Clinical Cardiology: New Frontiers
Exercise as Cardiovascular Therapy
Roy J. Shephard, MD, PhD, DPE; Gary J. Balady, MD
F or many years, cardiac physicians were strongly influ-
enced by Thomas Hilton’s “Rest and Pain” and advo-
cated prolonged rest for the majority of their patients.
However, the past 3 decades have seen a complete revolution
in this thinking, and moderate to vigorous exercise is now
prescribed not only for the prevention of ischemic heart
disease1 but also as a major component of treatment after
myocardial infarction,2 angioplasty and coronary bypass sur-
gery, and heart transplantation3 and in congenital heart
disease4 and stable congestive heart failure.5,6
This report defines exercise and physical activity, consid-
ering their impact on susceptibility to cardiovascular disease.
It also examines the physiological effects of regular exercise,
suggesting how exercise-induced changes might improve
cardiac performance. It discusses the influence of the type,
intensity, frequency, duration, and volume of exercise and
their respective contributions to the development of a rational
exercise prescription, commenting on problems of sustaining
compliance and the potential dangers of excessive exercise. A
final section of the article suggests possible avenues for
future research.
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Physical Activity, Exercise, and Fitness
To understand how physical activity and exercise fit into the
model of modern cardiovascular health, it is important to
understand specific terms and concepts. Physical activity has
been defined as any bodily movement produced by skeletal
muscles that results in energy expenditure. Exercise can be
defined as a subset of physical activity that is planned,
structured, repetitive, and purposeful in the sense that im-
provement or maintenance of physical fitness is the objective.
Physical fitness includes cardiorespiratory fitness, muscle
strength, body composition, and flexibility, composing a set
of attributes that people have or achieve that relates to the
ability to perform physical activity.7 Physical fitness is best
assessed by measures of maximal (or peak) oxygen intake
(V̇O2). Many studies estimate fitness levels by measurement
of either the peak work rate or MET level (where 1 MET5an
energy expenditure of 14.6 kJ z kg21 z min21, 3.5 kcal z kg21 z
min21) achieved during graded exercise tests.8 When defining
the amount of physical activity or exercise, an important
interrelation exists between the total dose of activity and the
intensity at which the activity is performed. Dose refers to the
From the Faculty of Physical Education and Health (R.J.S.) and Department of Public Health Sciences (R.J.S.), University of Toronto, Toronto, Ontario,
Canada; Toronto Rehabilitation Centre (R.J.S.), North York, Ontario, Canada; and the Section of Cardiology (G.J.B.), Boston University Medical Center,
Boston, Mass.
Correspondence to Prof Roy J. Shephard, MD, PhD, DPE, PO Box 521, Brackendale, BC V0N 1H0 (courier to 41390, Dryden Rd, Brackendale, BC
V0N 1H0). E-mail royjshep@mountain-inter.net
(Circulation. 1999;99:963-972.)
© 1999 American Heart Association, Inc.
Circulation is available at http://www.circulationaha.org
963
total amount of energy expended in physical activities that
require repetitive muscular movement (usually expressed in
kilojoules or kilocalories). Intensity can be defined in abso-
lute or relative terms. Absolute intensity reflects the rate of
energy expenditure during exercise and is usually expressed
in METS, kJ z min21 or kcal z min21. Relative intensity refers
to the relative percentage of maximal aerobic power that is
maintained during exercise and is expressed as a percentage
of maximal heart rate or a percentage of maximal oxygen
intake. For example, brisk walking at 4.8 km/h, 3 mph, has an
absolute intensity of approximately 4 METs. In relative
terms, this intensity is considered light for a 20-year-old
healthy person, but it is a hard intensity for an 80-year-old.8
One can achieve that same total dose of physical activity
by performing activities at a high intensity for a short
duration, or at a lower intensity for a longer duration.
Whether or not the health benefits are equivalent when
similar doses of activity are performed at different intensities
remains an area of great interest. The answer to this question
has important public health and clinical implications. Recent
guidelines on this topic8 reflect the current scientific knowl-
edge and consensus and conclude that variations in dose and
intensity will yield differing beneficial effects on fitness and
cardiovascular risk factors. These may translate to different
effects on cardiovascular morbidity and mortality rates.
Physical Activity and Exercise in the
Prevention of Cardiovascular Disease
Epidemiologic Observations
Several population-based studies show that incremental lev-
els of regular physical activity are inversely proportional to
long-term cardiovascular mortality when controlled for the
presence of other risk factors in both men and women.9 In
studies of male college alumni, the risk of death became
progressively lower as physical activity dose levels increased
from an expenditure of 2.1 to 14.7 MJ/wk, 500 to 3500
kcal/wk. There was a 24% reduction in cardiovascular mor-
tality in subjects whose energy expenditure was .8.4 MJ/wk,
2000 kcal/wk. Alumni who were initially inactive and later
increased their activity levels demonstrated significantly re-
duced cardiovascular risk compared with those who remained
inactive.10 In the large Nurses’ Health Study11 involving more
 964 Exercise as Cardiovascular Therapy
that 73 000 middle-aged women, physical activity was in-
versely related to the risk of coronary heart disease and
stroke. Among patients with known cardiovascular disease, a
meta-analysis of 10 randomized clinical trials examining the
effects of cardiac rehabilitation after myocardial infarction12
calculated a 24% reduction in all-cause mortality and a 25%
reduction in cardiovascular mortality in the exercise rehabil-
itation patients compared with control subjects. No differ-
ences in nonfatal myocardial infarction were apparent.
Higher levels of physical fitness, when measured with an
exercise tolerance test, are associated with a significantly
lower subsequent cardiovascular mortality rate among men
and women.13,14 The relative risk of coronary artery disease in
physically inactive compared with active individuals is
'2.0.9 Importantly, the relative risk for cardiovascular mor-
tality in the least fit or least active compared with the most fit
or active approaches 6.0.9 Paffenbarger et al15 have reported
encouraging data that demonstrate that when habitual physi-
cal activity levels are increased, subsequent mortality is
decreased relative to those who remain physically inactive.
These data strongly support the need to increase physical
activity and fitness levels among both women and men, with
the greatest decrease of mortality rates developing among
those who initially are the least fit.
The data regarding exercise intensity are much less clear
than those addressing dose. There is a growing body of
evidence that shows that regular moderate intensity activity
(17 to 29 kJ/min, 4 to 7 kcal/min), performed by men and
women of a broad age range, reduces cardiovascular mortal-
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ity rates.9,16 –19 A recent report involving 802 men (age 64 to
84 years) concludes that more intense activity (.4 METs)
was more strongly associated with lower cardiovascular
mortality rates than was less intense activity.17 However, Lee,
et al20 noted that only energy expended during vigorous
activity (.6 METs) was associated with a reduction of
mortality rates among male Harvard alumni.
Possible Biological Mechanisms for
Observed Benefits
The specific mechanisms by which physical activity and
physical fitness decrease mortality rates have not been well
elucidated. Physical activity has been associated with favor-
able modifications of cardiovascular disease risk through a
reduction in obesity, improved distribution of body fat, and
lower incidence of non–insulin-dependent diabetes.9 Regular
exercise also yields a modest but beneficial effect on blood
pressure and lipoprotein profiles.21,22 However, the beneficial
effect of physical activity cannot be accounted for solely by
means of risk factor reduction, since the association with
reduced mortality rates is independent of other coronary risk
factors.23
Exercise and Risk Factor Modification
Individuals who engage in regular physical activity have a
lower prevalence of cardiovascular risk factors. This is not
surprising because exercise has been found to yield beneficial
effects on several risk factors. Accordingly, exercise is
considered an important adjuvant therapy in risk factor
modification.
Hypertension
Two cohort studies have demonstrated that regular physical
activity prevents the development of hypertension.24,25 In
addition to preventing hypertension, regular exercise has been
found to lower blood pressure. In mildly hypertensive men,
short-term physical activity decreased blood pressure for 8 to
12 hours after exercise, and average blood pressure was lower
on exercise than on nonexercise days.26 In hypertensive black
men, moderate physical activity performed for 16 to 32 weeks
resulted in a decrease in diastolic blood pressure, which was
sustained even after reduction in antihypertensive medica-
tions. In addition, there was a significant decrease in left
ventricular hypertrophy as early as 16 weeks after the
initiation of exercise.27
Diabetes Mellitus
Physical activity has beneficial effects on both glucose
metabolism and insulin sensitivity. These include increased
sensitivity to insulin, decreased production of glucose by the
liver, larger number of muscle cells that utilize more glucose
than adipose tissue, and reduced obesity.28
Obesity
Exercise training appears to be an important contributor to
weight loss, although the effect of exercise is quite variable.
Most controlled exercise training studies show only modest
weight loss ('2 to 3 kg) in the exercise group. When diet is
added to exercise programs, the average weight loss is 8.5
kg.29 A well-controlled, 1-year randomized trial30 that in-
cluded 231 subjects demonstrated a significant 8.7-kg weight
loss, most of which was body fat, in the exercise and diet
intervention group and a significant 5.1-kg weight loss in the
diet-only group. Those in the control group increased their
weight by an average of 1.7 kg. These data strongly support
the role of both exercise and diet in weight loss programs.
Body composition and fat distribution are linked to cardio-
vascular mortality29 and are improved by exercise. Physically
active men and women have a more favorable waist-to-hip
ratio (,0.9) than do sedentary individuals.31
Lipids
The effect of exercise on lipid levels is an area of active
research. There is much variability in the results of exercise/
lipid-lowering studies, at least in part because of the hetero-
geneity of the study methods, populations, exercise interven-
tions, and the use of adjuvant interventions such as diet or
pharmacological lipid-lowering agents. A meta-analysis32 of
95 studies, most of which were not randomized controlled
trials, concluded that exercise leads to a reduction of 6.3% in
total cholesterol, 10.1% in LDL cholesterol, and 13.4% in
cholesterol/HDL cholesterol and 5% increase in HDL cho-
lesterol. It appears that the training intensities required to
yield modest improvements in lipids are not as high as those
that lead to improvements in fitness levels, as HDL appears to
increase across a broad spectrum of exercise intensities.33,34 A
recent randomized controlled trial of moderate-intensity ex-
ercise (equivalent to brisk walking of 16 km/wk, 10 miles/
wk), Step 2 AHA diet, and the combination of diet plus
exercise was conducted on 180 postmenopausal women and
197 middle-age men. Among those in the diet-plus-exercise

group, an 8% to 12% reduction in LDL and a 22% to 2%
change in HDL levels in women and men, respectively, were
noted after 1 year. LDL changes were greatest in the diet plus
exercise group.22
As estrogen causes an increase in HDL cholesterol, studies
regarding women are confounded by menopausal status and
estrogen use, which are frequently not reported. A recent
study examined the effects of vigorous exercise on HDL
cholesterol in women runners.34 HDL cholesterol levels
increased with increasing amounts of exercise and continued
to rise even in women who ran .64 km/wk. This dose-
response relation persisted in premenopausal and postmeno-
pausal women as well as in those receiving oral contracep-
tives and estrogen replacement therapy. Although the above
studies suggest an improvement in lipid profile with exercise
training, the effects are quite modest. These improvements
may have a favorable effect on cardiovascular risk; however,
exercise is unlikely to normalize cholesterol levels in patients
with genetically based lipid disorders.
Thrombosis
Emerging evidence suggests that exercise training favorably
affects the fibrinolytic system. Strenuous endurance exercise
for 6 months in healthy older patients resulted in a significant
improvement in hemostatic parameters, with a reduction in
plasma fibrinogen levels of 13%, an increase in mean tissue
plasminogen activator of 39%, an increase in active tissue
plasminogen activator of 141%, and a reduction of plasmin-
ogen activator inhibitor-1 of 58%.35 Other studies have shown
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favorable effects on fibrinolytic enzymes after exercise train-
ing in younger subjects36 and in patients after myocardial
infarction.37 Acute and chronic exercise affect platelet acti-
vation. Platelet activation is important in the pathophysiolog-
ical mechanisms of unstable coronary syndromes and acute
myocardial infarction. After acute strenuous exercise of
similar duration and intensity, platelet activation and hyper-
reactivity were increased in sedentary subjects but were
unchanged in physically fit subjects.38 After 12 weeks of
moderate-intensity exercise in middle-aged, overweight,
mildly hypertensive men, secondary platelet aggregation was
reduced by 52% compared with a 17% decrease in the control
group.39 Thus it appears that acute exercise can lead to
increased platelet activity, especially in sedentary individuals,
but regular exercise may abolish or improve this response.
Endothelial Function
The vascular endothelium plays an important role in the
regulation of arterial tone and local platelet aggregation, in
part, through the release of endothelium-derived relaxing
factor. Endothelium-derived relaxing factor release is stimu-
lated by various mechanisms, including the rise in shear stress
associated with acute and chronic increases in blood flow.40
Endothelium-dependent dilation is impaired in patients with
coronary atherosclerosis and in patients with coronary risk
factors, including hypercholesterolemia, diabetes mellitus,
cigarette smoking, and hypertension.41 Emerging evidence
suggests that exercise improves endothelial function. In
animal studies, treadmill exercise training leads to improve-
ment in endothelium-dependent vasodilation and increases in
the gene expression for nitric oxide synthase. Studies involv-
Shephard et al February 23, 1999 965
ing young, healthy army recruits and patients with heart
failure demonstrate improved brachial artery nitric oxide–
dependent, flow-mediated dilation after exercise training.42
No study has yet examined the effect of exercise training on
coronary artery endothelial function in humans.
Autonomic Function
The balance between sympathetic and parasympathetic activ-
ity modulates cardiovascular activity. Enhanced sympathetic
nervous system activity appears to be associated with an
increased risk of cardiac events, particularly in those patients
with known heart disease. Using measures of heart rate
variability, a well accepted noninvasive technique to assess
autonomic tone, cross-sectional studies of healthy men43
reported higher parasympathetic activity among those who
were physically trained and fit compared with those who
were not. Whether or not exercise affects autonomic tone
among patients with cardiovascular disease is unclear. How-
ever, improved measures of heart rate variability with exer-
cise training have been reported in patients with chronic heart
failure44 and in patients after myocardial infarction.45
Exercise Training Outcomes in Persons With
Cardiovascular Disease
Regular endurance or resistance training results in specific
changes in the muscular, cardiovascular, and neurohumoral
systems that lead to improvement in functional capacity
and/or strength. These changes are referred to as the training
effect and allow an individual to exercise to higher peak work
rates with lower heart rates at each submaximal level of
exercise. Exercise training at moderate intensity, 3 to 5 times
per week, leads to marked improvements in peak fitness
levels after 8 to 10 weeks among patients with heart disease,
much as in healthy individuals.2 To date, there are more than
20 published studies that have evaluated the efficacy of
exercise training among patients with impaired left ventricu-
lar function. Improvements of 18% to 25% in peak oxygen
intake and 18% to 34% in peak exercise duration have been
attained.6 Subjective symptoms, activity profile, and quality-
of-life scores are better after training as well.6
Several investigators have demonstrated a diminution of
the ischemic response at a given submaximal work rate in
cardiac patients after training. Moreover, several provocative
studies have reported a decrease in the ischemic response—
for example, angina, ST-segment depression,46 nuclear and
positron emission tomography scanning perfusion de-
fects47,48—at a given heart rate– blood pressure product after
training compared with the pretrained state. Improvement in
myocardial contractility in dysfunctional myocardial seg-
ments has been reported after exercise training as well.49
These findings suggest that there is an improvement in
myocardial oxygen supply (ie, coronary blood flow) at a
given level of myocardial oxygen demand. There are many
mechanisms or combinations thereof that may explain these
findings. Pathological studies in animals reveal that endur-
ance training causes an increase in the size of the superficial
coronary arteries and an increased myocardial capillary den-
sity. Recently, Belardinelli et al49 has reported an increase in
coronary artery collaterals in humans after exercise training.
 966 Exercise as Cardiovascular Therapy
However, other investigators have not noted these latter
changes. Importantly, 3 studies to date have demonstrated
angiographic evidence of regression of atherosclerosis as well
as reduction in the progression of atherosclerosis among
patients who were actively involved in a multifactorial risk
reduction program that includes exercise training.47,48,50 How-
ever, the observed absolute measures of atherosclerotic
change were small. Accordingly, improved myocardial per-
fusion may be due to changes in coronary vasomotor reac-
tivity. Recent data suggest that the beneficial effects of
exercise training on myocardial perfusion appear to yield
important benefits in clinical outcome, including a significant
reduction in adverse cardiac events.50,51
The time course during which the above changes take place
varies with respect to the specific variable and the specific
study. Improvements in functional capacity and myocardial
perfusion have been demonstrated to occur as early as 8
weeks after initiation of exercise training.49 Conversely,
atherosclerotic regression has been observed after 1 year of
exercise47 but has not been studied over shorter periods of
training. At this time, it is fair to state that the minimum
duration of exercise training that is required to yield the many
beneficial effects outlined above is not known and likely
differs for each variable.
Physiological Effects of Regular Exercise
From the viewpoint of the cardiac physician, regular exercise
has both indirect and direct effects on the cardiovascular
system, both of which can enhance functional capacity and
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reduce the likelihood of cardiac problems. The indirect
benefits may be realized at intensities of effort that have little
direct effect on myocardial function. Table 1 outlines the
benefits observed with regular exercise.
Indirect Effects
Important indirect benefits of exercise include a reduction in
cardiovascular risk factors (as discussed above), a strength-
ening of the skeletal muscles, and a change in certain aspects
of lifestyle, particularly a reduction of stress.
Muscle Strengthening
During vigorous effort, a high pressure is developed within
contracting muscle groups, and this tends to occlude muscle
blood flow; after-loading of the heart is increased, and this in
turn limits cardiac ejection fraction and stroke volume.
Occlusion of the intramuscular vessels begins when the
muscles are contracting at '15% of their maximal voluntary
force, and it becomes complete at some 70% of maximal
force.52 In many patients with heart disease, peak muscle
force has been weakened by bed rest and/or administration of
corticosteroids, and if muscle strength can be enhanced by
appropriate resistance exercise, there will be a corresponding
improvement in peak cardiac performance. Initially, gains of
strength reflect improved coordination of muscle contraction,
but as an exercise program continues, there is usually some
hypertrophy of the active muscle.
Lifestyle Change
The adoption of regular physical activity encourages other
advantageous changes of lifestyle, with a resulting reduction
TABLE 1. Possible Biological Mechanisms for
Exercise-Induced Reductions in All-Cause and Cardiac Mortality
Cardiovascular influences
Reduction of resting and exercise heart rate
Reduction of resting and exercise blood pressure
Reduction of myocardial oxygen demand at submaximal levels of physical
activity
Expansion of plasma volume
Increase in myocardial contractility
Increase in peripheral venous tone
Favorable changes in fibrinolytic system
Increased endothelium-dependent vasodilatation
Increased gene expression for nitric oxide synthase
Enhanced parasympathetic tone
Possible increases in coronary blood flow, coronary collateral vessels, and
myocardial capillary density
Metabolic influences
Reduction of obesity
Enhanced glucose tolerance
Improved lipid profile
Lifestyle influences
Decreased likelihood of smoking
Possible reduction of stress
Short-term reduction of appetite
in cardiac risk factors. However, benefits are relatively small.
In the case of cigarette smoking, endurance athletes are
usually nonsmokers, and involvement in endurance activity
can contribute to the process of smoking cessation. Absti-
nence from cigarettes often precedes involvement in physical
activity, both characteristics reflecting a health-conscious
personality.53 For a similar reason, many athletes consume
large quantities of both water-soluble (C) and fat-soluble (E)
vitamins, with potential benefit to the vascular system. The
possible role of exercise as an appetite suppressant remains
controversial.54,55 An acute bout of exercise can lead to a
temporary rise in both blood sugar and blood leptin levels,
with a short-term suppression of appetite54,56 and possibly an
increased thermic effect during subsequent ingestion of food.
Thus if exercise is performed just before a meal, it may be
helpful both in reducing food intake and in facilitating energy
expenditure. In a more long-term perspective, some investi-
gators argue that appetite increases to match the increase in
energy expenditure,54 whereas others maintain that an exer-
cise program does not necessarily enhance food intake.57
Weight loss may be promoted by a prolonged elevated
postexercise oxygen consumption,58 and in 1 recent study of
obese postcoronary patients this effect was large enough to
yield a substantial reduction of body fat without specific
dieting.59
Some forms of physical activity provide relaxation, with
favorable implications for cardiac health;60 indeed, many
people claim that the reason that they exercise is because it
makes them “feel better.” On the other hand, a strong desire
to win a game such as squash may provoke sudden death in
a coronary-prone individual,61 and obsessive efforts to fill an

exercise prescription under difficult circumstances can aug-
ment rather than reduce stress.
Direct Benefits
The direct cardiovascular benefits of regular physical activity
include a slowing of resting heart rate, a reduction of blood
pressure, an increase of peripheral venous tone, an expansion
of plasma volume, and an increase of myocardial contractil-
ity. There may also be an increase of coronary blood flow,
and an increase in the threshold for myocardial fibrillation.
Resting Bradycardia
A decrease in resting heart rate is perhaps the most obvious
manifestation of regular physical activity. Indeed, waking
pulse data provide a useful simple index of the response to
training. Underlying mechanisms include an altered auto-
nomic balance and an increase of stroke volume (below).
There is an increase of parasympathetic nerve activity,
possibly reflecting a resetting of the arterial baroreceptors.62
The intrinsic rate of contraction of the atria is also reduced,
and there may be a reduced drive from peripheral chemore-
ceptors, secondary to a strengthening of the skeletal mus-
cles. 63 Finally, there may be a downregulation of
b-adrenergic receptors in the myocardium.64
Training induces a parallel reduction of heart rate during
submaximal exercise. Practical implications include (1) an
increase in cardiac reserve and thus a boosting of functional
capacity, (2) a decrease in double product at any given rate of
working, thus reducing the likelihood of myocardial ische-
mia, and (3) a lengthening of the diastolic phase of the cardiac
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cycle, facilitating myocardial perfusion.
Reduction of Blood Pressure
Resting blood pressure and blood pressure at any given rate
of exercise are lower after training, this trend being aug-
mented by a strengthening of the skeletal musculature;
however, pressures remain unchanged at a fixed fraction of
maximal oxygen intake. Afterloading of the left ventricle is
reduced, allowing an increase of ejection fraction and stroke
volume. The peak cardiac output is thus augmented, with an
associated gain in functional capacity. Further, at any given
rate of submaximal exercise, the lower systolic pressure
yields a corresponding reduction in double-product and thus
reduces the risk of myocardial ischemia.
Increased Peripheral Venous Tone
Training induces an increased peripheral venous tone.65 This
increases central blood volume and thus ventricular preload-
ing; cardiac stroke volume is increased, and the likelihood of
hypotension after a bout of exercise is reduced. Ischemic
ST-segment depression and ventricular fibrillation can be
precipitated by the sudden fall in blood pressure at the end of
exercise. The increase in venous tone helps to limit this
problem, although the main remedies are a substantial “cool-
down” of light exercise and the avoidance of standing in a hot
shower area immediately after vigorous physical activity.65a
Plasma Volume Expansion
An expansion of plasma volume is an early response to
training, probably mediated by adjustments in the renin/aldo-
sterone system. Ventricular preloading is increased, contrib-
Shephard et al February 23, 1999 967
uting to the increase of cardiac stroke volume in the trained
individual. However, there may be an associated decrease in
the hemoglobin content of unit volume of blood, so that
oxygen transport per liter of cardiac output is unchanged or
even diminished.66
Increased Myocardial Contractility and Stroke Volume
Training induces some increase in myocardial contractility.67
This contributes to the increase in cardiac stroke volume. The
increase of myocardial contractility boosts the oxygen con-
sumption of the myocardium. However, it also reduces the
average ventricular dimensions, reducing wall tension and
thereby facilitating perfusion of the critical endocardial zone
by perforating branches of the coronary artery.
Training may increase cardiac stroke volume by 20% or
more, both at rest and during vigorous exercise. As discussed
above, mechanisms include an increase of preloading (caused
by increased peripheral venous tone and plasma volume
expansion) and a reduction of afterloading (strengthening of
the skeletal muscles and a reduction of systolic pressures). In
addition, there is an increase of myocardial contractility and
(if training is strenuous and prolonged) a ventricular hyper-
trophy. The enlarged heart of the endurance-trained athlete
was once considered a dangerous pathology, but it is now
recognized as a normal and desirable physiological response
to repeated bouts of endurance exercise.68 The increase of
stroke volume leads to a roughly proportional increase in
functional capacity. A given physical task can thus be
performed at a smaller fraction of the individual’s maximal
oxygen intake; the lower heart rate reduces double product
and thus the oxygen consumption of the myocardium, and
any tendency to myocardial ischemia is decreased. Treadmill
training can increase the ventricular fibrillation threshold,
although the mechanism underlying this change remains
unknown.69
Principles of Exercise Prescription
As with pharmacological therapy, exercise requires a pre-
scription, with a consideration of appropriate dosage and
possible side effects. Nevertheless, for most sedentary people,
any physical activity is better than none, and the prognosis is
substantially better for those who begin to exercise than for
those who do not. It may thus be unnecessary and even
counterproductive to insist on a detailed clinical and labora-
tory examination, together with fitness testing before exercise
is begun. Specific guidelines regarding medical screening and
evaluation before initiating a moderate-to-vigorous exercise
training program are provided in detail by the American
Heart Association70,71 and the American College of Sports
Medicine.72 The health of older adults may be quite well
served if they perform a little more exercise than the previous
week, incorporating this activity into their normal daily lives,
for example walking to the store and gardening with hand
tools. Assuming that a person feels no more than pleasantly
tired a few hours after such exercise, then the aim should be
to do a little more in each successive week until the desired
level of fitness is attained.
More specific recommendations concerning the type, in-
tensity, frequency, and duration of exercise are provided
 968 Exercise as Cardiovascular Therapy

TABLE 2. Exercise Prescription for Endurance and corticosteroids A variety of 8 to 10 muscle-resisted activities
Resistance Training should be performed to cover most of the major muscle
Endurance training groups of the body.
Frequency 3–5 d/wk Intensity
Intensity 55%–90% maximum HR or 40%–85% For many years, those prescribing exercise were strongly
maximum V̇O2 or HRR influenced by the views of Karvonen and associates73; limited
Duration 20–60 min studies on university students suggested that aerobic training
Modality was induced at a heart rate of 150 bpm but that a heart rate of
Lower extremity Walking 135 bpm had no training effect. These observations gave rise
to the dogma that the target intensity of effort needed to
Jogging/running
induce an aerobic training response corresponded to 60% to
Stairclimber
70% of the individual’s maximal oxygen intake. More recent
Upper extremity Arm ergometry data from the Cooper Clinic23 have shown that the largest
Combined Rowing reduction in overall mortality occurs on moving from the
Cross-country ski machine lowest to the next lowest quintile of fitness. Thus it is now
Combined arm/leg cycle suggested that (1) sedentary older adults can enhance aerobic
Swimming fitness by exercising at intensities as low as 40% of maximal
Aerobics oxygen intake,8 and (2) some health benefits are realized even
if the intensity of effort is insufficient to augment aerobic
Resistance training
power. It is further argued that attempts to reach the “target
Frequency 2–3 d/wk
zone” on first recruitment lead to discouragement through
Intensity 1–3 sets of 8–15 RM for each muscle group discomfort, injury, or lack of success; however, negative
Modality reactions are much less likely if a program is initiated at a low
Lower extremity Legs extensions, curls, presses intensity. The current initial recommendation is thus for a
Adductors/abductors moderate intensity of effort such as brisk walking.9
Upper extremity Biceps curls In terms of resistance training, the intensity of effort can be
Triceps extensions prescribed relative to the 1-repetition (1-RM) maximal vol-
untary force. Individual contractions should be made at 50%,
Bench/overhead presses
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later progressing to 60% of the 1-RM value. Initial intensities

Lateral pulldowns/raises
Benchovers/seated rowing
Modalities listed here are not all-inclusive. Maximum heart rate (HR)
indicates 220 minus age or peak HR on exercise test; V̇O2, measured oxygen
intake; RM, maximum number of times a load can lifted before fatigue.
HRR5(Peak2Resting HR)3Percent1Resting HR.
below, and a summary of the exercise prescription is provided
in Table 2.
Type
The prescription should include both aerobic and resistance
exercise. Initially, the preferred mode of aerobic exercise is
fast walking, progressing to jogging. Several reasons govern
this choice: (1) the energy cost of walking varies little from
one person to another, so that the desired dose of exercise can
be specified relatively precisely in terms of a distance to be
covered within a specified time, (2) the activity is familiar to
everyone and can be built into the normal day, and (3) there
is no need for special equipment, clothing, or experience. As
physical condition improves, and the individual becomes
familiar with the sensations associated with aerobic training,
other large muscle activities—for example, swimming, cy-
cling, rowing, cross-country-skiing, and aerobic dance— can
be introduced to provide variety. The energy costs for most of
these activities show a substantial interindividual variation,
and the intensity of effort must be monitored in terms of heart
rate (complicated by the administration of b-blocking agents)
or ratings of perceived exertion.
Resistance exercise is necessary to counter the muscle
atrophy induced by aging, bed rest, and administration of
as low as 30% 1-RM can be used in more frail or older
individuals. One-three sets of 8 to 15 repetitions should be
undertaken to exercise the front and back of each major
muscle group. Thus attention should be directed to movement
about each of the major joints, including hip flexion and
extension, knee flexion and extension, ankle dorsi-flexion
and plantar flexion, shoulder flexion and extension, and
elbow flexion and extension. In the absence of resistance
equipment, exercises for the same range of joints can be
improvised using inner tubes and elastic bands, cuff and hand
weights, free weights and dumb-bells, and wall pulleys.
Individual contractions should not be held for more than 5 to
6 seconds to avoid a large increase in cardiac afterloading.
Such training should be performed at least twice per week.8
Frequency
Aerobic exercise should be performed on most days of the
week. In the early days of cardiac rehabilitation, as many as
3 sessions per week may be undertaken at a cardiac rehabil-
itation center under close medical supervision. However, the
time involved in travel to and from such a center makes this
an impractical long-term arrangement for people living in
large cities. The supervised sessions can thus be tapered, first
to once per week, and then to once per month, with the
completion of an “exercise log” to encourage unsupervised
but prescribed exercise to a total of at least 5 sessions per
week. Fitness gains can probably be maintained by complet-
ing at least 3 sessions per week. It may be possible to build
much of the required activity into the daily routine—for
example, a walk to and from a commuter rail station; in any

event, such regular exercise is not easily forgotten or post-
poned. Muscle hypertrophy has a relatively slow acute time
course, and the current recommendation is that muscles are
best strengthened by at least 2 sessions of resistance exercise
per week.
Duration
Within limits, there is an inverse relation between the
intensity of aerobic effort and the required minimum duration
of exercise sessions. On the basis of the currently recom-
mended intensity of exercise, a minimum of 30 minutes of
exercise per day is required. Sedentary people initially find
difficulty in sustaining even moderate activity for 30 minutes,
and recent recommendations suggest that an almost equal
benefit can be obtained if the activity session is split into 2 or
even 3 parts.9
Total Energy Expenditure
As discussed earlier, many of the benefits of exercise depend
in part on the total volume of energy expended (dose). When
prescribing everyday activities, it is thus helpful to know their
approximate energy cost. Such information allows an assess-
ment of both the intensity of effort and the cumulative energy
expenditure. The energy cost of most activities depends on
both the body mass of the individual and the pace of the
activity. The issue of weight can be circumvented by using
MET units. However, the pace must be specified even for
something as simple as a walking prescription—for example,
a recommended distance to be covered in a specified time.
Fine tuning of the prescription, in the face of psychosocial
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stressors or adverse environmental conditions, can then be
based on such markers as perceptions of exertion, perceptions
of ventilation, or (in those with a normal heart rate response
to exercise) the immediate postexercise heart rate.
Exercise in Patients With Cardiovascular Disease
Much data have been accumulated regarding exercise training
in patients with cardiovascular disease, specifically those
with coronary artery disease, those with heart failure caused
by left ventricular systolic dysfunction, and those after
coronary artery bypass surgery.74 Very limited data are
available regarding patients with valvular disease. Patients
with cardiovascular disease should undergo medical evalua-
tion before initiating a regular exercise program of moderate
to vigorous intensity. An exercise tolerance test should be
performed to establish a safe and effective exercise intensity,
whereby 40% to 70% of heart rate reserve (peak exercise
heart rate minus resting heart rate) is added to resting heart
rate (Table 2). This yields the training heart rate range for
moderate intensity exercise. Further details regarding the
exercise prescription and monitoring in these patients is
described in detail elsewhere.70,75
Encouraging Compliance
Motivation remains a major challenge for cardiovascular
preventive programs. Often, initial recruitment from a seden-
tary but apparently healthy population is no greater than 30%
to 40%. As many as a half of those recruited to a specific
program were previously exercising elsewhere. Moreover, as
many as a half of those who are recruited are no longer
compliant 6 months later. The usual complaint is a “lack of
Shephard et al February 23, 1999 969
free time” or a “lack of equipment and facilities.” At first
inspection, these complaints may seem unreasonable, but
nevertheless the patient has judged that the perceived oppor-
tunity costs of the proposed exercise are too great relative to
the potential rewards.
Much motivational research is at present concentrated on
the “stages of change” hypothesis.76 Concerted and continued
effort is needed to evaluate and move each patient toward the
adoption of regular exercise. Health care providers may foster
this progression using strategies, such as: (1) an increase in
the immediacy of rewards by emphasizing current gains in
the quality of life rather than focusing on the postponement of
chronic disease and death (which may be many years distant)
and (2) a decrease in the opportunity costs of physical activity
by emphasizing everyday pursuits, such as rapid walking to
the store or the station, things that require no medical
examination, no preliminary travel, no special clothing, no
special equipment, and no expensive club membership.
Risks of Exercise
There are now clear guidelines as to the need for preliminary
clinical examination, contraindications to exercising, and
indications to halt an exercise or test session.71,72 The risk of
an adverse coronary event or death during exercise is low.
Each year '0.75 and 0.13 per 100 000 young male and
female athletes77 and 6 per 100 000 middle-aged men die
during vigorous exertion.78 Studies in Finnish men suggest
the incidence for all types of exercise is 1 per 11 million hours
at age 20 to 39, 1 per 1.3 million at age 40 to 49, and 1 per
900 000 at age 60 to 69; however, episodes are extremely rare
in women at all ages.78a Among patients in cardiac rehabili-
tation programs, who are carefully screened and supervised,
the incidence of myocardial infarction has been reported to be
1 per 294 000 person-hours, and the incidence of death was 1
per 784 000 person-hours.79 There is also evidence that heavy
exertion may trigger acute myocardial infarction. Several
studies79a,80,81 have found that the relative risk of myocardial
infarction within 1 hour after strenuous physical exertion was
2 to 6 times greater than that of patients who were sedentary
or less active during that hour. However, the risk was
inversely related to the amount of leisure time physical
activity performed by the subjects. Thus the more active the
individual, the lower the risk for development of acute
myocardial infarction during strenuous exertion.
There is some evidence that in healthy persons, very
prolonged exercise, such as participation in a triathlon, can
cause myocardial fatigue with a temporary depression of
myocardial function. However, complete recovery appears to
occur over a few days, with no evidence of permanent
harm.82,83 Questions have been raised about possible but
detrimental effects of exercise on left ventricular remodeling
and systolic function, particularly among those with left
ventricular dysfunction early after anterior myocardial infarc-
tion.84 However, several randomized controlled trials of
moderate to high intensity exercise training patients after
large myocardial infarction have not demonstrated adverse
effects on regional wall motion, left ventricular systolic
function, or left ventricular chamber dimensions after several
months of exercise.85,86
 970 Exercise as Cardiovascular Therapy
Despite concerns that excessive exercise may precipitate
muscle injury and sudden death, the main risk for the
sedentary person, and in particular for those with established
cardiac disease, is that the volume of activity undertaken will
be too small. Both in health and in disease, the overall
prognosis is better for the exerciser than for the sedentary
person.
Avenues of Future Research
The prediction of future trends is usually hazardous, and often
the authors of such predictions are quickly proven to be
wrong. Nevertheless, we may suggest several areas that seem
profitable topics for further investigation.
Sex Differences
How far are recently alleged sex differences in the nature of
cardiac disease and its treatment a real phenomenon? If real,
is the explanation a biological influence such as a difference
in hormonal milieu, or is there a sociocultural explanation
(for instance, differences in habitual patterns of physical
activity, demands of domestic life, and willingness to accept
chronic ill-health)?
Appropriate Dose of Exercise
Can a meta-analysis be undertaken to put together ineffective
individual attempts at determining an appropriate dose of
physical activity in men and women of various ages and in
various initial states of health? In particular, is there a
minimum threshold intensity and volume of activity, or is
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there some benefit with even a minimal increase in energy
expenditure?
Adjuvants to Exercise
How does a given dose of exercise interact with various
adjuvant treatments such as a restriction of total energy intake
or administration of supplements of vitamins C and E? Can
excessive exercise initiate endothelial activation, and if so,
how does this impact on the risk of cardiovascular disease?
Quality of Life Issues
There is a need to compare the effectiveness of exercise
relative to alternative treatments, such as surgery or pharma-
cotherapy, in terms not only of costs, but also the impact on
the quality-adjusted life expectancy of the individual. Such
analyses will likely stimulate research on the targeting of
exercise interventions to those who will benefit most from a
given type of physical activity, with an identification of those
who will react negatively to exercise (for example, identify-
ing the incipient cardiac catastrophe).
Motivation and Lifestyle Activities
Motivation to an adequate level of physical activity will
remain a major challenge to researchers in the context of
cardiovascular prevention. There will be a growing interest in
evaluating alternative approaches to treatment. Physicians
may be asked to move from outpatient clinics to exercise
facilities, where their advice may be more effective. Attention
will also focus on the negative aspects of the medicalization
of moderate physical activity, on the opportunity costs of
traveling to specialized facilities, and on the possibility of
meeting the energy requirements of good health by incorpo-
rating physical activity into normal daily life.
Conclusions
A recent editorial87 concluded that a physically active life-
style may be public health’s best buy. There is an urgent need
to translate this assessment into practical implementation that
will increase the physical activity habits of our patients—
both those who are sedentary but ostensibly healthy, and
those who have already developed clinical manifestations of
cardiac disease.
Acknowledgments
Dr Shephard’s studies are supported in part by grants from the
Defense and Civil Institute of Environmental Medicine, Toronto, and
the Toronto Rehabilitation Center.
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KEY WORDS: fitness n ischemic heart disease n physical activity
n prevention n rehabilitation n risk factors n training