Evidence of the Role of Physical Activity and Cardiorespiratory
QUEST, 1995,47,3 11-319
O 1995 American Academy of Kinesiology and Physical Education
Evidence of the Role of Physical
Activity and Cardiorespiratory
Fitness in the Prevention
of Coronary Heart Disease
Arthur S. Leon and Jane Norstrom
Epidemiologic evidence is presented on the now well-accepted contributions of
physical inactivity and reduced cardiorespiratoryfitness to risk of coronary heart
disease (CHI)), the principal cause of death and disability in the United States
and other Western industrializednations. The types and dose of physical activity
to reduce risk of CHI) and plausible biologic mechanisms for the partial protective effect are also reviewed.
Despite a progressive decline in the death rate from coronary heart disease
(CHD) since 1968, CHD remains the leading cause of death in the United States
and is a major contributorto disability, lost productivity, and medical costs (American
Heart Association, 1993). The underlying basis of CHD is atherosclerosis involving
the intimal linings of major coronary arteries. The pathogenesis of coronary atherosclerosis involves dysfunction and injury to endothelial cells; lipid (primarily low
density lipoprotein or LDL) insudation, alterations, and deposition; macrophage and
smooth muscle cell infiltration; fibrosis; and calcium deposition (Leon, 1995). This
disease process begins in childhood and progresses in severity over decades. The
resulting raised atherosclerotic plaques protrude into the artery lumen, progressively
reducing coronary blood flow. Rheologic damage to the plaques and endothelium
result in platelet adherence and aggregation, which in the presence of excess plasma
fibrinogen, reduced fibrinologic activity, and other hemostatic dysfunctions can lead
to thrombotic occlusion of an involved coronary artery. The resulting myocardial
ischemia can induce a fatal ventricular arrhythmia or cause myocardial necrosis
(i.e., myocardial infarction or heart attack).
As is true with most chronic diseases processes, CHD has a multifactorial
etiology (Leon, 1987, 1995; Pooling Project Research Group, 1978; Smith & Leon,
1992). Risk factors include elevated levels of blood total and LDL cholesterol,
reduced levels of high density lipoprotein (HDL) cholesterol, elevated levels of
Arthur S. Leon is with The Laboratory of Physiological Hygiene and Exercise Science,
School of Kinesiology & Leisure Studies at the University of Minnesota, 112 Cooke Hall,
1900 University Ave. SE, Minneapolis, MN 55455. Jane Norstrom is with Health Education
Services, Park Nicollet Medical Foundation, 5000 West 39th Street, Minneapolis, MN 55416.
LEON AND NORSTROM
systolic and diastolic blood pressure, diabetes mellitus, and obesity (particularly the
phenotype with a central or abdominal predominance of fat) (Bjorntorp, 1991). The
severity of atherosclerosis and risk of CHD progresses with age at a faster rate in
men than women until after menopause; however, by age 65 years women have a
higher rate of CHD than men (Becker & Corrao, 1992).
Low levels of physical activity (PA) and a reduction in cardiorespiratory
fitness or aerobic capacity, associated with the modem mode of living, are now
generally recognized as other important contributing factors to the etiology of CHD
and the emergence of CHD as a major public health problem. The evidence for this
statement is summarized below.
Physical inactivity is a prevalent risk factor in the United States. For example,
a recent survey by the Centers for Disease Control and Prevention revealed that
60% of American adults perform little or no recreational PA (Siegel, Brackbill, &
Frazier, 1991). The evidence supporting the contribution of PA and fitness to risk of
CHD, as well as premature death from all causes, is based primarily on observational
epidemiological studies, predominantly involving middle-aged or older men. There
is a paucity of research on this topic in women, and the results of existing studies
are mixed. Additional supporting evidence for the contribution of physical inactivity
to CHD are provided by postmortem studies; pooled data from secondary CHD
prevention trials; and experimental evidence from short-term animal and human
exercise training studies, which have identified possible protective mechanisms
associated with exercise.
Extensive reviews and critiques have been published of the more than 100
observational epidemiological studies appearing in the literature since the 1950s
(Berlin & Colditz, 1990; Leaf, 1991; Leon & Blackburn, 1977; Powell, Thompson,
Caspersen, & Kendrick, 1987). The initial pioneering epidemiologic studies published in the 1950s and 1960s primarily consisted of retrospective comparisons of
occupational PA levels based on job descriptions with CHD events determined from
death certificates or medical records (Brunner & Manelis, 1960; Kahn, 1963; Morris,
Heady, Raffle, Roberts, & Parks, 1953; Taylor et al., 1962; Zukel et al., 1959).
Although these first-generation epidemiologic studies contained many methodological shortcomings, their demonstration of an apparent inverse association between
occupational PA and risk of CHD served as the impetus for more sophisticated
investigations, an example of which was a landmark 22-year cohort study involving
San Francisco Bay longshoremen by Paffenbarger and colleagues (Paffenbarger,
Gima, Laughlin, Mary, & Black, 1971; Paffenbarger & Hale, 1975 ). In this study,
a threefold increase in death from CHD was associated with low energy expenditure
on the job as compared to high energy workout, which persisted after statistical
adjustment for age and several other risk factors for CHD in addition to reclassification for job changes.
Most recent epidemiologic studies have been prospective and have emphasized
leisure time PA, since few occupations require significant amounts of PA any longer.
Of particular interest are major large-scale longitudinal studies, using validated
measures of leisure time PA and CHD endpoints and statistical adjustments for many
possible confounding variables. These latest generation of prospective epidemiologic
studies include a 10-year follow-up of up to 18,000British male executive clerks and
civil service employees (Morris et al., 1973; Morris, Clayton, Everitt, Semmence, &
Burgess, 1990), a more than 20 year follow-up of about 17,000 male college alumni
(Paffenbarger, Hyde, Wing, & Hsieh, 1986; Paffenbarger et al., 1993; Paffenbarger,
Wing, & Hyde, 1978; Paffenbarger, Wing, & Steinmetz, 1984) a 7- and 10.5-year
PREVENTION OF HEART DISEASE
follow-up of middle-aged men at high risk for CHD, participating in the Multiple
Risk Factor Intervention Trial (MRFIT) (Leon & Connett, 1991; Leon, Connett,
Jacobs, & Rauramaa, 1987), and a 9.5-year follow-up of almost 8,000 middle-aged
men participating in the British Regional Heart Study (Sharper & Wannamethee,
The results of all of these studies unanimously support the postulated inverse
relationship of PA with risk of CHD, as well as with all-cause mortality. In addition,
a limited number of studies in the United States and Europe correlated cardiorespiratory fitness, or so-called aerobic power determined by exercise testing, with risk of
CHD (Blair et al., 1989; Bruce, Hossack, DeRouen, & Hofer, 1983; Ekeland et al.,
1988; Eeckssen, 1986; Peters, Cady, Bischoff, Bernstein, & Pike, 1983; Sandvik
et al., 1993; Slattery & Jacobs, 1988; Sobolaski et al., 1987; Wilhelmsen et al.,
1981). All of these studies observed a strong inverse, generally graded association
between fitness and risk of CHD. This includes an 8-year prospective study by Blair
et al. (1989) that involved over 10,000 initially healthy men and over 3,000 women,
who received maximal treadmill exercise tests at The Cooper Institute for Aerobics
Research in Dallas.
Pooled data and meta-analysis of the epidemiologic studies of "better" methodological quality have noted a consistent inverse association of both PA and of
aerobic power with risk of CHD. The risk of death from CHD increased about
twofold in those individuals who were physically inactive as compared to more
active individuals (Berlin & Colditz, 1990; Powell et al., 1987) and increased over
fivefold in the least fit as compared to the most fit (Blair, 1993). Adjustment for
other risk factors only slightly weakened these associations, suggesting independent
relationships. The largest reduction in relative risk of CHD appears to occur with
going from a sedentary to moderately-active lifestyle and from below average to
average fitness for one's age. In terms of energy expenditure the mass of observational data suggests that physical exertion of even moderate intensity (<6 METs),
if performed on the average for 30 minutes or more a day at a total energy cost of
1,050 to 2,000 kcal a week for an average-sized person, is associated with a reduced
risk of death from CHD (Haskell, 1985, 1994; Leon et al., 1987; Paffenbarger,
Wing, & Hyde, 1978). This can include short bouts of lifestyle-type of PA, such
as walking for transportation, stair climbing, and working around the house and
yard. Additional protective effects would be expected to accrue from regular higher
intensity PA of sufficient volume to improve maximal oxygen uptake, such as
recommended by American College of Sports Medicine guidelines (1991), based
on available epidemiologic studies and experimental data from training studies.
Additional supporting evidence for the apparent inverse relationship of PA to
risk of CHD comes from a limited number of major postmortem studies previously
reviewed (Leon, 1983; Leon & Blackburn, 1977). In these studies, the extent of
coronary atherosclerosis and of myocardial damage observed in men at autopsy was
correlated with antemortem, generally work-related PA habits. The following general
conclusions can be derived from these postmortem studies:
1. Death from CHD is twice as common and at an earlier age in men performing
light occupational tasks as compared to those performing heavy work.
2. The prevalence of severe coronary atherosclerosis is either unrelated to PA
or less severe in physically active men.
3. Physically active men have significantly larger coronary artery luminal areas
and less frequent complete or nearly complete coronary occlusions than less
LEON AND NORSTROM
4. Physically active workers generally have less evidence of ischemic myocardial
damage than less active workers.
Definitive experimental proof of the PA-CHD hypothesis by a large-scale,
randomized, controlled, primary prevention trial has been judged to be not feasible
due to the large sample size required and the problems of crossovers, adherence
and control of other risk factors, and prohibitive costs (Leon & Blackbum, 1977).
As an alternative, meta-analysis of pooled data from over 20 secondary prevention
trials in the United States and Europe, which included an exercise training component
or exercise advice, indicate a reduction of 20 to 25% in 1- to 3-year rates of mortality
from cardiovascular disease and from all causes in the treatment group, as compared
to control patients (O'Connor et al., 1989). However, the rate for nonfatal CHD
events was similar for the intervention and control patients, and the design of these
studies does not allow for the assessment of the independent contribution of the
exercise component. A recent encouraging finding is the demonstration of the
independent contribution of 1,600 kcal per week or more of PA in stopping the
progression or even partially reversing the severity of coronary atherosclerosis
demonstrated by serial angiograms in patients with known CHD (Hambrecht et al.,
Multiple plausible biological mechanisms have been identified from animal
research; small scale, short-term human experimental studies; and cross-sectional
comparisons of physically active versus sedentary people to help explain how PA
and cardiorespiratory fitness reduce the risk of initial CHD events, and improve
survival after a myocardial infarction. These mechanisms consist of anatomic, physiologic, and metabolic adaptations to PA and depend on the type, intensity, frequency,
duration, and length of the participation. These adaptations have recently been
extensively reviewed, along with the supporting evidence (Blair, Kohl, & Gordon,
1992; Leon, 1990, 1991), and are as follows:
1. Reduction in severity of coronary atherosclerosis both directly and through
favorable effects on other major coronary risk factors (i.e., loss of excess
weightbody fat, reduction in blood pressure, increase in HDL cholesterol
levels, improved insulin sensitivity, and increased glucose tolerance).
2. A reduction in myocardial oxygen demands at rest and during submaximal
physical effort by a decrease in heart rate and systolic blood pressure.
3. An increased myocardial oxygen supply through lengthening of diastole by
heart rate slowing, as well as perhaps by increasing vascularity.
4. A reduction in risk of coronary thrombosis by decreased platelet adhesiveness
and aggregability and promotion of fibrinolysis.
5. Reduced myocardial vulnerability to lethal ventricular arrhythmias in the
presence of advanced coronary atherosclerosis, even during heavy physical
exertion (Mittleman et al., 1993; Willich et al., 1993).
Some of these benefits may be due to the overlapping of effects of acute bouts of
exercise and others require chronic physical activity or exercise training.
The available epidemiologicand experimentaldata indicate that regular moderate intensity PA acts primarily to reduce susceptibility of people with existing
coronary atherosclerosis to fatal CHD by reducing vulnerability to ventricular ar-
PREVENTION OF HEART DISEASE
rhythmias and perhaps coronary thrombosis. A formal endurance exercise program,
sufficient to enhance cardiorespiratory endurance appears to be required to provide
the additional protective effects elucidated above. The ideal program, in order to
provide the full gamut of protective effects of PA against CHD, would be a combination of lifestyle or recreational PA on a nearly daily basis plus a formal endurance
exercise program several times a week to increase aerobic power.
Based on this impressive body of scientific evidence summarized above, many
expert groups worldwide have embraced the role of PA and fitness promotion as
important public health and medical practice objectives to reduce not only the burden
of CHD but also the occurrence of a number of other common medical conditions
reviewed by others in this issue of Quest. These organizations include the American
Heart Association (Fletcher et al., 1992), the U.S. Department of Health and Human
Services (1991) in their Healthy People 2000 health-promotionJdisease prevention
initiative, the U.S. Centers for Disease Control and Prevention and American College
of Sports Medicine (Pate et al., 1995), the U.S. Preventive Task Force (Harris,
Caspersen, DeFreise, & Estes, 1989), and the World Health Organization (Intemational Society and Federation of Cardiology, 1992).
Summary and Conclusions
Strong, consistent epidemiological evidence exists of an independent association between (a) low levels of both habitual PA and cardiorespiratory endurance
and (b) risk of fatal and CHD clinical events in middle-aged or older men with
limited supporting evidence also in women. Inactivity at work and during leisure
time essentially doubles one's risk of a fatal and nonfatal myocardial infarction,
independent of other risk factors. Low aerobic capacity has an even greater impact
on risk of CHD events than a sedentary lifestyle. Additional research has identified
multiple anatomic, physiologic, and metabolic adaptations to PA that provide plausible biologic mechanisms involved for the apparent partial protective effect of PA
and fitness against CHD.
The dose-response relationship between PA and risk of CHD and the various
protective mechanisms are also becoming better defined. Daily moderate intensity
lifestyle, recreational physical activities, and formal aerobic exercise programs contribute to protective benefits. To maximize protection against CHD, attention must
be paid to all major risk factors, along with performance of 30 minutes or more of
almost daily moderate routine and recreational PA plus a formal aerobic exercise
program, at least several times per week to promote cardiorespiratory fitness, for a
total weekly energy expenditure of 1,050 to 2,000 kcal for an average sized person.
The Activity Pyramid in Figure 1 has been developed by one of us (Norstrom)
as a model to graphically display this activity message for the purpose of public
education. The Activity Pyramid presents an ideal, stepwise, daily and weekly
activity scheme for promoting PA for the purpose of prevention of CHD and other
prevalent health problems related to physical inactivity. For an inactive individual,
the first step would be to increase nonstructured "everyday" activities at the base
of the Pyramid. The next step would be to incorporate more active recreational
pursuits and exercise into the weekly routine at least several times per week (middle
areas of the Pyramid). This step would provide the stimulus for improving one's
cardiorespiratory fitness. Ideally, this would include resistance exercises to improve
strength, as well as flexibility-promoting activities. For those who are presently
LEON AND NORSTROM
Figure 1 - The Activity Pyramid, a stepwise scheme for promoting regular physical
activity. Copyright 1995 by Park Nicollet Medical Foundation. Reprinted with permission.
only seasonably or sporadically active, the goal would be to become more consistently active by incorporating year-round activities, represented in the middle areas
of the Activity Pyramid. For a person already leading an active life, the goal would
be to emphasize a life-long maintenance program, including periodically exploring
new activities. The overall emphasis can be summed up as progressively adding
more physical activities and sitting less (peak of the Pyramid).
American College of Sports Medicine. (1991). Guidelinesfor exercise testing andprescription
(4th ed., pp. 93-109). Philadelphia: Lea and Febiger.
American Heart Association. (1993). Heart and stroke facts. Dallas: Author.
Becker, R.C., & Corrao, J.M. (1992). Coronary heart disease in women: Medical science
coming of age. Medicine, Exercise, Nutrition and Health, 1, 191-200.
Berlin, J.A., & Colditz, G.A. (1990). A meta-analysis of PA in the prevention of CHD.
American Journal of Epidemiology, 132, 612-628.
Bjorntorp, P. (1991). Metabolic implications of body fat distribution. Diabetic Care, 14,
Blair, S.N. (1993). C.H. McCloy Research Lecture: Physical activity, physical fitness, and
health. Research Quarterly of Exercise and Sports, 64, 365-376.
Blair, S.N., Kohl, H.W., & Gordon, N.F. (1992). How much physical activity is good for
health? Annual Review of Public Health, 13, 99-126.
PREVENTION OF HEART DISEASE
Blair, S.N., Kohl, H.W., ID, Paffenbarger, R.S., Jr., Clark, D.G., Cooper, K.H., & Gibbons,
L. (1989). Physical fitness and all-cause mortality: A prospective study of healthy men
and women. Journal of the American Medical Association, 262, 2395-2401.
Bruce, R.A., Hossack, K., DeRouen, T.A., & Hofer, V. (1983). Enhanced risk assessment
for primary coronary heart disease events by maximal exercise testing: 10years experience of Seattle Heart Watch. Journal of the American College of Cardiology, 2, 656673.
Brunner, D., & Manelis, G. (1960). Myocardial infarction among members of communal
settlements in Israel. Lancet, 2, 1049-1050.
Ekeland, L.G., Haskell, W.L., Johnson J.L., Whaley, P.S., Criqui, M.H., & Sheps, D.S.
(1988). Physical fitness as a predictor of cardiovascular mortality in asymptomatic
North American men: The Lipid Research Clinics Mortality Follow-Up Study. New
England Journal of Medicine, 319, 1379-1384.
Erickssen, J. (1986). Physical fitness and coronary heart disease morbidity and mortality: A
prospective study in apparently middle-aged men. Acta Medica Scandinavica, Supplement, 711, 189-192.
Fletcher, G.F., Blair, S.N., Blumenthal, J., Caspersen, C., Chaitman, B., Epstein, S., Falls,
H., Froelicher, E.S.S., Froelicher, V.F., & Pina, I.L. (1992). Benefits and recommendations for physical activity programs for all Americans: A statement for health professionals by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical
Epidemiology, American Heart Association. Circulation, 86, 340-344.
Hambrecht, R., Niebauer, J., Marburger, C., Gunze, M., Kalberger, B., Havor, K., Schlief,
G., Kubler, W., & Schuler, G. (1993). Various intensities of leisure time physical
activity in patients with coronary artery disease: Effect of cardiorespiratory fimess on
progression of coronary atherosclerotic lesions in patients with known coronary heart
disease. Journal of the American College of Cardiology, 22, 468-477.
Harris, S.S., Caspersen,C.J., DeFreise, G.H., & Estes, H. Jr. (1989). Physical activity counseling for healthy adults as a primary prevention intervention in the clinical setting:
Report of the United States Preventive Task Force. Journal of the American Medical
Association, 261, 590-598.
Haskell, W.L. (1985). Physical activity and health: Need to define the required stimulus.
American Journal of Cardiology, 5(Suppl.), 4D-9D.
Haskell, W.L. (1994). Health consequences of physical activity: Understanding and challenges
regarding dose-response. Medicine and Science in Sports and Exercise, 26, 694-660.
International Society and Federation of Cardiology. (1992). World Health Organization
position statement:Physical inactivity: A riskfactor for coronary heart disease. Geneva,
Switzerland: World Health Organization.
Kahn, H.A. (1963). The relationship of reported coronary heart disease mortality to physical
activity of work. American Journal of Public Health, 53, 1058-1067.
Leaf, D.A. (1991). Exercise and nutrition in preventive cardiology (pp. 145-177). Dubuque,
IA: Brown and Benchmark.
Leon, A.S. (1983). Epidemiologic aspects of physical activity and coronary heart disease.
Finnish Journal of Exercise Medicine, 2, 10-27.
Leon, A.S. (1987). Age and other predictors of coronary heart disease. Medicine Science in
Sports and Exercise, 19, 159-167.
Leon, A.S. (1990). Position paper of the American Association of Cardiopulmonary Rehabilitation: Scientific evidence of cardiac rehabilitation services with emphasis on patients
following myocardial infarction. Section 1: Exercise conditions component. Journal
of Cardiopulmonary Rehabilitation, 10, 79-87.
Leon, A.S. (1991). Physical activity and risk of ischemic heart disease-an update 1990. In
P. Oja & R. Telema (Eds.), Sport for all (pp. 251-264). Amsterdam: Elsevier.
LEON AND NORSTROM
Leon, A.S. (1995). Scientific rationale for preventive practices in atherosclerotic and hypertensive cardiovascular disease. In M.L. Pollock & D.H. Schmidt (Eds.), Heart disease
and rehabilitation (3rd ed., pp. 115-146). Champaign, IL: Human Kinetics.
Leon, AS., & Blackbum, H. (1977). The relationship of physical activity to coronary heart
disease and life expectancy. Annals of the New York Academy of Science, 301, 561578.
Leon, A.S., & Connett, J. (1991). Physical activity and 10.5 year mortality in the Multiple
Risk Factor Intervention Trial. International Journal of Epidemiology, 20, 690-697.
Leon, A.S., Connett, J., Jacobs, D.R., Jr., & Raurarnaa, R. (1987). Leisure-time physical
activity levels and risk from coronary heart disease and death: The Multiple Risk
Factor Intervention Trial. Journal of the American Medical Association, 258, 23882395.
Mittleman, M.A., Maclure, M., Tofler, G.H., Shenvood, J.B., Goldberg, R.J., & Muller, J.E.
(1993). Triggering of acute myocardial infarction by heavy physical exertion: Protection
by regular exertion. New England Journal of Medicine, 329, 1677-1683.
Morris, J.N., Chave, S.P.W., Adam, C., Sirey, C., Epstein, L., & Sheehan, D.J. (1973).
Vigorous exercise in leisure time and incidence of coronary heart disease. Lancet, 1,
Morris, J.N., Clayton, D.G., Everitt, M., Semmence, A.A., & Burgess, E.H. (1990), Exercise
in leisure time: Coronary attack and death rates. British Heart Journal, 63, 325- 334.
Moms, J.N., Heady, A., Raffle, P.A.B., Roberts, C.G., & Parks, J.W. (1953). Coronary heart
disease and physical activity at work. Lancet, 265, 1053-1057, 1111-1120.
O'Connor, G.T., Buring, S.E., Yusaf, S., Goldhaber, S., Olmstead, E.F., Paffenbarger, R.S.,
Jr., & Hennekins, C.H. (1989). An overview of randomized trials with exercise after
myocardial infarction. Circulation, 80, 234-244.
Paffenbarger,R.S., Jr., Gima, A.S., Laughlin, M.E., Mary, E., & Black, R.A. (1971). Characteristics of long-shoremen related to coronary heart disease and stroke. American Journal
of Public Health, 61, 1362-1370.
Paffenbarger, R.S., Jr., & Hale, W.E. (1975). Work activity and coronary heart mortality.
New England Journal of Medicine, 292, 5 15-550.
Paffenbarger, R.S., Jr., Hyde, R.T., Wing, A.L., & Hsieh, C-C. (1986). Physical activity, allcause mortality and longevity of college alumni. New England Journal of Medicine,
Paffenbarger, R.S., Jr., Hyde, R.T., Wing, A.L., Lee, I-M., Jung, D.L., & Kampert, J.B.
(1993). The association of changes in PA level and other lifestyle characteristics with
mortality among men. New England Journal of Medicine, 328, 538-545.
Paffenbarger, R.S., Jr., Wing, A.L., & Hyde, R.T. (1978). PA as an index of heart attack
risk in college alumni. American Journal of Epidemiology, 108, 161-175.
Paffenbarger, R.S., Jr., Wing, A.L., & Steinmetz, C.H. (1984). A natural history of athleticism
and cardiovascular health. Journal of American Medical Association, 252, 491-495.
Pate, R.R., Pratt, M., Blair, S.N., Haskell, W.L., Macera, A.A., Bouchard, C., Buchner, D.,
Ettinger, W., Health, G.W., King, A.C., Kriska, A., Leon, A.S., Marcus, B.H., Moms,
J., Paffenbarger, R.S., Jr., Patrick, K., Pollock, M.L., Rippe, J.M., Sallis, J., & Wilmore,
J.H. (1995). Physical activity and public health: A recommendation from the Centers
for Disease Control and Prevention and the American College of Sports Medicine.
Journal of the American Medical Association, 273, 402-407.
Peters, R.K., Cady, L.D., Jr., Bischoff, D.P., Bemstein, L., & Pike, M.C. (1983). Physical
fitness and subsequent myocardial infarction in healthy workers. Journal of the American Medical Association, 249, 3052-3056.
PREVENTION OF HEART DISEASE
Pooling Project Research Group. (1978). Relationship of blood pressure, serum cholesterol,
smoking habit, relative weight, and ECG abnormalities to incidence of major coronw
events: Final report of the Pooling Project. Journal of Chronic Diseases, 31,201-306.
Powell, K.E., Thompson, P.A., Caspersen, C.J., & Kenrick, J.S. (1987). Physical activity
and incidence of coronary heart disease. Annual Review of Public Health, 8, 253-287.
Sandvik, L., Erikssen, J., Thaulow, E., Erickssen, G., Mundal, R., & Rodahl, K. (1993).
Physical fitness as a predictor of mortality among healthy, middle-aged Norwegian
men. New England Journal of Medicine, 328, 533-537.
Sharper, A.G., & Wannamethee, G. (1991). PA and ischaemic heart disease in middle-aged
British men. British Heart Journal, 66, 384-394.
Siegel, P.Z., Brackbill, R.M., & Frazier, E.L. (1991). Behavioral risk factor surveillance,
1986-1990. Morbidity and Mortality Weekly Report, 40 (No. 55-4), 1-23.
Slattery, M.L., & Jacobs, D.R., Jr. (1988). Physical fitness and cardiovascular mortality: The
U.S. Railroad Study. American Journal of Epidemiology, 127, 571-580.
Smith, T.W., & Leon, A. (1992). Coronary heart disease: A behavioral prospective. Champaign, IL: Research Press.
Sobolaski, J., Komitzer, M., DeBacker, G., Dramaix, M., Abrarnowicz, M., Degre, S., Denolin,
H. (1987). Protection against ischemic heart disease in the Belgium Physical Fitness
Study: Physical fitness rather than physical activity.American Journal of Epidemiology,
Taylor, H.L., Klepetar, E., Keys, A., Parlin, W., Blackbum, H., & Puchner, T. (1962).
Death rates among physically active and sedentary employees of the railroad industry.
American Journal of Public Health, 52, 1697-1707.
U.S. Department of Health and Human Services. (1991). Healthy people 2000: National
health promotion and disease prevention objectives (DHHS Publication No. 91-50212).
Washington, DC: Public Health Service.
Wilhelmsen, L., Bjure, J., Ekstrom-Jodal, B., Aurell, M., Grimby, G., Svardsudd, K., Tibblin,
G., & Wendel, H. (1981). Nine years' follow-up of a maximal exercise test in a random
population sample of middle-aged men. Cardiology, 68(Suppl. 2), 1-8.
Willich, S.N., Lewis, M., Lowell, H., Amtz, H-R., Schubert, F., & Schroder, R. (1993).
Physical exertion as a trigger of acute myocardial infarction. New England Journal of
Medicine, 329, 1684-1690.
Zukel, W.J., Lewis, R.H., Enterline,P.E., Painter, R.C., Ralston, L.S., Fawcett, R.A., Meredith,
A.P., & Peterson, B. (1959). A short-term community study of the epidemiology of
coronary heart disease. American Journal of Public Health, 49, 1630-1639.