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- 1. 1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA
19103-2899 EXERCISE AND THE HEART, Fifth Edition ISBN-13:
978-1-4160-0311-3 ISBN-10: 1-4160-0311-8 Copyright 2006, Elsevier
Inc. All rights reserved. No part of this publication may be
reproduced or transmitted in any form or by any means, electronic
or mechanical, including photocopying, recording, or any
information storage and retrieval system, without permission in
writing from the publisher (Elsevier, 1600 John F. Kennedy
Boulevard, Suite 1800, Philadelphia, PA, 19103-2899). Library of
Congress Cataloging-in-Publication Data Froelicher, Victor F.
Exercise and the heart/Victor F. Froelicher, Jonathan Myers.5th ed.
p.;cm Includes bibliographical references and index. ISBN
1-4160-0311-8 1. Exercise tests. 2. Heart function tests. 3.
HeartDiseasesDiagnosis. I. Myers, Jonathan, 1957- II. Title. [DNLM:
1. Heart Diseasesrehabilitation. 2. Exercise Testmethods. 3.
Exercise Therapymethods. 4. Exertion. WG 141.5.F9 F926e 2006]
RC683.E.E94F76 2006 616.120754dc22 2005051641 Editor: Susan F.
Pioli Senior Editorial Assistant: Joan Ryan Publishing Services
Manager: Joan Sinclair Project Manager: Mary Stermel Design
Direction: Gene Harris Marketing Manager: Dana Butler Printed in
the United States of America Last digit is the print number: 10 9 8
7 6 5 4 3 2 1 Notice Knowledge and best practice in this field are
constantly changing. As new research and experience broaden our
knowledge, changes in practice, treatment and drug therapy may
become necessary or appro- priate. Readers are advised to check the
most current information provided (i) on procedures featured or
(ii) by the manufacturer of each product to be administered, to
verify the recommended dose or formula, the method and duration of
administration, and contraindications. It is the responsibility of
the practi- tioners, relying on their own experience and knowledge
of the patient, to make diagnoses, to determine dosages and the
best treatment for each individual patient, and to take all
appropriate safety precautions. To the fullest extent of the law,
neither the publisher nor the authors assume any liability for any
injury and/or damage to persons or property arising out of or
related to any use of the material contained in this book. The
Publisher
- 2. To Susan, my wife and best friend. VFF To my two older
brothers, Chris and Tim, who are no longer with us. Their intellect
eluded me but was always and continues to be a source of motivation
and inspiration. JM
- 3. Welcome to the fifth edition of Exercise and the Heart.
Since the fourth edition, there have been numerous important
documents published, including an update of the American Heart
Association (AHA)/American College of Cardiology (ACC) guidelines
on exercise testing, the American Thoracic Society/American College
of Chest Physicians Statement on Cardiopulmonary Exercise Testing,
an AHA Scientific Statement on Exercise and Heart Failure, an AHA
Scientific Statement on Physical Activity in the Prevention of
Cardiovascular Disease, new editions of the American Association of
Cardiovascular and Pulmonary Rehabilitation Guidelines, and the
American College of Sports Medicine Guidelines on Exercise Testing
and Prescription. Relevant information from these updated documents
has been incorporated into this fifth edition. The necessity of
practicing evidence-based medicine makes it critical that all of us
defer to the panels of experts who write these guidelines. In rare
cases in which the guidelines are inconsistent or we offer an
opinion or recommendation that dif- fers from the guidelines, we
alert the reader. As the field of cardiology has continued to
evolve, it is important to note some of the new or changed acronyms
in medicine. HF has been recommended as the acronym to replace CHF,
because CHF has confusingly repre- sented either chronic or
congestive (acute) heart failure. PCI (percutaneous coronary
intervention) has replaced PTCA, because currently many techniques
in addition to balloon angioplasty are performed by
interventionalists. AED (automated external defibrillator) and ICD
(implantable cardiac defibrillator) are used for the new biphasic
defibrillator products. CRT (cardiac resynchronization therapy) is
an implantable pacemaker for improving cardiac function that is
often combined with an ICD. ACS (acute coronary syndrome) is the
term now widely used to describe the spectrum of con- ditions
associated with acute myocardial ischemia, including unstable
angina pectoris and non-Q wave MIs. In this edition, weve tried to
incorporate the influence of the remarkable advances in cardiol-
ogy in the subject matter. These advances are listed below (not in
order of impact), because each by themselves has strongly
influenced exercise testing, exercise training, and clinical
exercise physiology. 1. Designation of ACSs 2. Biomarkers for
ischemia and volume overload/left ventricular dysfunction at point
of contact (troponin and brain natri- uretic peptide [BNP]) 3.
Advances in percutaneous coronary inter- ventions (PCI) culminating
in drug-eluting stents that have greatly reduced stent failure 4.
Evidence-based recommendations that PCI is better than thrombolysis
for acute myocardial infarction 5. Medications that convincingly
improve survival in patients with heart disease vii preface
- 4. viii Preface 6. Pacemakers for CRT 7. Further advances in
exercise training for patients with heart failure and other groups
previously excluded from rehabilitation 8. The basic role of
endothelial function in maintaining cardiovascular health and how
it is affected by exercise training 9. Human genomics studies
related to sudden death (LQT1) and training (ACE) 10. Advances in
cardiac defibrillators (implant- able and portable units) These
advances have actually interacted with one another, so it is best
to address them in groupings that impact health care in a similar
fashion. We address those that impact the diag- nostic use of
exercise testing first. Many patients who required diagnostic
exercise testing after the first appearance of symptoms now have
the diagnosis made based on an elevation of troponin. They
frequently go straight to cardiac catheteriza- tion. Many
cardiologists believe that advances in PCI make the noninvasive
diagnosis of ischemic chest pain moot, because angiography can be
used to make the diagnosis and treat the problem by averting all
steps in between. The lowered restenosis rate associated with
drug-eluting stents has removed, in their minds, all the rea- sons
not to diagnose and fix the problem all in one relatively low-risk
procedure. However, it is important to keep in mind that health
care costs continue to rise and fewer people are insured or able to
afford this invasive approach. As clinicians continue to deal with
the problems of cost-efficacy, we contend that the exercise test
remains the most logical gatekeeper to more expensive and/or
invasive diagnostic tests. When a biomarker that can be measured at
point of contact becomes val- idated as a way to increase the
sensitivity of the test along with multivariate scores, reasonable
clinicians apply the exercise test first. Although some would
disagree, we contend that the art of medical decision making and
the use of noninva- sive tests are currently more important than
ever. Next, let us consider the advances in health care that affect
the prognostic use of exercise testing. PCI for acute myocardial
infarction has been shown to be better for improving prognosis and
lessening myocardial damage than thrombolysis. The reason this is
so is that it is more effective than thrombolytic drugs in opening
coronary arteries blocked by thrombosis. Improved patency rates
mean that follow-up exercise testing is less likely to be needed
routinely after MI to determine who needs coronary angiography.
However, when the patient and physician want or need individualized
prognostic information, there is no test more valuable than the
standard exercise test. Several recent studies have confirmed that
exercise capac- ity alone has independent and significant prog-
nostic power regardless of the patients clinical history.
Surprisingly, the next two items, which relate to patients with HF,
have resulted in new ideas regarding cardiovascular physiology.
First, HF results in major metabolic and cellular changes that can
be improved by an exercise program. These alterations have provided
interesting insights into the exercise response, because changes in
endothe- lial function appear to be a major contributor to these
improvements. Second, implanted synchro- nous pacemakers have been
shown to improve both ventricular function and exercise capacity.
This is somewhat surprising, because previously it was thought that
myocyte damage was the pri- mary event leading to LV dysfunction
and that conduction disturbances were a result of this. However,
improvement in function resulting from correction of dysynchrony
suggests that damage to the conduction system can be the cause of
LV dysfunction and impair exercise capacity. There are two
important bench findings that are impacting our understanding of
cardiac pathophysiology. First, regular exercise can have a
powerful effect on endothelial dysfunction, and now this mechanism
is proposed as one of the major beneficial actions that exercise
has on health. Second, we are only on the threshold of using human
genomics to understand exercise and the heart. Congenital diseases
that cause exercise- related sudden death have been localized to
specific genes (for instance, LQT1). The ACE gene appears to be an
important determinant of the response to exercise training.
Finally, advances in defibrillators have had an important impact on
exercise for the public. Biphasic units resulting in lower energy
needs for defibrillation, long-life lithium batteries, and smart
arrhythmia algorithms are the basis for these advances.
Cardiopulmonary resuscitation (CPR) has been improved by AEDs, and
they are now widely used by the public, resulting in better
outcomes following arrhythmic events. These devices are now
ubiquitous and are mandatory at gyms and sporting events;
importantly, the AHA has developed guidelines for their use in
health clubs. However, studies on the number of sudden cardiac
deaths (50,000/year in the United States; approximately one fifth
of the number estimated initially and used as the impetus for AEDs)
and
- 5. Preface ix their location (most sudden deaths occur at home
and not in public places) have led to some reassessment of their
use. Randomized trials have demonstrated a survival benefit for
ICDs in most patients with LV dysfunction. Now patients with these
devices must be dealt with in the context of cardiac rehabilitation
and exercise laboratory settings. The following is our strongest
variance from the guidelines: Exercise testing should be used for
screening healthy, asymptomatic individuals along with risk factor
assessment. We plan to lobby with our colleagues on this point for
the following reasons: A number of contemporary studies have
demonstrated remarkable risk ratios for the combination of the
standard exercise test responses and traditional risk factors.
Other modalities without the favorable test characteristics of the
exercise test are being promoted for screening. Physical inactivity
has reached epidemic proportions, and the exercise test provides an
ideal way to make patients conscious of their deconditioning and to
make physical activity recommendations. Adjusting for age and other
risk factors, each MET increase in exercise capacity equates to a
10% to 25% improvement in survival. With this fifth edition, we
once again have assumed the writing by ourselves. Though it is
obvious which one of us was the main author for the various
chapters, we collaborated on all of them and take both blame and
credit. With the volume of studies on exercise testing and training
now all available on the world wide web, it is no longer practical
to review in detail as many individ- ual studies, however important
they are. Although we have been careful to update our citations, we
felt it necessary to keep the classic studies related to particular
issues. Wherever possible, we have tried to summarize the major
studies in tables, followed by a comment and then our overall view
or recommendation on a given issue. Once again we feel it is
important to provide the following precepts in the preface
regarding methodology even though the details are in the chapters:
The treadmill protocol should be adjusted to the patient; one
protocol is not appropriate for all patients. Exercise capacity
should be reported in METs, not minutes of exercise.
Hyperventilation before testing is not indi- cated but can be used
at another time if a false- positive test is suspected. ST
measurements should be made at ST0 (J-junction), and ST depression
should be consid- ered abnormal only if horizontal or downslop-
ing; most clinically important ST depression occurs in V5,
particularly in patients with a normal resting ECG. Patients should
be placed supine as soon as possible post exercise without a
cool-down walk in order for the test to have its greatest
diagnostic value. The 2- to 4-minute recovery period is critical to
include in analysis of the ST response. Measurement of systolic
blood pressure during exercise is extremely important, and exer-
tional hypotension is ominous; at this point, only manual blood
pressure measurement techniques are valid. Age-predicted heart rate
targets are largely useless because of the wide scatter for any
age; a relatively low heart rate can be maximal for a given patient
and submaximal for another. The Duke Treadmill Score should be
calculated automatically on every test except for the elderly.
Other predictive equations and heart rate recov- ery should be
considered a standard part of the treadmill report. To ensure the
safety of exercise testing and reassure the noncardiologist
performing the test, the following list of the most dangerous cir-
cumstances in the exercise testing lab should be considered:
Testing patients with aortic valvular disease or obstructive
hypertrophic cardiomyopathy (ASH or IHSS) should be done with great
care. Aortic stenosis can cause cardiovascu- lar collapse, and
these patients may be diffi- cult to resuscitate because of the
outflow obstruction; IHSS can become unstable due to arrhythmia.
Because of these conditions, a physical exam including assessment
of systolic murmurs should be done before all exercise tests. If a
significant murmur is heard, an echocardiogram should be considered
before performing the test. When patients without diagnostic
Q-waves on their resting ECG exhibit exercise-induced
- 6. x Preface ST segment elevation (i.e., transmural ischemia),
the test should be stopped; this can be associated with dangerous
arrhyth- mias and infarction. This occurs in about 1 of 1000
clinical tests. A cool-down walk is advisable in the follow- ing
instances: 1. When a patient with an ischemic cardio- myopathy
exhibits significant chest pain due to ischemia, because the
ischemia can worsen in recovery 2. When a patient develops
exertional hypo- tension accompanied by ischemia (angina or ST
depression) or when it occurs in a patient with a history of HF,
cardio- myopathy, or recent MI 3. When a patient with a history of
sudden death or collapse during exercise develops PVCs that become
frequent Appreciation of these circumstances can help avoid any
complications in the exercise lab. As in previous editions, there
are many pre- medical and medical students, graduate students,
residents, fellows, visiting professors, and inter- national
medical graduates who have contributed to the studies discussed in
this book. They are too numerous to mention individually, but their
work is cited extensively in this edition. One of the most
gratifying things about what we do is to have the opportunity to
host these individuals and gain the friendships that result through
the inevitable battles that occur in trying to answer a research
question. Because of this, we have main- tained a wide range of
contacts around the world, and many of them continue to collaborate
with us. A few individuals in particular warrant men- tioning here,
because their contributions to this edition are significant. They
include Paul Dubach from Switzerland, Euan Angus Ashley from
Scotland (now a Stanford cardiology fellow), and Kari Saunamaki
from Denmark. Takuya Yamazaki was our most recent research fellow
from Japan (of a list of many), and his desk is currently occu-
pied by Tan Swee Yaw from Singapore. Notable PhDs who keep a close
eye on our science are Barry Franklin, Paul Ribisl, and Bill
Herbert. We have profited both personally and professionally by our
association with all of these individuals and treasure the
friendships that began through research collaboration. Given this
background, we are targeting this book as a reference for the
clinical aspects of exer- cise testing and training. It is meant
for the serious student, academic, or health care provider who
wants to have available much of the knowledge in this field
summarized in one source. Hopefully it will find an appropriate
niche on the shelves in many exercise labs, cardiac rehabilitation
depart- ments, and educational training programs. We have tried to
incorporate the latest available guide- lines, position statements,
and meta-analyses. Our love of the subject has led to the
incorporation of details that some could consider minutia yet we
might have missed some work considered impor- tant by our
colleagues. We hope you enjoy this book and that it is helpful to
you. Victor F. Froelicher Jonathan Myers
- 7. 1 C H A P T E R one Basic Exercise Physiology Exercise
physiology is the study of the physiologic responses and
adaptations that occur as a result of acute or chronic exercise.
Exercise is the bodys most common physiologic stress, and it places
major demands on the cardiopulmonary system. For this reason,
exercise can be considered the most practical test of cardiac
perfusion and func- tion. Exercise testing is a noninvasive tool to
evaluate the cardiovascular systems response to exercise under
carefully controlled conditions. The adaptations that occur during
an exercise test allow the body to increase its resting metabolic
rate up to 20 times, during which time cardiac output may increase
as much as six times. The magnitude of these adjustments is
dependent upon age, gender, body size, type of exercise, fit- ness,
and the presence or absence of heart disease. Although major
adaptations are also required of the endocrine, neuromotor, and
thermoregula- tory systems, the major focus of this chapter is on
the cardiovascular response and adaptations of the heart to acute
exercise. Cardiovascular adaptations to chronic training in humans
and animals are reviewed in Chapter 12. It is important to
understand two basic principles of exercise physiology with regard
to exercise testing. The first is a physiologic princi- ple: total
body oxygen uptake and myocardial oxygen uptake are distinct in
their determinants and in the way they are measured or estimated
(Table 1-1). Total body or ventilatory oxygen uptake (VO2) is the
amount of oxygen that is extracted from inspired air as the body
performs work. Conversely, myocardial oxygen uptake is the amount
of oxygen consumed by the heart mus- cle. Accurate measurement of
myocardial oxygen consumption requires the placement of catheters
in a coronary artery and in the coronary venous sinus to measure
oxygen content. The determi- nants of myocardial oxygen uptake
include intramyocardial wall tension (left ventricular pressure
end-diastolic volume), contractility, and heart rate. It has been
shown that myocardial oxygen uptake can be reasonably estimated by
the product of heart rate and systolic blood pressure (double
product). This information is valuable clinically because
exercise-induced angina often occurs at the same myocardial oxygen
demand (double product) and thus is a useful physiologic variable
when evaluating therapy. When it is not the case, the influence of
other factors should be suspected, such as a recent meal, abnormal
ambient temperature, or coronary artery spasm. The second principle
of exercise physiology is one of pathophysiology: considerable
interaction takes place between the exercise test manifestations of
abnormalities in myocardial perfusion and function. The
electrocardiographic response to exer- cise and angina are closely
related to myocardial ischemia (coronary artery disease), whereas
exer- cise capacity, systolic blood pressure, and heart rate
responses to exercise can be determined by the presence of
myocardial ischemia, myocardial dysfunction, or responses in the
periphery. Exercise-induced ischemia can cause cardiac dys-
function that results in exercise impairment and an abnormal
systolic blood pressure response. Often it is difficult to separate
the impact of
- 8. ischemia from the impact of left ventricular dysfunction on
exercise responses. An interaction exists that complicates the
interpretation of the exercise test findings. The variables
affected by both myocardial ischemia and ventricular dysfunction
(i.e., exercise capacity, maximal heart rate, and systolic blood
pressure) have the greatest prognostic value. The severity of
ischemia or the amount of myocardium in jeopardy is known
clinically to be inversely related to the heart rate, blood
pressure, and exercise level achieved. However, neither resting nor
exercise ejection fraction nor a change in ejection fraction during
exercise correlates well with measured or estimated maxi- mal
oxygen uptake, even in patients without signs or symptoms of
ischemia.1,2 Moreover, exercise- induced markers of ischemia do not
correlate well with one another. Silent ischemia (i.e., markers of
ischemia presenting without angina) does not appear to affect
exercise capacity in patients with coronary heart disease. Although
not conclusive, radionuclide studies support this position.3
Cardiac output is generally considered the most important
determinant of exercise capacity, but studies suggest that in some
patients with heart disease, the periphery plays an important role
in limiting exercise capacity.1,4 Concepts of Work. Because
exercise testing fun- damentally involves the measurement of work,
there are several concepts regarding work that are important to
understand. Work is defined as force moving through a given
distance (W = F D). If muscle contraction results in mechanical
move- ment, then work has been accomplished. Force is equal to mass
times acceleration (F = M A). Any weight, for example, is a force
that is under- going the resistance provided by gravity. A great
deal of any work that is performed involves over- coming the
resistance provided by gravity. The basic unit of force is the
newton (N). It is the force that, when applied to a 1-kg mass,
gives it an acceleration of 1 m multiplied by sec2 . Since work is
equal to force (in newtons) times distance (in meters), another
unit for work is the newton meter (Nm). One Nm is equal to one
joule (J), which is another common expression of work. Because work
is nearly always expressed per unit of time (i.e., as a rate), an
additional unit that becomes important is power, the rate at which
work is performed. The bodys metabolic equiva- lent (MET) of power
is energy. Therefore, it is easy to think of work as anything with
weight moving at some rate across time (which is often analogous to
distance). The common biologic measure of total body work is the
oxygen uptake, which is usually expressed as a rate (making it a
measure of power) in liters per minute. MET is a term commonly used
clinically to express the oxygen requirement of the work rate
during an exercise test on a treadmill or cycle ergometer. One MET
is equated with the resting metabolic rate (;3.5 mL of O2/kg/min),
and a MET value achieved from an exercise test is a multiple of the
resting metabolic rate, either measured directly (as oxygen uptake)
or estimated from the maximal workload achieved using standardized
equations.5 Energy and Muscular Contraction. Muscular contraction
is a complex mechanism involving the interaction of the contractile
proteins actin and myosin in the presence of calcium. The British
scientist A.F. Huxley proposed that the myosin and actin filaments
in the muscle slid past one another as the muscle fibers shortened
dur- ing contraction. Huxley won the Nobel Prize for this concept,
which is still generally considered correct. The source of energy
for this contraction is supplied by adenosine triphosphate (ATP),
which is produced in the mitochondria. ATP is stored as two
products, adenosine diphosphate and phosphate, at specific binding
sites on the myosin heads. The sequence of events that occurs when
a muscle contracts has three other major players: calcium and two
inhibitory proteins, troponin and tropomyosin. Voluntary muscle
contraction begins with the arrival of electrical impulses at the
myoneural junction, initiating the release of calcium ions. Calcium
is released into the 2 E X E R C I S E A N D T H E H E A R T TABLE
1-1. Two basic principles of exercise physiology Myocardial oxygen
consumption ;Heart rate systolic blood pressure (determinants
include wall tension left ventricular pressure volume;
contractility; and heart rate) Ventilatory oxygen consumption (VO2)
;External work performed, or cardiac output a-VO2 difference* * The
arteriovenous O2 difference is approximately 15 to 17 vol% at
maximal exercise in most individuals; therefore, VO2 max generally
reflects the extent to which cardiac output increases.
- 9. sarcoplasmic reticulum that surrounds the muscle filaments.
The calcium binds to a special protein, troponin-C, which is
attached to tropomyosin (another protein that inhibits the binding
of actin and myosin), and actin. When cal- cium binds to
troponin-C, the tropomyosin mole- cule is removed from its blocking
position between actin and myosin. The myosin head then attaches to
actin, and muscular contraction occurs. The main source of energy
for muscular con- traction, ATP, is produced by oxidative
phosphory- lation. The major fuels for this process are
carbohydrates (glycogen and glucose) and free fatty acids. At rest,
roughly equal amounts of energy are derived from carbohydrates and
fats. Free fatty acids contribute greatly to the energy supply
during low levels of exercise, but greater amounts of energy are
derived from carbohy- drates as exercise progresses. Maximal work
relies virtually entirely on carbohydrates. Because endurance
performance is directly related to the rate at which carbohydrate
stores are depleted, major advantages exist for both: (1) having
greater glycogen stores in the muscle and (2) deriving a relatively
greater proportion of energy from fat during prolonged exercise.
Both of these benefits are conferred with training. Oxidative
phosphorylation initially involves a series of events that take
place in the cytoplasm. Glycogen and glucose are metabolized to
pyruvate through glycolysis. If oxygen is available, pyruvate
enters the mitochondria from the sarcoplasm and is oxidized to a
compound known as acetyl CoA, which then enters a cyclical series
of reactions known as the Krebs cycle. By-products of the Krebs
cycle are CO2 and hydrogen. Electrons from hydrogen enter the
electron transport chain, yielding energy for the binding of
phosphate (phosphorylation) from adenosine diphosphate to ATP. This
process, oxidative phosphorylation, is the greatest source of ATP
for muscle contraction. A total of 36 ATP molecules per glucose
molecule are formed in the mitochondria during this process. The
mitochondria can produce ATP for muscle contraction only if oxygen
is present. However, at higher levels of exercise, total body
oxygen demand may exceed the capacity of the cardio- vascular
system to deliver oxygen. Historically, anaerobic (without oxygen)
glycolysis has been the term used to describe the synthesis of ATP
from glucose under these conditions. Many researchers have
superseded this term with more functional descriptions, such as
oxygen independent, nonoxidative, or rapid glycoly- sis, because
anaerobic incorrectly implies that glycolysis occurs only when
there is an inadequate oxygen supply. Under such conditions,
glycolysis progresses in the cytoplasm much the same way as aerobic
metabolism until pyruvate is formed. However, electrons released
during glycolysis are taken up by pyruvate to form lactic acid.
Rapid diffusion of lactate from the cell inhibits any further steps
in glycolysis. Thus, oxygen- independent glycolysis is inefficient;
two ATP molecules per glucose molecule is the total yield from this
process. The fact that lactate accumulates in the blood during
rapid glycolysis is an important concept in exercise science. The
relative exercise intensity in which lactate accumulation occurs is
an impor- tant determinant of endurance performance. The degree to
which lactate accumulates in the blood is related to exercise
intensity and the extent to which fast-twitch (type IIB) fibers are
recruited. This subject is discussed further in Chapter 3. Although
lactate can contribute to fatigue by increasing ventilation and
inhibiting other enzymes of glycolysis, it can also serve as an
impor- tant energy source in muscles other than those in which it
was formed, and it serves as an important precursor for liver
glycogen during exercise.6-8 Muscle Fiber Types. The bodys muscle
fiber types are classified on the basis of the speed with which
they contract, their color, and their mito- chondrial content. Type
I, or slow-twitch fibers, are red in color and contain high
concentrations of mitochondria. Type II, or fast-twitch fibers, are
white in color and have low concentrations of mitochondria. Fiber
color is related to the degree of myoglobin, which is a protein
that both stores oxygen in the muscle and carries oxygen in the
blood to the mitochondria. Not surprisingly, slow-twitch fibers
with their high myoglobin content are more resistant to fatigue;
thus, a muscle with a high percentage of slow- twitch fibers is
well suited for endurance exercise. However, slow-twitch fibers
tend to be smaller and produce less overall force than fast-twitch
fibers. Fast-twitch fibers are generally larger and tend to produce
more force, although they fatigue more easily. Research suggests
that the speed of contraction for each fiber type is based largely
on the activity of the enzyme myosin ATPase, which sits in the
myosin head and to which ATP combines. It is important to note that
although the two fiber types can be separated by distinct char-
acteristics, both fibers function effectively for virtually all
physical activities. Evidence also suggests that slow-twitch and
fast-twitch fibers are not as dichotomous as previously thought. C
H A P T E R 1 Basic Exercise Physiology 3
- 10. Myosin ATPase activity and speed of contraction of some
slow-twitch fibers approximate those of fast-twitch fibers.
Moreover, type II (fast-twitch) fibers have been further divided
into three sub- categories: type IIA, type IIB, and type IIC. The
type IIA fiber mimics the type I fiber in that it has a high
capacity for oxidative metabolism. It has been suggested that the
type IIA fiber actually is a type II fiber that has been adapted
for endurance exercise, and endurance athletes are known to have a
relatively large number of these fibers.9 The type IIB fiber is a
true type II fiber in that it contains few mitochondria and is
better adapted for short bursts of activity. The type IIC fiber is
poorly understood; it may represent an uncommitted fiber, capable
of adapting into one of the other fiber types. Historically, it has
been thought that endurance athletes were obliged to be genetically
endowed with larger percentages of type I fibers, and that the
opposite was true of sprinters or jumpers. Numerous cross-sectional
studies have con- firmed these differences in fiber types between
endurance and sprint-type athletes since the advent of the muscle
biopsy technique. However, fiber types may in fact represent a
continuum, with some capable of adapting toward the characteristics
of another fiber. ACUTE CARDIOPULMONARY RESPONSE TO EXERCISE The
cardiovascular system responds to acute exercise with a series of
adjustments that assure (1) active muscles receive blood supply
appro- priate to their metabolic needs, (2) heat generated by the
muscles is dissipated, and (3) blood supply to the brain and heart
is maintained. This response requires a major redistribution of
cardiac output along with a number of local metabolic changes. The
usual measure of the capacity of the body to deliver and utilize
oxygen is the maximal oxygen uptake (VO2 max). Thus, the limits of
the cardiopulmonary system are historically defined by VO2 max,
which can be expressed by the Fick principle: VO2 max = maximal
cardiac output maximal arteriovenous oxygen difference Cardiac
output must closely match ventilation in the lung in order to
deliver oxygen to the working muscle. VO2 max is determined by the
maximal amount of ventilation (VE) moving into and out of the lung
and by the fraction of this ventilation that is extracted by the
tissues: VO2 = VE (FiO2 FeO2) where VE is minute ventilation, and
FiO2 and FeO2 are the fractional amounts of oxygen in the inspired
and expired air, respectively. (For the moment, this equation is
oversimplified, as the measurement of VO2 also requires a deter-
mination of expired CO2, as detailed in Chapter 3.) Therefore, the
cardiopulmonary limits (VO2 max) are defined by (1) a central
component (cardiac output) that describes the capacity of the heart
to function as a pump and (2) peripheral factors (arteriovenous
oxygen difference) that describe the capacity of the lung to
oxygenate the blood delivered to it and the capacity of the working
muscle to extract this oxygen from the blood. Figures 1-1 and 1-2
outline the many factors affecting cardiac output and arteriovenous
oxygen difference. An abnormality in one or more of these
components often characterizes the presence and extent of some form
of cardiovascu- lar or pulmonary disease. In the following, these
models are reviewed in the context of the cardio- vascular response
to exercise. Central Factors Figure 1-1 shows the central
determinants of maximal oxygen uptake. Heart Rate Sympathetic and
parasympathetic nervous system influences underlie the
cardiovascular systems first response to exercise, an increase in
heart rate. Sympathetic outflow to the heart and sys- temic blood
vessels increases and vagal outflow decreases. Of the two major
components of cardiac output, heart rate and stroke volume, heart
rate is responsible for most of the increase in cardiac output
during exercise, particularly at higher levels. Heart rate
increases linearly with workload and oxygen uptake. Increases in
heart rate occur primarily at the expense of diastolic, not
systolic time. Thus, at very high heart rates, diastolic time may
be so short as to preclude adequate ventricular filling. The heart
rate response to exercise is influenced by several factors,
including age, type of activity, body position, fitness, the pres-
ence of heart disease, medications, blood volume, 4 E X E R C I S E
A N D T H E H E A R T
- 11. and environment. Of these, the most important factor is
age; a decline in maximal heart rate occurs with increasing age.10
This decline appears to be due to intrinsic cardiac changes rather
than to neural influences. It should be noted that there is a great
deal of variability around the regression line between maximal
heart rate and age; thus, age-related maximal heart rate is a
relatively poor index of maximal effort (see Chapter 5). Maximal
heart rate is unchanged or may be slightly reduced after a program
of training. Resting heart rate is frequently reduced after
training as a result of enhanced parasympathetic tone. Stroke
Volume. The product of stroke volume (the volume of blood ejected
per heartbeat) and heart rate determines cardiac output. Stroke
volume is equal to the difference between end-diastolic and
end-systolic volume. Thus, a greater diastolic filling (preload)
will normally increase stroke volume. Alternatively, factors that
increase arterial blood pressure will resist ventricular outflow
(afterload) and result in a reduced stroke volume. During exercise,
stroke volume increases up to approximately 50% to 60% of maximal
capacity, after which increases in cardiac output are due to
further increases in heart rate. The extent to which increases in
stroke volume during exercise reflect an increase in end-diastolic
volume or a decrease in end-systolic volume, or both, is not
entirely clear but appears to depend upon ventricular func- tion,
body position, and intensity of exercise. In healthy subjects,
stroke volume increases at rest and during exercise after a period
of exercise train- ing. Although the mechanisms have been debated,
evidence suggests that this adaptation is due more to increases in
preloadand possibly local adapta- tions that reduce peripheral
vascular resistance than to increases in myocardial contractility.
In addition to heart rate, end-diastolic volume is determined by
two other factors: filling pressure and ventricular compliance. C H
A P T E R 1 Basic Exercise Physiology 5 FIGURE 1-1 Central
determinants of maximal oxygen uptake. (From Myers J, Froelicher
VF: Hemodynamic determinants of exercise capacity in chronic heart
failure. Ann Intern Med 1991;115:377-386.) FIGURE 1-2 Peripheral
determinants of maximal oxygen uptake. The a-V O2 difference is the
difference between arterial and venous oxygen. Hb, hemoglobin;
PAO2, partial pressure of alveolar oxygen; VE, minute ventilation.
(From Myers J, Froelicher VF: Hemodynamic determinants of exercise
capacity in chronic heart failure. Ann Intern Med
1991;115:377-386.)
- 12. Filling Pressure. The most important determi- nant of
ventricular filling is venous pressure. The degree of venous
pressure is a direct consequence of the amount of venous return.
The Frank- Starling mechanism dictates that, within limits, all the
blood returned to the heart will be ejected during systole. As the
tissues demand greater oxy- gen during exercise, venous return
increases, which in turn increases end-diastolic fiber length
(preload), resulting in a more forceful contrac- tion. Venous
pressure increases as exercise inten- sity increases. Over the
course of a few beats, cardiac output will equal venous return. A
number of other factors affect venous pressure, and therefore
filling pressure, during exercise. These factors include blood
volume, body position, and the pumping action of the respiratory
and skeletal muscles. A greater blood volume increases venous
pressure and therefore end-diastolic volume by making more blood
avail- able to the heart. Because the effects of gravity are
negated, filling pressure is greatest in the supine position. In
fact, stroke volume generally does not increase from rest to
maximal exercise in the supine position. The intermittent
mechanical constriction and relaxation in the skeletal mus- cles
during exercise also enhance venous return. Finally, changes in
intrathoracic pressure that occur with breathing during exercise
facilitate the return of blood to the heart. Ventricular
Compliance. Compliance is a mea- sure of the capacity of the
ventricle to stretch in response to a given volume of blood.
Specifically, compliance is defined as the ratio of the change in
volume to the change in pressure. The diastolic pressure/volume
relation is curvilinear; that is, at low end-diastolic pressures,
large changes in vol- ume are accompanied by small changes in
pressure, and vice versa. At the upper limits of end-diastolic
pressure, ventricular compliance declines; that is, the chamber
stiffness increases as it fills. Because of the difficulty in
measuring end-diastolic pressure during exercise, few data are
available concerning ventricular compliance during exercise in
humans. End-systolic volume is a function of two factors:
contractility and afterload. Contractility. Contractility describes
the forceful- ness of the hearts contraction. Increasing con-
tractility reduces end-systolic volume, which results in a greater
stroke volume and thus greater cardiac output. This process is
precisely what occurs with exercise in the normal individual; the
percentage of blood in the ventricle that is ejected with each beat
increases, owing to an altered cross-bridge formation.
Contractility is commonly quantified by the ejection fraction, the
percentage of blood ejected from the ventricle during systole using
radionuclide, echocardio- graphic, or angiographic techniques.
Despite its wide application as an index of myocardial con-
tractility, ejection fraction has been repeatedly shown to
correlate poorly with exercise capacity. Afterload. Afterload is a
measure of the force resisting the ejection of blood by the heart.
Increased afterload (or aortic pressure, as is observed with
chronic hypertension) results in a reduced ejection fraction and
increased end- diastolic and end-systolic volumes. During dynamic
exercise, the force resisting ejection in the periphery (total
peripheral resistance) is reduced by vasodilation, owing to the
effect of local metabolites on the skeletal muscle vasculature.
Thus, despite even a fivefold increase in cardiac output among
normal subjects during exercise, mean arterial pressure increases
only moderately. Volume Response to Exercise. Results of studies
evaluating the volume response to exercise have varied greatly.
Although the advent of radionu- clide techniques in the 1970s
offered promise for the noninvasive assessment of ventricular
volumes during exercise, the results have been disappointing.
Because of technical limitations, most of these studies have been
performed in the supine position. Early studies employing radio-
nuclide or echocardiographic techniques during supine exercise
among normal subjects reported that end-diastolic volume remained
constant or diminished slightly,11-14 increased in the order of
27%,15 or varied greatly depending on the subject.16-18 Among
patients with coronary artery disease exercised in the supine
position, increases in end-diastolic volume were observed among
patients with exercise-induced angina, whereas end-diastolic volume
did not change in patients who were asymptomatic. Sharma et al19
and Jones et al20 reported increases in both end-diastolic and
end-systolic volumes in patients who developed angina during
exercise. Slutsky et al11 reported that end-diastolic volume
remained unchanged in patients with coronary artery disease whether
or not they developed angina. Manyeri and Kostuk21 reported large
increases in both end-systolic and end-diastolic volumes during
supine exercise among 20 patients with coronary artery disease, 13
of whom developed angina during exercise. 6 E X E R C I S E A N D T
H E H E A R T
- 13. The ventricular volume response to upright exercise also
varies greatly, even in similar popu- lations. The results of some
of the major studies in this area are listed in Table 1-2. Among
normal subjects, end-diastolic volume has been reported to increase
greatly,15,21,22 increase moderately,23-27 or decrease slightly
during upright exercise.28-31 End-diastolic volume has been
reported to increase in the range of 8% to 56% among patients with
coronary artery disease, and end- systolic volume has been shown to
increase in the range of 16% to 94% in response to upright
exercise.21,23,32-37 Among normal subjects, end- systolic volume
has generally been reported to decrease in response to maximal
upright exercise (range 4% to 79%).21,23-33,38 Higginbotham et
al,22 however, observed a 48% increase in end-systolic volume among
normal subjects; others have reported lesser increases. Less is
known about the ventricular response to upright exercise in
patients with chronic heart failure. Sullivan et al,39 Tomai et
al,31 and Delahaye et al40 all observed increases in both
end-systolic and end-diastolic volumes from rest to peak exercise
ranging between 10% and 20% in patients with left ventricular
dysfunction. The inconsistent results concerning the ven- tricular
volume response to both supine and upright exercise have led
investigators to raise questions concerning the validity of
radionuclide techniques for assessing ventricular function. For
example, Jensen et al41 studied the individual variability of
radionuclide ventriculography in patients with coronary artery
disease with repeat testing for more than 1 year. Although
differences in end-diastolic volume measurements between initial
and repeat testing were small, the standard deviations of the
individual differences between tests at rest and peak exercise were
large, on the order of 38 and 49 mL, respectively. Variability in
the ejection fraction and end-systolic volume responses to exercise
were of a similar magnitude. In light of the apparent shortcomings
of the radionuclide techniques, investigators have C H A P T E R 1
Basic Exercise Physiology 7 TABLE 1-2. Ventricular volume response
to upright exercise using radionuclide of echocardiographic
techniques Percent Percent Investigator Population Technique change
EDV change ESV Rerych et al 197823 Normals (n = 30) RN Increase 10
Decrease 35 CAD (n = 20) RN Increase 56 Increase 94 Freeman et al
198134 Normals (n = 10) RN Increase 25 Increase 10 CAD (n = 22) RN
Increase 30 Increase 38 Wyns et al 198228 Normals (n = 10) RN
Decrease 8 Decrease 65 Manyeri and Kostuk 198321 Normals (n = 22)
RN Increase 31 Decrease 22 Crawford et al 198333 CAD (n = 10) Echo
Increase 8 Increase 22 CAD (n = 20) RN Increase 45 Increase 48
Kalischer et al 198436 CAD (n = 18) RN Increase 27 Increase 48 CAD
(n = 10) RN Increase 24 Increase 38 Hakki and Iskandrian 198543
Mixed (n = 117) RN Increase 15 Shen et al 198535 Normals (n = 17)
RN Increase 22 Increase 27 CAD (n = 14) RN Increase 26 Increase 29
Higginbotham et al 198622 Normals (n = 24) RN Increase 45 Increase
48 Iskandrian and Hakki 198624 Normals (n = 41) RN Increase 6
Decrease 35 Plotnick et al 198627 Normals (n = 30) RN Increase 4
Decrease 50 Renlund et al 198729 Normals (n = 13) RN Decrease 3
Decrease 79 Sullivan et al 198839 CHF (n = 20) RN Increase 20
Increase 20 Ginzton et al 198938 Normals (n = 14) Echo Decrease 26
Decrease 48 Younis et al 199025 Normals (n = 9) RN Increase 17
Decrease 4 Goodman et al 199126 Normals (n = 15) RN Increase 19
Decrease 14 Myers et al 199137 CAD (n = 8) Echo Increase 16
Increase 16 Schairer et al 199230 Normals (n = 15) Echo Decrease 4
Decrease 52 Tomai et al 199232 Normals (n = 12) RN Decrease 8
Decrease 42 Tomai et al 199331 Normals (n = 10) RN Decrease 8
Decrease 43 CHF (n = 10) RN Increase 12 Increase 14 Delahaye et al
199740 CHF (n = 13) RN Increase 15 Increase 23 Lapa-Bula et al
200241 CHF (n = 10) Echo Increase 4 Decrease 5 CAD, coronary artery
disease; CHF, chronic heart failure; Echo, echocardiography; EDV,
end-diastolic volume or end-diastolic volume index; ESV,
end-systolic volume or end-systolic volume index; RN, radionuclide
ventriculography.
- 14. employed alternative methods for quantifying ven- tricular
function during exercise. Crawford et al33 evaluated the
feasibility and reproducibility of two-dimensional echocardiography
for assessing left ventricular function during exercise. A 9%
test-retest difference in end-diastolic volume was demonstrated.
End-diastolic volume was reported unchanged from rest to peak
exercise in patients with coronary disease, but it increased
significantly (20%) from rest to peak exercise in normal subjects.
Ginzton et al38 compared athletes with sedentary subjects during
upright exercise using two-dimensional echocardio- graphy. After a
slight increase in end-diastolic volume submaximally in both
groups, end- diastolic volume decreased 39% and 35% at peak
exercise among athletes and sedentary subjects, respectively.
Although both groups decreased end-systolic volume progressively
during exercise, the reduction was greater among the athletes (70%
versus 52%). Thus, the ventricular volume response to exercise is
not entirely clear, but it appears to depend upon the type of
disease, method of mea- surement (radionuclide or
echocardiographic), type of exercise (supine versus upright), and
exer- cise intensity (submaximal versus maximal). Much of the
disagreement on this issue can no doubt be attributed to
differences in the exercise level at which measurements were taken.
With this in mind, some rough generalizations may be made
concerning changes in ventricular volume in response to upright
exercise. In normal subjects, the response from upright rest to a
moderate level of exercise is an increase in both end-diastolic and
end-systolic volumes of about 15% and 30%, respectively. As
exercise progresses to a higher intensity, end-diastolic volume
probably does not increase further,27 but end-systolic volume
decreases progressively. At peak exercise, end-diastolic volume may
even decline somewhat, while stroke volume is main- tained by a
progressively decreasing end-systolic volume. Based on six studies
that have quantified the volume response of patients with coronary
artery disease in the upright position,21,23,34-37 end-diastolic
volume has been reported to increase 16% to 56% during exercise.
The increase in end-systolic volume has been reported to range from
16% to 48%. An exception, however, is a study performed by Rerych
et al23 that reported a 94% increase in end-systolic volume.
Sullivan et al,39 Tomai et al,31 and Delahaye et al40 reported
approximately 20% increases in both end-systolic and end-diastolic
volumes from rest to maximal exercise during upright exercise among
patients with chronic heart failure, whereas Lapu-Bula et al42
reported that volumes changed minimally during exercise. Few other
data are available for this group in the upright position.
Peripheral Factors (a-VO2 Difference) Figure 1-2 shows the
peripheral determinants of maximal oxygen uptake. Oxygen extraction
by the tissues during exercise reflects the difference between the
oxygen content of the arteries (gen- erally 18 to 20 mL O2/100 mL
at rest) and oxygen content in the veins (generally 13 to 15 mL
O2/100 mL at rest, yielding a typical a-VO2 differ- ence at rest of
4 to 5 mL O2/100 mL, ;23% extraction). During exercise, this
difference widens as the working tissues extract greater amounts of
oxygen; venous oxygen content reaches very low levels and a-VO2
difference may be as high as 16 to 18 mL O2/100 mL with exhaus-
tive exercise (exceeding 85% extraction of oxygen from the blood at
VO2 max). Some oxygenated blood always returns to the heart,
however, as smaller amounts of blood continue to flow through
metabolically less active tissues that do not fully extract oxygen.
Generally, a-VO2 differ- ence does not explain differences in VO2
max between subjects who are relatively homogenous. That is, a-VO2
difference is generally considered to widen by a relatively fixed
amount during exercise, and differences in VO2 max have been
historically explained by differences in cardiac output. However,
some patients with cardiovascu- lar or pulmonary disease exhibit
reduced VO2 max values that can be attributed to a combination of
central and peripheral factors. Determinants of Arterial Oxygen
Content. Arterial oxygen content is related to the partial pressure
of arterial oxygen, which is determined in the lung by alveolar
ventilation and pulmonary diffu- sion capacity, and in the blood by
hemoglobin content. In the absence of pulmonary disease, arterial
oxygen content and saturation are usu- ally normal throughout
exercise, even at very high levels. This is true even for patients
with severe coronary disease or chronic heart failure. However,
often patients with symptomatic pul- monary disease neither
ventilate the alveoli adequately nor diffuse oxygen from the lung
into the bloodstream normally, and a decrease in 8 E X E R C I S E
A N D T H E H E A R T
- 15. arterial oxygen saturation during exercise is one of the
hallmarks of this disorder. Arterial hemo- globin content is also
usually normal throughout exercise. Naturally, a condition such as
anemia would reduce the oxygen-carrying capacity of the blood,
along with any condition that would shift the O2 dissociation curve
leftward, such as reduced 2, 3-diphosphoglycerate, PCO2, or
elevated temperature. Determinants of Venous Oxygen Content. Venous
oxygen content reflects the capacity to extract oxygen from the
blood as it flows through the muscle. It is determined by the
amount of blood directed to the muscle (regional flow) and
capillary density. Muscle blood flow increases in proportion to the
increase in work rate and thus the oxygen requirement. The increase
in blood flow is brought about not only by the increase in cardiac
output, but also by a preferential redistribution of the cardiac
output to the exercis- ing muscle. A reduction in local vascular
resist- ance facilitates the greater skeletal muscle flow. In turn,
locally produced vasodilatory mecha- nisms, along with neurogenic
dilatation resulting from higher sympathetic activity, mediate the
greater skeletal muscle blood flow. A marked increase in the number
of open capillaries reduces diffusion distances, increases
capillary blood vol- ume, and increases mean transit time,
facilitating oxygen delivery to the muscle. Cross-sectionally, fit
individuals have a greater skeletal muscle capillary density than
sedentary subjects. In addition, fit subjects may have a greater
capacity to redistribute blood flow toward the working muscle and
away from nonexercising tissue. The converse is true in many
patients with cardiovascular disease. For example, one of the
characteristics of the patient with chronic heart failure is an
exaggeration of the decondi- tioning response. These patients
exhibit a reduced capacity to redistribute blood, a reduced
capacity to vasodilate in response to exercise or following
ischemia, and a reduced capillary-to-fiber ratio. SUMMARY The major
cardiopulmonary adaptations that are required of acute exercise
make exercise testing a very practical test of cardiac perfusion
and func- tion. The rather remarkable physiologic adapta- tions
that occur with exercise have made exercise a valuable research
medium not just for the study of cardiovascular disease, but also
for studying physical performance in athletes and for studying the
normal and abnormal physiology of other organ systems. A major
increase and redistribution of cardiac output underlies a series of
adjustments that allow the body to increase its resting metabolic
rate as much as 10 to 20 times with exercise. The capacity of the
body to deliver and utilize oxygen is expressed as the maximal
oxygen uptake. Maximal oxygen uptake is defined as the product of
maximal cardiac output and maximal arterio- venous oxygen
difference. Thus, the cardio- pulmonary limits are defined by (1) a
central component (cardiac output) that describes the capacity of
the heart to function as a pump and (2) peripheral factors
(arteriovenous oxygen difference) that describe the capacity of the
lung to oxygenate the blood delivered to it and the capacity of the
working muscle to extract this oxygen from the blood. Hemodynamic
responses to exercise are greatly affected by the type of exer-
cise being performed, by whether or not disease is present, and by
the age, gender, and fitness of the individual. Coronary artery
disease is characterized by reduced myocardial oxygen supply,
which, in the presence of an increased myocardial oxygen demand,
can lead to myocardial ischemia and reduced cardiac performance.
Despite years of study, a number of dilemmas remain with regard to
the response to exercise clinically. Although myocardial perfusion
and function are intuitively linked, it is often difficult to
separate the impact of ischemia from that of left ventricular
dysfunc- tion on exercise responses. Indices of ventricular
function and exercise capacity are poorly related. Cardiac output
is considered the most important determinant of exercise capacity
in normal sub- jects and in most patients with cardiovascular or
pulmonary disease. However, among patients with disease,
abnormalities in one or several of the links in the chain that
defines oxygen uptake con- tribute to the determination of exercise
capacity. The transport of oxygen from the air to the mitochondria
of the working muscle cell requires the coupling of blood flow and
ventilation to cellular metabolism. Energy for muscular con-
traction is provided by three sources: stored phosphates (ATP and
creatine phosphate), oxygen- independent glycolysis, and oxidative
metabolism. Oxidative metabolism provides the greatest source of
ATP for muscular contraction. Muscular contraction is accomplished
by three fiber types that differ in their contraction speed, color,
and mitochondrial content. The duration and intensity C H A P T E R
1 Basic Exercise Physiology 9
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sources and fiber types are called upon. R E F E R E N C E S 1.
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Treadmill performance and cardiac function in selected patients
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Hammond HK, Kelley TL, Froelicher VF: Noninvasive testing in the
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ventricular function at rest and during bicycle exercise in the
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10 E X E R C I S E A N D T H E H E A R T
- 17. 11 C H A P T E R two Exercise Testing Methodology Despite
the many advances in technology related to the diagnosis and
treatment of cardiovascular disease, the exercise test remains an
important diagnostic modality. Its numerous applications,
widespread availability, and high yield of clini- cally useful
information continue to make it an important gatekeeper for more
expensive and invasive procedures. However, the many different
approaches to the exercise test have been a draw- back to its
proper application. Excellent guide- lines have been updated by
organizations such as the American Heart Association, American
Association of Cardiovascular and Pulmonary Rehabilitation, and
American College of Sports Medicine. These guidelines are based on
a multi- tude of research studies over the last 30 years and have
led to greater uniformity in methods. Nevertheless, in many
laboratories, methodology remains based on tradition, convenience,
equip- ment, or personnel available. New technology, while adding
convenience, has also raised new questions with regard to
methodology. For example, all commercially available systems today
depend upon computers. Do computer-averaged exercise electrocardio-
grams (ECGs) improve test accuracy, and should the practitioner
rely on this processed informa- tion or on the raw data? What about
the many computerized exercise scores that now can so easily be
calculated? Technology has changed the exercise-testing laboratory
environment, and concerns such as these have arisen. Though many of
these techniques are attractive, in many instances not enough data
are yet available to validate them, so they should be used
judiciously. Also, what about the various ancillary tests and the
nonexercise stress modalities? In this chapter, we will address
basic methodology and comment on the impact these advances in
technology have had. We start by listing the advantages and
disadvantages of exercise ECG testing. These considerations are
important because the health care provider must evaluate the
suitability of the various testing modalities in each situation.
ADVANTAGES AND DISADVANTAGES OF EXERCISE ECG TESTING ADVANTAGES OF
THE STANDARD EXERCISE ECG TEST 1. Low cost 2. Availability of
trained personnel 3. Exercise capacity determined 4. Patient
acceptability 5. Takes less than an hour to accomplish 6.
Convenience 7. Availability 8. Long history of use, validation of
responses, application of multivariate scores
- 18. SAFETY PRECAUTIONS AND RISKS The safety precautions
outlined by the American Heart Association are very explicit in
regard to the requirements for exercise testing. Everything
necessary for cardiopulmonary resuscitation must be available, and
regular drills should be performed to ascertain that both personnel
and equipment are prepared for a cardiac emergency. The classic
survey of clinical exercise facilities by Rochmis and Blackburn in
19711 showed exercise testing to be a safe procedure, with
approximately only one death and five nonfatal complications per
10,000 tests. Perhaps because of an expanded knowledge concerning
indications, contraindica- tions, and endpoints, data suggest that
maximal exercise testing is safer today than 30 years ago. In 1989,
Gibbons et al2 reported the safety of exercise testing in 71,914
tests conducted over a 16-year period. The complication rate was
0.8 per 10,000 tests. In a recent survey of 71 exer- cise testing
laboratories throughout the Veterans Administration Health Care
System including 75,828 tests, we observed an event rate of 1.2 per
10,000 tests.3 The fact that the event rate was similar between a
clinically referred population (the Veterans Administration, a
higher risk group), and a generally healthier population2
underscores the fact that the test is extremely safe. Gibbons et
al2 suggested that the low compli- cation rate in their study was
due to the inclusion of a cool-down walk, but we have observed a
low rate of ventricular tachycardia,4 and a low overall
complication rate3 despite having patients assume a supine position
immediately after the test and despite exercising higher risk
patients.This issue is addressed in more detail in Chapter 13, and
a sum- mary of these studies is presented in Table 13-6. However,
it is important to note that there have been reports of
complications, including acute infarctions and deaths, associated
with exercise testing. Although the test is remarkably safe, the
population referred for this procedure usually is at high risk for
coronary events. Irving and Bruce5 have reported an association
between exercise-induced hypotension and ventricular fibrillation.
Shepard6 has hypothesized the follow- ing risk levels for exercise:
(1) three or four times normal in a cross-country foot race, (2) 6
to 12 times normal when patients at risk for coro- nary artery
disease (CAD) are performing unac- customed exercise, and (3) as
high as 60 times normal when patients with existing CAD are per-
forming exercise in a stressful environment, such as a physicians
office. Cobb and Weaver7 esti- mated the risk to be over 100 times
in the latter situation and point out the dangers of the recov- ery
period. The risk of exercise testing in patients with CAD cannot be
disregarded even with its excellent safety record. Studies
documenting the risks of exercise training are presented in more
detail in Chapter 12. Indications to stop an exercise test, in
addition to the factors to consider in assessing the degree of
exertion, are outlined in Table 2-1. Most prob- lems can be avoided
by having an experienced physician, nurse, or exercise physiologist
stand- ing next to the patient, measuring blood pressure, and
assessing patient appearance during the test. The exercise
technician should operate the recorder and treadmill, take the
appropriate tracings, enter data on a form, and alert the physician
to any abnormalities that may appear on the monitor scope. If the
patients appearance is worrisome, if systolic blood pressure drops
or plateaus, if there are alarming ECG abnormalities, if chest pain
occurs and becomes worse than the patients usual pain, or if the
patient wants to stop the test for any reason, the test should be
stopped, even at a sub- maximal level. In most instances, a
symptom- limited maximal test is preferred, but it is usually
advisable to stop if 0.2 mV of additional ST-segment elevation
occurs, or if 0.2 mV of flat or downsloping ST-segment depression
occurs. In some patients estimated to be at high risk because of
their clinical history, it may be appropriate to stop at a submaxi-
mal level, as it is not unusual for severe ST-segment depression,
dysrhythmias, or both to occur in the postexercise period. If the
measurement of maximal exercise capacity or other information is
needed, it may be preferable to repeat the test later, once the
patient has demonstrated a safe performance of a submaximal
workload. Exercise testing should be an extension of the history
and physical examination. A physician obtains the most information
by being present to talk with, observe, and examine the patient in
12 E X E R C I S E A N D T H E H E A R T DISADVANTAGES OF EXERCISE
ECG TESTING 1. Limited sensitivity and specificity 2. Inability to
localize ischemia or coronary lesions. 3. No estimate of left
ventricular (LV) function 4. Not suitable for certain patients. 5.
Requires cooperation and the ability to walk or pedal a cycle
ergometer.
- 19. conjunction with the test. A brief physical exami- nation
should always be performed to rule out any contraindications that
exist. Accordingly, indi- viduals who supervise exercise tests must
have the cognitive and technical skills necessary to be competent
to do so. The American College of Cardiology, American Heart
Association, and the American College of Physicians, with broad
involvement from other professional organizations involved with
exercise testing, such as the American College of Sports Medicine,
have out- lined the cognitive skills needed to competently
supervise exercise tests.8 These skills include knowledge of
appropriate indications and con- traindications to testing, an
understanding of risk assessment, the ability to recognize and
treat com- plications, and knowledge of basic cardiovascular and
exercise physiology, along with the ability to interpret the test
in different patient populations. The need for physician presence
during exer- cise testing has been the subject of a great deal of
discussion in the past. In many cases, exercise tests can be
supervised by properly trained and competent exercise
physiologists, physical thera- pists, nurses, physician assistants,
or medical technicians who are working under the direct supervision
of a physician. However, the physician must be in the immediate
vicinity or on the prem- ises or the floor and available for
emergencies.8,9 In situations where the patient is deemed to be at
higher risk for an adverse event during exercise testing, the
physician should be physically pres- ent in the exercise testing
room to personally supervise the test. Such cases include, but are
not limited to, patients with recent acute coronary syndrome or
myocardial infarction (within 7 to 10 days), severe LV dysfunction,
severe valvular stenosis (e.g., aortic stenosis), or known complex
arrhythmias. The physicians reaction to signs or symptoms should be
moderated by the informa- tion the patient gives regarding his or
her usual activity. If abnormal findings occur at levels of
exercise that the patient usually performs, then it may not be
necessary to stop the test for them. Also, the patients activity
history should help determine appropriate work rates for testing.
CONTRAINDICATIONS Table 2-2 lists the absolute and relative con-
traindications to performing an exercise test. C H A P T E R 2
Exercise Testing Methodology 13 TABLE 2-1. Indications for
terminating an exercise test and assessment of maximal effort
Absolute Reasons or Indications to Terminate Acute myocardial
infarction Severe anginachest pain score of 4 out of 4 Exertional
hypotensiona drop in systolic blood pressure of 10 mmHg, or drop
below the value obtained in the standing position prior to testing,
particularly in patients who have heart failure, have had a prior
myocardial infarction, or are exhibiting signs or symptoms of
ischemia 1.0 mm ST elevation in leads without diagnostic Q waves
Serious arrhythmiasventricular tachycardia, third-degree heart
block Poor perfusion as judged by skin temperature and cyanosis
Neurologic signsconfusion, lightheadedness, vertigo Technical
problemsinability to interpret the ECG pattern; any malfunction of
the recording or monitoring device; inability to measure the
systolic blood pressure Patients request to terminate Relative
Reasons or Indications to Terminate The following indications may
be superseded if done so in the context of good clinical judgment.
Increasing chest painchest pain score of 3 out of 4 2.0 mm
horizontal or downsloping ST depression Pronounced fatigue or
shortness of breath Wheezing Leg pain or claudication Increase in
systolic blood pressure to 250 mmHg or increase in diastolic blood
pressure to 115 mmHg Less serious arrhythmias than those in
preceding list (frequent or mutifocal premature ventricular
contractions, supraventricular tachycardia, bradyarrhythmias)
Bundle branch block or another rate-dependent intraventricular
conduction defect that cannot be distinguished from ventricular
tachycardia Assessment of Maximal Effort As no single marker of
effort is usually specifically indicative of a maximal effort, it
is best to consider multiple responses. Borg scale 17-20 Signs of
fatigue, profound shortness of breath, or exhaustion Age-predicted
maximal heart rate, with a population-specific regression equation
Expired gas measurements, including respiratory exchange ratio
(>1.10)
- 20. Good clinical judgment should be foremost in deciding the
indications and contraindica- tions for exercise testing. In
selected cases with relative contraindications, testing can provide
valuable information even if performed submaximally. PATIENT
PREPARATION Preparations for exercise testing include the
following: 1. The patient should be instructed not to eat or smoke
at least 2 to 3 hours prior to the test and to come dressed for
exercise. 2. A brief history and physical examination (par-
ticularly for patients with systolic murmurs) should be performed
to rule out any contra- indications to testing (see Table 2-2). 3.
Specific questioning should determine which drugs are being taken,
and potential electro- lyte abnormalities should be considered. The
labeled medication bottles should be brought along so that they can
be identified and recorded. It is generally no longer con- sidered
necessary for most patients to stop taking their beta-blockers
prior to testing. If it is considered necessary to do so in
selected patients, they should be stopped gradually in order to
avoid the rebound phenomenon, which can be dangerous. The tapering
of beta-blockers should be over- seen by a physician. 4. If the
reason for the exercise test is not appar- ent, the referring
physician should be contacted such that this gets clarified. 5. A
12-lead ECG should be obtained in both the supine and standing
positions. The latter is an important rule, particularly for
patients with known heart disease, since an abnormality may
prohibit testing. On rare occasions, a patient referred for an
exercise test will instead be admitted to the coronary care unit.
6. The patient should receive careful explana- tions of why the
test is being performed and of the testing procedure, including its
risks and possible complications. A demonstration should be
provided of how to get on and off the treadmill and how to walk on
it. The patient should be told that he or she can hold on to the
handrails initially but then should use the rails only for balance
(discussed in the following section). TREADMILL The treadmill
should have front and side rails for patients to steady themselves,
and some patients may benefit from the helping hand of the person
administering the test. The treadmill should be calibrated at least
monthly. Some models can be greatly affected by the weight of the
patient and 14 E X E R C I S E A N D T H E H E A R T TABLE 2-2.
Contraindications to exercise testing Absolute Acute myocardial
infarction (within 2 days) Unstable angina not stabilized by
medical therapy Uncontrolled cardiac arrhythmias causing symptoms
or hemodynamic compromise Symptomatic severe aortic stenosis
Uncontrolled symptomatic heart failure Acute pulmonary embolus or
pulmonary infarction Acute myocarditis or pericarditis Relative*
Left main coronary stenosis or its equivalent Moderate stenotic
valvular heart disease Electrolyte abnormalities Uncontrolled
arterial hypertension Tachyarrhythmias or bradyarrhythmias
Hypertrophic cardiomyopathy and other forms of outflow tract
obstruction Mental or physical impairment leading to inability to
exercise adequately High-degree atrioventricular block *Relative
contraindications can be superseded if benefits outweigh risks of
exercise. In the absence of definitive evidence, a systolic blood
pressure of 200 mmHg and a diastolic blood pressure of 110 mmHg are
reasonable criteria.
- 21. will not deliver the appropriate workload to heavy
patients. An emergency stop button should be readily available to
the staff only. A small platform or stepping area at the level of
the belt is advisable so that the patient can start the test by
pedaling the belt with one foot prior to stepping on. After they
become accustomed to the treadmill, patients should not grasp the
front or side rails, as this decreases the work performed and thus
the oxygen uptake, which increases exercise time, resulting in an
overestimation of exercise capac- ity. Gripping the handrails also
increases ECG muscle artifact. For patients who have difficulty
letting go of the handrails, it is helpful to have them take their
hands off the rails, close their fists, and extend one finger on
each hand, touch- ing the rails only with those fingers in order to
maintain balance while walking. Some patients may require a few
moments before they feel com- fortable enough to let go of the
handrails, but we strongly discourage grasping the handrails after
the first minute of exercise. LEGAL IMPLICATIONS OF EXERCISE
TESTING In any procedure with a risk of complications, it is
advisable to make certain the patient understands the situation and
acknowledges the risks. Some physicians feel that informing
patients of the risks involved will occasionally make them overly
anxious or discourage them from performing the test. Because of
this, and the fact that a signed consent form does not necessarily
protect a physician from legal action, there has been less
insistence on consent forms. However, a great deal of case law
exists suggesting that a written informed consent before the
exercise test is important to protect the patient, physician, and
institution. Establishment of physician-patient communi- cation
before and after performance of the exer- cise test should be the
first legal consideration. A test should not be performed without
first obtaining the patients informed consent, after the patient is
made aware of the potential risks and benefits of the procedure. A
physician may be held responsible in the event of a major untoward
event, even if the test is carefully performed, in the absence of
informed consent. The argument can be made that the patient would
not have undergone the procedure had he or she been made aware of
the risks associated with the test. After the test, responsibility
rests with the physi- cian for prompt interpretation and
consideration of the implications of the test. Communication of
these results to the patient is necessarywith advice concerning
adjustments in lifestyleand this should be done immediately after
the test is performed. The second consideration should be adherence
to proper standards of care during performance of the test.
Exercise testing should be carried out only by persons thoroughly
trained in its admin- istration and in the prompt recognition of
prob- lems that may arise. A physician trained in exercise testing
and resuscitation should be read- ily available during the test to
make judgments concerning test termination. Resuscitative equip-
ment should always be available. As mentioned above, an updated
joint position statement from several professional organizations
was published in 2000, outlining the standards for physician
competence for performing exercise testing.8 BLOOD PRESSURE
MEASUREMENT Although numerous clever devices have been developed to
automate blood pressure measure- ment during exercise, none can be
recommended. The time-proven method of the physician hold- ing the
patients arm with a stethoscope placed over the brachial artery
remains the most reliable method to obtain the blood pressure. The
patients arm should be free of the handrails so that noise is not
transmitted up the arm. It is sometimes helpful to mark the
brachial artery. An anesthesiologists auscultatory piece or an
electronic microphone can be fastened to the arm. A device that
inflates and deflates the cuff on the push of a button can also be
helpful. If systolic blood pressure appears to be increasing
sluggishly or decreasing, it should be taken again immedi- ately.
If a drop in systolic blood pressure of 10 to 20 mmHg or more
occurs, or if it drops below the value obtained in the standing
position prior to testing, the test should be stopped. This is
particularly important in patients who have heart failure, a prior
myocardial infarction, or are exhibiting signs or symptoms of
ischemia. An increase in systolic blood pressure to 250 mmHg or an
increase in diastolic blood pressure to 115 mmHg are also
indications to stop the test. The clinical implications of abnormal
blood pressure responses to the exercise test are discussed in
detail in Chapter 5. C H A P T E R 2 Exercise Testing Methodology
15
- 22. ECG RECORDING INSTRUMENTS Many technologic advances in ECG
recorders have taken place. The medical instrumentation industry
has promptly complied with specifica- tions set forth by various
professional groups. Machines with high-input impedance ensure that
the voltage recorded graphically is equivalent to that on the
surface of the body despite the high natural impedance of the skin.
There remains some concern about mismatching lead impedance, which
can result in distortion. Optically isolated buffer amplifiers have
ensured patient safety, and machines with a frequency response from
0 to 100 Hz are commercially available. The 0 Hz lower end is
possible because DC coupling is technically feasible. Some ECG
equipment has monitoring and diagnostic modes, particularly
equipment used in coronary care units. The diagnostic mode follows
diagnostic instrument specifications with a fre- quency response
from 0.05 to 100 Hz. In the mon- itor mode, there can be distortion
of the ECG. The monitor mode is available to lessen the effects of
electrical interference, motion, and respiration on the ECG and
should not be used for exercise testing. The type of distortion is
affected by the ECG waveform that is presented. If the ECG wave-
form is a tall R wave without an S wave, the ST-segment distortion
can be different than if there is an R wave followed by a large S
wave. In general, an inadequate low-frequency response can greatly
decrease the Q- and R-wave amplitude and create S waves. Alteration
of the 25 to 45 Hz frequency response is the most common cause of
ST-segment distortion found in tracings with abnormal ST segments.
Some of the newer filter- ing techniques delay the appearance of
the ECG signal on the monitor screen by several seconds. WAVEFORM
AVERAGING Digital averaging techniques have made it possi- ble to
average ECG signals to remove noise. There is a need for consumer
awareness in these areas, since most manufacturers do not specify
how the use of such procedures modifies the ECG. Signal averaging
can actually distort the ECG signal. These techniques are
attractive because they can produce a clean tracing in spite of
poor skin preparation. However, the common expression used by
computer scientists, Garbage in, garbage out, has never been more
applicable than to the computerized ECG. The clean-looking exercise
ECG signal produced may not be a true represen- tation of the
actual waveform and in fact may be dangerously misleading. Also,
the instruments that make computer ST-segment measurements cannot
be totally reliable as they are based on imperfect algorithms. For
instance, the algorithm that measures QRS end at 70 or 80 msec
after the peak of the R wave can hardly be valid, partic- ularly
with a changing heart rate. Because of physician insistence on
having exercise tracings as clean as resting tracings,
manufacturers have taken some worrisome steps with filtering and
ECG presentation. One such approach is linked medians, in which
averages are connected together at the same R-R interval as raw
data. Even though these tracings are appropriately labeled, and
often presented with a channel of raw data as well, most physicians
do not realize that they are dealing with created waveforms instead
of raw data. ECG PAPER RECORDERS For some patients it is
advantageous to have a recorder with a slow paper speed option such
as 5 mm/sec. This speed makes it possible to record an entire
exercise test and reduces the likelihood of missing any
dysrhythmias when specifically evaluating patients with these
problems. A faster paper speed of 50 mm/sec can be helpful for mak-
ing accurate ST-segment slope measurements. Many different types of
ECG paper can be used. Wax-treated paper is known to retain an ECG
image for 20 years or longer; however, it is pressure- sensitive
and easily marked. Thermochemically treated paper is sturdy and
resists marking. There are many different types of thermochemically
treated paper, and the life expectancy of images recorded on them
is usually adequate. However, at least one instance of ECG paper
losing a recorded image resulted in legal action by a hos- pital
against a manufacturer. Ceramic-coated paper is very sturdy and
comparable in price to other ECG papers. It has a hard finish with
a high contrast, which makes it durable and easy to interpret.
Untreated paper is the cheapest ECG paper, but the ink-jet and
carbon-transfer tech- niques characteristically produce