your personal best starts declining, you will know your asthma is
starting to get worse.

Lung Disease 101
Question: What should I do if my personal best declines?

Answer: The first thing to do is to determine how much your personal best
is declining. A decline of 20–30% may indicate your asthma is beginning
to get worse. You and your medical professional should develop a plan of
action. This plan of action may include changing your medication. The goal
is to prevent an asthma attack.
Question: What is chronic obstructive pulmonary disease (COPD)?
Answer: COPD is a chronic disease of the airways in your lungs that gets
worse over time. Specifically, it is called chronic bronchitis and emphy-
sema. This makes it difficult to exhale.
Question: What causes COPD?
Answer: Continuous exposure to irritants to the airway, as well as to toxic chem-
icals, contributes to COPD, but tobacco smoke is the biggest offender.
Question: What is the difference between emphysema and chronic bronchitis?
Answer: The main difference between the two has to do with the chronic
cough and sputum production. If you have chronic bronchitis, you will
cough a lot and have sputum production. In emphysema, you will cough
little, if any, and not produce any sputum. In bronchitis, the airways are
inflamed; in emphysema, the airways (alveoli) are destroyed. These two
diseases often coexist simultaneously.
Question: What are the symptoms of COPD?
Answer: Cough and sputum production occur for 3 months of the year for at
least 2 years, there is shortness of breath with activity, swelling of the lower
extremities, and wheezing.
Question: Why do I feel so short of breath with any activity?
Answer: When you have COPD, you cannot completely empty the lungs of
air. With an increase in activity, the rate of breathing tends to increase also.
This increases the amount of air trapped in your lungs, making it even
harder to breathe.
Question: Can this disease be cured?
Answer: Only if you act very early. The disease progression can be slowed
down, but it cannot be reversed. It is very important to remove the cause,
such as exposure to a chemical or smoking.
Question: What is the treatment?
Answer: The treatment varies, depending on how sick you are. Bronchodilators,
antibiotics, airway clearance, chest-tapping exercises, and nutritional ther-
apy are common treatments.
Question: Are there any preventive measures I should take to stay healthy
after I have been diagnosed with COPD?
Answer: Yes. The following general measures should be followed: get a pneu-
mococcal vaccine every 6 years and an influenza vaccine each fall, practice
a healthy lifestyle, and exercise.
Question: How can I exercise when I feel short of breath?
Answer: Before you begin exercising, you should talk with your medical pro-
fessional regarding an exercise regimen specifically designed for you. The

important thing to know is that exercise cannot cure your lung disease, but
it will make you feel less short of breath when you do. Your strength and
endurance also will increase.
Question: Will I need to use oxygen at home?
Answer: Not everyone requires home oxygen. If you have a low blood oxygen
level at rest, during exercise, or at night, home oxygen will be prescribed.
Question: What is cardiopulmonary stress testing?
Answer: This is a test in which your heart and your lungs are tested/stressed
to determine the type and severity of your disease and how much exercise
is appropriate for your individual needs.
Question: How can I have a sexual relationship with my partner when I get so
short of breath just walking?
Answer: The most important thing is to communicate your fears and anxieties
to your partner. Discuss the issue with your medical professional when your
partner is present. Use energy management and plan ahead. Have inter-
course at your best time of the day. Do not eat a heavy meal before and use a
bronchodilator 10–15 minutes prior to intercourse. Allow your partner to be
more active. Use creative positioning. If you become short of breath during
intercourse, stop and let your partner take the active role.
Question: Is there anything I can do at home to make my workload easier?
Answer: Plan your daily activities in advance. Decide which are the most
important tasks and do them first. Delegate chores to family members. Take
rest periods during the day. Straighten rooms as you go. Most important,
work at your own speed and pace yourself.
Question: I’m hungry, but I get so short of breath when I eat. What should I do?
Answer: Eating too much at one time will cause your stomach to become too
full. This makes it hard for the lungs to expand and makes it difficult for you
to breathe. Try having several small meals instead. Avoid gas-producing
foods such as cabbage and beans. Eat in a relaxed environment and take
your time.
Question: What is cystic fibrosis?
Answer: Cystic fibrosis is a genetic disorder that results in chronic lung dis-
ease. It is passed on from both mother and father. Cough, recurrent pneu-
monia, and exercise intolerance are quite common.

6 Obesity
INTRODUCTION
The world population is growing fast: from 3 billion in 1960 to 6 billion in 2000
to 6.8 billion in 2010. If the world population continues to grow at the same pace,
by the end of this century it will reach 12 billion. At the current childbirth rate of
2.6 children per woman, the population will continue to grow unless the fertility rate
decreases or the mortality rate increases. Both are likely possibilities; the fertility
rate has been declining and obesity-related diseases have decreased life expectancy.
The current obese generation is expected to live a shorter life span than the previous
nonobese generation.
The U.S. population has the dubious distinction of being the fattest on the planet.
Between 2007 and 2008, the age-adjusted prevalence of obesity in the United States
(BMI > 30) was 33.8% overall: 32.2% among men and 35.5% among women. The
corresponding prevalence estimates for overweight and obesity combined (BMI ≥
25) were 68.0% overall: 72.3% for men and 64.1% for women.
According to the National Institutes of Health, obesity and overweight have become
the second leading cause of premature mortality (after cigarette smoking). The lowest
mortality rates for all causes are found in subjects having a BMI between 22.5 and
24.9 in men and 22 and 23.4 in women; the highest mortality rates are found in those
with a BMI > 40. A BMI > 25 increases the risk of cardiovascular death by 25%,
whereas the risk of cancer increases by 40–80% in the higher weight categories.
Obesity is the result of a positive caloric balance resulting in the accumulation
of fat when more energy has been consumed than expended. One pound of fat is
equivalent to 3500 kcal.
The prevalence of obesity in a given population should not be based on the desir-
able weight for that population, which varies according to personal preference and
culture, but rather on morbidity and mortality data. Based on life insurance statistics
relating height and weight to survival, insurance companies have proposed differ-
ent tables for desirable weights. These tables are widely used; however, the body
mass index (BMI)—the weight in kilograms divided by height in meters squared
(kilograms/square meters)—appears to be a better way to relate weight to height than
the height/weight tables. The calculated BMI above which there is a higher incidence
of mortality is identical for males and females, but changes with age as follows:
103
Suggested BMI Ranges

Age BMI
19–24 19–24
25–34 20–25
35–44 21–26
45–54 22–27
55–64 23–28
≥65 24–29
A trend toward an increase in weight and caloric consumption has been observed
for all age groups since 1918. Cultural trends are important, but there are other fac-
tors. The prevalence of obesity is higher in blacks, Latinos, females, older-age groups,
lower socioeconomic groups, and recent immigrants. Obesity is a serious health
problem. Among other conditions, it is associated with non-insulin-dependent diabe-
tes, hypertension, respiratory conditions, gallstones, biliary tract disease, obstructive
sleep apnea, primary hypoventilation, degenerative arthritis, and cancer.
The distribution of fat in obese subjects varies according to gender, probably sec-
ondary to the effect of progesterone, estrogen, and other hormones involved in the
regulation of lipoprotein lipase in different body sites. When females gain weight,
they accumulate fat in the femoral-gluteal area, causing the typical “pear shape” of
gynoid obesity. Males accumulate fat in the abdomen, causing “apple” or android
obesity. Individuals with android obesity are more prone to the metabolic conse-
quences of obesity and have a greater risk for diabetes, hypertension, stroke, and
coronary artery disease. However, some obese patients have no health problems
and live a normal life.
Obesity is the result of an imbalance between energy intake and energy expen-
diture. Energy expenditure above the normal resting energy level is determined by
muscular activity and a process called thermogenesis. The resting energy expendi-
ture (REE) is 65–75% of the total energy expenditure and can be estimated in calo-
ries per day by multiplying the ideal body weight in pounds by 10. Thermogenesis is
divided into obligatory and facultative thermogenesis. The energy cost of ingesting,
digesting, and processing the food is known as obligatory thermogenesis. The other
component of dietary thermogenesis is modulated by the sympathetic nervous sys-
tem and is called facultative thermogenesis.
The majority of the facultative thermogenesis is elicited by β-stimulation, which
occurs in the skeletal muscle and coincides with the uptake of glucose by the muscle and
rising plasma levels of epinephrine and nor-epinephrine. The ingestion of food causes
a rise in the concentration of catecholamines and an elevation of the resting energy
expenditure by 15% in lean subjects, but only 8% (or less) in many obese subjects.
There is evidence that close to 50% of obese subjects suffer from the previously
mentioned abnormality in facultative thermogenesis. This defect continues even
after the disappearance of obesity, suggesting that it is not the result of but rather
a contributing factor in the development of obesity. Facultative thermogenesis is

Obesity 105
decreased by the β-blocker propranolol and in insulin-resistant subjects. An abnor-

mality in β-receptor modulation and the resulting insulin resistance might be the
common denominator in diabetes, obesity, and hypertension. The effect of caffeine,
β-stimulants, and nicotine in appetite regulation and their role in the therapy of obe-
sity require further study.
Contrary to popular opinion, the REE is not always decreased in obesity; some
obese subjects, especially those who are free from obesity-related metabolic prob-
lems, have an increased REE because they have an increased lean body mass. For
each kilogram of excess body weight, the total energy expenditure is increased by
16 kcal/day. Furthermore, it has been estimated that for every pound of lean body
mass gained, resting energy expenditure increases by approximately 50 calories per
day. A diet very low in calories and/or carbohydrates causes loss of lean body mass,
resulting in a decrease in the REE.
DEFINING THE METABOLIC SYNDROME

The metabolic syndrome is a construct of risk factors that are of metabolic origin and
tend to cluster in individuals prone to obesity, diabetes type 2, and cardiovascular
disease. Findings from the Third National Health and Nutrition Examination Survey
estimated that 22% of the U.S. population has metabolic syndrome characteristics;
however, exactly what defines the metabolic syndrome is still a matter of controversy.
The finding that hypertension, hyperglycemia, and gout often coexist in the same
patient was first noted by Kylin in 1923, but the subject was brought to the forefront of
public attention by Reaven in 1988. Reaven linked insulin resistance with hypertension,
dyslipidemia, diabetes, and cardiovascular disease and labeled it “Syndrome X.” It was
later renamed the insulin resistance syndrome (IRS) and the metabolic syndrome.
In 1999 the World Health Organization (WHO) published the first criteria for the
diagnosis of the metabolic syndrome as follows: diabetes type 2 or impaired fasting
glucose or impaired glucose tolerance or insulin resistance with normal glucose plus
two of the following: (1) high triglicerides and low high-density lipoprotein (HDL),
(2) obesity or central fat distribution, (3) microalbuminuria.
In 2002 the American Association of Clinical Endocrinologists (AACE) and its
scientific arm (ACE) gathered several of their leaders in the field of insulin resis-
tance (including Dr. Reaven) in Washington, D.C. The result of this conference (ACE
position statement) was published in 2003 and included the following disclaimer:
“The research, diagnosis and treatment of IRS is rapidly evolving and we expect
changes in definitions and understanding as new evidence is presented. With regards
to this evolution, ACE and AACE hope that healthy debate will not be misconstrued
as fractious controversy.” The controversy continues to this day.
Commenting on insulin resistance and the metabolic syndrome, the American
College of Endocrinology explained that the insulin resistance syndrome concept
was designed to help physicians predict, prevent, and treat conditions such as car-
diovascular disease, diabetes, fatty liver, polycystic ovary syndrome, and certain
cancers. Metabolic abnormalities are more likely to occur in individuals who are

insulin resistant. In addition, it has been argued that the term metabolic syndrome is
vague and unclear and that, unlike the term insulin resistance syndrome, it does not
imply an underlying pathophysiology relationship among the factors in that cluster,
but only an association. The arguments for and against these two names appear to be
purely academic. The term metabolic syndrome seems to be a more practical con-
struct and the term insulin resistance syndrome more academically demanding.
The major opinion seems to adhere to the concept of the metabolic syndrome as
a powerful unifying hypothesis of the metabolic factors underlying the development
of both atherosclerotic cardiovascular disease and diabetes; a minority opinion holds
that insulin resistance alone is the fundamental feature. Other clinical elements may
stem from this metabolic defect. In actual practice, much of this apparent difference
may simply be one of emphasis (see Grundy 2005).
The clause on insulin resistance made by the WHO was unattractive criteria and
was not included in the National Cholesterol Education Program’s Adult Treatment
Panel III (NCEP-ATP III), which settled for: abdominal obesity + dyslipidemia +
hypertension + increased plasma fasting blood glucose.
An Italian study using both the World Health Organization and ATP III criteria
for metabolic syndrome (the Bruneck study) found that both definitions identified
subjects at greater cardiovascular risk and that neither was superior in predicting
cardiovascular risk.
In summary, the metabolic syndrome is an evolving construct. It is less demand-
ing and more inclusive than the insulin resistance syndrome. It does not predict
cardiovascular risk as well as some of its individual components, such as diabetes
type 2, insulin resistance, dyslipidemia, and hypertension. Furthermore, it is inferior
to the Framingham score in predicting overall risk (among other things because the
metabolic syndrome does not include age and smoking), but it draws attention to
several abnormalities that cluster around central obesity, such as:
• Insulin resistance
• Abnormal fasting glucose
• Abnormal glucose tolerance
• Diabetes type 2
• High triglycerides/low HDL
• Hypertension
There are several others, such as:
• Mitochondrial dysfunction
• Increased production of reactive oxygen species
• Increased fatty deposition in organs, including liver (fatty liver disease),
and muscle
• Hyperuricemia or hypyeruricosuria
• Microalbuminuria
• Prothrombotic state
• Rennin-angiotensin activation

Obesity 107
• Autonomic dysfunction
• Obesity-related growth hormone impairment
• Excessive production of cortisol-related products in the adipose tissue
• Abnormal cytokine production by adipose tissue and adipose tissue
macrophages
• Up-regulation of NF-KB
• Increased inflammatory burden usually translated as high CRP levels
The metabolic syndrome develops from the interaction between metabolic sus-
ceptibility and predisposing/precipitating factors of which the most common is
a hypercaloric Western diet high in processed carbohydrates and saturated fats,
especially when combined with decreased physical activity. Obesity in individuals
susceptible to insulin resistance leads to the insulin resistance syndrome; however,
in addition to the identified metabolic abnormalities caused by insulin resistance,
there are other biological consequences of obesity, such as adipokines, abnormali-
ties, and an increased inflammatory burden.
The benefit of an expanded understanding of the metabolic syndrome is greater
awareness of the possibility of the multiple pathogenesis that could lead to disease,
organ impairment, and possibly death. The concept of the metabolic syndrome does
not replace the concept of the insulin resistance syndrome but rather complements it.
The therapy of insulin resistance includes medications that lower insulin resistance,
but the therapy of the metabolic syndrome includes medications for insulin resis-
tance plus a variety of other medicines. These other medications address the other
problems associated with it, such as medicines to decrease inflammation, improve
autonomic function, reduce appetite, induce weight loss, improve mitochondrial
function, increase energy expenditure, etc.
It is very unlikely that a single therapy will cure obesity. The survival value of
storing energy is such that the body has many ways of “protecting” us against weight
loss. Therefore, the therapy of obesity should be multifactorial. It is not enough to tell
the patient to eat less and exercise more; in addition, we need:
• To identify the total daily energy expenditure and the number of daily calo-
ries that would cause a weight loss of 1–2 lb per week
• A diet prescription high in fruits and vegetables that will provide the above
number of calories while avoiding hunger, improve carbohydrate metabo-
lism, and reduce cardiovascular risk
• A cognitive-behavioral therapy program to change the patient’s faulty think-
ing and unhealthy behaviors and habits that sabotage efforts to lose weight
• Increased daily activity
• Exercise
• Pharmacological interventions to address a variety of problems, such as:
• Excessive appetite
• Food addiction
• Depression
• Low metabolic rates

• Mitochondrial dysfunction
• Insulin resistance
• Dyslipidemia
• Hypertension
• Dysautonomia
• In selected populations, bariatric surgery
Management
Eating behavior is critical for permanent weight loss. The entry of food in the gastro-
intestinal tract stimulates vagal receptors, inhibits the production of ghrelin by the
stomach, and increases the production of several intestinal peptides that act as a neg-
ative feedback to stop eating. Hormones and cytokines produced by adipose tissue
and other peripheral organs not only modulate feeding but also influence energy
expenditure. The neurons that integrate the homeostatic signals that regulate appetite
and eating behavior are located in the hypothalamus and brainstem; however, eating
behavior is also influenced by factors other than energy needs.
Hunger and “liking to eat” are different but closely linked. Hunger is physiologi-
cally driven by the biologic homeostatic mechanisms that regulate energy consumption
and expenditure; eating because we like to eat is mediated by different neurological
pathways and has different neurotransmitters. However, they are also linked to the
appetite centers of the hypothalamus and brainstem. Visual smell and taste signals,
the environment where we eat, the expectations we have in regards to the taste of
food, and even the quality of the tablecloth and plates we use influence appetite.
Taste receptors convey taste information to the brainstem (nucleus of the tractus
solitarius and the parabrachial nucleus). Taste signals then convey this information
to the thalamus and from there to the frontal cerebral cortex, amygdala, and lat-
eral hypothalamus. The tongue provides information regarding texture and the five
basic elements of taste: sweet, salt, bitter, sour, and the delicious taste of glutamate.
Although we have no taste receptor for fat, fat tastes very good—not because of the
taste of fat itself (pure fat is insipid) but rather because of its silky texture and prob-
ably its water-repellent properties. These properties concentrate the elements of taste
in the aqueous solution of saliva.
However, what really differentiates fine dining from simple eating is not only but-
ter but also aromas. The olfactory sense has an artistic flair that the tongue does not
understand. The nose has about 350 different receptors and can detect thousands of
different smells. When we eat—especially when we eat warm food—the warm air of
the oral cavity rises to the back of the nose and then we sense the aromatic smells of
fish and meat, the different spices with which we embellished them, and all the other
flourishes of flavor of the culinary art.
The experience of eating is a lot more than the actual taste and olfactory sensa-
tions. The electrons emanating from the tongue and nose do not create the experi-
ence of taste; rather, it is the pattern the brain creates with them and their relations
to other patterns. Taste begins in the food we eat; the rest is imagined and invented.
A good deal of appetite is driven by pleasure. It is hedonic and this is the hedonistic

Obesity 109
aspect of appetite, mediated by the same neurotransmitters that give us most of other
pleasures: opiates and dopamine.
The restaurant industry understood the principles regulating the hedonic aspect of
appetite hundreds of years before neurophysiologists and psychologists were able to
discern it. Good taste is largely dependent on context, the decorations, the fine china,
the presentation of the waiter, and even the name of the food—pate de foie gras
tastes better than Strasbourgh pie (as it was formerly known), which in turn tastes
better than goose’s liver; filet de boeuf en croute tastes better than “meat covered
with mushrooms.” If we bottle plain wine in two different bottles—a very expensive
bottle of Bordeaux wine and a bottle of a vulgar table wine—and ask experts who
have been blinded to these facts (and believe that they are tasting different wines) to
compare the taste of wine from each bottle, they are more likely to “taste and smell”
the woody, complex, and well balanced taste associated with expensive Bordeaux
wines in the wine that was expensively bottled and “identify” the weaknesses and
faults associated with cheap wines in the other. What we expect to taste in something
partially determines its taste.
The subjective contribution to appetite is strong—sometimes stronger than the
objective homeostatic signals. This is why we continue to eat when we are not hun-
gry anymore. We eat when we are depressed, when we are bored, and when we just
want to feel good because the emotions associated with food and the ideas and the
cultural context associated with food give us pleasure and make us feel better.
Psychotropic drugs affect feeding behavior. Naloxone, an opiate inhibitor, not
only enhances the anorectic effect of CCK but also decreases the cravings of the
addict, including food addicts, because it reduces the endorphin release trigger by
food and thus reduces the hedonic aspect of appetite. Dopaminergic drugs decrease
appetite by activating dopamine neurons in the mesolimbic pathways and thus
inhibit the motivation to eat in order to obtain the dopamine “reward” provided
by eating—another aspect of the hedonic pattern of appetite regulation. Serotonin
enhancers such as selective serotonin reuptake inhibitors (SSRIs) suppress dop-
aminergic pathways; however, they also activate melanocortin-4 receptors, blunt
emotions, and curb obsessive thinking—all of which are associated with decreased
appetite. Unfortunately, the strongest serotonin enhancers, which are also the stron-
gest appetite suppressants, reduce motivation, blunt affect, and, in some patients,
decrease sexual desire, arousal, and orgasm.
More important than psychotropic medications are behavioral and cognitive inter-
ventions to change the cognitive context, the faulty thinking, and the self-defeating
behaviors of the overweight and obese. A weight loss plan is destined to fail unless
the subject is able to motivate himself or herself daily; masters behavioral strate-
gies for behavior change, especially during difficult times; and changes the faulty
thinking that drives the negative emotions and inappropriate behaviors that sabotage
weight loss efforts—specifically, efforts to diet and exercise.
Weight loss requires the following:
• Identification of the number of daily dietary calories that cause a weight

loss of 1–2 lb per week. This is usually an amount equal to the REE. It is
best to measure it, but if this is not possible, the REE can be approximated

by multiplying ideal weight in pounds (not the weight that the patient wants,
but rather the weight associated with a BMI of 23) by 10. For example, a
person with an ideal weight of 124 lb has an REE of 124 × 10, or 1,240
calories per day. A diet of 1,240 calories will cause a weight loss of 1 lb per
week; exercise would help to accelerate and, most importantly, maintain
the weight loss and lean body mass.
• A diet prescription that will provide a number of calories equal to the REE
while avoiding hunger. It is impossible to battle hunger, an implacable
enemy that, in the long run, will always frustrate efforts to lose weight.
There is only one way to eat fewer calories while avoiding hunger: to eat
foods that are bulky and low in calories. Advice such as “what you eat is
not as important as the size of the portions” and “eat less but eat frequently”
is misguided. Patients need to differentiate eating because they are hungry
from eating in order to satisfy psychological needs. The first is only satisfied
by eating; the second can be manipulated with medications and cognitive-
behavioral therapy. It is important that subjects eat when they are hungry
to satisfy the hunger stimulus; the only way to do it without gaining weight
is to eat more vegetables and fruits, less oils and fats, and fewer sweets and
processed carbohydrates. We have known this for a very long time—since
the days when Hippocrates was teaching medicine—and yet we continue
to ignore it. There are no better foods than vegetables and fruits to increase
fiber in the diet and add bulk for satiety.
• A prescription to increase the number of daily activities above the seden-
tary level coupled with daily exercise in such a way that, when combined,
the subject “burns” approximately 500 calories daily. Daily activities can
be increased by always parking far from the driving destination, walking
the whole mall or supermarket before making a purchase, walking when
answering the phone rather than taking the call sitting down, etc. The sim-
plest form of exercise is walking, but any activity that engages large muscles
continuously counts. This includes dancing, as well as bicycling or using a
manual wheelchair rather than an electric one, for a few hours every day.
This is not easy but there is no way around it.
What we know indicates that obesity can occur as the result of one or more factors:
• Genetic
• Metabolic
• Cultural
• Racial
• Socioeconomic
• Seasonal
• Psychological
In a recent study of 540 Danish subjects, a strong correlation was found between the
BMI of the subjects and the BMI of the biologic, but not the adoptive, parents, thus

Obesity 111
suggesting that genetic factors are more important than environmental factors in the
pathogenesis of obesity.
As Americans grow larger, the ideal image for female beauty has become increas-
ingly lean. Our beauty queens and fashion models are considerably thinner than they
were in the past. The result of this dichotomy is an increasing dissatisfaction with
how we look. Psychological problems are common in obese subjects; however, the
emotional problems faced by the obese are likely to be secondary to cultural biases
against the obese and the patient’s preoccupation with his or her image rather than
intrinsic psychological problems. Two well-recognized psychiatric conditions could
lead to obesity: bulimia and depression.
Some patients may suffer from a condition characterized by depression and weight
gain during the fall and winter seasons. These patients have shown a tendency to
crave carbohydrates, overeat, and gain weight during the fall and winter months. The
condition called seasonal affective disorder (SAD) improves when the exposure to
sunlight is increased. Exposure to 2 hours of bright light (2500 lux) between 6 a.m.
and 2 p.m. improves depression and reduces carbohydrate cravings within 2–4 days
of the initiation of treatment. Unfortunately, symptoms recur within 2–4 days after
cessation. Exercising outdoors combines the benefits of increased energy expendi-
ture and exposure to bright light.
The pathogenesis of depression associated with carbohydrate craving is not clear,
but it appears that it involves neurotransmitters including serotonin. Medications
used to treat depression include drugs that either stimulate or inhibit serotonin activ-
ity. They have opposite effects on appetite and weight control. Medications such
as amitriptyline, chlorpromazine, and lithium reduce serotoninergic neurotransmis-
sion. These drugs increase appetite and cause weight gain. Drugs such as fluoxetine
enhance serotoninergic neurotransmission, decrease appetite, and cause weight loss.
In addition, the antidepressants that inhibit serotonin reuptake and serotonin recep-
tor stimulants increase serotonin levels, resulting in a reduction in carbohydrate
cravings and weight loss.
The relationship between depression and carbohydrate craving has led some to
speculate that frequent carbohydrate snacking causes pleasure because it relieves the
discomfort of a decreased serotonin activity. This is the alleged mechanism of action
behind the “nocturnal eating syndrome,” where patients with this problem suffer
from mild depression and eat more than 50% of daily calories at the end of the day
(at dinner and before going to bed). The proposed pathophysiology is an increased
need for serotonin as the brain prepares to sleep and the recommended therapy is
serotonin enhancers. This syndrome should not be confused with sleep eating—a
parasomnia related to sleep-walking. The role of food as a mood-altering substance
requires further study.
The ingestion of food has important hedonic effects mediated by the release of
endorphins and dopamine in the hypothalamus and amygdala and can be decreased
with endorphin antagonists (such as naltrexone) and dopamine enhancers such as
Bupropion. The effect of caffeine, β-stimulants, and nicotine in appetite regulation
and its role in the therapy of obesity require further study.

Since the cause of obesity is multifactorial, any form of therapy should consider
the person as a whole and address the different factors that are responsible for the
condition of obesity in any given individual. Behavioral, social, and cultural factors
require proper attention. Depression should be aggressively treated. If an antidepres-
sant is needed, serotoninergic or dopaminergic agents can be prescribed. Medications
that contribute to obesity, such as β-blockers, corticosteroids, certain antipsychotics,
and phenothiazines–antidepressants should be removed if at all possible.
Mitochondrial dysfunction is commonly seen in the insulin-resistant obese;
whether this is the cause or effect of insulin resistance remains debatable. However,
it precedes obesity and is commonly found in the pre-obese first-degree relatives of
subjects with type 2 diabetes. Patients with this problem have a decreased number
of mitochondria in the liver and muscle coupled with a decreased amount of mito-
chondrial enzymes; they exhibit a decrease in mitochondrial oxidation, coupled with
an increase in anabolism of cellular glycosylated products; an increased dependency
for glucose utilization in the cytoplasm; an increase in the amount of intracellular
triglycerides and ceramides; and a decrease in the resting energy expenditure and
maximal aerobic exercise capacity. The best treatment for this condition is exercise,
which single-handedly corrects all of these problems.
Diets continue to be the most popular form of treatment for obesity even
though the evidence against their efficacy is abundant. The maximum weight
loss of patients participating in various diet studies is 8.5% of their entrance
weight, but the majority of those patients regain some or all of the weight lost,
and many report weight gain within the next 2 years. Dietary treatments for
obesity result in a recidivism rate of 70–95%. This lack of success stems
mainly from an unclear understanding of the mechanisms that cause obesity and
a simplistic approach to therapy. Any diet that forces the patient to be hungry is
destined to fail.
Dietary manipulations that allow the subject to eat to satiety are best. This can
be achieved with a variation in the U.S. Department of Agriculture’s food guide
pyramid by increasing the consumption of fruits and vegetables, decreasing the con-
sumption of carbohydrates, and eliminating hypercaloric processed foods as much
as possible. The original food guide pyramid recommendation of 6–11 servings
of carbohydrates could result in weight gain. Increasing the amount of nondigest-
ible fiber in fruits and vegetables makes it difficult to overeat. Furthermore, fruits
and vegetables are high in all kinds of antioxidants and vitamins. Unfortunately,
many vegetables and carbohydrates are eaten with oil-rich dressings; this practice
should be avoided.
We recommend that first-line treatment for obesity be dietary modification and
exercise, followed by weight-reduction medications only when the patient is unable
to lose weight and still needs to lose additional weight to reduce health risks. Many
weight loss plateaus can be overcome by increasing the lean muscle mass via weight-
training programs. Obese, healthy patients who exercise and do not have a major risk
factor for heart disease are at no greater risk than individuals of normal body weight.
Unfortunately, the majority of obese individuals do not exercise and have more than
one major risk factor for heart disease.

Obesity 113
For permanent weight loss, energy intake should be restricted to accomplish a

gradual weight loss of no more than 2.0 lb/week coupled with an exercise program.
This will allow preservation of the REE and may increase or at least maintain lean
body mass. Recommended guidelines for adult weight loss programs should incor-
porate the following:
• Include food palatable to the patient and within the patient’s sociocul-
tural background.
• Provide a negative dietary caloric balance not to exceed 500–1,000 calo-
ries daily.
• Include behavior modification and cognitive therapy techniques.
• Encourage eating habits that can be maintained for life.
• Exercise and increase daily activities to expend a minimum of 500 calo-
ries daily.
Exercise Issues
Obese subjects lose weight when they exercise; lean subjects do not. Lean indi-
viduals regulate their caloric intake according to their activity—the higher the
energy expenditure is, the greater the energy consumption is. Obese subjects do
not increase caloric intake in direct proportion to their energy expenditure. A
very low-calorie diet without exercise can lead to the loss of lean tissue, which
is metabolically active tissue and important for maintenance of the REE. A low-
calorie diet, in combination with an exercise program, preserves lean tissue and
increases energy consumption and the weight loss it causes consists primarily of
adipose tissue.
The rationale for prescribing exercise in moderately obese individuals is fivefold:
• Biochemical changes in the skeletal muscles that result from exercise include
increases in the activity of mitochondrial enzymes, capillary density, and
the number and density of mitochondria. Fat oxidation and oxygen deliv-
ery are enhanced during submaximal exercise. These changes are mostly
apparent in the slow-twitch or red fibers that have the highest capacity for
oxidative metabolism.
• Physical activity in obese individuals improves the metabolism of glucose,
insulin, and lipids.
• Exercise can result in an increase in muscle mass and energy expenditure.
There is a high correlation between lean body weight and caloric expendi-
ture. The energy expenditure during exercise is related to the intensity and
duration of the activity; however, obese individuals should be instructed
to exercise at a comfortable intensity that emphasizes duration and fre-
quency of exercise. It is the volume of exercise (i.e., duration, intensity,
and frequency) performed that accounts for total caloric expenditure.
A relative perceived exertion (RPE) of no greater than 14 is recommended
(see Appendix A, Method 5). Other methods using target heart rate to pre-
scribe exercise can also be applied (see Appendix A).

• Exercise will reduce body fat. Studies investigating the effects of physical
activity on moderately obese individuals have reported decreases in body
weight between 2.6 and 14.3 kg, most of which was body fat. The reduction
in body fat is mainly due to a decrease in the size of individual fat cells.
• Exercise can depress food consumption in the obese; high-intensity exercise
has the greatest effect.
It is difficult to report on the effects of physical activity and diet because a

review of the literature reveals a wide variety of experimental protocols, such as
diversity within the obese individuals and varying activity modalities, intensities,
durations, and frequencies. It is generally agreed that physical training should be
performed daily for an extended duration to maximize caloric expenditure. A mini-
mum goal of 300–500 kcal should be expended during each exercise session, total-
ing 2100–3500 kcal/week.
WEIGHT TRAINING GUIDELINES FOR OBESITY

When patients who are obese undergo weight training, secondary risk factors associ-
ated with obesity are of the utmost concern. Patients with uncontrolled hypertension
(systolic ≥ 160 mmHg or diastolic ≥ 100 mmHg), brittle diabetes, or heart disease
should avoid weight training until they are cleared by their physician. Other con-
traindications to weight training include

frequent repetitions is recommended. Circuit training involves moving from exer-
cise to exercise at a consistent pace. This will develop muscle endurance and
strength. To control blood pressure and prevent the elevation of after-loads on the
heart, isometric or static components should be minimized when the weight-lifting
exercise is performed by breathing on exertion and using a weight that can be lifted
without stopping halfway through the motion. Weight lifting has been reported to
minimize the loss of lean body mass during caloric restriction, thereby maintaining
metabolic rates.
join a gym or fitness center. Exercises that can be performed at home and guidelines
for patients are illustrated in the weight loss workbook CD.

Obesity 115

[100 – (# reps × 2.5)] = % 1RM

weights and stretch elastic bands.
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Appleyard, S. M. 2003. A role for the endogenous opioid beta-endorphin in energy homeosta-
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EXERCISE PRESCRIPTION FOR OBESITY

Frequency
Exercise a minimum of five times per week, preferably daily.
Modality
Activities that have a low isometric or strenuous component and work
the large muscles are recommended. Walking is an excellent modal-
ity because it does not require any special equipment. Stationary or
active bike riding and swimming are also acceptable aerobic activities,
especially if the patient has joint problems. Try combining different
modalities during the exercise session. Weight training is recom-
mended to prevent the loss of muscle tissue and maintain the rest-
ing metabolic rate.
Duration
Begin with a time that is comfortable—perhaps 10 minutes. Gradually

Obesity 117
Intensity
chart in Appendix A, Method 5. A perceived exertion between very
light and hard, an RPE of 10–14, is recommended. When weight train-
ing is undertaken, use a weight that can comfortably be handled for
10–15 repetitions. Do one to two sets for each muscle group. See the
information on weight loss workbook CD for further instructions.
Other Instructions
• Patients should avoid exercising during the hottest part of the day.
pain immediately.
follow-up visit.
COMMON QUESTIONS ON OBESITY (A PATIENT’S PERSPECTIVE)

Question: What is ideal body weight (IBW)?
Answer: Ideal body weight represents a body weight that is a healthy weight
for you. It is usually calculated at your doctor’s office using a height and
weight chart; however, there are more accurate methods available to deter-
mine your ideal body weight. When your IBW is about 20% above the
recommended value, or 120%, your risk for certain diseases such as heart
disease, hypertension, and diabetes increases.
Question: How, exactly, is IBW calculated?
Answer: There are several methods used to calculate IBW. The method men-
tioned before uses a weight-to-height table and takes your age and body
frame size into account. Although this method is fast and inexpensive, it
does not consider the amount of lean mass or muscle tissue you may have.
This is important because muscle weighs more than fat, and if you are very
athletic and muscular, it may cause you to exceed your IBW recommenda-
tion when using a table. A person can be overweight without being overly
fat and therefore not be at a greater risk for disease. Methods that account
for lean mass are hydrostatic or underwater weighing and the “skin-fold
technique,” which measures pinches of skin.
Question: How can I lose weight and achieve my ideal body weight?
Answer: The first step in weight loss is setting a realistic goal. A maximum
weight loss goal of 2 lb per week accompanied by an exercise program is
recommended. By adding exercise to your weight loss program, you will
increase your chances of keeping the weight off. If your weekly weight
loss exceeds 2 lb per week, the additional weight lost is usually water and

lean body mass or muscle tissue. Exercising while you are on a weight loss
program will help to prevent the loss of muscle tissue. This will keep your
metabolic rate (the rate at which you burn calories) throughout the day at a
higher level, adding to your chances for success.
Question: Are there any medications that can help me lose weight?
Answer: Yes, there are several medications that can assist in weight loss. The
anorectic medications can be used as an adjunct to therapy; however, they
are only approved for short-term use.
Question: How should I balance my diet to get all the nutrients I need?
Answer: Ask your health care provider to recommend that a registered dieti-
tian meet with you. The dietician will develop a weight loss plan that is low
in calories and manageable for your lifestyle. It should include foods that
are tasty and low in fat. Emphasis should be placed on fruits, vegetables,
and carbohydrates (breads and grains).
Question: Why is it that I eat the same things that other people eat and yet I
gain weight and they do not?
Answer: Many factors contribute to obesity, such as genetics, cultural and
social influences, and psychological stressors. It is true that some individu-
als are blessed with a fast metabolism and can eat more food than the aver-
age person and not gain weight. However, the most common explanation
for obesity is simply that more calories are being consumed than needed or
expended. Those “other people” are probably eating less than they seem to
be or you are eating more calories than you realize.
Question: Do I need to exercise; if so, how much should I exercise?
Answer: Yes! Exercise is the key factor. Exercise helps you to maintain your
muscle mass, and that is important to maintain your metabolic rate. You
should try to exercise at least five times a week and burn between 300 and
500 calories during each session. By following the guidelines in the weight
loss workbook, you will burn about 1,500 calories per week from exercise. A
pound of fat contains 3,500 calories, but remember that you are also reducing
your caloric intake. Your goal should be to lose no more than 2 lb per week.
Question: What type of exercise is good?
Answer: Follow the recommendations in the weight loss workbook. Pick a
modality you enjoy doing and will maintain. Pick an aerobic exercise that
involves large muscle groups and is challenging to your heart. Examples
are walking, swimming, and cycling. Do weight training to maintain your
muscle mass.
Question: Once I lose weight, how do I keep from gaining it back?
Answer: Change your current eating behaviors by emphasizing a healthy diet
and an exercise plan. Studies report that adherence to a simple exercise
program will drastically increase your chances for success.
Question: Why is it so important to achieve and maintain my IBW?
Answer: Obesity increases the risk for many diseases, including high blood
pressure, stroke, heart attack, diabetes, sleep apnea, and osteoarthritis. By
losing weight, you decrease the relative risk for developing these diseases.
Even a modest weight loss will alleviate problems associated with obesity.

7 Vascular Disease
BACKGROUND
The subjects of this chapter are arteriosclerosis and atherosclerosis. The first is also
known as arteriosclerotic vascular disease (ASVD) and the second refers to the pro-
cess of atheroma formation within the walls of arteries. These two concepts are
related and common usage has made them synonymous. Arteriosclerosis, from the
Greek words arteria (artery) and sklerosis (hardening), obviously means hardening
of the arteries; atherosclerosis specifies hardening of the arteries due to the presence
of atheromas, from the Greek athere (porridge or gruel) and oma (inside). The most
common cause of vascular disease is atherosclerosis.
Atherosclerosis begins at an early age and progresses slowly and silently until the
blood supply to the organs or the affected artery becomes insufficient to meet
the demands of the tissues it feeds, and symptoms arise. Very often the first symptom
of atherosclerosis is a sudden event: A vulnerable plaque ruptures, causing the forma-
tion of a thrombus and the blood flow stops. In the absence of collateral circulation,
an acute thrombotic event leads to death of the tissue that the artery serves. In 65% of
men and 47% of women, the first symptom of coronary atherosclerosis is myocardial
infarction or sudden cardiac death. The rest, or approximately 50% of patients with
significant coronary artery disease (CAD), suffer from chest pain caused by activity
and relieved by rest (angina) prior to the acute event. This is also the case in patients
with atherosclerotic cerebral-vascular disease (CVD). Stroke symptoms typically
start suddenly, over seconds or minutes, and progress rapidly.
The sudden onset and progression, without premonitory symptoms, make CAD
and CVD the most dramatic and probably important of all vascular diseases, but these
conditions do not exist in isolation. A patient with vascular disease in the arteries of
the heart or the brain may also have vascular disease in the periphery. Patients with
peripheral vascular disease (PVD) experience muscle pain caused by exercise relieved
by rest (claudication). This is more common in the lower than the upper extremities.
Atherosclerosis also coexists in the arteries of the gastrointestinal tract, kidneys, and all
others; therefore, the study of the pathogenesis and treatment of atherosclerosis applies
to the pathogenesis and treatment of all arteriosclerotic vascular diseases (ASVDs).
Many infarctions involve very small arteries and are asymptomatic, leaving only
a scar that might be detected in imaging techniques of the heart, brain, kidney, or
other organs. Repeated small infarcts lead to progressive dysfunction without the
classical symptoms of infarction leading to ischemic cardiomyopathy, cerebral-
vascular dementia, or progressive renal failure.
119
Cardiac stress testing can detect the presence of CAD when the amount of disease
is advanced enough; there is no similar test to explore the possibility of cerebrovas-
cular, renal, or intestinal vascular disease. Approximately 10% of the population
over the age of 70 has intermittent claudication. Claudication may be defined as “the
inadequate delivery of oxygen to the muscles, resulting in pain.” Currently, the exact
number of individuals with PVD is not known; however, it has been estimated that
2.6 per 1,000 men and 1.1 per 1,000 women are affected with it. Furthermore, 25%
of all patients with coronary artery disease have concomitant PVD.
From the inside out, the layers of an artery include the endothelium, the tunica
intima, the tunica media, and the tunica adventitia. The intima is made of endothe-
lial cells on top of a thin layer of elastic subendothelial connective tissue called the
internal elastic lamina. The media is made of connective tissue and smooth muscle
surrounded by a thick elastic band called the external elastic lamina; the adventitia,
the outer layer, is made of connective tissue and contains small vessels (vasa vaso-
rum) and nerves.
Atherosclerosis often begins in childhood with lipid deposits within the intima,
just under the endothelium. At first, the process is visible only under the microscope;
the intima appears thickened with an increase in the amount of extracellular matrix
(collagen) and the presence of a few smooth muscle cells and macrophages. As the
process continues, a fatty streak becomes visible to the naked eye.
As the fatty streak advances, more muscle cells migrate from the media. The
number of white cells and amount of extracellular matrix increase and a fibrous cap
is formed under the endothelium covering the atherosclerotic process until the fatty
streak has evolved into a fibrous plaque.
The smooth muscle cells and white cells within the fibrous plaque are prone to an
early death (increased apoptosis). Their dead bodies degenerate and cause increased
migration of macrophages to clean the field (increasing the amount of inflamma-
tion) and a greater migration of smooth muscle cells eventually. The combination of
necrosis and lipids forms a necrotic lipid-rich core within the arterial wall; vessels
from the adventitia grow into the media and the plaque is now said to be advanced.
As time goes by, calcium is deposited within the necrotic lipid-rich core. Those cal-
cifications will eventually show up macroscopically as whitish deposits and in radio-
logical images.
Arteries with advanced lesions remodel when the external elastic lamina expands
the size of the lumen. When it is relatively preserved, the process is called positive
remodeling; when the external elastic lamina shrinks, the process is called nega-
tive remodeling. Positive remodeling is thought to be a compensatory process that,
unfortunately, often leads to the formation of aneurisms.
PATHOGENESIS
Endothelial dysfunction and dyslipidemia are the most important risk factors for
atherosclerosis. Endothelial dysfunction is the initial step; it is often caused by dys-
lipidemia but it can exist on its own. It is often associated with insulin resistance and
has been documented in young family members of patients with atherosclerosis in
the absence of other comorbidities.

Vascular Disease 121
The vascular endothelium produces nitric oxide (NO), a potent vasodilator with a very
short life span (≤5 seconds). It is currently impossible to assess NO in vivo; therefore, the
techniques used to study endothelial dysfunction rely on documentation of the vasodilat-
ing action of NO. For example, changes in blood flow of a limb following the admin-
istration of a stimulus that increases NO, such as insulin, acetylcholine, or poststress
vasodilation induced by inflating and deflating a blood pressure cuff. The term endothe-
lial dysfunction is thus synonymous with the term impaired vascular reactivity.
Family history (genetic factors) is the single most important cause of endothelial
dysfunction. Impaired vascular reactivity has been documented in normal, young, first-
degree relatives of subjects with coronary artery disease and subjects with type 2 diabe-
tes (and no other risk factors). Dyslipidemia can cause endothelial dysfunction and, when
combined with a positive family history, it compounds the risk of atherosclerosis.
There is nothing we can do about our family history. Likewise, other risk factors,
such as gender, for atherosclerosis are beyond our control. Males are more likely to
suffer from atherosclerosis than females. However, as in many other diseases, genes
are not destiny. Family history and male gender predispose to atherosclerosis, but
there are many others precipitating and aggravating factors that can be prevented,
decreased, or eliminated, as shown in Table 7.1.
Among risk factors, the most important ones are chronic cigarette smoking,
hypertension, insulin resistance, obesity, and a sedentary lifestyle. Those risk fac-
tors feed each other, compounding the risk. For example, insulin resistance is made
worse by a sedentary lifestyle, and both lead to obesity, hyperglycemia, high tri
glycerides and low high-density lipoprotein (HDL) levels, and hypertension. Obesity
leads to sleep apnea, which leads to fragmented sleep and hypertension, but cigarette
smoking alone increases the risk of atherosclerosis by 200%. The combination of
risk factors increases the risk exponentially; two risk factors increase the risk by
400% and three risk factors by 700%.
TABLE 7.1
Risk Factors for Atherosclerosis
Modifiable Risk Factor Unmodifiable Risk Factor
Insulin resistance Aging
Hyperglycemia Male gender
High LDL levels Family history of diabetes type 2
Low HDL levels Family history of CAD
LDL/HDL > 3:1 Family history of CVD
High triglycerides levels Family history of PVD
Cigarette smoking Familial hypercholesterolemia
Hypertension
Abdominal (central) obesity
High inflammatory burden
High homocysteine levels
Hypothyroidism
Insufficient or fragmented sleep
Sedentary lifestyle

Recent research has illuminated the mechanism by which insulin resistance con-
tributes to endothelial dysfunction. The traditional concept of insulin resistance is a
decreased sensitivity to the metabolic effect of insulin; however, insulin has actions
other than metabolic ones—among them the regulation of NO and endothelin pro-
duction by the endothelium, the stimulation of several arterial tissue growth factors,
and the promotion of atherosclerotic mediators. The binding of insulin to its cellular
receptor triggers the phosphorylation and activation of two cellular pathways; one
of them, the phosphatidylinositol 3-kinase (PI 3-kinase) branch of insulin signaling,
leads to NO production in the endothelium (promoting vasodilatation). PI 3-kinase
activation is also responsible for the metabolic effects of insulin and causes GLUT-4
translocation and glucose uptake by the muscle and other cells.
The other pathway, the mitogen-activated protein kinase (MAP-kinase) branch of
insulin signaling, regulates endothelial growth, mitogenesis, and the expression of sev-
eral atherosclerosis mediators such as plasminogen activator inhibitor type-1 (PAI-1), cel-
lular adhesion molecules (ICAM and VCAM), E-selectin, and increased synthesis of the
vasoconstrictor endothelin. There is normally a balance between arterial vasodilatation
mediated by NO and prostacyclines and arterial vasoconstriction mediated by endothe-
lin (the most potent vasoconstrictor). However, resistance to insulin in the metabolic
pathway (PI 3-kinase) may cause hyperinsulinemia and increased MAP-kinase signal-
ing, disrupting the balance in favor of vasoconstriction and endothelial dysfunction.
The abnormal endothelial function resulting from a decrease in NO synthesis and
an increase in MAP-kinase activity results in a greater endothelial permeability to low-
density lipoprotein (LDL), a plasma protein that carries cholesterol and triglycerides.
Several endothelial enzymes, along with endothelial free radicals, oxidize the free
fatty acids released from cholesterol and triglycerides; it is all downhill from there.
The oxidized fatty acids induce several factors, such as the vascular cell adhesion
molecule-1 (VCAM-1), which recruits circulating macrophages that enter the arte-
rial wall to remove the oxidized LDL and prevent injury. However, what begins as a
protective action to remove oxidized cholesterol changes into a major problem. The
macrophages release inflammatory cytokines, initiating an inflammatory process that
activates another adhesion molecule, the intracellular adhesion molecule-1 (ICAM-1),
and activates P-selectin, a platelet and endothelial receptor that mediates adhesion
between vascular cells, thus promoting a greater influx of macrophages into the artery.
Unfortunately, the macrophages and T-lymphocytes are unable to control the
influx and remove the oxidized cholesterol within the arterial wall. Their lipid con-
tent increases and becomes abnormal (foam cells). Ultimately, they die, releasing
cytokines, proteases, and prothrombotic molecules and inducing mitochondrial dys-
function in the endothelium, migration of smooth muscle from the adjacent tunica
media, blood vessel proliferation from the tunica adventitia, and an increase in the
production of collagen and fibrous tissue with the formation of the fibrous cap that
covers the atherosclerotic plaque.
If the fibrous cap ruptures, blood enters the atheroma and forms clots inside (and
sometimes outside) the arterial wall; the atheromatous plaque grows and the lumen
of the vessel narrows. Bleeding and sudden expansion of the atheromatous plaque
can also be caused by thrombosis of the vasa vasorum, the unstable small vessels
that have grown into the plaque from the adventitia.

Paradoxically, plaque rupture usually occurs in arteries that are not severely nar-
rowed and have a lumen that is ≤50% of the original size. Those vulnerable plaques
have less calcium and less fibrous tissue but more inflammatory activity than their
harder, more stable counterparts. Symptoms begin when the harder arteries narrow
the lumen by 70–80% or when the vulnerable plaque ruptures.
Vascular angiography and other imaging techniques typically identify vessels with
severe narrowing; many of them can be stented or dilated and vascular occlusion can
thus be prevented. However, neither vascular angiography nor any other imaging tech-
nique can predict which of the mildly narrowed vessels will lead to plaque rupture and
acute closing. Most myocardial infarctions, strokes, and other acute vascular events
are caused by plaque ruptures in vessels with a luminal narrowing of 20–50%.
PHARMACOLOGICAL TREATMENT
Pharmacological therapy should address all the risk factors that contribute to athero-
sclerosis. Since no single medication can achieve such a task, combination therapy is
inevitable. The goals of pharmacological therapy are to
• Decrease LDL to <100 mg/dL but, if triglycerides are >200, decrease

LDL to <70 mg/dL; levels should be measured every 6 weeks until goal is
achieved, then every 6 months
• Increase HDL to >40 mg/dL in males and >50 mg/dL in females
• Decrease triglycerides to <150 mg/dL
• Decrease the inflammatory burden
• Decrease hypertension to <120/80 mm Hg or <130/80 in patients with dia-
betes or known vascular or renal diseases
• Promote cigarette abstinence
• Decrease insulin resistance
• Improve diabetes control
• Decrease homocysteine levels to <6.3 μmol/L (0.85 mg/L)
• Treat hypothyroidism
Levels of LDL are increased in patients with atherosclerotic disease and are posi-
tively correlated with its severity. A group of medications whose name ends in statin
(collectively called statins) reduces levels of LDL and mortality. The newest one
(rosuvastatin) has been shown (with ultrasound evaluation) to increase the lumen of
atherosclerotic coronary arteries. In addition to lowering LDL, statins are known to
have antioxidants and anti-inflammatory effects. There have been approximately 15
large studies between the Scandinavian Simvastatin Survival Study (4S) and the Effect
of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis
(ASTEROID) Study. With one exception (the ALLHAT-LLT study of pravastatin vs.
usual care), which reported less favorable results, all of them have shown a mortal-
ity reduction between statin and placebo of 25–30%, except in patients with type 2
diabetes, in whom the benefits were almost twice as large. The 4S study showed a
mortality reduction of 30% overall and 54% for patients with type 2 diabetes.

HDLs increase cholesterol transport away from the arteries and protect endothe-
lial function. There is an inverse relationship between HDL levels and atherosclerotic
cardiovascular risk. The risk of atherosclerosis increases (and decreases) with HDL
levels less (and higher than) 45 mg/dL in men and 55 mg/dL in women. In other
words, the risk ratio for cardiovascular risk is higher than 1 in males and females
with HDL lower than 45 and 55, respectively. It is 1 with levels of 45 and 55, respec-
tively, and lower than 1 with levels higher than 45 and 55, respectively. The relation-
ship is almost linear; for every change of 5 in the HDL above or below 45 and 55 for
males and females, the risk ratio increases or decreases by 0.2. Subjects with very
high HDL levels do not develop atherosclerosis in spite of diets rich in animal fat
(such as the Native Americans of Alaska and Northern Canada) and those individu-
als with HDL levels > 75 mg/dL live much longer than the general population, a
condition referred to as the “longevity syndrome.”
Niacin (vitamin B3) increases the levels of HDL by 10–30%. It also increases
LDL particle size (see later discussion) and has shown clinical benefits; however,
pharmacological doses (available by prescription and over the counter) might have
unpleasant side effects.
The benefits of lowering triglyceride levels are difficult to evaluate because high
triglyceride levels are often associated with low HDL levels; however, a triglyceride
level > 200 mg/dL is thought to be atherogenic. A likely reason why hypertrygliceri
demia is atherogenic is due to the effect of triglyceride levels on LDL particle size;
the higher the triglyceride levels are, the smaller is the LDL particle size, and large
LDL particles are less atherogenic than small ones. It is not the amount of LDL
but rather the number of LDL particles that favors atherosclerosis. Given a certain
amount of LDL, the number of LDL particles is considerably fewer if the LDL par-
ticles are large. Consider two groups of balls, each weighing the same: The group
made of basketballs will have fewer balls than the group made of tennis balls. It is
not difficult to imagine that smaller triglyceride “balls” can more easily squeeze
through the endothelial membrane.
The National Cholesterol Education Program (NCEP) suggests the use of medi-
cations if the triglyceride levels cannot be brought below 200 by diet and exercise
alone. The most effective medications are omega-3 fatty acids, fibrates, statins, and
niacin. Omega-3 fatty acids can lower triglyceride levels by 20–45% and have no
serious side effects.
Markers of inflammation such as C reactive protein (CRP) levels are directly
associated with the risk of atherosclerosis and the formation of vulnerable plaques.
CRP is blood protein manufactured by the liver whose function is to bind to bacte-
ria and dead cells and facilitate complement binding and thus assist phagocytosis.
CRP is manufactured proportionally to the blood levels of interleukin-6 (IL-6), a
cytokine produced by macrophages and enlarged adipocytes. An elevated CRP usu-
ally means elevated IL-6 and, by extension, elevation of all the other inflamma-
tory cytokines such as IL-1 and tumor necrosis factor-alpha (TNF-α). Inflammatory
cytokines increase the risk of atherosclerosis by enhancing the expression of cell sur-
face molecules, such as VCAM and ICAM, inducing proliferation of smooth muscle

and collagen tissue and increasing oxidation injury by increasing the production of
reactive oxygen species.
Arterial macrophages injured by oxidized cholesterol release a variety of inflam-
matory cytokines. Macrophages are also found in adipose tissue surrounding dead
lipocytes arranged in crowns around them (crown formations). These macrophages
are the source of most of the inflammatory cytokines originating in adipose tis-
sue, although large adipocytes, especially those located within central (visceral)
stores, are also known to release inflammatory cytokines (adipokines). Patients with
obstructive sleep apnea (OSA) often demonstrate high CRP levels; it is not clear if
the reason is obesity (increased production of lipokines), insulin resistance (condi-
tions that often coexist with OSA), or increased oxidative injury caused by recurrent
episodes of hypoxemia and reoxygenation following each apnea/hypopnea event.
The most interesting development linking inflammation and atherosclerosis is
the possibility of infection within atherosclerotic plaques. Although we can culture
only very few of the millions of bacteria within our bodies, we know they are there
because we can see their genetic fingerprint. We have assumed that those bacteria
live in the skin, bowel, and mouth—the parts of our bodies that are exposed to the
outside environment.
Testing for bacterial rDNA signatures by polymerase chain reaction in specimens
obtained during atherectomy has revealed the DNA fingerprint of bacteria within
the arterial walls, with a mean of 12 bacteria per lesion. Therefore, bacterial infec-
tion might play an important role in atherosclerosis. More evidence comes from a
variety of studies showing that chronic infections increase the risk of atherosclerotic
disease. Antimicrobial therapy for 1 week in patients admitted with unstable angina
decreased the incidence of myocardial infarction, and the prior use of a quinolone in
patients with type 2 diabetes (for at least 14 days within 3 years prior to the study)
decreased the incidence of hospitalization for coronary artery disease.
Medications such as statins (simvastatin, rosuvastatin, etc.) and glitazones (piogli-
tazone, rosiglitazone, etc.) have anti-inflammatory properties. The antidiabetic effects
of salicylates have been known for a long time; their anti-atherogenic effect has been
attributed to the fact that salicylates decrease platelet adhesiveness. However, there is
a possibility that salicylates, and probably other anti-inflammatory medications such
as xanthines, might have a beneficial effect due to their anti-inflammatory proper-
ties. Although salicylates are useful, blood thinning by other means is not. In 2001,
Price showed that “warfarin-induced artery calcification is accelerated when vita-
min D is added in toxic doses to rats.”
Patients with hypertension have a 60% increased risk of atherosclerosis. Obviously
decreasing hypertension is beneficial, but some medicines are better than others.
Increased plasma levels of angiotensin II increase smooth muscle and collagen pro-
liferation, promoting atherosclerosis. Angiotensin-converting enzyme inhibitors
and angiotensin receptor blockers decrease the negative effects of angiotensin II.
Angiotensin-converting enzyme (ACE) inhibitors protect endothelial function even in
patients who are normotensive, and they are part of the recommended therapy of patients
with diabetes type 2 because their angiotensin blocking has renal protecting effects.

Tobacco is the single greatest source of preventable death in the United States;
contrary to popular belief, the products of tobacco combustion—not nicotine—cause
lung disease and cancer. Nicotine increases the release of dopamine and other adren-
ergic substances and therefore causes an increase in blood pressure and heart rate
and likely plays a role in the pathogenesis of hypertension, stroke, and impotence.
However, its role in the pathogenesis of atherosclerosis is small, if any. Nevertheless,
cigarette smoking increases the risk of atherosclerosis 200%; the reasons are multiple
but the most important is the increased amount of oxidation injury caused by carbon
monoxide. Therefore, nicotine products (such as nicotine patches, nicotine gums, and
electronic cigarettes) and medication that mimics the effects of nicotine in the brain
(such as the dopamine reuptake inhibitor bupropion) are useful because they reduce
the smoking craving of the addict and increase the likelihood of eventual abstinence.
Resistance to the metabolic effects of insulin is caused by a pathway-specific
impairment of the PI3-K system. The compensatory elevation of insulin levels results
in a reciprocal increase in the activity of the MAPK-dependent insulin signaling
pathway. The imbalance between the two systems is atherogenic due to a decrease
in NO production (which is under the domain of the PI3-K signaling system) and an
increase in endothelin-1 levels and growth promotion (which is under the domain of
the MAPK signaling system). Interventions that decrease insulin resistance and lower
insulin levels have an antiatherosclerotic effect. The most important ones are the
insulin sensitizers glitazones and metformin. The first one not only decreases insu-
lin resistance but also has significant anti-inflammatory actions; it decreases CRP
and IL-6 and increases the levels of adiponectin and antiatherosclerotic adipokines.
Metformin also improves insulin resistance and, unlike the glitazones, it is associated
with weight loss and decreased plasma levels of endothelin-1.
Not only insulin resistance but also elevated blood glucose levels have a proathero-
genic effect. Hyperglycemia promotes endothelial dysfunction through endothe-
lial glucotoxicity secondary to the formation of advanced glycation end products
(AGEs), increased activity of the hexosamine biosynthetic pathway, and increased
oxidative stress. The higher traffic through the hexosamine pathway increases the
synthesis of glucosamine, which worsens insulin resistance, and accumulation of
ceramides, which have been linked to cellular dysfunction and early cellular death.
Oxidative injury also worsens insulin resistance by decreasing PI3-K signaling; this
leads to decreased NO production and increased endothelin-1 production, altering
the NO/ENT-1 ratio in favor of atherogenesis.
Homocysteine is an amino acid synthesized from methionine and recycled back
to methionine. Genetic factors are responsible for the elevated homocysteine levels
found in 10% of the population, but deficiencies of folic acid, pyridoxine, and vitamin
B12 can also increase homocysteine levels. Homocystein degrades the function and
structure of arterial proteins, including collagen, elastin, and proteoglycans. High lev-
els of homocysteine are associated with a higher incidence of negative cardiovascular
events such as strokes and myocardial infarction. Therapy with folic acid and vitamin
B6 and B12 lowers homocysteine levels but has not been proven to improve outcomes
except for a reduction in the incidence of strokes, probably because the proteins cor-
rupted by homocysteine remain degraded for life. However, it makes sense to stop this
corrosive process, therapy with folic acid and vitamins B6 and B12 supplementation is

indicated with the goal of lowering homocysteine levels to <6.3 μmol/L (0.85 mg/L) if
possible. High-intensity exercise might increase homocysteine levels in athletes, who
might benefit from diet vitamin supplementation as well.
Hypothyroidism increases cholesterol levels and the risk of atherosclerosis; sub-
clinical hypothyroidism (elevated TSH but normal T4 levels) may increase the risk
of cardiovascular disease. In a meta-analysis, the Cochrane Collaboration found
an improvement in the lipid profile and left ventricular function in patients with
subclinical hypothyroidism and a meta-analysis published in the Annals of Internal
Medicine in June 2008 showed a possible increase in the risk of coronary artery dis-
ease and cardiovascular mortality in patients. Given the evidence, it is advisable to
treat patients with hypothyroidism to decrease the risk of atherosclerotic disease, and
it is probably a good idea to treat those with subclinical hypothyroidism, too, until
there is stronger evidence otherwise.
DIET AND EXERCISE MANAGEMENT

Dietary changes to decrease atherosclerosis include a reduction in the consump-
tion of products rich in cholesterol and saturated fats and an increase in the con-
sumption of fruits and vegetables. In patients with elevated LDL levels, a reduction
of simple sugars, and alcohol in patients with elevated triglycerides. All of these
in insulin-resistant patients, and an adjustment in the consumption of calories to
achieve ideal weight. Pure vegetarian (vegan) diets are controversial because the
internal production of cholesterol increases to compensate for the reduced intake.
Other dietary interventions include increasing the consumption of foods rich in
omega-3 fatty acids such as fish (especially tuna and salmon), flax seeds, raspberry,
canola oil, and pecan and hazel nuts, as well as avoiding processed foods, especially
those with processed fat, which changes the natural cis-fats into atherogenic trans-fats.
Certain dietary supplements might be beneficial: Omega-3 supplements, vita-
mins C, B6, B12, and folic acid have been found to be useful. Contrary to popular
belief, vitamin E has no proven beneficial effects.
Exercise is useful for multiple reasons:
• It helps patients lose weight.

• It is especially important in maintaining weight loss; without exercise,
weight is easily regained.
• It reduces blood pressure.
• It reduces mortality from coronary artery disease.
• It decreases triglycerides.
• It increases HDL.
• It reduces insulin resistance.
• It improves glycemic control in diabetic subjects.
Exercise for patients with atherosclerotic risk factors, such as high blood pressure
and diabetes, and in patients with kidney and coronary artery diseases is covered in
Chapters 1–4. We will now concentrate on the evaluation and treatment of patients
with peripheral vascular disease (PVD).

PERIPHERAL VASCULAR DISEASE

The diagnosis of PVD has been based mainly on the patient’s subjective complaints
of lower leg or calf pain while walking. Diminished palpation of the peripheral pulses
has been a standard technique in the diagnosis of PVD. More recently, with the devel-
opment of Doppler flow meters, blood flow can be detected through human skin by
pulsed ultrasound. This has resulted in a far better objective measure to diagnose PVD.
For example, measurements taken at the femoral, popliteal, anterior, and posterior tib-
ial arteries in patients suspected of having PVD can be used to diagnose the disease.
To rule out PVD, brachial artery and posterior tibial artery pressures can be com-
pared. This is termed the ankle/arm index. The brachial artery pressure is taken
by standard auscultatory methods, while ankle pressures are taken by Doppler. An
ankle/arm index (ABPI) is then generated by dividing the highest of the tibial sys-
tolic pressure or the dorsalis pedis artery pressure in the ankle or foot by the higher
of the two brachial systolic pressures in the arms. Normal individuals have an ABPI
of 0.9–1.3; values outside that range should be investigated because they suggest the
presence of decreased blood flow in the arms or the legs. When performed appropri-
ately, the ABPI has a sensitivity and specificity of 90 and 98%, respectively, for the
detection of peripheral vascular disease. Treadmill exercise for 6 minutes increases
the sensitivity of the ABPI. Some individuals may have a normal ankle/arm index
at rest, but become grossly abnormal immediately following exercise. Medical man-
agement for patients with PVD includes pentoxifylline, dipyridamole, and aspirin.
Pentoxifylline, like other xanthines, is a phosphodiesterase inhibitor; it reduces
inflammation, decreases platelet aggregation, and induces vasodilatation and is there-
fore useful in patients with intermittent claudication and in patients with cerebral-
vascular disease. Pentoxifylline also decreases TNF-α, a property that enhances its
anti-inflammatory profile and improves its efficacy in conditions such as steatohepa-
titis and alcoholic hepatitis.
Dipyridamole is another phosphodiesterase inhibitor; like pentoxifylline, it inhib-
its the formation of thromboxane and proinflammatory cytokines and lowers CRP
levels. It decreases inflammation and platelet aggregation and, by increasing the lev-
els of adenosine, it induces vasodilatation.
Pentoxifylline and dipyridamole induce vasodilatation in healthy arteries; arterio-
sclerotic arteries dilate less well or not at all. This could cause a vascular steal phe-
nomenon where the dilated artery “steals” blood flow from the diseased artery, thus
aggravating the ischemia. The steal phenomenon is more concerning in patients with
cerebrovascular and coronary disease than in patients with intermittent claudication.
Acetylsalicylic acid (aspirin) decreases platelet aggregation by inhibiting the pro-
duction of thromboxane, which binds one platelet with another.
These medications are often used in combination to increase each other’s effects.
EXERCISE ISSUES
Due to the high prevalence of CAD and other risk factors, a stress test is recom-
mended before beginning a structured exercise program (see Appendix B). Patients
who are suspected of being limited by leg pain should be tested on a cycle ergometer

to rule out CAD. This will allow an increase in myocardial oxygen consumption
without leg claudication as a limiting factor.
Once CAD has been ruled out, an exercise prescription that includes education,
modality, progression, intensity, duration, and frequency components should be
prescribed. Fewer than 10% of physician office visits include exercise educational
information. Smoking cessation is the first step in treating PVD. Patients should
be made aware of the numerous studies unanimously demonstrating that exercise
results in significant symptomatic improvement in patients with claudication. Thus,
there will be no doubt that exercise will increase performance by increasing maxi-
mal walking time (MWT) and claudication pain time (CPT). There is no evidence
to suggest that severe ischemia during exercise results in tissue damage in the
leg muscles; however, the mechanisms for improvement are still incompletely
defined. As with all patients who are prescribed exercise, to maintain adherence,
they should be instructed to keep detailed records of their exercise program in their
PVD workbook.
Walking is the best modality when prescribing exercise in patients with PVD,
based on the training principle of specificity, which states that training must closely
approximate the activity. Walking specifically works the gastrocnemius muscles,
which are generally the first muscle group affected by lower extremity occlusive dis-
ease. Swimming or cycling is not recommended as the primary modality to improve
CPT or MWT. However, stationary cycling and swimming may be prescribed to
maximize cardiovascular training when leg pain limits continual exercise. These
methods will be discussed further in the next section on progression.
Patients with PVD will exhibit a wide variability of MWTs. Progression of the
exercise prescription must not be started too abruptly because patients may be non-
compliant. We recommend that patients try to increase their total walking time by a
minimum of 2 minutes each week. During each exercise session, the patient should
be instructed to walk to the point of severe leg discomfort (not pain) because exer-
cise-induced ischemia may be the stimulus for adaptive responses. Walking should
be prescribed on a 3+ to 4+ basis using the following claudication scale:
Claudication Ischemia Scale

1 Light, barely noticeable
2 Moderate, bothersome
3 Severe, very uncomfortable
4 Severe discomfort, cannot continue
Once a level of 3+ to 4+ has been reached, the patient should be instructed to

discontinue activity (rest period) until the pain subsides. If a cardiovascular effect is
desired, the patient should be instructed to continue an activity, such as stationary
cycling, that does not result in leg pain. This activity should be continued until leg
pain subsides, allowing the patient to maintain the target heart rate. At this point,
walking should be resumed. The patient’s ultimate goal should be to have enough
symptomatic improvement in the claudication to allow him or her to walk long
enough to achieve a cardiovascular training effect.

Once the patient can walk continuously for at least 20–30 minutes, prescrib-
ing exercise intensity should involve a target heart rate. We recommend that
40–60% of the heart rate reserve or VO2 reserve be used when a target heart rate for
cardiovascular benefits is prescribed (see Appendix A, Methods 2 and 9 for details).
This intensity corresponds to the minimum intensity that will produce a cardiovas-
cular conditioning effect. As stated earlier, the majority of patients will be limited by
leg pain. Achieving and maintaining a target heart rate may be difficult, especially
in the early stages of an exercise program. Therefore, most patients initially will not
achieve a cardiovascular training effect. However, by prescribing exercise at a 3+ to
4+ level on the claudication scale, improvements in MWT and CPT, which are the
primary goals of the exercise program, will result.
The optimal duration of an exercise session has not been well defined for patients
with claudication. In order to achieve and maintain a cardiovascular training effect,
at least 20 minutes at the target heart rate is needed 3 days per week. However,
patients with claudication who are not interval training on another modality to main-
tain a target heart rate will be resting for a significant period of time during each
exercise session. For example, patients with claudication on average stopped after
approximately 3 minutes because of discomfort, which resolved after about 6 min-
utes. Thus, during a 1-hour session, the patient was only walking for 20 minutes. Our
recommendation is to start with a goal of 10 minutes of total walking time for each
session. About 20–30 minutes per exercise session will be needed to accomplish this
for most patients. The ultimate goal is to progress to 60 minutes of continuous walk-
ing at the prescribed target heart rate.
There are two major considerations when determining frequency. First, the sever-
ity of the patient’s disease should be taken into consideration. In cases of severe leg
pain, more than one daily session may be needed. The second consideration is the
intensity. Since most patients with PVD will be exercising at a moderate intensity,
or a target heart rate equivalent to 40–60% of heart rate reserve or VO2 reserve,
patients can recover more readily. This allows for exercise to be incorporated into
their daily routines. In an attempt to minimize attrition, we recommend that patients
exercise in alternating cycles a minimum of two to three times per week, to the point
of severe leg discomfort (i.e., 3+ to 4+), followed by a more comfortable intensity of
2+ on alternate days.
WEIGHT TRAINING GUIDELINES FOR PERIPHERAL

VASCULAR DISEASE
When patients with peripheral vascular disease undergo weight training, resting and
peak blood pressures are of the utmost concern. Patients with uncontrolled hyper
tension (systolic ≥ 160 mmHg or diastolic ≥ 100 mmHg) should avoid weight train-
ing. Other contraindications to weight training include


for patients are illustrated in the vascular disease workbook CD.

[100 – (# reps × 2.5)] = % 1RM

The preceding methods for prescribing intensity can be used for any weight-lift-
ing equipment: free weights (barbells and dumbbells), weight machines, or hand
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EXERCISE PRESCRIPTION FOR PERIPHERAL VASCULAR DISEASE

Frequency
Exercise a minimum of three times per week to a claudication pain level
of 3+ to 4+, preferably on alternating pieces of exercise equipment to
maintain a target heart rate. On the other days of the week, exercise to a
claudication pain level of no less than 2+ with rest or exercise periods
in between.
Modality
Walking is the preferred method; however, stationary or active bike riding
and swimming are also acceptable modalities for maintaining the heart
rate when leg pain requires the patient to stop exercising. Resistance
training with weights may be beneficial for improving body strength
and endurance, but only if the blood pressure is under control.

Duration
Begin with a time that is comfortable—initially, perhaps 10 minutes.
Gradually increase the exercise time by 2–4 minutes each week until 60
minutes can be achieved without stopping. Be sure to instruct the patient
to walk as long as possible before resting or using another modality.
Intensity
The intensity should be prescribed using the claudication chart in the work-
book. If the patient cannot exercise continuously, instruct him or her to
exercise to a claudication pain level between 3+ and 4+ at least three
times per week. If exercise can be performed continuously for 20 min-
utes, prescribe a target heart rate using Method 2, Appendix A.
Other Instructions
pain immediately.
follow-up visit.
COMMON QUESTIONS ON PERIPHERAL VASCULAR DISEASE

Question: What is peripheral vascular disease (PVD)?
Answer: This condition is associated with cramping and/or pain in the legs,
calves, or feet. These symptoms develop due to a lack of oxygen to the muscle.
The pain may occur intermittently when you are walking. As this condition
advances, the pain becomes constant and is then termed “claudication.”
Question: What places me at risk for this disease?
Answer: The risk factors include high cholesterol, cigarette smoking, high
blood pressure, and obesity.
Question: What can I do to help prevent or control this condition?
Answer: Several lifestyle modifications should be initiated. These modifica-
tions include smoking cessation, weight loss, and a regular exercise pro-
gram that emphasizes walking.
Question: Why does it hurt when I walk?
Answer: The arteries in your legs are narrowed or blocked and this prevents
blood and oxygen from reaching the muscles in your legs. The pain comes
from lack of oxygen and build-up of a compound called lactic acid.

Question: Are there any medications that will help?

Answer: Several medications can be used to help with the symptoms of clau-
dication. These medications work by thinning the blood and allowing easier
flow through the narrowed arteries. Food high in omega-3 fatty acids and
carnitine, a vitamin-like compound, may also help.
Question: Are there tests to determine if I have intermittent claudication?
Answer: Yes. The easiest and least invasive technique is the ankle-brachial
pressure index. This test measu res the blood pressure (using a blood pres-
sure cuff) in the ankle and compares it to the blood pressure in your arm.
The pressure in your ankle should be higher than the pressure in your
arm. If the arm pressure exceeds the ankle pressure or the ratio is less
than 1.00, you probably have claudication. These measu rements should
be taken after walking.
Question: What can I do to manage this disease?
Answer: Management includes a combination of the lifestyle modifications
mentioned before, medication, and a regular exercise regimen.
Question: How can I exercise when it hurts so badly even to walk?
Answer: The key is to start slowly and rest until the pain goes away. Follow
the aerobic exercise guidelines in the PVD workbook.
Question: How does exercise help?
Answer: Exercising helps by improving the resting blood flow, improving
your circulation, increasing your walking time, and increasing tolerance to
the pain in your legs.
Question: What is the best exercise?
Answer: Walk, walk, walk! This form of exercise is optimal because it spe-
cifically works the muscles that hurt. In addition, it is easy, inexpensive,
and does not require any special equipment. Secondary forms of exercise
include bike riding and swimming to condition the heart.
Question: How do I get started on an exercise program?
Answer: Your medical professional will help you find the mode of exercise
that is best for you. Together, you can negotiate the appropriate exercise,
duration, frequency, and intensity. A good starting time is approximately
10 minutes, gradually increasing the time by 2 minutes every week. Follow
the instructions in the PVD workbook.

8 Osteoporosis
and Arthritis
OSTEOPOROSIS
Background
Osteoporosis is a disease characterized by low bone mass and microarchitectural
deterioration of bone tissue leading to enhanced bone fragility and a consequent
increase in fracture risk. Both men and women are at risk for osteoporotic frac-
tures; however, osteoporosis is more common in females. In North America, one
in three women over the age of 70 will have vertebral fractures. Furthermore, one in
three women over the age of 85 will suffer a hip fracture, compared to one in six
males of the same age.
Factors that influence fracture risk include skeletal fragility, frequency and sever-
ity of falls, and tissue mass surrounding the skeleton. Prevention of osteoporotic
fractures, therefore, is focused on the preservation or enhancement of the material
and structural properties of bone, the prevention of falls, and the overall improve-
ment of lean tissue mass. Mechanical force acting when the muscles and gravity pull
on the bones is the only factor known to regulate bone mass and strength.
The diagnosis of osteoporosis is based on clinical history and radiological data.
The measurement of bone mineral density provides a useful method for the evalua-
tion of the risk for fracture; that is, a 10% decrease in bone mineral density doubles
the risk for a fracture.
Management
Many diseases and drugs are known to cause osteoporosis; however, in most cases, no
cause can be identified. Osteoporotic fractures usually occur at sites that are mainly
trabecular bone: vertebrae, ribs, distal forearm, and proximal femur. Bone mass in
the elderly depends on the rate of involutional bone loss and on the peak bone mass
(i.e., the bone mass present around the third decade of life). Factors relating to the
attainment of peak bone mass include congenital factors, diet, hormones, physical
activity, lifestyle factors, drugs, and diseases.
A therapeutic intervention aimed at increasing peak bone mass is conceivable
only by controlling factors such as estrogen status, dietary calcium intake, and physi-
cal activity. Estrogen administration is realistic only in conditions characterized by
hypoestrogenism. Calcium intake appears to be relevant up to the so-called thresh-
old intake (1000–1500 mg/day; higher allowances do not seem to offer additional
135
advantages, although recent observations have challenged this concept. Exercise

affects only the regions of the skeleton under mechanical stress.
The diet and exercise that help older women preserve their bones can also help
middle-aged or younger women lessen their chances of developing osteoporosis
in later years. Diets adequate in calcium intake are very important. Pregnant and
breast-feeding women, as well as women from adolescence to the mid-20s, need
about 1200 mg of calcium each day. Women who have not yet reached menopause
need about 1000 mg of calcium a day. For postmenopausal women not on estrogen
replacement therapy, for women over 65 years, and for pregnant or nursing women,
the recommended daily intake of calcium jumps to 1500 mg.
Dairy products fortified with vitamin D are the most important source of calcium
in the diet. Leafy green vegetables, nuts, and seafood are also important sources
of dietary calcium. One cup of skim milk contains 300 mg of total calcium; drink-
ing 3.3 cups will provide about 1000 mg of calcium. Women who cannot digest
milk or for other reasons do not include adequate calcium in their diets can take
supplements.
Women are most vulnerable to rapid bone loss after menopause, when their body’s
natural supply of estrogen drops dramatically. Estrogen protects against bone loss,
improves calcium absorption, and enhances the effect of exercise on the bones.
Osteoporosis is probably the most important health problem of healthy older
women after the age of menopause. Women who live the longest are the most likely
to develop osteoporosis and fractures. Estrogen therapy can prevent osteoporosis (and
coronary artery disease), but it increases the risk of endometrial carcinoma 6 times
during the first 5 years and 15 times in long-term users. Estrogen also increases the
risk of breast cancer. Women on estrogen therapy for 10 years or more are 43% more
likely to die of breast cancer than women who did not take estrogen.
Since the risk of coronary artery disease in women is considerably higher than the
risk of breast cancer, taking estrogen to decrease the risk of death by heart disease
is worth the smaller risk of breast cancer. Women with a family history of breast
cancer are obviously at a much higher risk for developing breast cancer. Women who
have a low risk of developing heart disease should weigh the decision to take estro-
gen against the risk of uterine and breast cancer and the risk of osteoporosis. Cyclic
estrogen therapy is recommended for women with coronary risk factors without a
previous history of phlebitis or pulmonary embolism and without a family history of
breast cancer. Adding progesterone to the last 12 days reduces the risk of endome-
trial hyperplasia and uterine cancer.
There is a considerable interest in drugs that would offer protection against osteo-
porosis and heart disease without increasing the risk of uterine or breast cancer.
Alternatives to estrogen include drugs such as tamoxifen and raloxifene, which were
originally anticancer drugs. Tamoxifen offers protection against osteoporosis but not
against heart disease. It might also protect against breast cancer. Raloxifene prevents
osteoporosis and it might also decrease the risk of breast cancer; however, unlike
tamoxifen, it has the cardiovascular benefits of estrogen. Alendronate promotes bone
growth without increasing the risk of cancer but lacks the cardiovascular advantage
of estrogen and raloxifene. Alendronate inhibits bone resorption and normalizes

Osteoporosis and Arthritis 137
bone turnover rates; 10 mg is as effective as 20 mg and more effective than 5 mg.

It should be taken with a liberal amount of water and the patient should avoid lying
down after ingestion to prevent the possibility of esophagitis.
Calcium and vitamin D supplements combined with exercise are by far the most
effective method to reduce the risk of osteoporosis and cardiovascular disease. Daily
doses of at least 1000 mg/day of calcium carbonate and 500–800 units of vitamin
D3 do not increase urinary calcium excretion and do not induce hypercalcemia.
Furthermore, they significantly decrease the risk of femoral fracture in older women
and prevent the loss of mineral density in the lumbar spines of patients treated with
low-dose corticosteroids.
Exercise Issues
Numerous human and animal studies have reported that exercise will positively
influence the composition and mechanical properties of bone. However, high-inten-
sity exercise may retard bone growth, resulting in stress fractures. The load-bearing
capacity of bone reflects both its material properties, such as density and modulus,
and the spatial distribution of bone tissue. These features of bone strength are all
developed and maintained in part by forces applied to bone during daily weight-
bearing activities and exercise.
Functional loading through physical activity exerts a positive influence on bone
mass in humans. The extent of this influence and the types of programs that induce
the most effective osteogenic stimulus are still uncertain. While it is well estab-
lished that a marked decrease in physical activity (e.g., bed rest) results in a profound
decline in bone mass, improvements in bone mass resulting from increased physical
activity are less conclusive. Results vary according to age, hormonal status, nutrition,
and exercise prescription.
Athletes have greater bone mass and strength than sedentary individuals. Runners
and weight lifters tend to have stronger bones than swimmers because water reduces
the gravitational force on the bone. To improve and maintain bone mass, regular
weight-bearing exercise should be emphasized. This is important for women and men
of all ages, especially older women or women who have never exercised. Individuals
should start out slowly and build up to the recommended guidelines listed on the
aerobic exercise page.
Resistance training performed twice a week for 6 months at 70% of a one repetition
maximum preserves bone mineral density of lumbar vertebrae and the femoral neck.
Resistance-training programs should be undertaken cautiously, focusing on strength.
ARTHRITIS
Arthritis is generally defined as inflammation of joint tissues. The most common
forms of arthritis are osteoarthritis (OA), defined as a progressive, irreversible
degeneration of the articular surfaces of the joints, and rheumatoid arthritis (RA),
which is an autoimmune process resulting in inflammation of the synovium. Both
types result in painful inflammation and swelling of the joints with limited range

of motion. Typically, RA patients experience flare-ups and OA patients experience

discomfort continuously. Medications usually include analgesics and nonsteroidal
anti-inflammatory medications with possible glucocorticoid and immunosuppres-
sive agents for RA patients.
There is no evidence that links exercise and increased incidence of osteoarthritis.
To the contrary, there is an increasing body of support to back the theory that exer-
cise benefits patients with arthritis. Exercise can, however, aggravate arthritis when
it is not done properly or during acute joint pain in patients with RA.
Patients with all forms of arthritis benefit from an exercise program by improv-
ing their joint motility and muscle strength. The type of exercise should be care-
fully chosen in cooperation with the medical professional to obtain maximum
improvements in strength, flexibility, and endurance without exacerbating the
patient’s symptoms.
WEIGHT TRAINING GUIDELINES FOR OSTEOPOROSIS

AND ARTHRITIS
When patients with osteoporosis and/or arthritis undergo weight training, be pre-
pared for a high degree of day-to-day variability. Patients with rheumatoid arthritis
may have “flare-ups” on some days and should not be encouraged to weight train
beyond their interpretation of discomfort. Patients with osteoporosis should be cau-
tious when using free-weights because any loss of balance could result in a fall and a
possible fracture. For patients with osteoporosis, up to 60–75% one repetition maxi-
mums should be encouraged. Patients with arthritis should not perform one repeti-
tion maximums. Other contraindications to weight training include

for patients are illustrated in the osteoporosis and arthritis workbook CD.


[100 – (# reps × 2.5)] = % 1RM

of the 1RM. An example using this equation to determine the 1RM follows:
1. Pick a weight the individual can lift comfortably.

2. Let us say that 35 lb was lifted eight times.
3. Use the equation [100 – (8 × 2.5)] = % 1RM.
4. 100 – 16 = % 1RM or 80%.
5. 35 lb is 80% of the 1RM.
6. The 1RM can be determined by 35 lb/0.80.
7. Therefore, the 1RM would be equal to 44 lb.
8. The weight that should be lifted corresponding to 30–50% of the 1RM is
12–20 lb.
The preceding method for prescribing intensity can be used for any weight-lift-
weights and stretch elastic bands. Most patients, however, will be too weak to use
free weights. The rate of perceived exertion (RPE) of 11–16 prescribed for aerobic
work should not be exceeded when lifting weights.
RECOMMENDED READING
Adams, G. M. 1990. Exercise physiology laboratory manual, 25. Madison, WI: Brown &
Benchmark.
Buckley, L. M. 1996. Calcium and vitamin D3 supplementation prevents bone loss in the spine
secondary to low-dose corticosteroids in patients with rheumatoid arthritis. Annals of
Internal Medicine 125:961–968.
Durstine, J. L., L. E. Bloomquist, S. F. Figoni, et al., eds. 1997. ACSM’s exercise management
for persons with chronic diseases and disabilities. Champaign, IL: Human Kinetics.
Hartard, M. 1996. Systematic strength training as a model of therapeutic intervention. A con-
trolled trial in postmenopausal women with osteopenia. American Journal of Physical
Medicine and Rehabilitation 75 (1): 21–28.

EXERCISE PRESCRIPTION FOR OSTEOPOROSIS AND ARTHRITIS

Frequency
Exercise a minimum of three times per week. Do not exercise patients who
are experiencing intense joint pain or are having an arthritic flare-up.
Modality
Activities that require the patient to support his or her own weight are
recommended to build and maintain bone mass in osteoporosis. For
example, walking does not require any special equipment. Stationary or
active bike riding and swimming are also acceptable modalities and are
recommended for patients with arthritis and joint pain. Weight training
may be beneficial. See the section on weight training in this chapter.
Duration
Begin with a time that is comfortable—perhaps initially 10 minutes.
Intensity
The intensity can be prescribed by following the RPE chart in Appendix A,
Method 5. An RPE between 11 and 16 or a perceived exertion between
light and somewhat hard is recommended.
Other Instructions
pain immediately.
follow-up visit.
COMMON QUESTIONS ON OSTEOPOROSIS

Question: What is osteoporosis?
Answer: Osteoporosis is a progressive disease in which your bones gradually
become weak and thin. The bones commonly affected are those in the neck,
spine, ribs, forearm, and hip.
Question: What happens to the bones in osteoporosis?

Answer: Because of the loss of bone mass, the bones become fragile and may
break easily. Bone mass is at its peak by age 35 and then begins to decline
after the age of 40 in women and after the age of 50 in men.
Question: How did I get osteoporosis?
Answer: Factors that can cause you to develop osteoporosis are age, smoking,
menopause, inadequate calcium intake, heavy alcohol use, lack of exercise,
and family history. Other factors that can lead to osteoporosis include an
overactive or enlarged thyroid, problems digesting food nutrients, inflam-
mation of the liver, certain cancers, drugs such as steroids and anticonvul-
sants, and lung disease.
Question: Are women the only ones who get osteoporosis?
Answer: No. Men also can develop osteoporosis, although usually about
10 years later than women.
Question: Why are women more likely to get osteoporosis?
Answer: Women are more vulnerable to bone loss following menopause, when
their natural estrogen levels drop significantly. Estrogen protects the bones
and when the level of estrogen decreases, a woman becomes more sus-
ceptible to bone loss. The rate of bone loss is most rapid in women within
2 years of menopause.
Question: How do I know if I have osteoporosis?
Answer: Osteoporosis may be initially picked up on x-ray or by taking a
diagnostic measurement of your bone density. You may even simply have
a backache that does not go away or you may have a bone fracture.
Question: What can I do to prevent osteoporosis?
Answer: The key is to build bone mass early on by not smoking, doing regular
exercise, taking calcium and vitamin D supplements, and avoiding heavy
alcohol consumption. After menopause, you may be advised by your doctor
to take a medication to reduce the amount of bone loss.
Question: How much calcium should I get daily?
Answer: Pregnant women, women who are breast feeding, or women in their
mid-20s require 1200–1500 mg every day. Premenopausal women should
take in 1000 mg and menopausal women should have 1500 mg. Taking
vitamin D with calcium improves absorption. Low-fat dairy products such
as milk, yogurt, cheese, and ice cream are good sources of calcium. Other
good sources are dark-green leafy vegetables, sardines, tofu, and nuts.
Question: Can taking estrogen to increase or maintain my bone mass
cause cancer?
Answer: Estrogen has been related to both uterine cancer and breast cancer.
Studies have shown that another medication, progesterone, taken in con-
junction with estrogen significantly reduces the chance of uterine cancer
(close to 0%) in those women who have not had hysterectomies. Some stud-
ies report a small increase in breast cancer risk on hormone replacement.
Question: How does exercise help with osteoporosis?
Answer: Exercise helps to promote bone mass and bone growth and to prevent
or slow bone mass loss.

Question: What kind of exercise is the best?

Answer: Regular exercise that requires you to bear your own weight, such
as low-impact aerobics, is good. Bicycling, either stationary or active,
and swimming are also acceptable types of exercise. Exercise should be
done at least three times a week. Start slowly and gradually increase the
duration. Refer to the sections on aerobic exercise and weight training in
the workbook.

9 Cancer, the Immune
System, and AIDS
CANCER
Background
All cancerous cells share a common characteristic: the ability to proliferate and
spread throughout the body. Cancer, including hereditary cancer, is caused by errors
made during DNA replication. People with a family history of cancer inherit a pre-
disposition to cancer due to a DNA mutation. However, this is not enough to cause
cancer; additional mutations (either spontaneous or triggered by carcinogens) are
necessary for the disease to emerge. Given the enormous amount of DNA that is rep-
licated every second, it is no surprise that errors are made. The surprising fact is how
few are made: Only one base in every 100,000 replicated bases is incorrect.
Cells have a proofreading system that checks for mistakes and, when one rep-
lication mistake is found, an enzyme (exonuclease) corrects it. But there is more:
The cellular quality control mechanism has a plan B, used when proofreading is
not enough, called mismatch repair. As the name implies, certain enzymes replace
the incorrect base, matching with the correct one. If this also fails, there is still a
plan C: The mutated cell is marked for early cellular death (apoptosis) and, if this
is not enough, circulating tumor-killing cells recognize the abnormal cellular pro-
teins that have resulted from the DNA abnormalities and activate the tumor-killing
immune system.
When this also fails and the mutation results in uncontrolled growth, we have
a tumor in our midst. However, not all mutated, rapidly growing cells that escape
the tumor-killing cells are cancerous cells. For a cell to become cancerous, it has to
activate cell-growth-promoting genes (oncogenes) and inactivate tumor-suppressing
genes, impair the process of apoptosis, and escape the tumor-killing cells. It also has
to be able to invade adjacent tissue and metastasize to distant organs.
Cancer is a disease that occurs due to a series of DNA mistakes resulting in
uncontrolled cell division, although at this point the tumor is still benign. Then,
other mutations allow the uncontrolled cells to overcome the natural barriers that
keep specialized cells within the geographic boundaries of their organs and to
invade adjacent organs. These locally invasive tumors have low-grade malignancy;
a good example is basal cell carcinoma of the skin. Finally, additional mutations
allow tumor cells to metastasize to other tissues.
Errors made during replication lead to greater errors in subsequent replications
and eventually cancer cells, which have a very abnormal DNA and therefore do not
143
obey the rules of cellular social life. They grow out of control, do not respect proper
boundaries, and do not interact appropriately with other cells, including cells of the
immune system. Cancer is actually a myriad of hundreds of diseases sharing these
features. The ultimate treatment goal is to prevent cancer and, when this is not pos-
sible, to eliminate the cancer cells or inhibit their growth, thus achieving a cancer-
free or remission state.
Many benign tumors and cancers are caused by viruses. An invading virus injects
its DNA into the host cell to replicate itself; this often results in altered cellular
growth. Examples of virally induced benign tumors are the common wart and papil-
lomas; examples of virus-induced cancers are cancer of the cervix, caused by the
human papilloma virus, and Kaposi’s sarcoma, which is caused by the HIV virus.
However, viral infection has been implicated in the genesis of several other cancer
types such as cancer of the prostate and cancer of the breast.
Hereditary tumors such as prostate, breast, and colon cancer are difficult to pre-
vent; early detection and early removal of those cancers is the only way to prevent
local invasion and metastasis. Many common cancers, such as cancer of the mouth,
esophagus, stomach, and colon, are caused by carcinogens present in tobacco, food,
alcohol, as well as other environmental sources such as asbestos, food additives, etc.
Cancer of the skin is caused by ultraviolet light (UVL). Cancers linked to lifestyle
risk factors can be prevented with lifestyle modification, such as avoiding tobacco
and alcohol use, protecting the skin against UVL exposure, eating a diet rich in
vegetables and fruits and low in saturated fats, preventing weight gain and obesity or
losing excessive weight, and engaging in daily exercise.
AIDS
Background
Acquired immune deficiency syndrome (AIDS) is a disease caused by the human
immunodeficiency virus (HIV), a retrovirus that infects cells of the immune system
such as CD4 T-lymphocytes, macrophages, dendritic cells, and others. Eventually,
the number of CD4 T-cells becomes severely depleted and, when their numbers
reach a critical low, it renders the organism susceptible to opportunistic infections
and tumors.
HIV progression may be divided into three stages:
• Asymptomatic HIV seropositive

• Early symptomatic HIV
• AIDS
The latest statistics show that 33.2 million people suffer from the disease. HIV
virus originated in West Africa and the continent of Africa is the most severely
affected by the disease; approximately three fourths of all AIDS-related deaths
occur in Africa. The most important risk factors are engaging in unprotected sex,
especially anal sex, and sharing needles with HIV-infected people. Contaminated

Cancer, the Immune System, and AIDS 145
blood transfusions are no longer a problem in America but continue to be a problem

in Africa.
The goal of therapy is to prevent the disease. When this fails, the goal is to
decrease the number of HIV viruses with antiretroviral therapy, to prevent oppor-
tunistic infections once the number of CD4 lymphocytes reaches a critically low
number, and to prevent or minimize cachexia.
ANXIETY AND DEPRESSION IN PATIENTS

WITH CANCER AND HIV INFECTIONS
The diagnosis of cancer and HIV infection causes a considerable amount of anxiety
and depression. In addition to the existential threat, these two diseases (more than
any other) are associated with evil and are thought to be particularly gruesome. We
speak of malignant disease, we talk of invasions, we call cancer victims heroes,
we encourage them to fight, and families ask them not to give up. Physicians and
other caregivers address issues related to therapy in militaristic terms: Radiographs
show that patients have been infiltrated by tumor, and we speak of the weapons
we have in the war against cancer, such as radioactive (radiotherapy) and chemical
(chemotherapy) weapons. It is no wonder that cancer patients are terrified.
In addition to the burden of their disease, HIV-infected patients suffer from soci-
etal prejudice and rejection. HIV has replaced tuberculosis as the most feared infec-
tious disease, but, unlike tuberculosis, AIDS is looked upon as a form of divine
punishment. The heroines of La Boheme and La Traviata had tuberculosis, but that
did not decrease their romantic appeal. Doc Holliday remains a Western myth undi-
minished by his tuberculosis, and the setting of Thomas Mann’s The Magic Mountain
is a tuberculosis sanatorium for the rich and sophisticated. Unlike the tuberculosis of
Verdi and Mann, HIV is seen as dirty, sinful, and dangerous; people feel shame when
confronted with the facts of a family member’s illness and try to hide it or simply lie
about it. Cancer and HIV infection are associated with a great deal of distress.
We should distinguish between the words stress, eustress (normal or good stress),
and distress. Stress in itself is not necessarily bad; many of our most productive
moments and achievements have been obtained under stressful conditions. Stress
can be good when it is processed and dealt with in a healthy way, but it can be nega-
tive when the subject experiencing it cannot cope with it.
Stress is a form of hyperarousal; the brain and cardiovascular, endocrine, muscu-
lar, digestive, and all other systems of the body participate to direct and concentrate
attention to the problem at hand and facilitate decision making and rapid action. The
body as a whole responds to the stressing stimulus, and a change in one system causes
changes in others. Unfortunately, the hyperarousal response often continues for too
long and wears the person down (distress), reducing his or her capacity to adapt.
Not only the body but also the body and the environment as a whole adapt to
stress in a reciprocal fashion; a change in the person leads to changes in the environ-
ment and vice versa (action ↔ environment). It is not the strongest or the biggest that
survives and thrives under stress, rather, it is the one who is better able to adapt to it.
Distress is what happens when the adaptation to stress (by the person ↔ environment)

is not possible or is incomplete. The physical and psychological consequences of the

failure to adapt involve the function of almost every bodily system and the subjective
manifestation of the system when viewed as a whole. Distress has negative emotional
consequences (anxiety and depression) and decreases self-esteem.
Self-esteem is one of the aspects of the cognitive objectivation of the self. When
the cognitive capacity (our powers of thinking) is directed to our self, the self
becomes an object. Under conditions of distress, the analysis of the self yields a neg-
ative report, and the self is viewed as socially defective, physically inadequate, etc.
The combination of negative emotions and low self-esteem further decreases the
capacity to adapt and to foster maladaptive cognitive and behavioral reactions. This
leads to a vicious cycle of negative self-concepts ↔ distress until a pathologic pla-
teau is reached.
The treatment of the distress often encountered in patients with chronic illness
is multidisciplinary and includes psychotherapy, social work, and medications.
However, there is no better medicine for anxiety, depression, low self-esteem, and
stress than daily exercise. Moderate-intensity aerobic training leads to a significant
reduction in anxiety and depression and is associated with an improvement in self-
confidence and the capacity to deal with problems. For information and references
regarding the somatopsychic effects of exercise, we recommend Chapters 8 and
14 of Kate F. Hayes’s book, Working It Out. Using Exercise in Psychotherapy (see
Recommended Reading section).
Benefits of exercise include
• Decreased anxiety
• Decreased depression
• Improved physical fitness, leading to improved self-concept
• Improved capacity to function (exercise capacity), leading to an improved
sense of competence and goal attainment
• Improved physical appearance and capacity to function, leading to improved
sense of security and self-sufficiency
• Improved self-esteem associated with improved sense of competence and
self-sufficiency, leading to healthier behaviors
• Decreased hyperaroused state and improved symptoms of conditions asso-
ciated with it, such as hypertension, cardiovascular disease, chronic back
pain, insomnia, inflammation, and autoimmune disorders
There is unequivocal information regarding the positive effects of exercise train-
ing in the treatment of anxiety and depression. Less is known about the effect of
exercise in regard to cancer prevention and cancer recurrence and even less about
the effects of exercise in the immune system, especially as it refers to the treatment
of HIV-infected persons.
EXERCISE AND CANCER

Physical activity can decrease the risk of cancers of the colon and breast and probably
cancer of the endometrium (lining of the uterus) and cancer of the lung. Although the

optimal levels and duration of exercise are difficult to determine due to differences
between studies, as a rule of thumb, 30–60 minutes of moderate to vigorous physical
activity per day is needed to protect against cancer and cancer recurrence.
Physical activity may protect against cancer in multiple ways. These include
dietary and weight loss changes associated with increased physical activity such as
decreased caloric intake, decreased body fat, and increased gastrointestinal transit
time (decreasing the time the bowel is exposed to carcinogens). Other ways include
exercise-induced hormonal changes such as changes in sex hormone metabolism,
improved insulin sensitivity, and reduced insulin mediated growth factors and by
modulating the immune system.
For more information and references regarding exercise and cancer, please
visit the National Cancer Institute Web site (http://www.cancer.gov/cancertopics/
factsheet/prevention/physicalactivity). Most of the information presented here was
obtained from that site on June 3, 2010.
Colon Cancer
More than 50 studies have examined the association between colorectal cancer and
habitual exercise. They have consistently found that adults who increase their physi-
cal activity in intensity, duration, or frequency can reduce their risk of developing
colon cancer by 30–40% relative to those who are sedentary, regardless of body
mass index (BMI). The greatest risk reduction is seen among those who are most
active and those who engage in high-intensity activity.
Breast Cancer
Over 60 studies have examined the relationship between exercise and breast cancer.
Most studies indicate that physically active women have a lower risk of developing
breast cancer than inactive women, but the amount of risk reduction varies widely
(between 20 and 80%). High levels of moderate and vigorous physical activity dur-
ing adolescence may be especially protective, but women who increase their physical
activity after menopause may also experience a reduced risk compared with inactive
women. A number of studies also suggests that the effect of physical activity may be
different across levels of BMI, with the greatest benefit seen in women in the normal
weight range (BMI < 25 kg/m2) and in direct proportion to the intensity and duration
of exercise.
Endometrial Cancer
About 20 studies have examined the role of physical activity on endometrial can-
cer risk. As the research on colon cancer and breast cancer has shown, women
who are physically active have a reduced risk of endometrial cancer (20–40%),
with the greatest reduction in risk among those with the highest levels of physi-
cal activity. Unlike the breast cancer data, however, the benefits are not affected
by age.

Lung Cancer
At least 21 studies have examined the impact of physical activity on the risk of lung
cancer. Overall, these studies suggest an inverse association between physical activ-
ity and lung cancer risk, with the most physically active individuals experiencing
about a 20% reduction in risk. An analysis of many existing studies found evidence
that higher levels of physical activity protect against lung cancer, but was unable to
control fully for the effects of smoking or respiratory disease in estimating the mag-
nitude of the potential benefit. The relationship between physical activity and lung
cancer risk is less clear for women than it is for men.
Cancer Survival
One study found improved cancer survival following the diagnosis of breast cancer
in women who exercised moderately. Two studies have suggested a protective associ-
ation of physical activity after colon cancer diagnosis. The breast cancer study found
that walking at an average pace for 30–60 minutes daily improved survival when
compared with more survival rates for sedentary women. This is similar to the gen-
eral recommendation in regards to cancer prevention (exercise 30–60 minutes daily).
Although these studies suggest protective effects of physical activity, more research
is needed to understand what levels of physical activity provide these benefits.
EXERCISE AND THE IMMUNE SYSTEM

Although there have been hundreds of studies on exercise and the immune system,
there is little direct evidence on its connection to illness. Epidemiological evidence
suggests that moderate exercise has a beneficial effect on the human immune system,
while extreme exercise impairs it. Moderate exercise has been associated with a 29%
decreased incidence of upper respiratory tract infections (URTIs). On the other hand,
some (but not all) studies of marathon runners and other elite athletes have found that
prolonged high-intensity exercise is associated with an increased risk of URTI.
There is a change in the immune function following exercise training; the immune
systems of athletes and nonathletes are similar, but athletes may have a slightly ele-
vated natural killer cell count and cytolytic action. Given the beneficial effect of
exercise in regards to cancer risk, this change is clinically significant. Additionally,
biomarkers of inflammation (such as C reactive protein [CRP]), which are associ-
ated with chronic diseases, are reduced in active individuals relative to sedentary
individuals. Therefore, the effects of exercise in the immune system might be medi-
ated by its anti-inflammatory effects. However, the opposite might also be true: A
depression of the immune system following an acute bout of exercise may be one of
the mechanisms for the anti-inflammatory effect.
Toll-like Receptors
The effect of exercise on inflammation and the immune system might be mediated by
the effect of exercise on toll-like receptors (TLRs). These are a class of proteins that

play a key role in the innate immune system and there is evidence that this system
is altered by exercise. TLRs are single, membrane-spanning, noncatalytic receptors
that recognize structure molecules derived from foreign cells such as microbes. Once
microbes have breached physical barriers such as the skin or intestinal mucosa, they
are recognized by TLRs, which activate a cellular immune response.
TLRs receive their name from their similarity to the protein coded by the toll
gene identified in Drosophila in 1985 by Christiane Nüsslein-Volhard. When the
protein was identified the researchers spontaneously shouted out in German “Das
ist ja toll!” This translates as “that’s amazing” or “that’s great!” Thus, the word
“toll receptor” originates in the German word for great, and they are great receptors
indeed. TLRs are present in animals, plants, and bacteria; they are one of the most
ancient components of the immune system.
TLRs are pattern recognition receptors (PRRs); they recognize molecules that
are broadly shared by abnormal cells such as bacterial pathogens but distinguishable
from host molecules. This is collectively referred to as pathogen-associated molecular
pattern (PAMP). Together with the IL-1 receptor, TLRs form a receptor superfamily,
known as the interleukin-1 receptor/toll-like receptor superfamily. All members of
this family have a so-called TIR (toll-IL-1 receptor) domain in common.
Three subgroups of TIR domains exist. Proteins with subgroup 1 TIR domains
are receptors for interleukins that are produced by macrophages, monocytes, and
dendritic cells and all have extracellular immunoglobulin (Ig) domains. Proteins
with subgroup 2 TIR domains are classical TLRs, and bind directly or indirectly to
molecules of microbial origin. A third subgroup of proteins containing TIR domains
consists of adaptor proteins that are exclusively cytosolic and mediate signaling from
proteins of subgroups 1 and 2.
Heat Shock Proteins

Another system altered by exercise is a class of functionally related proteins whose
expression is increased when cells are exposed to stress such as high temperatures
(or any other type of stress); they are called heat shock proteins (HSPs). Beginning in
the mid-1980s, investigators recognized that many HSPs function as molecular chap-
erones and play a critical role in protein folding, intracellular trafficking of proteins,
and coping with proteins denatured by heat and other stresses.
Production of high levels of heat shock proteins can also be triggered by exposure
to different kinds of environmental stress conditions, such as infection and expo-
sure of the cell to toxins such as ethanol, arsenic, trace metals, ultraviolet radiation
light, starvation, dehydration hypoxia and many others stresses, including exercise.
Consequently, heat shock proteins are also referred to as stress proteins and their up-
regulation is sometimes described more generally as part of the stress response.
The mechanism by which heat shock or other environmental stressors such as exer-
cise activate the heat shock factor has not been determined. However, some studies
suggest that an increase in damaged or abnormal proteins brings HSPs into action.
Exercise can alter the immune response in the manner presented next. Please note
the similarities and differences between the effects of two different stressors on the
immune system: infection and exercise:

Pathogen → stress signal → HSP

Pathogen and/or HSP → activation of toll receptors → phagocytosis and
degradation of pathogen to immunogenic peptides, which are then pre-
sented to the T-cell lymphocyte histocompatibility receptors → cytokine
production → inflammation and activation of immune system
Exercise → HSP + modulation of toll receptors
↓→ Better recognition/processing of cancer cells
Decreased production of cytokines
↓
Decreased inflammatory activity and decreased production of CRP
CACHEXIA
Background
Weight loss occurs when caloric requirements exceed the caloric intake. This occurs
when the patient is not ingesting or absorbing enough calories, the energy produc-
tion is increased, or a combination of the two occurs. Within the last category, a
group of patients suffer from a cluster of metabolic problems that include increased
resting energy expenditure, decreased protein synthesis, increased protein degra-
dation, muscle wasting, hypocholesterolemia, hypoalbuminemia, normochromic–
normocytic anemia, and insulin resistance. This syndrome is called cachexia and it
is associated with increased mortality.
The weight loss associated with cachexia is different from starvation-induced
weight loss. During starvation, the caloric intake is not enough to maintain body
weight; the organism adapts by reducing the resting energy expenditure, losing pri-
marily fat stores and preserving lean body mass. Cachexia is characterized by weight
loss secondary to a disproportionate reduction of lean body mass with relative pres-
ervation of fat stores and increased energy expenditure.
The average rate of protein turnover varies among tissues; certain enzymes last
only minutes, whereas muscle protein lasts several days. In a normal 70 kg adult,
280 g of protein is synthesized and degraded every day. Cellular protein synthesis
and degradation are carefully balanced. Signals that stimulate degradation include
inactivity, fasting, acidosis, certain hormones, and cytokines. Most cellular protein
degradation consumes ATP and includes a linkage to a protein cofactor—ubiq-
uitin—that labels other proteins for proteasome recognition. Proteasomes are large
protein complexes located in the nucleus and the cytoplasm whose function is to
degrade proteins.
During fasting, muscle protein is mobilized for gluconeogenesis, but after a
few days, muscle degradation decreases, lipolysis increases, and metabolic rate is
decreased. The mechanism responsible for cachexia is part of the metabolic response
to injury and, as such, it is present in a variety of acute illnesses such as multiple
trauma and infections. When the trigger event is removed, cachexia is removed along
with it. Cachexia is also present in a variety of chronic pathologic states including
cancer, sepsis, and advance stages of cystic fibrosis, AIDS, chronic obstructive pul-
monary disease, and others.

During illness, the muscles become amino acid donors. Some of those amino
acids are used for gluconeogenesis and others for protein synthesis. The mobilization
of amino acids from muscle is part of the adaptation to illness, but in conditions of
chronic cachexia, muscle loss continues unabated and visceral proteolysis follows.
These secondary events become more important than the trigger event. In fact, death
seems to be determined more by the amount of lean body mass lost than by any
other particular problem. Death usually coincides with the loss of 50% of the lean
body mass; under such conditions even a minor infection can result in death.
Many of the metabolic problems associated with cachexia result from the actions
of cytokines—in particular, tumor necrosis factor (TNF/cachectin) and interleu-
kins (IL)-1 and -6. Cytokines are part of a neuro-humoral-hormonal information
system responsible for the coordination of different organ functions and the preserva-
tion of the “internal milieu.” Cytokines are produced by a variety of cells, including
lymphocytes, monocytes, macrophages, and the central nervous system (microglia,
which are related to macrophages). Cytokines cause anorexia, increase metabolic
rate, suppress lipoprotein lipase (IL-1), increase gluconeogenesis (IL-1), increase
muscle proteolysis (TNF), decrease synthesis of albumin, and increase production
of acute phase protein (IL-1 and TNF). Cytokines alone do not stimulate proteolysis;
rather, this action requires the presence of other mediators such as glucocorticoids
and thyroid hormones. Factors opposing the catabolic effects of cytokines and glu-
cocorticoids are insulin and growth hormone.
Populations at greatest risk for cachexia include diabetics and the elderly. Insulin
resistance increases with age and levels of growth hormone decrease; therefore, pro-
tein synthesis decreases and protein degradation increases as people grow older.
Management
Beyond treating the underlying disease and providing dietary supplements, there is
no effective therapy to treat cachexia. A common-sense approach includes:
• Removal of etiologic factors such as treatment of infections, etc.

• Optimization of conditions known to aggravate cachexia such as diabetes,
hyperthyroidism, renal failure, and metabolic acidosis
• Avoiding overuse of catabolic medications such as corticosteroids when-
ever possible
• Appropriate nutrition: micronutrients (vitamins and minerals), caloric
replacement equal to the daily energy expenditure, and protein replace-
ment 1–1.5 g per kilogram of body weight; providing proteins in excess of
1.5 g/kg does not improve nitrogen balance, but rather simply increases the
production of urea and waste products
• Consideration of insulin, growth hormone, anabolic steroids, and megestrol,
which have short-term benefits but controversial long-term uses
Animal studies suggest that β2-adrenergics and phosphodiasterase inhibitors might

reduce proteolysis and improve lipolysis.

Exercise Issues
Muscle mass and function are improved, even in the elderly, during resistance exer-
cise training; these changes occur as a result of increased protein synthesis. Moderate
weight lifting by these individuals does not appear to increase the rate of muscle
protein breakdown. The mechanisms for improved synthesis are not clear; however,
exercise is the best natural way to stimulate production of human growth hormone,
which increases proportional to the intensity of exercise. A rating perceived exertion
(RPE) of no greater than 14 is recommended. (See Appendix A, Method 5 for a dis-
cussion about the RPE chart.)
AIDS
Management
Drug therapy should include both exercise and nutritional guidance. Infections that
may result from HIV are treated with a variety of medications, such as antiviral,
antibacterial, gastrointestinal, and anticancer medications.
Exercise Issues
Exercise prescription for AIDS patients may vary depending on the progression of
the disease. For example, during stage one, metabolic parameters are within normal
limits and therefore no limitations need to be placed on the individual. During stages
two and three, functional capacity will be reduced, requiring a more individualized
exercise prescription and lower intensities as outlined at the end of this chapter.
It is important to begin an exercise program as early as possible to increase the
CD4 cells, possibly delay symptoms, and increase muscle strength and size. The pos-
itive effects of aerobic exercise on psychological and immunological function among
gay men seropositive for HIV-1 have been studied. It appears that interval training
at 70–80% of maximal heart rate (see Appendix A, Method 1) elicited a significant
increase in T-helper/inducer (CD4) cells and the inducer subset (CD45RA+CD4+),
which activate suppressor/cytotoxic (CD8) cells. Exercise could minimize the
decrease in cellular immunity in patients infected with HIV-1 (LaPerriere 1990,
1991). Other benefits of exercise may include increases in lean body mass, improve-
ment in mood state, and increased energy for the activities of daily life.
Exercise training at a higher intensity than 80% of the heart rate reserve (see
Appendix A, Method 2) increased strength and aerobic fitness, but did not change
total lymphocyte counts and CD4+ and CD8+ cell counts and ratios (Rigsby 1992).
The studies of Rigsby and LaPerriere suggest that the intensity of aerobic train-
ing could have a significant effect on the immune system’s response to exercise.
Johnson (1990) has previously shown that the lactate threshold is lower and the slope
of the heart rate VO2 max relationship is increased in HIV-positive individuals. This
observation revealed a significant amount of cardiovascular deconditioning in HIV-
positive individuals (or occult cardiac disease). It also demonstrated the unreliability

of heart rate formulas to identify the lactate threshold and prescribe exercise above
or below such a threshold (see Appendix A, Method 7).
The effect of exercise on the immune system might be modulated by the endo-
crine response to exercise, which varies considerably with the exercise intensity.
Exercise results in a decline in plasma insulin and an increase in concentrations of
glucagon, epinephrine, norepinephrine, cortisol, and growth hormone. The extent
of these hormonal alterations is accentuated as the intensity of exercise increases.
The hormonal profile observed during exercise is rapidly reversed during the first
minutes of recovery, except for the increments in cortisol and growth hormones.
Cortisol levels do not rise significantly with exercise, but they progressively increase
during the recovery period. Plasma growth hormone increases with exercise and
continues to increase during the recovery period. An RPE of no greater than 14 is
recommended (see Appendix A, Method 5).
CANCER
Management
The treatment for cancer may involve chemotherapy, which can have an overall cyto-
toxicity on all cells in the body. Fatigue may result from the destruction of red blood
cells during chemotherapy, muscle atrophy, and mitochondrial dysfunction. Patients
on intensive chemotherapy may become easily fatigued, complicating exercise per-
formance. Common side effects as a result of chemotherapy and cancer may include
bone fractures, cardiac or pulmonary damage, anemia, low platelet counts, tumor–
host competition for nutrients, dehydration, electrolyte imbalances, peripheral nerve
damage, myopathy, and infections.
Exercise Issues
The goal of any exercise program for the treatment of cancer should be to enhance
immune function and prevent or minimize muscle wasting, thus counteracting the
detrimental and physiological effects of cancer and chemotherapy. Eventual return
to precancer functional capacity should be a goal for individuals in remission. In
patients undergoing treatment, the goal of exercise should be to maintain enough
endurance and strength to perform the everyday activities of living. Most of the ben-
efits resulting from exercise are musculoskeletal and psychological. Patients who are
in remission will benefit more than those who are undergoing treatment; however,
patients undergoing treatment will benefit as well.
Peak exercise capacity is normally 3–5 METs (metabolic equivalents). Non-weight-
bearing activities are usually recommended due to muscle wasting and increased
risk of bone fractures. The exercise intensity should be prescribed at 40–65% of
the peak heart rate, the heart rate reserve, the VO2 max or reserve, or just below the
anaerobic threshold, depending on the patient’s ability (see Appendix A, Methods 1,
2, 6, 7, and 9). A rating perceived exertion of no greater than 12 may be used as a
guide when exercise testing is not possible.

The frequency and duration of exercise are determined by the clinical status
of the patient. Factors involved in the clinical status of the patient may include the
possibility of intravenous lines becoming dislodged, malaise, nausea, fatigue, mus-
cle weakness, and numbness in the extremities. The modality of exercise can vary
from stationary cycle to treadmill to weight training, preferably using machines. If
weight training is prescribed, high-repetition, low-weight circuit programs that do
not exceed the aerobic RPE of 14 or within the range of 30–50% of the 1RM also are
recommended (see Appendix A, Method 10).
WEIGHT TRAINING GUIDELINES IN CHRONIC INFECTIONS

When patients with chronic infections undergo weight training, be prepared for a
high degree of day-to-day variability. Contraindications to weight training include

• Aerobic capacity of less than 5 METs with severe AIDS-related disease
for patients are illustrated in the AIDS and AIDS-related diseases workbook CD.
recommend the following method to prescribe the intensity. All exercise or repeti-
tion sets may be performed one or two times or in one or two sets—for example:
Choose a weight that can be lifted comfortably 10–15 times. When 15 repetitions
can be comfortably performed, the weight may be increased to an amount that can
be lifted at least 10 times. Most patients have a very low 5-MET capacity. Therefore,
weight training should be supervised when possible and consist of low weight and
high repetitions as described previously. Weight also can be prescribed as a percent
of the patient’s 1RM, or repetition maximum, typically 30–50%. See Appendix A,
Method 10, for a detailed explanation of the formula.
The preceding method for prescribing intensity can be used for any weight-lift-
weights and stretch elastic bands. Most patients, however, will be too weak to use
free weights. The RPE of 14 prescribed for aerobic work should not be exceeded
when lifting weights. See Appendix A, Method 5.

REFERENCES
Johnson, J. E. 1990. Exercise dysfunction in patients seropositive for the human immunodefi-
ciency virus. American Review of Respiratory Disease 141:618–622.
La Perriere, A. R. 1990. Exercise intervention attenuates emotional distress and natural killer
cell decrements following notification of positive serologic status for HIV-1. Biofeedback
Self-Regulation 15:229–242.
———. 1991. Aerobic exercise training in an AIDS risk group. International Journal of Sports
Medicine (Suppl. 12) 1:S53–S57.
Rigsby, L. W. 1992. Effects of exercise training on men seropositive for the human immuno
deficiency virus-1. Medicine and Science in Sports and Exercise 24:6–12.
RECOMMENDED READING
Antoni, M., N. Schneiderman, M. Fletcher, D. Goldstein, G. Ironson, and A. La Perriere. 1990.
Psychoneuroimmunology and HIV-1. Journal of Consulting and Clinical Psychology
58:38–49.
Calles-Escandon, J. 1984. Fuel-hormone metabolism during exercise and after physical train-
ing. Clinics in Chest Medicine 5:3–11.
Costelli, P. 1995. Muscle protein waste in tumor-bearing rats is effectively antagonized by
a β2-adrenergic agonist (clenbuterol): Role of the ATP-ubiquitin-dependent proteolytic
pathway. Journal of Clinical Investigation 95:2367–2372.
Ferrari, R. 1991. Temporal relations of the endocrine response to exercise. Cardioscience
2:131–139.
Gleeson, M. 2007. Exercise and immune system. Journal of Applied Physiology 103:693–699.
Hayes, K. F. 1999. Working it out: Using exercise in psychotherapy. Washington, D.C.:
American Psychological Association.
La Perriere, A. R. 1997. AIDS. In ACSM’s exercise management for persons with chronic
diseases and disabilities, ed. J. L. Durstine, L. E. Bloomquist, S. F. Figoni, et al. chap.
23. Champaign, IL: Human Kinetics.
National Cancer Society. http://www.cancer.gov/cancertopics/factsheet/prevention/physicalactivity
Yarasheski, K. E. 1993. Acute effects of resistance exercises on muscle protein synthesis rate in
young and elderly men and women. American Journal of Physiology 265:E210–E214.
Ziegler, T. R. 1994. Strategies for attenuating protein-catabolic responses in the critically ill.
Annual Review of Medicine 45:459–480.
EXERCISE PRESCRIPTION FOR CHRONIC INFECTIONS:

CACHEXIA, AIDS, AND CANCER
Frequency
Exercise a minimum of three times per week. Try to alternate the exercise
days to allow plenty of time for recuperation. The number of times the
patient exercises per week may be determined by the clinical status.
Modality
Weight-supportive machines such as stationary cycling or rowing are the
preferred method. Combining as many different modalities as possible

during the aerobic exercise is recommended. A rigorous weight-train-

ing program may be harmful; however, moderate weight training may
be beneficial to prevent muscle wasting and should be done with light
weights that allow 10–15 repetitions per exercise. An RPE of 14 should
not be exceeded when weight training.
Duration
Begin with a time that is comfortable—initially 10 minutes. Gradually
20–60 minutes is achieved without stopping. Training in intervals with
rest periods may help the patient to achieve this goal.
Intensity
The intensity can be prescribed by following the RPE chart in Appendix A,
Method 5. An RPE of no greater than 14 or between light and somewhat
hard is recommended.
Other Instructions
pain immediately.
follow-up visit.
COMMON QUESTIONS ON DISEASES OF THE IMMUNE SYSTEM

(CHRONIC INFECTIONS, CACHEXIA, AND AIDS)
Question: What is cachexia?
Answer: Cachexia is a state of emaciation associated with many diseases. It is
characterized by loss of weight and muscle despite adequate ingestion of food.
Question: What causes cachexia?
Answer: Certain diseases or conditions cause involuntary weight loss, such as
cancer, AIDS, chronic infections, and severe heart and lung diseases.
Question: What causes my weight loss?
Answer: There may be several reasons why you are losing weight. The first
may be that you are not consuming enough calories or that the calories
are not being absorbed and digested properly. Another reason may be that,
due to a cancer or other disease, the amount of energy you produce has
increased and the amount of tissue breakdown has increased. The elderly

may not be eating enough simply because of difficulties with chewing, lack
of teeth, a reduced appetite, depression, or isolation.
Question: How much weight loss should be concerning?
Answer: If 5% of your body weight has been lost over a 6-month period without
your attempting to lose the weight or without using diet pills. For example,
if you weigh 150 lb and your weight drops by 7.5 lb without your changing
your dietary habits or increasing your exercise, there may be a problem.
Question: How does the requirement for calories change?
Answer: A disease can change the way nutrients are used in the body. This may
result in an increased consumption of calories in the body and increased
protein turnover in the muscles. You will not know this is occurring until
the weight loss is apparent.
Question: How does HIV cause weight loss?
Answer: The body responds to HIV infection by increasing the amount of
energy it needs to function. You will probably be unaware that your body is
using so much energy to function and will not increase your daily calories.
There is more energy going out than calories coming in and this results in
weight loss. A second reason why weight loss occurs is because of other
infections associated with the virus: for example, infections of your stom-
ach and intestines such as gastrointestinal candidiasis, CMV infections, and
diarrhea. They increase your body’s energy needs and will cause weight
loss. Much of this weight loss will be muscle loss.
Question: Why do you lose weight with cancer?
Answer: There are many reasons why you lose weight if you have cancer.
One reason is because your body releases something called “tumor necro-
sis factor.” This causes changes in your body that result in the breakdown
of muscle and a loss of weight. In addition, the chemotherapy and radia-
tion may cause mouth ulcers and stomach problems and change the taste of
food—all leading to a lack of interest in eating.
Question: Are medications available to prevent weight loss?
Answer: Yes. If the reason for your weight loss is an infection, then a medica-
tion may be prescribed to kill the infection. If the problem is a lack of inter-
est in eating, medications used to increase the appetite as well as caloric
intake are prescribed. If there is a lot of breakdown in muscle mass, there
are drugs on the market, such as anabolic steroids, testosterone, and human
growth hormone, that might help this condition.
Question: Can I exercise?
Answer: Yes, you can exercise; however, before you begin an exercise pro-
gram, discuss it with your medical professional. He or she will determine
the appropriate amount of exercise for you. For more information, refer to
the sections on aerobic exercise and weight training in the AIDS and AIDS-
related diseases workbook.
Question: How can exercise help with cachexia?
Answer: Exercise helps increase muscle mass and functional capacity and
improves your ability to fight off infections. In addition, exercise has a posi-
tive impact on your psychological well-being.

10 The “Golden Years”
EXERCISE IN THE HEALTHY ELDERLY
Background
As we grow older (i.e., >65 years old), we accumulate a number of deficits caused
by degenerative illnesses for which we compensate in different ways until the day
comes when compensation is no longer possible, our physiologic reserve has been
decreased to the point that homeostasis can no longer be achieved, and death fol-
lows. If medicine has fulfilled its goal, by the time of death, those diseases that could
have been prevented have been prevented, those that could have been cured have
been cured, and, through the duration of the person’s life, the functional capacity
has been increased and the symptoms of disease decreased as much as possible. The
functional capacity and the amount of pain and suffering give the patient a certain
level of excellence called the quality of life. The primary objective of exercise
in the elderly is to treat their medical problems and improve their functional
capacity, thus improving their quality of life.
The following changes occur as we age:
• Decreases are seen in

• Maximal heart rate and cardiac output
• Maximal oxygen uptake
• Vital capacity
• Reaction time
• Muscular strength and lean body mass
• Flexibility
• Glucose tolerance
• Resting metabolic rate
• Increases are seen in
• Resting and exercise blood pressure
• Residual volume
• Percent body fat
• Recovery time
Little or no change is apparent in the resting heart rate.

Most adults who have experienced an illness severe enough to deprive them of
their ability to function independently report feelings of helplessness (inability to
159
satisfy basic needs), hopelessness (inability to see any purpose in living), and use-
lessness (low self-worth). Approximately 44% of the population over age 65 has
some degree of physical disability. When those patients realize that they will not
be able to achieve what they want to, they often develop feelings of low self-worth.
Reactions from the insulted self-esteem might include anger, depression, decreased
psychomotor activity, anxiety, withdrawal, and other symptoms. Inactivity brings
muscle wasting, weakness, contractures, pain, fear of falling, fear of further injury,
fear of more pain, and eventually resignation to the role of invalid and refusal to
exercise or to engage in physical activities. This further decreases the level of fitness
and worsens chronic medical problems.
The poor fitness levels in our elderly population are a result of sedentary lives
and the presence of medical problems such as diabetes, hypertension, COPD,
heart failure, and peripheral vascular disease. But even the healthy among the
aged are unfit. Exercise capacity in the apparently healthy elderly population
is so low that activities of daily living may use >50% of the person’s maximal
exercise capacity!
Management
Exercise is therapeutic. It is indicated in the management of the majority of the dif-
ferent medical problems that affect the elderly and has many other practical benefits.
The age-related changes listed earlier are secondary to a decrease in resting energy
expenditure, a decrease in the thermic response to food, decreased catecholamine-
induced lipolysis, reduced muscle mass, and decreased triiodothyronine levels. The
decrease in body weight after 70 is most likely related to decreased caloric intake.
Physical activity, especially when combined with adequate dietary calcium and
protein intake, retards osteoporosis, increases muscle mass and muscle strength,
improves functional capacity, and decreases the risk of falls. Further improvements
are reported in sleep patterns, appetite, bowel function, self-image, cognitive func-
tion, and decreased depression, anxiety, and need for drug therapy. The metabolism
of medications and the ability of the kidneys to excrete drugs might be impaired;
therefore, drugs remain in the body for longer periods of time. It is important to iden-
tify individuals who self-medicate and/or do not follow medication instructions. Any
side effects resulting from medical prescriptions must be managed prior to undertak-
ing exercise.
Exercise Issues
A medical evaluation is advisable for all elderly patients before they engage in a
vigorous exercise program. Individuals wishing to participate in vigorous exercise
(i.e., activities greater than 60% of their VO2 max, or maximum capacity) should
have a medical examination and clinical exercise stress test before starting an exer-
cise program. Particular attention should be given to their mental status, muscu-
loskeletal system, cardiovascular system, pulmonary system, and the status of the
different chronic medical problems that might be present. As many as 70–80% of
all relative or absolute contraindications to exercise are detected during a routine

The “Golden Years” 161
history and physical. They include cardiopulmonary or metabolic instability, neuro-

logic problems, severe arthritis, etc. (see Appendix B).
A cardiopulmonary stress test (see Appendix B) will further identify the
majority of individuals with medical problems and minimize the risk for under-
taking exercise in the elderly. Other benefits include evaluation of exercise
capacity and cardiac and pulmonary reserve and identification of an appropriate
exercise heart rate.
Due to the wide range of fitness levels associated with the elderly, there is consid-
erable variability among methods of expressing exercise intensity. Prescribing exer-
cise by heart rate may not be the best method. The inability of older individuals to
self-monitor their pulse and concomitant medical problems such as diabetic neuropa-
thies and chronic arrhythmias may limit the usefulness of this method. If exercise
intensity is prescribed using a target heart rate, we recommend measuring the maxi-
mal heart rate from a cardiopulmonary stress test as opposed to predicting it from
age (see Appendix A for detailed methods to prescribe aerobic exercise intensity).
A fitness evaluation should include a cardiopulmonary stress test, as well as a
flexibility and strength assessment. Flexibility exercises should be slow and static
in nature. Weight training is strongly recommended and is outlined in detail in the
following sections. Improvements in muscular strength and endurance have been
reported to result from resistance training in the elderly. However, the changes
in muscular strength are mainly due to a more efficient neuromuscular facilitation
instead of muscular hypertrophy.
Resistance training, especially upper body exercises, is strongly encouraged in
healthy elderly patients to enhance their activities of everyday living. We recom-
mend that resistance-training sessions be performed either concomitantly or on
alternate days with aerobic exercise, at least 2 days per week. If resistance training
is performed at the same time as aerobic training, it should follow the aerobic exer-
cise. This will ensure that the core temperature of the body has had adequate time to
warm up, enhancing flexibility and reducing the chances of musculoskeletal injuries.
Performing one set of 10–15 repetitions is recommended.
Exercises that involve major muscle groups, like the chest, arms, and shoulder
muscles for the upper body and the leg, hamstring, and quadriceps for the lower body,
should be performed. The intensity should not exceed the prescribed target heart rate,
or rating perceived exertion (RPE) of 10–16. If the resistance exercises are performed
on the same day as aerobic exercise, the sessions should not exceed 30–45 minutes in
duration. The duration of resistance training, performed on alternating days, can be
lengthened depending on the individual’s tolerance and recovery ability.
When they are available, resistance machines are recommended over free
weights. Balance and overloading injuries are less likely. Individuals with arthritic
flare-ups are advised not to exercise with weights until their inflammation has
become inactive. Weight-training exercises that can be done at home are illustrated
in the “Golden Years” workbook, as part of the included (CD).
Many elderly persons are so unfit that they will not be able to exercise aerobically
at the prescribed RPE of 10–16 (Appendix A, Method 5) for more than a few min-
utes. These patients will benefit from a program that will alternate several minutes
of exercise with several minutes of rest, slowly increasing the exercise time until the

person is able to exercise for 20 minutes without interruption. Increasing the exercise
time by 2 minutes per session per week is recommended.
The very frail elderly should only exercise under supervision and special atten-
tion should be given to symptoms of exercise-induced cardiopulmonary or meta-
bolic decompensation and/or overuse injuries. If exercise causes injury or illness, the
exercise program should be temporarily halted until the condition has been treated.
A new exercise evaluation and prescription should take place before the person is
allowed to exercise again.
The presence of stable medical problems has no effect on muscle metabolism in the
elderly. However, the elderly recover more slowly than the young and the slow rate of
recovery is not improved with an exercise program. Research on exercise in the elderly
has documented that once an appropriate exercise has been prescribed, there is a vir-
tual absence of reports of serious cardiovascular or musculoskeletal complications. In
fact, approximately 34% of the population 65 years and older engage in regular exer-
cise. Exercisers are slightly younger; have a more positive health perception, higher
income, and higher education; and are more likely to report fewer than two of the fol-
lowing medical conditions: heart disease, hypertension, arthritis, and emphysema.
Exercise in the elderly needs to be tailored to the individual exerciser according to
the subject’s preference of exercise activities and the objectives of exercise. Moderate
and high exercise intensities (>60% of the VO2 max) yield higher cardiovascular
benefits, while lower intensities and higher volumes of exercise are more suitable
for obesity management. Weight-bearing exercises are best for osteoporosis; non-
weight-bearing exercises, such as swimming, are recommended for individuals with
osteoarthritis; and group exercises, such as ballroom dancing, for social benefits.
The idea is to offer a menu of exercise activities likely to stimulate participation and
reduce the likelihood of attrition.
WEIGHT TRAINING GUIDELINES DURING THE GOLDEN YEARS

When older individuals undergo weight training, special attention should be given to
the abilities of the person. Some may be extremely deconditioned, while others may
have other conditions (e.g., obesity, hypertension, back problems) that may limit their
ability to exercise. Contraindications to weight training include:

Most strength gains are the result of neuromuscular familiarization to the exercise.
However, some gains in strength can be attributed to muscle hypertrophy. To control
blood pressure and prevent the elevation of after-loads on the heart, isometric or static
components should be minimized when the weight-lifting exercise is performed by

The “Golden Years” 163
breathing on exertion and using a weight that can be lifted without stopping halfway
through the motion.
for patients are illustrated in the “Golden Years” workbook.

[100 – (# reps × 2.5)] = % 1RM

be exceeded when lifting weights.
RECOMMENDED READING
Chavez Velazquez, Z. 1993. Benefits of physical exercise in the elderly. Revista Cubana de
Enfermeria Enferm 9:87–97.
Elward, K. 1992. Benefits of exercise for older adults. A review of existing evidence and current
recommendations for the general population. Clinical Geriatric Medicine 8:35–50.
———. 1992. Factors associated with regular aerobic exercise in the elderly population.
Journal of the American Board of Family Practitioners 5:467–474.
McCully, K. K. 1991. Muscle metabolism in older subjects using 31P magnetic resonance
spectroscopy. Canadian Journal of Physiological Pharmacologists 69:576–580.
Merck & Co. 1995. Merck Manual of Geriatrics, 2nd ed., 397–409. Whitehouse Station, NJ:
Merck & Co.
Mitchell, R. 1994. The average daily energy expenditure of elderly males and females. Asia
Pacific Journal of Public Health 7:218–223.
Panton, L. B. 1996. Relative heart rate, heart rate reserve, and VO2 during submaximal exer-
cise in the elderly. Journal of Gerontology A: Biological Sciences and Medical Sciences
51:M165–M171.
Vallbona, C. 1984. Physical fitness prospects in the elderly. Archives of Physical Medicine and
Rehabilitation 65:194–200.

EXERCISE PRESCRIPTION DURING THE GOLDEN YEARS

Frequency
Exercise a minimum of three times per week, but no more than 5 days per week.
Try to alternate the exercise days to allow plenty of time for recuperation.
Modality
Walking is the preferred method and does not require any special equip-
ment. Stationary or active bike riding and swimming are also accept-
able modalities, especially if a patient has joint pain. Try combining
different modalities during the exercise session. Weight training may
be beneficial. Include weight training at least two times per week, pref-
erably immediately after the aerobic exercise. See the “Golden Years”
workbook for detailed illustrations.
Duration
Begin with a time that is comfortable—perhaps initially 10 minutes.
Intensity
The intensity should be a perceived exertion between light and hard, an
RPE of 10–16.
Other Instructions
pain immediately.
follow-up visit.

11 The Physically Inactive
EXERCISE RECOMMENDATIONS FOR HEALTHY
BUT PHYSICALLY INACTIVE INDIVIDUALS
Background
Physical activity is defined as movement that involves contraction of the muscles.
Examples include activities such as housework, gardening, walking, and climbing
stairs. Exercise is defined as a more planned activity and includes activities such as
swimming, cycling, running, tennis, golf, and working out at a health club.
Physical Activity and Exercise: What Is the Difference?

Most daily physical activity is considered light to moderate in intensity. For exam-
ple, jogging, running, or maintaining activity without stopping for long periods of
time will improve cardiovascular health. In most cases, exercise at an intensity of
40–60% of maximum heart rate will accomplish this. That is why it is important to
exercise within the target heart rate range when doing cardio, for example, to reach
a certain level of intensity. However, that being said, any activity at all is better than
nothing at all: “It is better to stand than sit.”
Physical Activity and Exercise: Understanding Intensity

How can someone tell if an activity is considered moderate or vigorous in intensity?
He or she can do what is called the “talk test.” If a person can talk while performing
exercise, it is moderate. If an individual needs to stop to catch his or her breath after
saying just a few words or cannot sing a song, the activity is more on the vigorous
side. The level of exercise intensity when using the talk test may depend on the fit-
ness level. For example, for a sedentary person, walking may be more vigorous than
jogging would be for a more conditioned person. Another example is dancing the
waltz. This would be considered moderate intensity, but aerobic ballroom dancing
would be considered vigorous. Again, it is not just the choice of activity, but also how
much exertion it requires.
An exercise program should include the following elements designed to
improve health:
• Cardiorespiratory endurance
• Muscular strength (see Appendix A, Method 10)
• Flexibility or stretching
165
The healthy population interested in exercise can further be divided into two
groups: the exercisers and the athletes. Exercisers seek fitness as an end in itself. Fit
is defined as suitable or well adapted to do something; exercise fitness refers to the
ability to do physical work. They aim to improve their endurance, speed, strength,
flexibility, and health.
Athletes seek improvement in performance. They push the limits of safety and risk
injury to excel in their particular sport, sometimes sacrificing one goal to obtain another.
For example, weight lifters disregard speed and endurance and sometimes they risk los-
ing their health by taking anabolic steroids in their quest for greater strength and power.
With the athletic subject, exercise testing will provide significant information
to generate an appropriate exercise prescription and optimize the efficiency of the
training program with minimal risk of over- or undertraining. Exercise testing for the
athlete is done to measure the VO2 max, the anaerobic threshold (AT), and the exer-
cise economy defined as the oxygen consumption at different work intensities. See
Appendix B for more detailed information on stress testing and Appendix A for
exercise prescription methods. We recommend aerobic exercise at a rating perceived
exertion (RPE) of 12–16 (see Appendix A, Method 5).
Exercise testing and prescription should address the needs of the subject being
tested. There is considerable variability among exercisers: There are schoolchildren,
middle-aged adults, cardiac patients, young executives, etc. The exercise prescrip-
tion should include flexibility, aerobic exercise, and strength training. Exercise for
flexibility can be done before the warm-up and during the cool-down periods. It is
important to maintain or improve the range of joint motion and prevent injury.
Strength training should be specific to the needs of the patient. For example,
a cardiac patient may do better by exercising aerobically to vasodilate and warm
up the core temperature of the body prior to strength training. Furthermore, police
officers, firefighters, and manual laborers obtain more benefit from strength training
than individuals in sedentary occupations.
Initially, low weights and aerobic exercise intensities below the AT are indicated,
progressing to higher weights and higher intensities. As the level of fitness and
motivation increase, the intensity of the aerobic activity increases to the point that
60–80% of the training is done at or just below the AT (see Appendix A, Method 7).
The amount of training done above the AT depends on the physiologic profile and the
expected performance goals. For example, interval training above the AT increases
speed and cardiovascular recovery times.
The exercise prescriptions in this chapter were developed for the patient who is
free of risk factors for heart disease—that is, healthy, but deconditioned. The follow-
ing guidelines have been developed from the American College of Sports Medicine
(ACSM) recommendations:
• ACSM risk factors for heart disease:

• For men, >45 years; for women, 55 years
• Family history of heart disease prior to 55 years
• Smoking, hypertension, or hypercholesterolemia
• Diabetes
• Sedentary lifestyle

The Physically Inactive 167
• Benefits of regular physical activity:

• Improved cardiorespiratory function and reduced coronary artery disease
• Decrease in morbidity and mortality
• Improved psychological profile and self-esteem
• Reduction in hospitalizations and health care costs
WEIGHT TRAINING GUIDELINES FOR PHYSICALLY

INACTIVE INDIVIDUALS WITHOUT DISEASE
When out-of-shape or deconditioned sedentary individuals undergo weight train-
ing, special attention should be given to the abilities of the individual. Some may be
extremely deconditioned, while others may have conditions that limit their ability to
exercise. Contraindications to weight training include

When weight lifting takes place, circuit training using moderate weights with frequent
repetitions is recommended. Circuit training involves moving from exercise to exercise at
a consistent pace. This will develop muscle endurance and strength. Most strength gains
are the result of neuromuscular familiarization to the exercise. However, some gains in
strength can be attributed to muscle hypertrophy. To control blood pressure and prevent
the elevation of after-loads on the heart, isometric or static components should be mini-
mized when the weight-lifting exercise is performed by breathing on exertion and using
a weight that can be lifted without stopping halfway through the motion.
for patients are illustrated in the nonexerciser workbook section.

[100 – (# reps × 2.5)] = % 1RM


be exceeded when lifting weights.
RECOMMENDED READING
American Association of Cardiovascular and Pulmonary Rehabilitation. 1991. Guidelines for
cardiac rehabilitation programs, 2nd ed., chap. 3. Champaign, IL: Human Kinetics.
EXERCISE PRESCRIPTION FOR PHYSICALLY INACTIVE

INDIVIDUALS WITHOUT DISEASE
Frequency
Modality
The greatest improvement in cardiovascular conditioning will result when
aerobic exercises are performed that involve the large muscles. These
muscles should be worked in a rhythmic or aerobic fashion. Examples
of such activities are walking, running, swimming, hiking, rowing,
dancing, and cross-country skiing. Virtually any activity that meets
the previous requirements and maintains an elevated heart rate will
improve cardiorespiratory fitness. Resistance or weight training should
be added to improve musculoskeletal strength. See the guidelines on
weight training.
Duration
Begin with a time that is comfortable—initially about 10 minutes. Gradually
Intensity
If a maximal stress test is available, the intensity should be between 60 and
90% of maximum heart rate or 40–85% of the maximum functional capac-
ity (VO2 max) or heart rate reserve (see Appendix A). An RPE between
12 and 16, or somewhat hard to very hard, should accomplish this.
Other Instructions
pain immediately.

The Physically Inactive 169
follow-up visit.

12 Pregnancy
BACKGROUND
Many women who are active prior to their pregnancy desire to stay active throughout
their pregnancy. With an increasing frequency, women are turning to their physicians
for advice about exercising during their pregnancy and postpartum. Unfortunately,
exercise standards for prescribing exercise during pregnancy are vague. They are
based primarily on common sense and intuition. Furthermore, research is lacking on
the effects of exercise during pregnancy and postpartum. Women have been forced
to turn to nonprofessionals for advice about exercise (e.g., the “personal trainer”).
Therefore, the medical basis for an exercise prescription during pregnancy is often
inappropriate, inaccurate, or incomplete.
Physically active women who are contemplating pregnancy may feel a strong need
to continue their exercise program, but may also be concerned that the exercises may
have an adverse effect on the course and outcome of their pregnancy. There are no
conclusive data to suggest that pregnant women should limit exercise intensity
and lower target heart rates because of potentially adverse effects. Furthermore,
there is evidence supporting the notion that regular exercise will improve the out-
come of pregnancy.
Some studies have reported a conditioning effect as a result of strenuous exer-
cise concomitant with a decrease in gestational length, maternal weight gain, and
birth weight. However, these changes did not negatively impact the course of labor
and delivery or immediate neonatal course. Finally, other studies have reported that
women who exercise regularly return to their prepregnancy weight, strength, and
flexibility sooner than those who do not exercise regularly. Following is a list of com-
monly reported benefits of exercising during pregnancy:
• Reduction in severity and frequency of back pain

• Reduced stress, anxiety, and depression
• Controlled weight gain
• Improved digestion and decreased constipation
• Greater energy for daily activities
• Reduction in postpartum belly
Currently, approximately 50% of women of reproductive age exercise regularly;

over 90% plan to continue to remain active during and following their pregnancies.
171
MANAGEMENT
Many changes occur during pregnancy that will affect the exercise prescription.
First are the changes to connective tissue. Under the influence of hormones such as
progesterone, estrogen, and elastin, connective tissues become softer and more eas-
ily stretched. This may render the joints more susceptible to injury. Problems with
balance may also occur as the body’s center of gravity changes due to an enlarging
uterus and breasts. This may place an increased stress on the sacroiliac and hip
joints, causing balance problems and increasing the risk for falls.
Next, cardiovascular changes occur due to increases of about 30% in maternal
blood volume. Furthermore, heart rate and cardiac output will be elevated at rest.
Hematocrit levels also will be lower during pregnancy, but will tend to hemoconcen-
trate during exercise. The significance of these changes when prescribing exercise
will be discussed in the next section on exercise issues.
The third change occurs in nutrition. Patients should increase their caloric
intake by 300 additional calories each day to meet the needs for pregnancy.
Using exercise to promote weight loss during pregnancy should be discouraged.
Most women who do not breast feed gain about 6 pounds postpartum once their
weight stabilizes. Repeated pregnancies can result in this weight gain reaching
medically significant levels. The risk of dehydration increases during pregnancy.
Patients should be advised to drink plenty of liquids before and after exercising
to prevent dehydration.
Respiratory responses represent the fourth change during pregnancy. As the end
of pregnancy approaches, the enlarging uterus displaces the diaphragm upward.
This reduces lung volumes, causing dyspnea in some women. However, pulmonary
function at rest remains normal. An increase in tidal volume and increased minute
ventilation are commonly seen. In part, they compensate for the increased oxygen
demands and CO2 production, but pregnancy is often associated with mild hyperven-
tilation at rest and during exercise.
Last, endocrine factors change. Hypoglycemia is always a concern because preg-
nant women utilize carbohydrates at a greater rate during exercise. Increased insu-
lin resistance can cause gestational diabetes. Epinephrine and norepinephrine levels
increase significantly during exercise. Increases in these hormones may affect uter-
ine muscle activity and contractions and precipitate premature labor. Women at risk
for premature labor should therefore avoid vigorous exercise.
MANAGING THE PREGNANT ATHLETE

As a general rule, we do not recommend routine exercise testing for the pregnant
woman. It is of limited clinical value unless it has a very specific medical need, such
as identifying exercise tolerance, pulmonary function, heart disease, or drug effec-
tiveness. However, a very specific group of women may benefit from exercise testing
during pregnancy. Serial exercise testing should be a regular part of care for all female
athletes who feel they must maintain an intense exercise program during pregnancy.
A baseline evaluation should occur before pregnancy to obtain a valid refer-
ence point, followed by multiple tests at the beginning of each trimester thereafter.

Pregnancy 173
The modality of exercise testing should coincide with the athlete’s current training.
Variables to be assessed could include the following:
• Oxygen consumption
• Arterial pressure
• Lactate
• Catecholamine and glucose levels
• Rectal temperatures (restricting the rise to 38°C)
• Body fat assessments (skinfolds); at least 2.5 kg weight gain in the first
16 weeks, continuing throughout
• Measurement of the fetal response to activity (should be relatively unaffected)
• Ultrasound examination to rule out multiple gestation and confirm normality
This information would be ideal to have for planning and maintaining a safe
exercise regimen. Several specific conditions to be aware of during exercise testing
include the following:
• Due to a pregnancy-induced decrease in venous tone, venous pooling may

result and postural hypotension and syncope may occur; therefore, meas
ures should be undertaken to prepare for this and exercise should not be
discontinued abruptly.
• The testing environment should be maintained at 19–22°C with humidity
under 50%.
• Appropriate footwear should be used to prevent foot strike injuries.
EXERCISE ISSUES
There is no scientific foundation for the specifics of exercise prescription during
pregnancy; however, it is important to note that the current data do not indicate that
any type of exercise is hazardous to the mother or fetus. There are some caveats
to address when exercising during pregnancy, and these will be discussed later in
this section. Our planned program of exercise during pregnancy is designed to be
applicable to all women who do not have absolute contraindications, regardless of
their current physical condition. Furthermore, we do not recommend commencing
an intense exercise regimen during pregnancy if a woman is in poor physical
condition or for the purpose of weight reduction. Low-impact activities such as
swimming and stationary cycling are recommended for individuals who have never
exercised before and wish to begin exercising during pregnancy.
Ideally, an exercise program should include a variety of modalities: walking,
swimming, stationary cycling, and possibly modified forms of dancing and calis-
thenics. Resistance training can also be included as part of the exercise program.
It is important that the physician assess the individual abilities of the patient and
prescribe the best modalities.
Contraindications for exercising during pregnancy are a matter of common sense
and include the following:

• Pregnancy-induced hypertension
• Premature rupture of membrane
• Early labor during current pregnancy
• Persistent bleeding
• Intrauterine growth retardation
Once the individual has been cleared for exercise, frequent communication
with her physician is essential. If any of the following changes are apparent dur-
ing exercise, the patient should seek medical advice before continuing with her
exercise program:
• Any sign of bloody discharge or a “gush” of fluids from the vagina

• Sudden swelling of the ankles, hands, or face
• Unexplained, persistent headaches, visual problems, or dizzy spells
• Elevated pulse or blood pressure that persists following exercise
• Heart palpitations or arrhythmias
• Abdominal pain
• Insufficient weight gain: <1.0 kg/month during the last two trimesters
Exercise intensity prescriptions by heart rate have typically had an upper cut-off
limit of 140 beats per minute for the mother. However, we recommend using the per-
ceived exertion (RPE) scale (see Appendix A, Method 5) at an intensity of no greater
that 15. Studies have reported that women naturally will decrease the intensity and
duration of their exercise as pregnancy advances. The frequency of exercise should
be at least 3 days per week. This will provide ample health benefits. The duration
of exercise should be for at least 20 minutes. Continuous activity is preferred to
intermittent activity.
There are certain caveats to be aware of when exercising. During the first tri-
mester, the closure of the neural tube occurs. Intense exercise in a hot environment
greater than 19–22°C and humidity greater than 50% can result in a hyperthermic
response and may interfere with the closure of the neural tube. However, this is
unproven in humans. Women should avoid exercising in the supine position after the
first trimester. The enlarging uterus may interfere with venous return by compress-
ing the vena cava; this can cause supine hypotensive syndrome, and cardiac output
and uterine circulation may decrease, increasing the risk of placental abruption.
Many of the physiological and morphological changes of pregnancy persist
for 4–6 weeks postpartum; therefore, prepregnancy exercise routines should be
resumed gradually.
WEIGHT TRAINING GUIDELINES DURING PREGNANCY

When pregnant women undergo weight training, general fatigue may prevent it from
being performed in a consistent manner. Contraindications are the same as those
listed previously in the section on exercise issues. Keep in mind that supine exercises
should not be performed after the first trimester.

Pregnancy 175
and ability. Weight machines and free weights can be used when the patient is able
to join a gym or fitness center.
When selecting the proper intensity, it is important that the amount of weight lifted
be based on the ability of the individual rather than on an arbitrary weight. We recom-
mend two methods to determine the intensity. Weight lifting should not be prescribed
for individuals who were not lifting prior to their pregnancy. All exercise or repeti-
tion sets may be performed one or two times or in one or two sets—for example:

[100 – (# reps × 2.5)] = % 1RM

weights and stretch elastic bands. The RPE of 15 prescribed for aerobic work should
not be exceeded when lifting weights.
RECOMMENDED READING
ACOG guidelines for exercise during pregnancy. http://www.birthingnaturally.net/exercise/
acog.html
American College of Obstetrics and Gynecology. http://www.acog.org/publications/patient_
education/bp119.cfm
Clapp, J. F. 1989. Pregnancy. In Exercise in modern medicine, ed. B. A. Franklin, S. Gordon,
and G. C. Timmis. Baltimore, MD: Williams & Wilkins.
EXERCISE PRESCRIPTION DURING PREGNANCY

Frequency
Exercise a minimum of three times per week, but no more than 5 days per
week. Do not insist on exercise if the patient feels excessively fatigued.

Modality
Depending on the exercise history, it is acceptable to begin with walk-
ing, jogging, or running. To encourage the continuation of exercise,
non-weight-bearing activities such as stationary cycling and swim-
ming are recommended when weight-bearing exercise can no longer
be tolerated. Try combining different modalities during the exercise
session. However, if the patient has not been weight training, a rigor-
ous weight-training program may be harmful. See the guidelines on
weight training for more information.
Duration
Begin with a time that is comfortable. Try to achieve 20–60 minutes of
aerobic exercise, resting as needed. Decrease the duration so the patient
is not completely exhausted at the end of the exercise session as the
pregnancy advances.
Intensity
The intensity should be prescribed using the RPE chart. A perceived exer-
tion no greater than hard (heavy) or 15 is recommended. If the patient
is taking her pulse during exercise, it should not exceed a heart rate of
140–150 beats per minute.
Other Instructions
pain immediately.
follow-up visit.
• Instruct the patient to stop exercising immediately if she feels faint or dizzy
or has heart palpitations.

13 Wheelchair-
Dependent Patients
BACKGROUND
Medical conditions associated with wheelchair dependency are stroke, multiple scle-
rosis, muscular dystrophy, and traumatic spinal cord injuries that result in paralysis.
This chapter will focus primarily on issues pertaining to spinal cord injuries.
Spinal cord injuries are classified as complete or incomplete depending on the
level of function. Complete damage results in little or no central nervous system
outflow from autonomic or somatic areas. The higher the spinal cord injury, the more
paralysis. For example, damage to the cervical region can result in quadriplegia,
whereas damage to the thoracic or lumbar regions can result in paraplegia.
EXERCISE ISSUES
Physical activity for individuals with spinal cord injuries can be challenging, but
very rewarding. Individuals with higher, more complete lesions—that is, quadri-
plegics—will be more limited than paraplegics (individuals with lower spinal cord
injuries). A sedentary lifestyle in wheelchair-dependent individuals can result in
secondary conditions such as cardiovascular disease, muscle wasting, osteoporosis,
decubitus ulcers, and peripheral vascular claudication.
Individuals with lesions in the cervical and thoracic regions above T1 (quadri
plegics) will have reduced sympathetic outflow to the heart and lungs. This results in
a reduction in cardiac output. Exercise-induced cardioacceleration and myocardial
contractility are therefore limited. Furthermore, the vasoconstriction reflex in nonac-
tive muscles is not apparent. Reductions in cardiac output limit blood flow to active
muscles, which results in early onset of peripheral fatigue. A low anaerobic threshold
at <40% of the VO2 max or early anaerobiosis diminishes aerobic capacity.
Exercise or physical activity is difficult for quadriplegics with higher level, com-
plete cervical lesions. Since these individuals are sympathectomized with limited
chronotropic and inotropic mechanisms, exercise prescriptions that use target heart
rates are inaccurate. Quadriplegics unable to perform unassisted exercising could be
referred for functional electrical stimulation (FES), which involves the application
of surface-applied electrodes (TENs units) to lower limb muscles (e.g., hamstrings,
quadriceps, and gluteals).
FES candidates must have intact and functional motor units (lower motor neurons
and the muscle fibers they innervate). A stretch reflex or muscle spasticity is usually
177
present in these individuals. Muscle contractions can be elucidated by placing the

electrodes directly over the motor points (where motor nerves enter the muscle).
With the use of a computerized link, these muscle contractions can be channeled to
perform knee extensions and cycle ergometer pedaling. However, because FES tech-
nology is peripherally induced and bypasses the central nervous system, increases
in heart rate, blood pressure, and vasoconstriction, as well as diminished sweating
mechanisms in nonactive muscles, do not result.
In some patients, autonomic dysreflexia can result in elevated blood pressures
(i.e., >175 mmHg). These individuals are at risk and should not exercise. Blood pres-
sure should be monitored during the initial FES sessions, and patients should not
attempt FES exercise in hot environments. The scientific literature contains little
information about the benefits and protocols for optimal FES prescriptions. FES
strength training exercises are usually performed to exhaustion, with intervals of
rest for two or three sets. Aerobic exercise protocols utilize power outputs that allow
continuous muscle contractions for 15–30 minutes. FES cycle ergometer exercise
appears better utilized for developing endurance than strength.
Exercises prescribed for individuals with paraplegia can utilize FES for lower
body conditioning while doing upper body motions concurrently. The advantages of
utilizing both methods include the following:
• Greater muscle mass involvement

• Higher metabolic rates
• Reduced venous pooling
To formulate an exercise prescription for paraplegic individuals, heart rate and/or

relative perceived exertion methods can be used (see the RPE chart in Appendix A,
Method 5). This prescription can be preceded by an exercise test, typically using an
arm crank or arm ergometer in paraplegic individuals. Protocols to measure maxi-
mal VO2, or fitness level, heart rate, and blood pressure can be either continuous or
discontinuous. It is important to remember that arm cranking elicits peak VO2 levels
about one third those of lower body testing. Maximal heart rates for arm exercise
also are 10–20 beats lower when compared to lower body testing.
Therefore, this should be taken into consideration when predicting maximal heart
rate from age (see Appendix A, Methods 1 and 2). For example, if an exercise test
is needed, an arm-crank protocol may begin with an initial power output of 0–5 W.
Intensity may be increased by raising the braking force every 1– 2 minutes in incre-
ments of 5–10 W. Maximal watts are normally limited to 25–30 W. Exercise can
then be prescribed using one of the methods listed in Appendix A.
Concerns for exercise in quadriplegics and paraplegics involve circulatory
“hypokinesis.” This may result in venous pooling and reduced stroke volumes.
Secondarily, disruption of the central sympathetic vasomotor and cardioacceleratory
mechanisms may occur. Quadriplegics may exhibit vasomotor dysfunction that is
dependent on the withdrawal of vagal activity for increases in exercise heart rates.

Wheelchair-Dependent Patients 179
WEIGHT TRAINING GUIDELINES FOR

WHEELCHAIR-DEPENDENT PATIENTS
When people with spinal cord injuries undergo weight training, autonomic dysre-
flexia may present a major area of concern. Other contraindications to weight train-
ing include:

Individuals can expect similar gains in strength and muscle size when compared
to sympathetically intact individuals provided they are able to perform the lifts at
similar relative intensities. To control blood pressure and prevent the elevation of
after-loads on the heart, isometric or static components should be minimized when
the weight-lifting exercise is performed by breathing on exertion and using a weight
that can be lifted without stopping halfway through the motion.
join a gym or fitness center. Weight-lifting exercises are best applied to paraple-
gic individuals who are able to use their upper body muscles.

[100 – (# reps × 2.5)] = % 1RM


RECOMMENDED READING
Glaser, R. M., and G. M. Davis. 1989. Wheelchair-dependent individuals. In Exercise in
Williams & Wilkins.
EXERCISE PRESCRIPTION FOR WHEELCHAIR DEPENDENCY

(QUADRIPLEGIA) FUNCTIONAL ELECTRICAL STIMULATION
Frequency
Exercise a maximum of three times per week. Try to alternate the exercise
days to allow plenty of time for recuperation.
Modality
Functional electrical stimulator cycle ergometer and/or closed-loop electri-
cal stimulator for knee extensions are recommended.
Duration
Aerobic protocol should utilize an intensity that allows the individual to
eventually achieve 15–30 minutes of continuous pedaling. Intervals
will most likely be required to achieve this time. Begin slowly, with
5- to 10-minute exercise sessions. Anaerobic or knee extensions should
be performed utilizing a weight that allows a maximum of 20 repeti-
tions or to exhaustion for a maximum of three sets.
Intensity
Initially begin FES cycle ergometry with 0 kg and increase gradually until
exhaustion. Knee extension exercise should not exceed 15 kg. Begin
with 0 kg and increase as tolerated.
Other Instructions
• Avoid performing FES in warm environments.
• Record progress to show the doctor at the next follow-up visit.
• Stop exercising immediately if faintness or dizziness is experienced.
• Check blood pressure at least during the initial exercise sessions.
EXERCISE PRESCRIPTION FOR WHEELCHAIR

DEPENDENCY (PARAPLEGICS)
Frequency

Wheelchair-Dependent Patients 181
Modality
Hybrid exercises utilizing simultaneous FES ergometer cycling and arm
cranking are recommended.
Duration
Duration of FES protocol as stated under FES quadriplegia guidelines.
Arm cranking can be continuous or discontinuous to coincide with
FES duration.
Intensity
FES intensity as stated under FES quadriplegia guidelines. Arm cranking
should begin at an intensity that allows a minimum of 5 minutes of
continuous arm cranking and be increased as tolerated.
Other Instructions
• Avoid performing FES in warm environments.
• Record progress to show the doctor at the next follow-up visit.
• Stop exercising immediately if faintness or dizziness is experienced.
• Check blood pressure at least during the initial exercise sessions.

14 Prepubescent Children
HEALTHY CHILDREN
Background
This chapter will provide information about prepubescent children. We are routinely
asked by parents whether it is safe for their children to be exercising and at what
intensity. Today, pressure and monetary support from parents hoping their child will
become a highly paid superstar can place stress on children to perform at a young
age. Currently, there is no apparent underlying physiological factor that would make
children less suitable than adults for prolonged, continuous activities. For a more
thorough investigation in the major differences in physiological responses between
children and adults, see Zwiren (1993). According to the American Academy of
Pediatrics (AAP), “If children enjoy the activity and are asymptomatic, there is
no reason to preclude them from training for or participating in such events.”
Management
Children can exercise at a variety of intensities and durations. However, if given a
choice, they prefer short-term, intermittent activities that have a high recreational
component: For example, soccer is preferable to treadmill running and bicycling
outdoors is better tolerated than stationary cycling. Furthermore, children seem to
tolerate repeated activities that last a few seconds and have short rest periods. The
least physiologically tolerable types of activities are ones that are highly intense and
last from 10–90 seconds.
The metabolic rate of children is high at a given submaximal walking or running
speed. Therefore, children produce excessive body heat when exercising. An imma-
ture cardiovascular system with a low skin-blood-flow capacity results in a poor
capacity for sweating. This, along with a large surface–to–mass ratio in children,
results in a low tolerance to warm weather and a greater susceptibility to heat stress.
Furthermore, the high surface area–to–body mass ratio of children accelerates heat
loss during exposure to the cold and can increase the risk of hypothermia.
It takes children about 10–14 days to acclimate to a hot environment. Clothing
should be lightweight and have the ability to breathe to allow for the evaporation of
sweat. When air temperature and humidity levels are high, activities lasting longer
than 30 minutes should be reduced, and fluid replacement of 100–150 mL every
183
15–30 minutes should be provided whether the child is thirsty or not. Cold water is
better absorbed; a beverage should not contain more than 25 g/L of sugar.
Activities that involve repeated mechanical stress over a long period of time can
result in overtraining. Children may be more prone than adults to musculoskeletal
problems due to overuse. Risks factors include:
• Any abrupt change in intensity, duration, or frequency of exercise of more

than 10% per week
• A musculotendinous imbalance in strength and flexibility
• Anatomic malalignment of lower extremities
• Improper footwear/running surface
Exercise Issues
The goal of the exercise prescription for children should focus on keeping the child
active, rather than increasing the functional capacity or VO2 max.
Recommended activities are those that require moving the whole body, such as
running, swimming, and cycling activities. These should be performed at an intensity
not greater than a rating perceived exertion (RPE) of 13 (see Appendix A, Method 5).
Because of difficulty in monitoring heart rates with children, the perceived exertion
scale is a more practical method for monitoring intensity. To make up for the lower
intensity, the frequency can be increased to daily and the duration may be expanded
to more than an hour. Furthermore, because children are involved in a variety of
activities throughout the day, a specific time should be set aside for sustained aero-
bic activities. These changes will maximize the volume of energy expended, which
would be beneficial for obese children.
Fitness Testing
Typically, fitness testing in children involves the measurement of skill-related fitness
components such as agility and balance tests. Some children, however, may require
a stress test to determine their maximal exercise capacity or health-related aspect of
their fitness. Adult-based equations that predict the VO2 max should not be applied
to children; the VO2 max should be measured directly.
Children who are 7 years or younger perform a stress test better on a treadmill
than on a stationary cycle. Treadmill activity is self-driven and does not require as
great an attention span when compared to a stationary cycle. Underdeveloped knee
extensors, coupled with premature muscular fatigue and the inability to maintain
a specific cadence on a stationary cycle, are more likely to prevent children from
producing their best effort. If a cycle must be used, we recommend an electronically
braked cycle so that the workload is held constant and is not dependent on any given
pedaling rate. The recommended pedaling rate is 60–70 revolutions per minute.
WEIGHT TRAINING GUIDELINES FOR CHILDREN

Resistance or strength training in children is not contraindicated. However, power
lifting or participation in heavy 90–100% of a 1RM lift can be harmful to the

Prepubescent Children 185
musculoskeletal system, especially if the epiphyseal plates and long bones are still
growing. If children do decide to participate in resistance training, strength and
endurance gains can be obtained. These gains result mainly from a neuromuscu-
lar familiarization, rather than muscle hypertrophy, because testosterone is not in
adequate supply in the body.
An appropriate resistance training program should be supervised by well-trained
adults and not the average personal trainer found in a fitness center. High repeti-
tion, 10–15 reps, and low resistance should be emphasized. Flexibility and proper
technique should be taught to balance out a healthy resistance training program.
Following are some recommendations for developing a sound resistance training
program in children:
• No matter how big the child is, remember that, physiologically, he or she
should still be treated as a child.
• Teach proper breathing techniques (i.e., no valsalva maneuvers, exhale
on exertion).
• Focus lifting techniques on proper form and slow, continuous movements.
• Lift weights than can be lifted at least 10 times.
• Increase intensity by increasing the number of repetitions to 15, then
increasing the weight.
• Perform one or two sets of 8–10 different exercises. Emphasize large mus-
cle groups, utilizing compound muscle groups.
• Limit resistance training to twice per week.
When prepubescent children undergo weight training, it is important not to encour-

age them to perform maximal lifts. Weight training is usually performed to increase
fitness and improve performance, with gains in strength accompanied by a minimal
risk of injury. Children should be supervised by adults at all times. Other contraindi-
cations to weight training include:

The type of weight-lifting equipment used depends on the child’s preference and
ability. Weight machines and free weights can be used when the child is of age able
to join a gym or fitness center.
lifted be based on the ability of the child rather than on an arbitrary weight. We

recommend the following method to prescribe the intensity. All exercise or repetition
sets may be performed one or two times or in one or two sets. For example, choose
a weight that can be lifted comfortably 10–15 times. When 15 repetitions can be
comfortably performed, the weight may be increased to an amount that can be lifted
at least 10 times. Weight training should be supervised and consist of low weight and
high repetitions as described before.
and stretch elastic bands. The RPE of 13, prescribed for aerobic work, should not be
exceeded when weight lifting.
REFERENCE
Zwiren, L. D. 1993. Exercise prescription for children. In American College of Sports Medi
cine resource manual for guidelines for exercise testing and prescription, 2nd ed., ed.
J. L. Durstine, A. C. King, P. L. Painter, et al. Philadelphia, PA: Lea & Febiger.
RECOMMENDED READING
EXERCISE PRESCRIPTION FOR PREPUBESCENT CHILDREN

Frequency
Children can exercise every day. However, if exercise involves a structured,
strenuous aerobic program, be sure to allow at least 2 days per week for
recuperation. If weight lifting is prescribed, no more than two to three
times per week is recommended.
Modality
Exercises that work the large muscles continuously are recommended—for
example, activities that involve walking and running, such as soccer and
basketball. Stationary or active bike riding and swimming are also accept-
able. Although different modalities can be combined during the exercise
session, a rigorous program of lifting heavy weights may be harmful.
Duration
Activities that are repeated and last a few seconds, incorporating short rest
periods, are recommended. A total time of at least 20–30 minutes is rec-
ommended each day. Intense activities lasting 10–90 seconds may not be
well tolerated. Activities that involve repeated mechanical stress, such
as endurance runs, may result in injury and overtraining. Allow plenty
of time for recuperation if these types of activities are prescribed.

Prepubescent Children 187
Intensity
The intensity should not be greater than an RPE of 13 or, more importantly,
one that is comfortable for the child and can be sustained for at least
20 minutes. When lifting weights, perform no more than two sets per
body part, with 10–15 repetitions.
Other Instructions
• Instruct the child to report any weight gain, shortness of breath, or chest
pain immediately
• Record progress.
• Stop exercising immediately if faintness, dizziness, or heart palpitations
are reported.
• Warm up and cool down prior to exercising for at least 5–10 minutes at a
comfortable intensity.
• Do not perform heavy maximal lifts when resistance training and do not
increase the amount of weight lifted until 15 repetitions can be performed
with the current weight.
• Bring plenty of water if the child is not used to exercising in a hot
environment.
• Limit the exercise duration to short bouts, with plenty of rest, for 10–14 days
until the child is acclimatized to the heat.

Appendices

Appendix A: Exercise
Prescriptions and “the Charts”
Appendix A is designed to assist the interested health professional with writing exer-
cise prescriptions. This appendix is referenced with the appropriate method in the
“Exercise Issues” section of each chapter and can be used to prescribe exercise based
on the recommendations in each chapter. For a more detailed explanation on using
metabolic equations to predict exercise capacity and prescribe exercise, the reader is
referred to a book by David P. Swain and Brian C. Leutholtz, Exercise Prescription:
A Case Study Approach to the ACSM Guidelines 2nd ed. Human Kinetics, 2007.
The majority of the methods described allow exercise to be prescribed by target
heart rate. However, some patients should not be prescribed exercise by a target heart
rate. The window of intensity for calculating target heart rates is commonly 40–85%
of VO2 max, heart rate reserve, or VO2 reserve. Exercise for a deconditioned patient
should be prescribed on the lower end of the intensity window.
We recommend that patients who wish to exercise via target heart rate be instructed
to check their pulse at the wrist counting the first beat as ‘zero.’ Palpating a pulse at
the neck or using the carotid arteries may result in the activation of the baroreceptor
reflex, thus slowing the heart rate and resulting in syncopy or dizziness. Teaching
a patient to palpate the pulse for 6 seconds and then adding a zero is the simplest
method. However, 10- and 15-second counts (then multiplying by 6 and 4, respec-
tively) can be used to increase the accuracy. Never encourage the use of the thumb for
palpating a pulse because it has a pulse of its own that may confuse the patient. The
middle and index fingers are recommended.
METHOD 1: THE AGE-PREDICTED METHOD

The age-predicted method for calculating a target heart rate is one of the simplest
methods. It is widely used in aerobic classes and can be found on charts on the walls
of most health clubs. The principle is based on the fact that the heart’s maximum
rate is 220 beats per minute (bpm) and that this maximum rate declines by a beat
each year. This 1 bpm yearly decrease is probably a result of the heart stiffening
and becoming less compliant. There is a standard deviation of ±10 beats per minute
for any one individual. Although it is acceptable, this method may underestimate or
result in a “low” target heart rate when compared to other methods. An example
using the age-predicted method follows:
191
192 Appendix A: Exercise Prescriptions and “the Charts”
You want your 62-year-old patient to exercise at 60% of his maximum heart rate.
What would be his target heart rate (HR)?
Answer: 95 bpm
Solution: target HR = (0.60) (220 – age)
target HR = (0.60) (220 – 62)
target HR = (0.60) (158)
target HR = 95
It is important to be aware of any medications that would affect the heart rate
(e.g., (β-blockers) that your patient may be taking. Prediction of maximal heart
rate using this method would then be inaccurate. Maximal heart rate would need
to be measured from a maximal stress test (see Appendix B). This method should not
be applied to patients with peripheral neuropathies or chronotropic incompetence.
METHOD 2: HEART RATE RESERVE OR KARVONEN METHOD

The heart rate reserve (HRR), or Karvonen method, takes into account the patient’s rest-
ing heart rate. It can be used by either predicting or measuring the maximal heart rate
(see Method 1). The resting heart rate should be determined when the patient has been in
a state of quiet rest for several minutes. The patient should not be overheated, dehydrated,
or under the influence of recently consumed caffeine, nicotine, or other drugs that influ-
ence heart rate. An example using the HRR or Karvonen method is as follows:
You want your 76-year-old client, who has a maximum heart rate of 144 bpm and
a resting heart rate of 80 bpm, to exercise at a 75% intensity level. What would the
target heart rate be?
Answer: 128 bpm

Solution: target HR = (0.75) [(220 – age) – resting HR] + resting HR
target HR = (0.75) [(220 – 76) – 80] + 8 0
target HR = (0.75) (144 – 80) + 80
target HR = (0.75) (64) + 80
target HR = 48 + 80
target HR = 128
This method should not be applied to patients with peripheral neuropathies or chro-
notropic incompetence. Maximal heart rates should not be predicted using age if the
patient is taking a medication that may change the resting heart rate (e.g., β-blockers).
METHOD 3: THE RATE PRESSURE PRODUCT METHOD

The rate pressure product (RPP) method is a unique way to individualize an exercise
prescription using a target heart rate. The RPP is equivalent to the product of HR and
systolic blood pressure. It is a noninvasive way to measure the myocardial oxygen

Appendix A: Exercise Prescriptions and “the Charts” 193
consumption, or MVO2. There are no units associated with the RPP index; however,
it is very reproducible for prescribing exercise for patients with ischemic thresh-
olds, without being limited to these patients. This method should not be applied to
patients with peripheral neuropathies or chronotropic incompetence. Furthermore,
this method requires a maximal exercise stress test to measure maximal systolic
blood pressure.
For example, a patient is a candidate for an exercise program and prescription.
The following data were reported after a maximal exercise test was performed:
maximal systolic blood pressure: 155 mmHg

maximal heart rate: 128 bpm
resting systolic blood pressure: 110 mmHg
resting heart rate: 65 bpm
maximal RPP = max systolic BP 3 max HR/100
resting RPP = resting systolic BP 3 resting HR/100
maximal RPP = (155 3 128)/100 = 198
resting RPP = (110 3 65)/100 = 71
Using the RPP to calculate an exercise prescription involves plugging the RPP
into the Karvonen equation (see Method 2) and setting up a proportion. The RPP is
divided by 100 to simplify the calculation. With the preceding data, a target heart
rate using an intensity level of 50% can be calculated as follows:
Solution: target RPP = (0.50) (peak RPP – resting RPP) + resting RPP
target RPP = (0.50) [(198 – 71)] + 71
target RPP = (0.50) (127) + 71
target RPP = 63 + 71
target RPP = 134
Next, plug the 50% target RPP (134) into a proportion to determine the target
heart rate as follows:
Maximum RPP = 198 Maximum RPP = 128

target HR =
target RPP = 134 target RPP = X
Cross multiplying and solving for “X” gives a target HR of 86 bpm. Notice that if
Method 1 had been used, a target heart rate similar to the patient’s resting heart rate,
or 64, would result—grossly underpredicting a training target heart rate.
METHOD 4: SYSTOLIC BLOOD PRESSURE METHOD

The systolic blood pressure (SBP) can be used to monitor exercise intensity in place
of heart rate. This method is extremely useful when prescribing exercise for patients
with hypertension and patients prone to hypertension (e.g., cardiac transplant and

peripheral vascular disease). The method requires a maximal exercise test to deter-
mine the peak SBP and then plugging the SBP into the Karvonen equation (see
Method 2). Using Method 1 (the age-predicted method) may result in a target SBP
that is lower than the patient’s resting SBP and therefore is not recommended. An
example using this method is illustrated as follows:
Assume the maximal SBP is 185 mmHg, the resting SBP is 140 mmHg, and the
intensity is 60%. Using the Karvonen equation (Method 2):
Answer: 167 mmHg

target systolic blood pressure = (0.60) (peak SBP – resting SBP) + resting SBP
(0.60) (185 – 140) + 140
(0.60) (45) + 140
27 + 140
167
METHOD 5: THE CHARTS

Perceived exertion charts offer a convenient way to monitor and prescribe exercise
intensity. They are the method of choice when prescribing exercise to a patient who
may be unwilling or unable to monitor his or her pulse during exercise. Three charts
are presented in this section: (1) a rating perceived exertion chart (Borg chart) or rat-
ing of perceived exertion (RPE), (2) a dyspnea scale, and (3) a claudication scale. It
is important to instruct the patient on the use of these charts.
How to Use the Charts

The exercise intensity should be determined following 3–5 minutes of aerobic or
weight-training activity, when the body has had time to adjust to the exercise inten-
sity. Concentrate on how the exercise feels—all over. Do not just think about a cer-
tain area of the body. For example, if someone is walking or riding a bike, that
person should think about how the whole body feels when he or she is exercising—
not just the muscles being used, which in this case are in the legs.
Individuals who are very anxious, or type A individuals, may underestimate their
actual intensities. Furthermore, about 10% of the population will be unable to use
the charts accurately.

Rating of Perceived Exertion

6 No exertion at all
7
Extremely light
8
9 Very light
10
11 Light
12
13 Somewhat hard
14
15 Hard (heavy)
16
17 Very hard
18
19 Extremely hard
20 Maximal exertion
Source: Adapted from Noble, B. J., G. A. V. Borg,

I. Jacobs, R. Ceci, and P. Kaiser. 1983. A
category-ratio perceived exertion scale:
Relationship to blood and muscle lactates
and heart rate. Medicine and Science in
Sports and Exercise 15:523–528.
Dyspnea Scale
10 Maximal
9 Very, very severe
7 Very severe
5 Severe
4 Somewhat severe
3 Moderate
2 Slight
1 Very slight
0.5 Very, very slight; nothing
Source: Adapted from Faryniarz, K., and D. A.

Mahler. 1990. Writing an exercise pre-
scription for patients with COPD. Journal
of Respiratory Diseases 11:638–644.

Claudication Scale
0 No claudication pain
1 Initial, minimal pain
2 Moderate pain
3 Intense pain
4 Maximal pain, cannot continue
METHOD 6: MAXIMAL OXYGEN CONSUMPTION

(THE VO2 MAX OR MAXIMAL FUNCTIONAL CAPACITY)
The VO2 max is considered the gold standard when describing the fitness level of an
individual. It is determined by measuring expired gases during a cardiopulmonary
stress test. There is a linear relationship between heart rate and VO2. This relationship
allows exercise to be prescribed using a target heart rate corresponding to a percent-
age of the patient’s functional capacity. For example, the window of intensity used is
typically 40–85% of the functional capacity. For more deconditioned patients, 40%
would be used; 85% is used after conditioning improves. After a cardiopulmonary
stress test is performed, the heart rate is extrapolated from the corresponding VO2
and an exercise target heart rate is then applied. For more a more detailed discussion
on the VO2 max, see Appendix B, “Cardiopulmonary Stress Testing” section.
METHOD 7: THE ANAEROBIC THRESHOLD

The anaerobic threshold is defined as the point in an incremental cardiopulmo-
nary stress test where ventilation takes a sharp rise from linearity. This point or
“event marker” is hypothesized to occur when the intensity of exercise results in a
rapid rise in lactic acid. This lactic acid is buffered and exhaled as CO2, resulting in
the rise in ventilation.
Exercise that is prescribed at or just under the anaerobic threshold is tolerable for
most patients. Exercise intensity above the anaerobic threshold may result in fatigue
and the inability to continue. An improvement in conditioning can occur when a
target heart rate is prescribed at or just under the anaerobic threshold. To calculate
the anaerobic threshold, a cardiopulmonary stress test measuring expired gasses is
needed. A target heart rate corresponding to the rapid rise in ventilation can be used
to prescribe intensity. It is important to recognize that there may be an initial “false”
rise in ventilation due to hyperventilation. For a more detailed discussion on the
anaerobic threshold, see Appendix B, “Cardiopulmonary Stress Testing” section.
METHOD 8: VENTILATION
Exercise also can be prescribed based on a percentage of a patient’s ventilation. A
heart rate corresponding to 70–80% of the maximum voluntary ventilation (MVV)
or anaerobic threshold, whichever heart rate is lower, is recommended in chronic

lung disease (see Method 7). For a more detailed discussion on the anaerobic thresh-
old, see Appendix B, “Cardiopulmonary Stress Testing” section.
METHOD 9: THE VO2 RESERVE

The use of the VO2 reserve was adopted by the American College of Sports Medicine
in 1998. It basically says that the heart rate reserve (HRR), or Karvonen formula, is not
equivalent to a percentage of the VO2 but rather to the VO2 reserve. The VO2 reserve
formula is calculated as follows: target VO2 = (intensity fraction)(VO2 max – VO2
rest [3.5 can be substituted here]) + VO2.
METHOD 10: WEIGHT LIFTING FORMULA

1. Choose a weight the individual can lift comfortably.
2. Let us say that 35 lb was lifted eight times.
3. Use the equation [100 – (8 × 2.5)] = % 1RM.
4. 100 – 16 = % 1RM or 80%.
5. 35 lb is 80% of the 1RM.
6. The 1RM can be determined by 35 lb/0.80.
7. Therefore, the 1RM would be equal to 44 lb.
8. The weight that should be lifted corresponding to a percentage of the 1RM,
for beginners, is usually 30–50% of the 1RM. In this case, it is 12–20 lb.

Appendix B: Exercise Testing
The purpose of Appendix B is to elaborate on the exercise prescription methods

outlined in Appendix A. We will differentiate between a cardiac stress test and a
cardiopulmonary stress test, outlining the value each plays in exercise prescription.
MEDICAL SCREENING PRIOR TO EXERCISE

Medical screening for the purpose of disease prevention and health promotion is
indicated in the evaluation of all persons but its role and methods in the evaluation of
subjects prior to engaging in an exercise program are controversial.
Young, apparently healthy people under the age of 40 do not need a special visit
to their physician before engaging in an exercise program; however, at the first avail-
able opportunity, attention should be given to the detection of factors that would
increase the risk of exercise, such as smoking, family history of heart and other
diseases, high blood pressure, elevated cholesterol, sedentary living, etc. Physical
examination should include a determination of the blood pressure and a search
for signs of diseases of the heart, lungs, circulation, and musculoskeletal system.
Laboratory work should include the routine tests for detection of common occult
diseases such as a complete blood count, urinalysis, and blood levels of glucose,
cholesterol, and creatinine.
CARDIAC STRESS TESTING

The role of a cardiac stress test in apparently healthy individuals is very contro-
versial. The American College of Sports Medicine (ACSM) recommends a cardiac
stress test in all persons older than 40 years old before the initiation of a vigorous
exercise program. This recommendation is controversial because the cardiac stress
test is negative in many patients with coronary artery disease even in the presence of
coronary risk factors and is abnormal (falsely positive) in many patients with normal
hearts, especially women. In a population of 3,617 patients, aged 35–59 years, who
had no symptoms but were known to have elevated cholesterol levels, the cardiac
stress test had a sensitivity of only 18%. Nevertheless, many patients known to be at
risk of medical problems associated with exercise would benefit from exercise test-
ing. Contraindications to exercise testing are as follows:
Absolute Contraindications
• Recent change in the ECG suggesting myocardial infarction
• Unstable coronary artery disease
199
200 Appendix B: Exercise Testing
• Third-degree arterioventricular block
• Acute congestive heart failure
• Severe aortic stenosis
• Dissecting aneurysm
• Thrombus or embolus
• Acute infection
• Psychosis
Relative Contraindications
• Resting blood pressure > 200/110
• Moderate valve disease
• Electrolyte abnormalities
• Fixed-rate pacemaker
• Ventricular aneurysm
• Uncontrolled metabolic disease
• Chronic infectious disease
• Muscular disorders that are augmented by exercise
• Advanced or complicated pregnancy
CARDIOPULMONARY STRESS TESTING

Cardiopulmonary stress testing is a cardiac stress test with the extra benefit of meta-
bolic monitoring. The cardiac stress part of the test is used to assess the likelihood or
severity of coronary artery disease. The addition of metabolic monitoring provides
a better understanding of how the heart, the circulation, the lungs, and the musculo
skeletal system coordinate their activities to meet the energy requirements of the
work performed by the muscles.
Shortness of breath on exertion can occur as a result of muscle, cardiac, or pulmo-
nary disease. Cardiopulmonary exercise testing allows the examiner to differentiate
among all of the preceding components and determine the cause of symptoms in
patients with more than one illness. The cardiopulmonary stress test allows a physi-
cian to diagnose the cause of functional impairment, measure the severity of such
impairment (the person’s capacity to do aerobic work), monitor the results of treat-
ment, prescribe exercise to rehabilitate people with disease, and guide the training
of athletes.
Patients can be tested on the bicycle or the treadmill for lower extremity exercise
and the arm ergometer or the rowing machine for upper extremity exercise. The
information obtained during the exercise test can be extrapolated to other forms of
exercise as long as the exercise involves the use of large muscle groups. In the next
few sections, we will review the principles pertinent to cardiopulmonary stress test-
ing and how to use that information to prescribe exercise.

Appendix B: Exercise Testing 201
Aerobic Fitness
The main requirement for endurance exercise is aerobic fitness. This is the ability
of the heart, lungs, and circulation to supply the muscles with oxygen and remove
waste products. Whether a patient is a couch potato or a fit athlete, suffers from
heart or lung disease, or is the model of health, there is an aerobic training program
for that person that is optimally efficient and safe. Cardiopulmonary exercise test-
ing provides the information needed to prescribe it. For example, a person who is
aerobically fit can generally exercise comfortably at 40–60% of the VO2 max for an
extended period of time (e.g., 20–60 minutes).
Aerobic Exercise
During exercise, the skeletal muscles obtain the energy necessary to work by con-
verting carbohydrates and fat into energy. Carbohydrates and free fatty acids are
the fuel utilized by the muscle to produce energy. The word “aerobic” indicates the
requirement of oxygen. Exercise is aerobic when all of the energy used during its
performance is obtained from the burning of carbohydrates and fat with oxygen. The
higher the intensity of exercise is, the higher the amount of energy (i.e., carbohydrate)
needed and the higher the amount of fuel and oxygen needed to produce it. Because
aerobic exercise can be sustained for a long time, the phrase aerobic exercise is often
used to mean steady exercise performed over a relatively long period of time.
The VO2 max
Aerobic capacity is synonymous with endurance and reflects the ability to do aerobic
exercise. The extent of a person’s aerobic capacity can be gauged by measuring how
much oxygen he or she used during maximal exercise; this is called the VO2 max
(short for the maximal utilization of oxygen). The VO2 max reflects the functional
condition of the person. It illustrates the ability of the lungs to transfer oxygen to
the blood, the heart to pump the blood, and the circulation to take it to the muscle.
The VO2 max indicates the effectiveness of the lungs, heart, and blood vessels to
function as a unit during maximal work. It measures how fit a person is when doing
aerobic work and is considered the “gold standard” of fitness.
Oxygen Economy
Oxygen economy is synonymous with work efficiency and it expresses the ability to
do muscular work using relatively little oxygen. Strength, flexibility, body weight,
and proper technique are important components of efficiency. A flexible, lightweight,
and well-trained runner can run faster using the same amount of oxygen as a stiff,
heavy, and clumsy runner. To improve oxygen economy is to become more efficient
and it is obtained by losing body fat, increasing strength and flexibility, and perfect-
ing technique. The slope of the curve (VO2 × work) reflects this factor. The flatter the
slope is, the greater is the oxygen economy.

Anaerobic Exercise
Exercise that does not depend on the burning of oxygen to generate energy is called
“anaerobic.” When the intensity of work is relatively low (e.g., <50% of the VO2 max),
energy is derived entirely through the aerobic biochemical pathway. However, when
an increasing work rate reaches a certain point, aerobic mechanisms alone are insuf-
ficient to produce all the energy needed and the anaerobic mechanism is activated.
The aerobic production of energy is 18 times more efficient than the anaerobic.
The energy used during anaerobic exercise is either borrowed from the energy stored
in the muscle or produced by transforming carbohydrates and fat into lactic acid. The
amount of anaerobic work performed is proportional to the amount of lactic acid
accumulated and the magnitude of the oxygen debt.
Oxygen Debt
Like a battery, muscle has an energy charge. The muscle maintains the energy charge
in the form of chemical energy kept in the phosphate bonds of molecules such as ade-
nosine tri-phosphate (ATP). If it is necessary to do high-intensity work over a short
time (such as lifting a heavy weight, jumping, or running the 100-meter dash), the
muscle borrows energy from that energy charge to get the job done. Later, the energy
utilized is “paid back” by burning sugar or fat with oxygen. The amount of oxygen
utilized to pay back the borrowed energy completely is called the oxygen debt.
High-intensity anaerobic exercise done over a very short period of time decreases
the energy charge of the muscles and creates an oxygen debt, but it does not produce
a large accumulation of lactic acid. For example, a 15-second sprint will not gener-
ate any significant lactic acid production; however, sustained high-intensity work
leads to the production and buildup of lactic acid and a large oxygen debt.
For example, when a person runs as hard as possible for 4 minutes, 65% and 35%
of the energy used come from anaerobic and aerobic sources, respectively. The total
amount of anaerobic work done over those 4 minutes will generate a large amount
of lactic acid and a large oxygen debt. Marathon runners pace themselves just below
the lactic acid buildup pace. Almost all the energy used during such exercise comes
from aerobic sources; unless the runner increased the pace by the end of the race (as
most of them do), there would be little or no lactic acid accumulation and little or no
oxygen debt.
The Anaerobic Threshold

As the exercise intensity increases, there is a point, or “event marker,” when the lac-
tate concentration in the serum begins to rise. This is the beginning of the so-called
“anaerobic threshold” (AT) zone, defined as the oxygen consumption where serum
lactic acid accumulation increases proportionally to exercise intensity, and the slope
of the ventilation rises from a linear state. Exercise intensities below the AT zone do
not cause the production of enough lactic acid to result in fatigue; however, exercise
intensities above the AT zone result in a progressive accumulation of lactic acid, a

progressive fall in the serum bicarbonate level, and a progressive increase in the
heart rate and minute ventilation.
Exercise intensities above the AT zone cannot be sustained without fatigue. The
AT zone is usually found somewhere between 50 and 85% of the VO2 max. The closer
the AT zone is to the VO2 max, the faster the pace that can be maintained without
fatigue. A low AT indicates an impairment in the oxygen delivery system secondary
to anemia, heart disease, or circulatory problems in the systemic or pulmonary cir-
culation. Less commonly, a low AT occurs as the result of muscular disease.
Heart Rate and Exercise

The heart rate (HR) is a good indicator of how hard a particular muscle group is
working. It does not reflect the amount of work done by the muscle; rather, it reflects
the intensity of the work. For example, if a particular activity is done using only
one arm, the intensity of the work is twice as much as the same amount of work done
using both arms. The amount of aerobic work the arm does is reflected in how much
oxygen the arm uses to do that work.
Since the HR reflects the intensity of the work, the HR is higher when only
one arm is used. Trained athletes have a lower HR at rest; this is secondary to an
increased stroke volume and other factors. One should develop the habit of checking
HR as soon as one wakes up in the morning and keeping a record of it. Overtraining
and illness will increase morning HR. As a rule of thumb, a morning HR five beats
higher than average might reflect illness or overtraining. Similar information can
be obtained by monitoring the HR at the same exercise intensity. For example,
monitoring the HR after 5 minutes of walking on a treadmill at the same speed and
elevation, and compared to previous data.
HR, AT, and Perceived Exertion

Since the HR increases in proportion to the level of exertion, people who frequently
check their HR when they exercise learn to associate the heart rate with a particular
level of exertion. Exercise below the anaerobic threshold is perceived as easy or
mild; at this exercise intensity, the exerciser can engage in conversation and articu-
late long sentences. If the subject stops exercising, his or her breathing will become
as easy as it was at rest as soon as the exercise stops.
Exercise near the AT is felt as hard or very hard (moderate or moderately severe).
Depending on whether the exercise intensity corresponds to the lower or the upper
end of the AT zone, conversation is impaired and is limited to short sentences. If the
exerciser stops exercise, he or she will continue to be short of breath for a period of
time, paying back an oxygen debt.
Exercise intensities above the anaerobic threshold are felt as extremely hard, can-
not be sustained, and invariably lead to fatigue within a short period of time. The
formulas discussed in Appendix A to predict maximum HR and training HR are not
100% accurate; they give only a ballpark approximation ±10–15 beats, but they do
not require a cardiopulmonary stress test. The best way to know the HR at the two
extremes of the AT is to measure it with a cardiopulmonary stress test.

EXERCISE TESTING FOR PEOPLE WITH COMMON

CARDIOPULMONARY PROBLEMS
Heart Failure
Exercise testing of patients with heart failure reveals a cardiac output that is com-
pletely HR dependent and a maximal HR reached at a relatively low level of work.
Exercise causes the pressure within the pulmonary circulation to increase, especially
in patients with severe heart failure; however, this change does not correlate well
with dyspnea. Patients with heart failure have a low AT and a low VO2 max. The AT
is less than 40% of the predicted VO2 max.
The AT and the VO2 max correlate very well with the severity of heart failure:
• Mild heart failure or no heart failure at all corresponds to a VO2 max >

20 cc/kg/min
• Mild to moderate heart failure, 16–20 cc/kg/min
• Moderate to severe heart failure, 10–15 cc/kg/min
• Severe heart failure, 6–9 cc/kg/min
• Very severe heart failure, correlates with <6 cc/kg/min
Improvement or lack of improvement can be measured objectively by the changes

in the AT and VO2 max.
Pulmonary Vascular Impairment

Patients with pulmonary vascular disease (e.g., pulmonary hypertension, pulmo-
nary embolism, scleroderma, etc.) respond to exercise in a manner similar to that
of patients with heart failure. Exercise testing in these patients is likely to reveal
a low work capacity (low VO2 max), and low AT (less than 40% of the predicted
VO2 max).
Subtle changes allow the examiner to differentiate patients with pulmonary vas-
cular impairment from patients with heart failure. They are elevated ventilatory
equivalents (VE/VO2 and VE/VCO2) and elevated dead space ventilation (VD/VT)
measured at the AT (ventilatory equivalents) and during maximal exercise (VD/VT).
Other abnormalities observed in patients with pulmonary arterial disease include
an elevated alveolar arterial O2 tension difference and a large arterial end tidal CO2
tension difference. As with the patient with chronic heart failure, the severity of the
pulmonary vascular disease correlates well with the VO2 max and the AT.
Using a Cardiopulmonary Stress Test to Prescribe Exercise for Patients

with Heart Failure or Pulmonary Vascular Impairment
Patients with stable disease can engage in exercise activities of low to moderate
intensity corresponding to a heart rate at or below the AT zone. Exercise activities in
the middle or the upper parts of the AT zone should be discouraged. Exercise activ
ities above the anaerobic threshold zone can be dangerous.

Restrictive Pulmonary Diseases

Patients with restrictive disease are characterized by having low lung volumes with
normal flow rates. The diffusion capacity differentiates the patient with restrictive
disease located diffusely within both lungs from patients with localized disease or
restrictive disease located outside the lungs (i.e., pleura or chest wall). During exer-
cise, the tidal volume (the amount of air exhaled with each breath) increases until it
reaches about half of the vital capacity (the amount of air exhaled from a maximal
inspiration to a maximal exhalation); further increases in respiration volume are
obtained by increasing the respiratory rate.
Respiratory rates higher than 40 breaths per minute can be observed in this group
of patients. Patients with restrictive disease might have problems transferring oxygen
from the lungs to the arterial blood. The magnitude of the abnormality of O2 trans-
fer cannot be predicted with resting data obtained in the pulmonary function lab,
although there is a gross correlation between the severity of the impairment in the
diffusion capacity and the magnitude of the abnormality observed during exercise.
Patients with a diffusion capacity of <50% of the predicted are more likely to have a
low arterial oxygenation during exercise.
Obstructive Impairment
Patients with obstructive lung disease are characterized by decreased flow rates. These
patients have traditionally been divided into two groups. The type A patients are the
“pink puffers” who suffer from emphysema, have large lungs, loss of elastic recoil, and
impaired gas transfer because they have destroyed many of their alveolar units and have
a reduced alveolar surface area for gas exchange; their arterial O2 and CO2 tensions are
usually normal or low. The type B patients, or the “blue bloaters,” suffer from chronic
bronchitis, have smaller lungs than the type A patients, and have a normal alveolar sur-
face area, although gas transfer is impaired because their lungs are poorly ventilated.
The arterial O2 tension is normal or low, their arterial CO2 tension is normal or high.
Exercise causes the arterial oxygen tension to change in opposite directions.
Patients with emphysema have a tendency to decrease the arterial O2 tension; patients
with bronchitis have a tendency to improve it. Changes in the exercise arterial O2 ten-
sion cannot be predicted from the resting data alone, although there is a gross cor-
relation with the FEV1. Patients with an FEV1 of <1.0 L are more likely to decrease
the arterial O2 tension with exercise. During exercise, the tidal volume increases but,
unlike patients with restrictive disease, it seldom reaches half of the vital capacity.
The respiratory rate also increases, but seldom exceeds 40 breaths per minute.
The poor level of physical fitness often seen in patients with lung disease com-
pounds the disability. Muscular weakness causes dyspnea on exertion. As the respira-
tory impairment worsens, the increasing level of dyspnea further limits the patient’s
work capacity until it interferes with the performance of everyday activities such
as walking, climbing stairs, shopping, etc. As the patient becomes less active, mus-
cles become weaker; this further worsens the dyspnea.
An exercise program will not correct the pulmonary problems of the patient, but
it will improve exercise capacity. If a cardiopulmonary stress test and metabolic

monitoring data have been obtained, an exercise prescription for patients with lung
disease can be issued using one of the following methods:
1. Exercise at a target heart rate equal to the anaerobic threshold or at

70–80% of maximal voluntary ventilation (MVV), whichever is less.
The pulmonary status of some patients is so impaired that they cannot
achieve the AT. If the patient were able to achieve the AT, he would benefit
from exercise at an intensity that would elicit a heart rate response equal to
the HR observed at the AT or slightly below. Patients who are not able to
obtain the AT or utilize close to 100% of their breathing capacity at the AT
benefit from exercise prescribed at a heart rate that corresponds to 70–80%
of the MVV.
2. Exercise at an intensity within the AT zone. Patients with mild pulmonary
disease obtain a greater training effect if they exercise within the AT zone.
In a study of hospitalized patients with mild COPD, Casaburi et al. (1991)
reported significantly greater improvements in exercise variables, including
a reduction in minute ventilation, in a group of patients who trained within
the AT compared to a group that trained below the AT.
3. Exercise at near-maximal intensity. The principle of high-intensity exer-
cise training is based on the observation that patients with moderate to
severe COPD can sustain ventilation at a high percentage of their MVV. In
one study, Punzal et al. (1991) reported that 52 patients trained at an inten-
sity of 95% of their MVV. Although most individuals could sustain this
intensity for only a few minutes, they significantly increased their endur-
ance. As a group, the patients reported a significant increase in exercise
time and less breathlessness and fatigue. Interestingly, whether or not a
given patient reached AT during the initial stress test had no effect on the
efficacy of the training.
4. Use ratings of dyspnea to define intensity. The majority of patients with
moderate to severe respiratory disease are limited by exertional dyspnea.
It is therefore possible to prescribe exercise intensity based on subjective
dyspnea ratings. The dyspnea rating chart is similar to the Borg chart of
perceived exertion; it varies from 0.5 or very, very slight to 10, correspond-
ing to very, very severe. A dyspnea rating of 3, or moderate, corresponds
to a VO2 max of approximately 50% of the VO2 max. A dyspnea rating of
6–7, or severe to very severe, corresponds to a VO2 max of approximately
85%. In a preliminary study, Horowitz and Mahler (1993) demonstrated
that patients with COPD can achieve a target VO2 within ±15%, based on
dyspnea ratings obtained from a cardiopulmonary stress test. The accuracy
of using the dyspnea rating scale to determine exercise intensity in patients
with COPD is better at higher intensities. This approach provides a specific,
easily quantified guideline for patients to self-monitor their intensity of dys-
pnea during routine exertional tasks. Moreover, the use of a dyspnea scale
and the prescription of exercise at a given dyspnea level instill in the patient

the understanding that it is appropriate and acceptable to experience dys-

pnea during exercise training. The dyspnea and rating perceived exertion
(RPE) charts are in Appendix A, Method 5. A copy of the data collection
sheet we have developed for use during a cardiopulmonary exercise test can
be found at the end of this appendix.
REFERENCES
Casaburi, R., A. Patessio, F. Ioli, S. Zanaboni, C. F. Donner, and K. Wasserman. 1991. Reduc
tions in exercise lactic acidosis and ventilation as a result of exercise training in patients
with obstructive lung disease. American Review of Respiratory Disease 143:9–18.
Punzal, P. A., A. L. Ries, R. M. Kaplan, and L. M. Prewitt. 1991. Maximum intensity exercise
training in patients with chronic obstructive pulmonary disease. Chest 100:618–623.
EXERCISE PRESCRIPTION
Name:_ ____________________________________________ Age:_ ____________
I.D. #:_ ____________________________________________ Sex:______________
Date:_ _____________________________________________ Height:___________
M.D.:______________________________________________ Weight:___________
Referring physician:___________________________________________________
History:_ ___________________________________________________________
Before: After: % Chg.

PFTs FVC =______________ FVC =______________ % =_ ________
(liters) FEV1 =______________ FEV1 =______________ % =_ ________
MVV =_____________ MVV =_____________ % =_ ________
FEV1/FVC =_________ FEV1/FVC =_________ % =_ ________
Aerobic: Measured
VO2 max (liters)
VO2 max/pred. 85%
HR max (220 – age)
HR @ 60% HRR
HR @ 70% VE max
HR @ AT *
O2/HR (mL/beat) *
AT as % of VO2 max >40%
VO2 @ AT *
Reason for stopping the test:

Breathing reserve: Normal Measured

1 – (VE max/MVV) >30% ______________________
MVV – VE max > 15L ______________________
Respiratory: Predicted
VE (liters)
VD/VT: Rest/Max 0.35/0.25
VE/VO2: VE/VCO2 24–26
Pulse oximetry: Rest/max >88%
Cardiac: BP: Rest:_ _______________ Max:_ _______________

EKG: __________________________________________
Impression:
(AT = anaerobic threshold, HRR = heart rate reserve)

Appendix C: Training Injuries
Exercise is not without risk, but injuries related to exercise are uncommon. The
most common exercise-related injuries consist of musculoskeletal problems caused
by trauma or overuse. Exercise-related injuries are usually limited to athletes and
persons who train at high intensities. This appendix presents a summary of such
injuries organized by organ system.
CARDIOCIRCULATORY SYSTEM
Exercise can increase heart size and cause changes in the electrocardiogram sugges-
tive of hypertrophy or infarction in the absence of disease. The so-called “athlete’s
heart” functions better than the “normal” heart, although these changes are often
confused for evidence of disease by inexperienced examiners.
Strenuous exercise can cause myocardial infarctions in patients with coronary
artery disease; this is the reason why exercise testing is recommended in patients
suspected of having coronary artery disease. Unfortunately, cardiac stress testing is
an insensitive method to detect coronary artery disease (see Appendix B, “Medical
Screening Prior to Exercise”). Since coronary artery disease and cardiac arrhyth-
mias are the most common cause of death related to exercise, patients who experi-
ence symptoms suggestive of cardiac arrhythmias or coronary artery disease such
as palpitations, dizziness, light-headedness, or pain or discomfort in the chest, upper
abdomen, jaw, or left arm should consult their physician.
ENDOCRINE SYSTEM
Abnormalities in the menstrual cycle are commonly seen in female athletes who have
low body fat levels (<20%). Menstrual cycles return to normal with weight gain. The
abnormality is related to decreased estrogen production. The most important prob-
lem associated with the lower estrogen level is not the absence of the menstrual cycle
but rather the demineralization of the bones (osteoporosis) caused by it. Patients with
diabetes might experience hypoglycemia (see Chapter 2).
EYES
There is no evidence of exercise-induced eye-related injuries except for those caused by
direct trauma to the eyes. Exercise does not cause or aggravate diabetic retinopathy.
209
210 Appendix C: Training Injuries
GASTROINTESTINAL SYSTEM
Exercise often causes heartburn-like symptoms caused by the reflux of acid from the
stomach into the esophagus. Because exercise increases bowel motility, it is good
for people who suffer from constipation, but it can cause abdominal cramps and
occasional diarrhea (runner’s trots). Gastrointestinal bleeding has been observed in
marathon runners and in exercisers who suffer from ulcerative colitis when they are
in the midst of an exacerbation of the disease.
HEMATOLOGIC SYSTEM
There are no exercise-related hematological problems except for the possibility of
iron deficiency with or without anemia in athletes. Individuals with chronic gastro
intestinal blood loss may experience iron-deficiency anemias. Athletes may experi-
ence an iron deficiency without anemia. The so-called “sports anemia” is not a true
anemia; it has been reported in endurance athletes who drastically increase their
training intensities in the early phases of their exercise programs. Sports anemia
results from an increase in plasma volume, which can benefit cardiac output; how-
ever, it also causes a diluted hemoglobin concentration in the blood. Iron deficiency
without anemia, when corrected, does not improve performance.
MUSCULAR PAIN OR INJURY

Strenuous exercise causes some degree of muscular injury proportional to the inten-
sity, duration, and type of exercise. The muscular pain that often follows exercise is
related to the injury experienced by the muscle fibers and the collagen harness that
holds the muscle fibers together. The best way to prevent muscle pain is to exercise in
moderation and to continue to exercise; with time, the soreness will go away. There
are situations when extensive, life-threatening muscle injuries occur; those cases
have usually occurred in military settings and during very strenuous competitive
sports when untrained subjects perform a very large volume of exercise, often under
adverse climatic conditions.
MUSCULOSKELETAL SYSTEM
Injuries can occur as a result of accidents and trauma. In that case, pain and disabil-
ity occur suddenly and medical attention usually follows. Physicians are well trained
to evaluate, diagnose, and treat these types of conditions. Occasionally, pain occurs
not as a result of accidents or trauma, but rather due to abnormal alignment or over-
use of a body part. It could also be the result of faulty equipment and/or technique.
This pain usually begins slowly; the cause is difficult to recognize and it is com-
monly misdiagnosed and mistreated. Faulty alignment alone is not sufficient to
cause injury and pain. It must be associated with limitations in flexibility. This is
why many people exhibit faulty alignment yet have no symptoms and others with
apparently normal alignment develop symptoms. When a joint has good flexibility,

Appendix C: Training Injuries 211
minor alignment problems will not cause a problem. However, a joint that lacks
flexibility—even if it is well aligned—will not be able to withstand the stresses of
exercise. The ligaments and other tissues surrounding the joints that lack flexibility
may suffer minute tears as a result of activity. Over time, these microtears lead to
inflammation, swelling, and pain. Pain can cause compensatory changes in align-
ment to minimize the discomfort.
Proper assessment of flexibility, alignment, and muscle strength cannot be done
when the subject is experiencing pain. One must wait until the painful episode has
subsided to evaluate the problem correctly. An exercise program whose objective is
to improve endurance, strength, and flexibility is not enough. The program should
also aim to restore proper muscle balance and develop correct alignment.
It is beyond the scope of this book to illustrate the exercises needed to cor-
rect faulty biomechanics; nevertheless, the reader should take notice of this
problem. One particular exercise, however, will be commented on because it is
so commonly done incorrectly: strengthening of the abdominal muscles. Weak
abdominal muscles are quite prevalent and result in low-back pain, which is a
very important cause of disability. When strengthening the abdominal muscles,
most people prescribe sit-ups. Actually, when done incorrectly, sit-ups can aggra-
vate the back pain. The sit-up, when done with the feet blocked and the knees
extended, is a very strong hip-flexor exercise. The hip flexors are usually stronger
than the abdominal muscles and this contributes to the back pain. In order to
exercise the abdominal muscles without activating the hip flexors, it is necessary
to perform only the spine flexion phase (trunk curl) of the exercise and avoid the
hip flexion (sit-up) phase altogether. Blocking or restraining the feet during the
exercise increases the possibility of activating the hip flexors and should not be
permitted. Furthermore, the knees should always be bent or flexed.
Pronation and supination of the foot are easily diagnosed by observing the runner’s
gait. Exercises to minimize these abnormal motions are relatively simple. For supina-
tors, rise up on the toes with the feet pointed inward. This activates the peroneus longus
and brevis, which oppose supination. Pronators should do this “rise-up-on-the-toes”
exercise with the feet pointing out. This exercise strengthens the tibialis posterior,
which opposes pronation. Both exercises strengthen the soleus and gastrocnemius.
OVERUSE INJURIES
There are two types of overuse injuries: the acute and the chronic. Acute injuries,
as the name indicates, happen acutely, usually as the result of trauma. The exerciser
knows immediately that something went wrong and develops pain, swelling, and the
inability to function. Disability ensues and the victim almost always seeks medi-
cal help (if the pain is bad enough). There are other types of sports injuries which
develop slowly over the course of many small traumas to the bones or tendons. In
the beginning, the pain is mild and easily tolerated, as well as ignored. It is often
disregarded by the athlete as a mere nuisance. The exerciser adapts to the discomfort
until the pain becomes severe enough to command attention and prevents not only
exercise but also the activities of daily living.

The other overuse injuries are chronic. They occur very often and are responsible
for 30–50% of all sports injuries. Unlike the acute injuries, they are often misdiag-
nosed and mistreated. Overuse injuries are almost always caused by biomechanical
problems, poor training, or faulty equipment. Treatment with rest and anti-inflamma-
tory medications usually corrects the problem, but if the biomechanical abnormality
is not recognized and corrected it is likely to reoccur. An example of a biomechani-
cal abnormality is excessive pronation of the foot causing shin splints or knee pain.
Poor training usually means “too much, too soon”—such as the stress fracture of
the tibia of a runner who has increased his number of miles per day too rapidly. It
could also result from poor technique, such as leading with the elbow and extending
the wrist during the tennis backhand stroke; over an extended period of time, this
could result in tennis elbow. Improper equipment involves judgment errors like run-
ning on a hard surface or using too large a racquet or wearing the wrong shoes.
Overuse injuries can affect any of the tissues involved in locomotion: the tendons,
the bones, the bursae, the ligaments, the muscles, and even the nerves. Contrary to
popular opinion, physical activity is not harmful to the joints, overuse is seldom the
cause of arthritis, and exercise plays an important role in the therapy and rehabilita-
tion of patients with joint problems.
TENDINITIS
Tendons connect muscles to bone. They have very poor circulation, which makes
them very susceptible to injury. Tendinitis is more likely to develop when poor align-
ment causes excessive friction between tendon and bone, when there is too much
stress (too much or too soon), or when the tendon is weak. The treatment of tendini-
tis consists of rest and ice for the first 3 days, followed by heat. Anti-inflammatory
agents can be useful. Steroid injections are permissible once, seldom twice, and never
three times. Steroids should never be injected into the tendon itself—only around it.
Ultrasound can be used to drive medications into the inflamed area. Deep friction
massage could help to improve circulation and stretch the tendon. Once the inflam-
mation has subsided, a program of strength and stretching exercises is necessary to
prevent recurrence.
Bursitis
Bursitis is the inflammation of a bursa. Bursae are little sacs filled with an oily liquid
located in areas where tendons or skin rub against bone. Overuse causes excessive
rubbing of the tendon or skin against the bone, resulting in tendinitis, bursitis, or both.
Occasionally, bursitis can be caused by direct trauma to the bursa. When a bursa is
inflamed, it becomes thick and the oily liquid inside fills with calcium, changing it
into a grinding paste. If the inflammation continues, the bursa can turn into a rigid
scar filled with calcium. Bursitis is treated with rest and anti-inflammatory medica-
tions. Swelling bursae with calcium deposits can be rapidly improved (and calcium
deposits disappear) with needle aspiration of the fluid and injection of steroids. If the
process is too far advanced and does not respond to therapy, another possible form
of treatment might be surgery.

Stress Fractures
Bones have a remarkable ability to grow and repair themselves. When a person begins
training or increases the intensity of training, the forces applied to the bone by the
action of the muscles and gravity create tension in some areas and compression in oth-
ers. This directs the cells to build new bone in some areas and remove the old bone.
The end result is the creation of new bone that is better suited to the new demands.
Too much or too rapid an increase in training can create problems. When new
bone formation cannot keep pace with the bone removal, a stress fracture might
develop. The most frequent sites of stress fractures are in those areas that receive
considerable stress from weight-bearing forces, such as the foot bones, shin bones,
and the thigh bone close to the hip joint. People who suffer from kidney diseases,
malnutrition, or secondary amenorrhea (cessation of menstruation) or who have
undergone a period of prolonged immobilization have weaker bones and a greater
risk of stress fractures.
Stress fractures cause pain on palpation (touching) first, followed by pain during
activity. X-rays of the area usually do not show any abnormalities if they are taken
during the first 3 weeks of the fracture. However, bone scans are almost always posi-
tive. The average time of healing for a stress fracture is 7–8 weeks. Medications other
than painkillers are seldom needed, except in malnourished persons who lack mag-
nesium, calcium, or vitamin B and in amenorrheic females, who might require hor-
monal replacement. Exercise may be continued but should be modified. Runners are
advised to stop running and begin swimming or cycling until they are free of pain.
Then, walking, jogging, and a slowly progressive running program can be initiated.
The majority of stress fractures can be prevented. Physical training should be pro-
gressive, with periods of rest to allow the body to recover. One should avoid sudden
increases in training. Training should be slowly progressive and cyclic. A minimum
of 1 day a week for rest and alternating weeks of high-intensity training with weeks
of easy training and cross training in different sports will prevent stress fractures.
Overuse Injuries of the Arm and Hand

Lateral Epicondylitis (Backhand Tennis Elbow)
Backhand tennis elbow is tendinitis at the origin of the extensor carpi radialis muscle
at the elbow. Patients with this condition develop pain in the lateral (outer) aspect of the
elbow in the arm. This phenomenon is caused by frequent, quick extension movements
of the wrist—movements associated with the backhand stroke. This type of stress
causes small, frequent tears of the tendon. Aggravating factors include using a heavy
racquet or ball, too much tension on the strings of the racquet, oversized grip, and play-
ing on cement or other fast surfaces. The diagnosis is made when the examiner finds
pain upon palpation a little distal (away) from and anterior (in front of) to the lateral
(outside) epicondyle. (The lateral epicondyle is the bony prominence on the upper and
outer part of the elbow.) Resisting extension of the wrist reproduces or aggravates the
pain. Treatment of this condition is the same as the treatment of any other tendinitis.
To prevent backhand tennis elbow, proper technique and equipment should be
used. Strengthening and stretching prior to returning to the game following a respite

and appropriate warm-up before playing are very important. Poor technique, such as
using the arm and the wrist to pull the ball rather than keeping the wrist and elbow
rigid, increases the likelihood of worsening tennis elbow.
Medial Epicondylitis (Forehand Tennis Elbow, Pitcher’s Elbow)

Medial epicondylitis is a tendinitis of the forearm flexors (pronator teres and the
flexor carpi muscles). Patients with this condition develop pain on the inside of the
elbow of the arm. Pitcher’s elbow is caused by frequent, quick flexion and inward
rotation movements of the hand such as throwing a baseball or serving a tennis ball.
The diagnosis is made when the examiner elicits pain, on palpation, inside the elbow
over the bony prominence located in that area. The pain is aggravated by flexing and
inwardly rotating the hand against resistance. The treatment is the same as that out-
lined for tendinitis. Proper strengthening and stretching before returning to the sport
plus appropriate warm-up before playing are important in preventing this problem
from recurring.
Little League Elbow

Young people who abuse their elbows (e.g., Little League pitchers) have a variant of
the pitcher’s elbow. The tendons of the forearm flexors insert in the growth center of
the inside of the elbow. The constant irritation may cause a mild growth deformity
of that bone followed by pain and tenderness. A prolonged episode of rest (1 month
or more) is usually needed. Restart throwing slowly and increase the workout very
gently. This condition can be very resistant to treatment.
Bicipital Tendinitis
Bicipital tendinitis is an inflammation of the biceps tendon near the shoulder where
it runs inside a bony groove. Repeated motions such as throwing and swinging the
arm can rub the tendon against the bony groove, resulting in inflammation. The pain
is felt in the front of the arm part of the shoulder when the player brings the arm back
as he or she prepares to throw the ball. Treatment is as outlined for tendinitis, fol-
lowed by strengthening and stretching exercises of the arm and shoulder.
Tendinitis of the Dorsal Aspect of the Wrist

Tennis players with improper backhand technique (see sections on tennis elbow)
or any other activity that requires quick, forceful use of the wrist extensor muscles
can cause tendinitis of the dorsal tendons of the wrist. In addition to the treatment
outlined in the section on tendinitis, splinting of the wrist to rest it properly is usu-
ally necessary; this is followed by a program of strengthening and stretching. Deep
friction massage is very useful in this type of tendinitis.
Tendinitis of the Thumb Extensor (DeQuervain’s Tendinitis)

The thumb extensor muscle extends the thumb and allows one to give the “thumbs
up” signal. The extensor’s tendon can be easily seen when the thumb is extended.
This can become swollen and inflamed. Stretching the tendon when it is inflamed
will make the pain worse. This is what happens when the thumb is pushed toward
the little finger (Finkelstein’s test). The treatment is similar to that for other forms of

tendinitis. Splinting and one or two steroid injections might be necessary. Bad cases
might require surgery to free the tendon from the surrounding scar tissue.
Olecranon Bursitis
Between the skin of the elbow and the bone there is a bursa (see section on bursitis).
This bursa is quite useful because we seem to be constantly “elbowing” objects—
soft and hard. Occasionally, the trauma becomes too intense for the bursa to handle
and it becomes inflamed, swollen, and easily visible under the skin of the arm just
above the elbow. At times, the olecranon bursa can become infected. The swelling
looks the same, but the area hurts and might feel warm when it is touched. Painful
olecranon bursitis suggests infection and requires immediate medical attention.
Shoulder Pain
Unlike the hip, which resembles a baseball inside a cup, the shoulder looks more like
a baseball (the cup of the humerus) inside a large spoon (a shallow depression in the
scapula). The hip joint is a very stable joint, but the shoulder joint is not. If it were not
for the multiple ligaments and powerful muscles around it, the shoulder joint could
be easily dislocated. This is why muscle imbalance about and around the shoulder
predisposes to and perpetuates shoulder injuries.
The roof of the shoulder is formed by two bones and a strong ligament. The col-
lar bone joins with the acromium (a bony extension of the shoulder blade) forming a
horseshoe-like roof on the top of the shoulder. The shoulder can move around more
than any other joint in the body. Because of this phenomenal mobility and the large
number of tendons and muscles around it, a total of eight bursae are needed to keep
the joint, the tendons, and the bones well lubricated and prevent injuries. Overuse
pain in the shoulder is usually the result of bursitis or tendinitis.
Rotator Cuff Tendinitis

The rotator cuff is a combination of four tendons from four different muscles that
go from the shoulder blade to the head of the arm. Their job is to rotate the arm.
They are used mostly with overhead throwing types of motions such as swimming,
pitching, tennis serving, etc. We cannot see the rotator cuff because it is located
under the acromium. Tendinitis of the rotator cuff causes recurrent pain and stiffness
in the shoulder, radiating into the front and upper part of the arm and aggravated
by activity. Between the rotator cuff and the acromium is a bursa. When this bursa
is inflamed, the person cannot elevate the hand past 90° due to pain brought on by
squeezing the inflamed bursa against the bone. Bursitis in this area is usually sec-
ondary to tendinitis in the rotator cuff. The treatment of rotator cuff tendinitis is the
same as the treatment of any tendinitis, followed by stretching and strengthening of
all the shoulder muscles.
Overuse Injuries of the Lower Extremities

Shin Splints
Patients with this condition develop pain and discomfort in the anterior (front) part of
the leg. Initially, the pain occurs during the warm-up, disappears with exercise, and

returns after the workout. Later on, the pain begins during the warm-up, continues
during exercise, and sometimes bothers the patient during daily activities. The pain is
caused by the repetitive pulling of the soleus muscle and possibly the tibialis posterior
on the shin bone (tibia), resulting in small tears and inflammation in the area where
these muscles attach to the bone. The several possible biomechanical predisposing
factors include pronation of the foot, stiff tibialis posterior and soleus muscles, and
running on hard surfaces. The diagnosis is made by eliciting tenderness on palpation
of a 3- to 6-centimeter area on the posterior and inside part of the lower one third of
the shin bone. Shin splints must be differentiated from stress fractures of the tibia as
well as a condition called “compartment syndrome” (discussed later).
Rest and gradual resumption of sports activities, coupled with anti-inflammatory
medication, are the appropriate treatments. Steroid injections do not help. Rehabili
tation consists of strengthening and stretching the leg muscles, especially the soleus
and the tibialis posterior. The correction of any biomechanical abnormality, if pres-
ent, and the avoidance of running on hard surfaces—plus the use of appropriate
shock-absorbing shoes—will help in preventing future recurrences.
Stress Fractures of the Tibia

For the definition and cause of stress fractures, please see the earlier “Stress
Fractures” section. A person with a stress fracture of the tibia has a very well local-
ized and defined area of tenderness over the shin bone. This pain is so well defined
that it could hurt during palpation of an area no greater than 1 inch; palpating above
and below that 1 inch does not cause pain. Initially, the pain is mild and there is only
tenderness on palpation; in time, however, it will occur when the person plays the
offending sport. Ultimately, it will hurt constantly.
The well-defined nature of this pain helps to differentiate stress fractures of the
tibia from shin splints and compartment syndrome. X-rays are often negative during
the first 6 weeks, but bone scans are positive as early as 3 days after the injury. False
positive scans are infrequent. Treatment consists of rest until the patient is free of
pain, at which point regular activities can be gradually resumed. If the pain returns,
the patient should slow down and then try a gradual resumption of activity.
Compartment Syndrome
With exercise, the muscles swell with blood. There is a group of muscles in the leg
located in a very tight compartment that is limited by the tibia inside, the tibia on the
other side, and a thick fascia (membrane) in the back. When those muscles swell with
exercise, the pressure inside the compartment increases, squeezing shut the circula-
tion and pinching a nerve that runs through it. The result is pain in the leg just outside
the shin bone that is occasionally associated with numbness and tingling in the lower
leg and the back of the foot. This pain usually occurs consistently during exercise
or after about 15 minutes of running, cycling, or doing aerobics. Compartment pain
might develop as a result of injury and subsequent swelling of this area. This is a
medical emergency and the patient should go to an emergency room immediately.
There is no good treatment for compartment syndrome other than surgery to decom-
press the area.

Overuse Injuries of the Knee

The most frequently injured area of the body and the joint most frequently requiring
surgery is the knee (25% of all sports injuries and 75% of all sports-injury-related
surgeries). Pain in the knee can be caused by a variety of problems involving any one
of the many structures that comprise this joint—for example:
• problems in the bone (two round prominences at the lower end of the femur
that articulate with two shallow cups at the upper end of the tibia)
• the cartilage that coats the bone (meniscus), which lies between the bones
• the crossing ligaments inside the knee (cruciate ligaments), which prevent
the joint from sliding to the front or back
• the ligaments located on either side of the knee (lateral and medial liga-
ments), which prevent the joint from bending sideways
• the sac that surrounds the knee and produces the oily fluid that lubricates
it (synovial sac)
• the small bone that rides on top of the knee, over which rides the quad-
riceps tendon
• any of the multiple tendons and their bursae as they insert around the joint
Considering the mobility of the knee joint and the amount of force it withstands, it
is surprising that injuries do not occur more often. However, when injury does occur,
it could affect any of the structures mentioned before. Overuse injuries make up 85%
of knee problems and the majority of these are related to the way in which the patella
(knee cap) slides up and down the femur.
Chondromalacia Patella (Extensor Mechanism Injury)

Sixty percent of patients with overuse injury knee problems complain of pain that is
very difficult to pinpoint. It is felt inside, outside, or below the patella. The inability
to pinpoint where it hurts and the absence of any other abnormality such as swelling,
fluid in the knee joint, etc. suggests that the cause of the pain is patellofemoral. The
patella is firmly attached to the tendon of the quadriceps muscle, which runs from
the lower thigh, over the patella, and into the upper leg. The patella provides a point
of leverage and, by changing the angle of the tendon, increases the strength of the
quadriceps by 30%. Flexion and extension movements of the leg move the patella up
and down, sliding in a groove built for this purpose in the lower end of the femur.
Several alignment problems cause the patella to rub excessively against the fem
oral groove, resulting in inflammation and, in severe cases, wearing down the car-
tilage that lines the underside of the patella. Pronation of the foot causes the knee
to rotate to the inside as the patella rubs on the outside of the femoral groove.
Sometimes, knee pain begins following a period of inactivity. For example, an ankle
sprain forces one to take it easy for several weeks and, because of this lack of activ-
ity, the quadriceps become weak. The quadriceps pull the patella inward (vastus
medialis). This part of the muscle usually becomes weaker.
Thus, when running or dancing begins again, the patella begins to rub against the
outer edge and lacks the balancing effect of the vastus medialis muscle. Interestingly

enough, cycling is a good exercise to strengthen the vastus medialis. Therefore, for
lateral (outside) patellofemoral pain resulting from a period of inactivity and begin-
ning after running or walking has been started again, the amount of running should
be decreased and more cycling substituted. Strengthening the vastus medialis might
correct the problem.
Patellar Tendinitis (Jumper’s Knee)

The pain experienced by athletes with this condition is very well localized. One can
touch the sore part, which is the lower end of the tendon that goes from the patella
to the tibia. It is called jumper’s knee but it could happen to anyone who is involved
in running and jumping sports like running, soccer, basketball, volleyball, etc. The
same alignment problem described in chondromalacia patella predisposes to patellar
tendinitis. The treatment is similar to that of any other form of tendinitis.
Osgood–Schlatters Disease
The place in the tibia where the patellar tendon attaches happens to be a growth
center. Bones grow at either end in certain areas called growth centers. If a person’s
bones are growing and he or she develops patellar tendinitis (see previous section),
the inflammation will cause the growth center to swell into a tender lump. Treatment
is the same as that for patellar tendinitis.
Hamstring Tendinitis
The hamstrings are the largest muscle group in the back of the thigh and are com-
posed of three different muscles. The tendons of those muscles can be easily pal-
pated in the back of the knee. The semimembranosus and semitendinosus muscles
are located toward the medial side and the biceps femoris muscle is located toward
the lateral side. These tendons are very strong and are called hamstrings because
hogs were hung from them to be slaughtered. Any of these tendons can be injured
if the hamstring muscles or hip flexors are out of balance and are too tight or the
subject embarks on activities that overstretch the hamstrings, such as running in low-
heeled shoes, running barefoot in the sand, or running downhill.
Semimembranosus Tendinitis
One of the two hamstring tendons runs on the inside and the back of the knee. The
semimembranosus muscle prevents excessive external rotation of the leg. Excessive
pronation of the foot as well as internal rotation of the femur places too much stress
on this tendon and predisposes to tendinitis. The pain is felt on the inside and back
of the knee and increases by palpation and activity. Treatment is the same as for any
tendinitis followed by stretching and strengthening of the hamstring muscle group.
Semitendinosus Tendinitis and Pes Anserinus Bursitis

The semitendinous is the other hamstring muscle located on the inside and the back
of the knee. It swings around a little and joins two other tendons—the gracilis and
the sartorius—as it inserts on the inside of the knee just in front of the medial liga-
ment. The bursa that lubricates those tendons is called the pes anserinine bursa.
Inflammation of the semitendinosus tendon (tendinitis) or the pes anserinine bursa

causes pain on the inside of the knee just below the joint line. Predisposing factors
include tightness of the hamstrings, knock-knees (genu valgum), pronation of the
foot, and external tibial torsion.
Popliteal Tendinitis
We have mentioned before that pronation of the foot can cause pain in the back and
inside of the knee (semimembranosus tendinitis), on the inside of the knee (pes anseri-
nus bursitis), and on the front of the knee (patellofemoral pain). It can also cause pain
in the outside of the knee by placing stress on the tendon of a very short muscle that
originates in the back of the tibia and ends in a short tendon that crosses the outside of
the knee and inserts on the outside of the end of the femur. Poplitial tendinitis causes
pain on the outside of the knee, especially when a person is running downhill.
Iliotibial Band Tendinitis (IBT)

The most common cause of pain on the outside of the knee is inflammation of the
IBT. The exact frequency of occurrence of IBT is not known, but several studies have
estimated it to be between 7%–50% of all cases of knee pain. The IBT is a very long
and strong tendon that runs from the hips on the outside of the thigh to the outer part
of the tibia. With flexion and extension of the knee, the IBT moves like a windshield
wiper over the bony prominence on the outside of the knee. People who have a tight
IBT, bow legs (genu varum), pronation of the foot, or leg length inequality (on the
longer leg) or who do a lot of downhill running increase the amount of rubbing and
are predisposed to inflammation.
However, the most common cause of IBT pain is error in training. In approxi-
mately 50% of cases of IBT pain, the runner can trace the onset of the pain to a
single, unusually severe training event (i.e., too many hills or too long of a run).
Downhill running is a particularly stressful activity and is a salient cause of IBT. The
pain is felt on the outside of the knee—sometimes a little lower (over the outside part
of the upper shin bone). The pain is worse immediately after the foot hits the ground
and just before the foot passes the midline (the knee is in 30%–40% of flexion). The
treatment consists of correction of alignment problems, if possible; avoiding training
errors; and following the routine therapy of tendinitis outlined earlier.
Overuse Injuries of the Hip and Thighs

The hip bone is very large and accommodates the thigh bone, which is the largest of
all bones, in a very stable joint that resembles a ball inside a cup. The hip joint does not
require tendons and muscles to keep it together as do the shoulder and knee joints.
The hip and femur hold the key to proper posture. The muscles of the abdomen
and the powerful muscles of the back and thigh attach to them. The hamstring in the
back of the thigh flexes the leg over the thigh. The quadriceps muscles in the front
of the thigh extend the legs. The gluteus muscles (there are three of them) rotate the
hip and legs outward and extend the thigh backward. The adductors are a group of
muscles located on the inside part of the upper thigh and the groin. They connect
the lower part of the pelvis (pubis) with the inside of the femur. Their job consists
of pulling the legs together. The psoas major connects the vertebrae in the lower

back with the upper inside part of the femur (lesser trochanter). Together with the
iliacus muscle, which connects the upper rim of the pelvis (iliac crest) with the lesser
trochanters, they flex the thighs on the trunk (flexing the thighs on the trunk occurs
when one does sit-ups). All of these muscles can be stressed and their tendons can be
inflamed in different ways.
Distance runners, ballet dancers, and gymnasts are more prone than other ath-
letes to injuries of the adductors, extensors, and rotators of the hips and thighs. Pain
in the upper back of the thigh could be the result of a strain of a hamstring origin on
the posterior lower part of the pelvic bone (ischial tuberosity). People with one leg
shorter than the other are predisposed to this problem in the shorter leg. Pain in the
inside and upper part of the thigh could indicate strain in the tendons of the iliacus
and psoas where it connects with the femur (lesser trochanter), or it could be the
result of a strain of the origin of the adductor muscles. Pain in the groin could repre-
sent inflammation at the site where the right and left pelvis meet (pubic symphysis).
This is more common in women runners who cross their arms when they run, creat-
ing a rotational strain in the pelvis. In some cases, this type of strain could result in
a stress fracture of the pelvis.
Young athletes who are still in the growing phase can experience inflammation of
the growing centers of the hip. This can occur in the upper part of the hip (iliac crest;
anterior, superior, and inferior iliac spines) and in the site of insertion of the ham-
strings (see preceding discussion). Runners can sometimes develop stress fractures
of the femoral neck (the upper part of the thigh bone). This type of stress fracture is
difficult to diagnose because although the pain might not be felt in the hip, it might
travel through the nerve and be felt elsewhere. This is an unusual case of a rather
severe hip problem that manifests with pain in the knee.
Trochanteric Bursitis
If one touches the upper and outer part of the thigh, somewhere between the front
and back pockets of one’s pants, a bony prominence will be found. It is called the
greater trochanter of the femur. The gluteal maximum muscle is located just behind
it and the tensor fascialata muscle is located just in front. The fascialata, a very strong
ligament, originates about that level and runs over the trochanter and down toward
the knee on the outer part of the thigh. There is a bursa located over the trochanter
that can be inflamed either by direct trauma (such as falling on it) or by rubbing the
ligaments over it. This is more likely to occur in people who have one leg longer than
the other (in the longer leg), tight fascialata, or any condition that causes pelvic tilt
with elevation of the pelvis in the injured site (e.g., scoliosis).
Back Pain
Without the bones in the back (vertebral column), it would be impossible to stand
up, get up from a chair, or even get out of bed. Remove the vertebral column and
we are like a boat without a mast—not able to do anything or go anywhere. Unlike
the boat’s mast, the vertebral column is capable of bending forward, backward, and
laterally and rotating around itself. This is possible because the backbone is not a
stiff pole, but rather a collection of blocks (vertebrae) separated by a round cushion

that functions as a shock absorber and gives the spine flexibility. This cushion is
very tough on the outside and filled with a jellylike substance. These “cushions” are
called the intervertebral discs, but they look more like a jelly-filled Danish pastry.
The vertebrae and disks stay in line by a very ingenious arrangement. Each ver-
tebra overlaps the one below it in the back. The place where they connect with the
vertebra above and below is a small joint called the facet joint. However, this is not
enough to provide support to the weight of the upper body, especially if someone
has decided to lift weights. An enormous amount of pressure can be applied to the
vertebral column and the facet joints, which stay in place thanks to very tough liga-
ments located in front and back of the vertebrae plus the balancing forces of power-
ful muscles that connect the backbone with the pelvis in a manner very similar to the
way that a mast is held in place by cables in all four directions.
The muscles connecting the vertebral column with the pelvis determine the
posture of the trunk. They are very powerful and are often recruited to help with
activities that weaker muscles cannot handle. If we are doing bench presses and the
pectoralis and triceps are having difficulty, we recruit the back muscles and arch our
back to get better leverage. The same thing happens with shoulder presses. If the
deltoid cannot handle the weight, we tend to arch our back; when we are doing sit-ups
and the abdominal muscles fatigue, the iliopsoas takes over and flexes the spine over
the thighs. (This is why if we want to emphasize only the abdominal muscles, we
should not hook our feet under something because doing so activates the iliopsoas
and makes the work easier for the abdominal muscles.)
One of the most common causes of back pain is improper technique coupled with
weakness of muscles elsewhere; this prompts the exerciser to use the back muscles
unnecessarily and excessively. Interestingly enough, people with back pain often
refer to their back as being weak, adding insult to injury. Back muscles are very
seldom weak, even in people who lead sedentary lives, because carrying the weight
of the upper body around as we go about our normal routine is enough to keep these
muscles in decent shape. It is the rest of the body that is usually at fault and in need
of strengthening.
Deconditioning is one of the most important causes of back pain. The two key
muscles that keep the spine straight are the spinal muscles in the back, which connect
the backbone to the pelvis, and the abdominal muscles in the front that connect the
rib cage, which in turn connects to the backbone. But, perhaps of more importance,
the abdominal muscles keep the abdominal organs tight inside the abdomen, pro-
viding additional support to the spine. The spinal muscles are usually always strong,
but the abdominal muscles can become weak if not exercised. Weak abdominal
muscles result in forward displacement of the abdomen and arching of the back.
Let us present an example of why this situation leads to back pain. Push one of
your fingers back gently so that you feel slight pressure in the finger joint. It does not
hurt, does it? But if you keep your finger bent like that day after day, the strain over
the joint will be too much and pain will eventually begin. It is just a matter of time. It
is the same with the lower spine. Weak abdominal muscles lead to overextension of
the spine and eventually overload the facet joints, which eventually causes degenera-
tive arthritis and chronic back pain.

Two types of conditions can result in back pain:
• The vertebrae, discs, and ligaments are normal. The pain in this case is
secondary to muscle imbalance, tight hamstrings, tight iliopsoas, weak
abdominal muscles, obesity, deconditioning, poor exercise technique, or
a combination of two or more of these, resulting in facet overload and
muscle spasms.
• The vertebrae, discs, and ligaments are normal, but the subject has suffered
an abnormally high mechanical load. The result is a strain of the ligaments
or muscles of the back, a rupture of a disk, a fracture of a bone, etc.
Minor daily activities can trigger the problem. Examples of problems in the ver-
tebral column include scoliosis (abnormal curvature of the spine), spondylolysis
(defect of the part of the vertebra that supports the facet joint), spondylolisthesis
(one vertebra slips over the other and shifts forward), or degenerative arthritis of
the spine. The treatment of back pain varies according to its source. If the pain
is secondary to muscle imbalance and deconditioning, then the proper treatment is
appropriate training and reconditioning. If back pain is secondary to the sprain of a
muscle or a ligament, the patient usually develops a considerable amount of pain and
reflex muscle spasm leading to disability. Painkillers, muscle relaxants, local heat,
and gentle stretching will eventually solve the problem.
A ruptured disc is a more severe problem. When the tough, outer part of the disc
gives way and the pressurized jelly inside bulges out, the bulged disc can put pres-
sure against the spinal cord or the nerve roots as they leave the spine. When that hap-
pens, the pain might not be limited to the back, but might radiate down the arms or
legs. Numbness and tingling in the arms and legs are not uncommon findings as well.
Coughing, sneezing, and movements of the nerve roots (when lifting the straightened
leg up) aggravate the pain. If this is happening, the injured individual must consult
a physician immediately as surgery might be indicated to save the person from fur-
ther injury and even paralysis. Any back pain that has not improved with over-the-
counter painkillers, heat, and stretching should be evaluated with appropriate x-rays
to rule out underlying medical problems.
Degenerative disc disease can result in chronic and very frustrating back pain
that often does not improve with medications. Surgery very often fails to correct
this problem and it should be reserved for patients with severe disability after all
other forms of treatment have failed. Physical and psychological techniques have a
high success rate. Back pain in patients with scoliosis occurs intermittently and sel-
dom requires more than transient modification of sports activities. Spondylolysis and
spondylolisthesis might require surgery to provide stability to the spine.
Overuse Injuries of the Foot and Ankle

The foot is poorly understood, often neglected and abused, and, generally speak-
ing, not appreciated. Poems have been written about the hands, the face, the thorax,
and even the ankles. But few poets will find the foot attractive enough to write love
poems about it. The feet are thought of as being ugly and malodorous, and yet are

asked to perform an incredible amount of work. The foot, like a faithful dog, takes
this all in stride, seldom complaining.
For the sports medicine physician, the foot is fascinating—a biomechanical
wonder. It has 26 bones, articulated in such a way as to allow movements and power
sufficient to get us where we are going, to execute a dancing step, or leap to a basket.
It has an intricate shock absorption mechanism and quite a few tendons and power-
ful ligaments that allow it to move in different directions while keeping the body
balanced. It is an impressive machine, especially when one considers that most
people work their feet all their lives and never have any problems in spite of all the
things they do to them. However, occasionally things do go wrong and, when they
do, it is usually because of problems outside the foot that have caused abnormal
mechanical stress on the foot. The result might be plantar fasciitis, bunions, stress
fractures, etc.
On the other hand, when the foot is not performing well—for example, if it rolls
inward too much (pronation)—all sorts of problems can occur—not in the foot, mind
you, but elsewhere. It could be the ankle (Achilles tendinitis), or the leg (shin splints),
or the knee (patellofemoral pain). So, it is best to begin our review of injuries of the
foot and ankle with a review of the normal biomechanics of walking and running.
The walking and running stride have three common phases: foot strike, pronation,
and push-off. The difference between walking and running is that, in walking, one
foot is always in contact with the ground; in running, there is an extra phase, the float
phase, after the push-off, when neither foot is touching the ground. Forty percent of
runners and 100% of walkers land on their heel when the foot strikes the ground. Forty
percent of runners land on the full foot and the other 20% on the balls of their feet.
After foot strike, the foot absorbs the shock by rotating inward (pronation) and
unlocking the joints and flattening the arch. In the process, it becomes more flexible
and adapts to the surface of the ground. Pronation lasts until the foot crosses the
gravity center, when it becomes rigid again. It passes from pronation to supination
(rolls outward) and pushes off with the first (great) and second toes. With pronation
there is a flattening of the subtalar joint (the joint directly below the ankle joint), a
mild bowing of the Achilles tendon, and an inward rotation of the leg. Excessive
pronation causes stress in the Achilles tendon and shin bone, and rotational stress in
the knee joint.
Plantar Fasciitis
The plantar fascia is a tough band of fibrous tissue that goes from the heel bone to the
bones in the base of the toes. It is quite thick and, when the foot is rested, it arches
the foot like the string of a bow. When the foot lands, the plantar fascia gives some
as the foot lands, absorbing some of the shock. People with high arches have tight
fascia (like a tight bow) and are prone to develop small tears of the plantar fascia.
Excessive tightness of the calf muscles has been identified as a cause of plantar
fasciitis. The pain is felt in the bottom of the foot, usually close to the heel. In mild
cases, the pain is felt only after running. As the condition gets worse, the pain is felt
while walking and while running.
Treatment consists of rest, custom-made arch supports (orthotics), and stretch-
ing the calf muscles and Achilles tendon. The pain of plantar fasciitis should not

be confused with the pain caused by a pinched calcaneus (calcaneal neuritis). The
neuritis pain is different. It is also a plantar pain but it has a burning quality to it (see
the “Nerve Entrapment” section).
Achilles Tendinitis
The Achilles tendon is a very large and tough tendon. However, like all tendons, it is
not very elastic. If the calf muscles are short and tight (common in women who wear
high-heeled shoes), if a person has purchased new low-heeled shoes and has been
doing a lot of running in them, or if someone suffers from pronation (which bows the
tendon inward, rubbing it against the bone), the tendon might become overstressed
and, eventually, inflamed.
Initially, the patient will feel a mild discomfort when getting out of bed in the morn-
ing. Later on, it will hurt when the person runs but goes away when he or she stops, only
to hurt again for a little while on rising. People usually ignore this pain until it becomes
constant. Treatment consists of heel lifts to reduce the pain, the correction of pronation if
present, and, when the pain has subsided, stretching and strengthening the calf muscles.
Haglund’s Syndrome
A syndrome is a set of symptoms or signs that occur together. Haglund’s syndrome
is a combination of a painful bump (or lump) at the insertion of the Achilles tendon.
People with this problem usually have a combination of bursitis and Achilles ten-
dinitis. The result is swelling and pain. Treatment is the same as that for Achilles
tendinitis.
Metatarsal Stress Fractures

Metatarsal stress fracture has also been called “march” fracture and is the typical
stress fracture. The metatarsal bones are five bones that connect the bones in the
middle of the foot (tarsals) with the toes. The repeated stress of marching eventually
results in fracture of one of these bones. As expected, this problem is common in
young recruits about 3 weeks after they begin boot camp training. However, it can
happen to anyone engaged in any other running and/or jumping sports such as run-
ning, aerobic dancing, etc.
The most serious of the metatarsal stress fractures is the stress fracture of the fifth
metatarsal (the great toe is the first toe and the small toe is the fifth) especially when
the fracture has occurred in the part of the bone that is close to the midfoot. That part
of the fifth metatarsal has very poor circulation and does not heal well. If the fracture
has occurred in this area, it should be immobilized with a non-weight-bearing cast.
If, in spite of the cast, the fracture does not heal, it might require surgical attention.
Navicular Stress Fractures

The navicular is the bony prominence on the back of the foot on the great toe side. It
is the uppermost bone in the top of the midfoot. Fractures of tarsal navicular (there
is another navicular in the wrist) are a real problem. This bone has very poor circula-
tion and these fractures are very difficult to heal, resulting in prolonged disability.
As usual, the problem begins with mild pain in the top of the foot that is made worse
by activity and relieved by rest.

X-rays are usually negative in the early stages. If routine x-rays of the foot are
negative, a bone scan of both feet (for comparison) should be obtained. Several bio-
mechanical abnormalities have been suspected of setting the stage by concentrating
too much stress on the navicular. Abnormalities can include a short great toe, limited
dorsiflexion of the ankle, and limited subtalar joint motion. Fractures of the navicu-
lar are treated with a non-weight-bearing cast for 6–8 weeks. Surgery is indicated
when there is no union of the fragments after that time.
Orthotics
By now it has become obvious that pronation is a biomechanical abnormality that
often results in overuse injuries of the lower extremity, and one might be tempted
to correct it whenever it is found to prevent problems in the future. A word of cau-
tion, however: Pronation sometimes occurs as a compensatory mechanism to correct
some other abnormality, such as poor dorsiflexion of the foot. Correcting the prona-
tion could lead to other problems. Keep in mind two rules of thumb before buying
over-the-counter orthotics: (1) “if it’s not broken, don’t fix it”—in other words, if it
does not hurt, leave it alone; and (2) if someone is having pain and thinks orthotics
are needed, the foot should be properly evaluated by a professional.
NERVE ENTRAPMENT
There are a few nerves in the body that run a peculiar course through bony channels,
between ligaments, or through muscles where they can be squeezed, trapped, or
pinched. Weight lifters and rowers can overdevelop the forearm muscles and squeeze
either the median nerve or the radial nerve near the elbow. Cyclists and athletes who
frequently use the wrist can pinch the median nerve (carpal tunnel syndrome) or the
ulnar nerve (handlebar palsy) in the wrist. The constant pounding of the foot against
pavement in runners can cause entrapment of the posterior tibial (shin) nerve or the
peroneal tendon in the foot. The result is pain and/or abnormal sensations (such as
numbness and tingling) or weakness. These are the same symptoms found in patients
with diseases in the spine. Someone who develops any of these symptoms should see
a physician immediately. One should not risk ignoring a spine problem.
Sometimes the opposite happens. A patient with a pinched nerve could be con-
sidered to have a spinal problem. The sciatic nerve runs very close to the piriformis
muscle (a small muscle located under the gluteus, which is the largest muscle in the
buttocks). In 20% of the population, the sciatic nerve runs through the piriformis
muscle. Occasionally, the nerve is squeezed by this muscle, resulting in buttock pain
that runs down the back of the leg and the foot. Since the majority of patients with this
type of pain suffer from diseases of the lumbar (lower back) spine, it would be rela-
tively easy to attribute the pain mistakenly to the back. To make matters more confus-
ing, the “straight-leg raising” test (sciatic pain induced by raising the straight leg) is
positive in patients with this piriformis syndrome and is also positive with sciatica.
The diagnosis is made when the alert examiner demonstrates that the pain can also
be induced by raising the leg with the knee bent and by maneuvers that stretch the
piriformis muscle. Treatment for nerve entrapment varies among anti-inflammatory

medications, steroid injections, surgery, and rehabilitation exercises. Each case

requires individual attention because the same problem can be treated differently in
different people.
Carpal Tunnel Syndrome

This is the most common type of nerve entrapment. The median nerve and the flexor
tendons of the fingers travel together through a tunnel located in the middle of the
palmar aspect of the wrist. Inflammation of the tendons can “trap” the nerve in
the tunnel, causing pain, numbness, and tingling of the palm of the hand and the
fingers. Tapping the carpal tunnel causes pain and confirms the diagnosis. Treatment
consists of immobilization (splinting), anti-inflammatory medications, and stretch-
ing. Injection of steroids might help. Recalcitrant cases might need surgery to free
the nerve.
PULMONARY
Exercise-induced asthma is the most common pulmonary problem associated with
exercise. This occurs in 12% of the population and is discussed in Chapter 5.
SKIN
Skin-related problems are usually mild and easily preventable. They include irri-
tation of the nipples, which is commonly seen in joggers (jogger’s nipple) and is
caused by the friction of clothing on the nipples; this can be prevented by covering
the nipples with a band-aid. Irritation of the inner part of the thighs and the axillae
is caused by the friction of skin on skin and can be prevented with petroleum jelly
(Vaseline). Tinea pedis (athlete’s foot) and tinea cruris (jock itch) are also common
skin problems. They can be treated with applications of tolnaftate cream or another
over-the-counter remedies. Bleeding under the toenails (runner’s toe, tennis toe) can
be prevented by wearing shoes one-half size larger. Occasionally, exercise can cause
itching and a skin rash that is often diagnosed as an allergy to sweat. This condition
is called” exercise-induced urticaria” and is caused by histamine release.
URINARY SYSTEM
Exercise-induced hemodynamic and hormonal changes cause renal vasoconstriction
and a considerable reduction in the glomerular filtration rate. Medications that cause
renal vasoconstriction could theoretically predispose the athlete to exercise-induced
renal injury, but such cases are very rare. Common exercise-induced urinary prob-
lems, including proteinuria and microscopic hematuria, are benign conditions. The
only danger lies in the possibility of confusing this benign problem with a more
serious urinary condition such as nephritis. Exercise-induced renal failure can occur
as a complication of rhabdomyolysis (see section on muscular injury), dehydra-
tion secondary to heat-related injuries, and excessive vasoconstriction caused by a

combination of strenuous exercise and the use of renal artery vasoconstrictors such
as nonsteroidal anti-inflammatory medications.
THERMAL INJURIES
The energy produced during exercise is converted into work and heat. The body is not
an efficient machine: Only 25% of the energy produced is translated into mechanical
work; the rest is converted to heat. Elimination of heat is accomplished by radiation,
convection, conduction, and evaporation, of which evaporation of sweat is the most
important. Cold and windy days increase the efficiency of radiation and convection
mechanisms; humid days decrease the effectiveness of evaporation. All forms of
heat elimination are enhanced by thermoregulatory mechanisms that cause cutane-
ous vasodilation, raising the skin temperature. Dehydration, advanced age, and the
administration of medications that interfere with thermoregulation (such as diuretics
and anticholinergics) are predisposing factors for heat-related injuries.
There are three heat-related syndromes: (1) heat cramps, (2) heat exhaustion, and
(3) heat stroke. Heat cramps are dehydration-induced muscular cramps associated
with exercise. Patients with heat exhaustion experience fever (usually greater than
103°F), nausea, cramps, headaches, and light-headedness, and the patient sweats
freely. Patients with heat stroke have symptoms similar to those of patients with heat
exhaustion except that they are confused, their skin is flushed and dry, and they are
more likely to be hypotensive. Prevention of heat-related injuries includes proper
hydration and avoidance of exercise during hot and humid days. Drinking water
before and during exercise is very important; adding salt and/or other electrolytes to
the ingested fluids is usually not necessary. For more detailed guidelines on hydra-
tion see ACSM.org.
Cold-related injuries include exposure, hypothermia, and frostbite. Exposure to
cold weather or immersion in cold water lowers the core temperature and can cause
hypothermia (core temperature below 35°C [95°F]). The symptoms of hypothermia
include confusion, slurred speech, lack of coordination, and shivering, followed
by muscular rigidity, lethargy, coma, metabolic acidosis, and cardiac arrhythmias.
Areas most likely affected by frostbite include the toes, fingers, ears, nose, and
penis. Symptoms begin with pain; this is followed by numbness and the affected
area appears pale and waxy. Areas at risk of frostbite should be slowly rewarmed in
warm water (42°C). During rewarming, the affected area becomes hyperemic and
painful. Victims of hypothermia should be covered with blankets and transferred to
a warm place. Rapid rewarming with electric blankets or immersion in warm water
are not indicated and could be dangerous since they would not alter core temperature
and would redistribute blood flow to the skin.
RECOMMENDED READING
Garrick, J. G., and P. Radetsky. 1988. Peak condition. New York: Harper & Row.
McRae, R. 1983. Clinical orthopedic examination, 835. London: Churchill Livingstone.
Novich, M. M., and B. Taylor. 1983. Training and conditioning of athletes. Philadelphia, PA:
Lea & Febiger.

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S E C O N D E D I T I O N

Boca Raton London New York

CRC Press is an imprint of the

No claim to original U.S. Government works

Printed in the United States of America on acid-free paper

International Standard Book Number-13: 978-1-4398-2760-4 (Ebook-PDF)

Section 1 “Postmodern” Medicine: Teaching

Section 2 Curing, Healing, and Maintaining Health

Chapter 1 High Blood Pressure: The Silent Killer................................................ 9

Chapter 3: Kidney Disease..................................................................................... 49

© 2011 by Taylor & Francis Group, LLC

Chapter 4: Heart Disease....................................................................................... 59

© 2011 by Taylor & Francis Group, LLC

Chapter 5: Lung Disease........................................................................................ 85

Chapter 6: Obesity................................................................................................ 103

© 2011 by Taylor & Francis Group, LLC

Weight Training Guidelines for Obesity........................................... 114

Chapter 7: Vascular Disease................................................................................ 119

Chapter 8: Osteoporosis and Arthritis............................................................... 135

Chapter 9: Cancer, the Immune System, and AIDS......................................... 143

© 2011 by Taylor & Francis Group, LLC

Lung Cancer................................................................................. 148

Chapter 10: The “Golden Years”........................................................................ 159

Chapter 11: The Physically Inactive................................................................... 165

© 2011 by Taylor & Francis Group, LLC

Exercise Prescription for Physically Inactive Individuals

Chapter 12: Pregnancy......................................................................................... 171

Chapter 13: Wheelchair-Dependent Patients..................................................... 177

Chapter 14: Prepubescent Children.................................................................... 183

© 2011 by Taylor & Francis Group, LLC

Method 3: The Rate Pressure Product Method................................. 192

© 2011 by Taylor & Francis Group, LLC

© 2011 by Taylor & Francis Group, LLC

Walk and be happy; walk and be healthy.

Two hours and 30 minutes (150 minutes) of moderate-intensity aerobic

Muscle-strengthening activities on 2 or more days a week that work all major

One hour and 15 minutes (75 minutes) of vigorous-intensity aerobic activity

Muscle-strengthening activities on 2 or more days a week that work all major

An equivalent mix of moderate- and vigorous-intensity aerobic activity and

Muscle-strengthening activities on 2 or more days a week that work all major

• Physical inactivity is a major risk factor for cardiovascular disease.

The principal recommendation from this conference was essentially identical to

© 2011 by Taylor & Francis Group, LLC

• Physical activity reduces the risk of premature mortality, in general, and of

A more comprehensive review of physical activities guidelines can be found at the

© 2011 by Taylor & Francis Group, LLC

© 2011 by Taylor & Francis Group, LLC

© 2011 by Taylor & Francis Group, LLC

Ignacio Ripoll, MD, FACP, FACCP, is associate professor of internal medicine at

Medical science is in a process of constant change; for example: at the time of

© 2011 by Taylor & Francis Group, LLC

© 2011 by Taylor & Francis Group, LLC

knowledge of the disease and its treatment

© 2011 by Taylor & Francis Group, LLC

THE EXERCISE PRESCRIPTION AND ADHERENCE

The Six “Aces” of Exercise Adherence

© 2011 by Taylor & Francis Group, LLC

• Antecedents: patients’ previous exercise, medical, and social history,

© 2011 by Taylor & Francis Group, LLC

© 2011 by Taylor & Francis Group, LLC

© 2011 by Taylor & Francis Group, LLC

• Normal: BP ≤ 119/79 mmHg

As the name suggests, pre-HTN is a precursor of HTN. During aerobic exercise,

Section 1 “Postmodern” Medicine: Teaching

If antihypertensive therapy in conjunction with hygienic measures (i.e., weight reduc-