Journal Logo


Is physical activity or physical fitness more important in defining health benefits?


Author Information
Medicine and Science in Sports and Exercise: June 2001 - Volume 33 - Issue 6 - p S379-S399
  • Free


Physical activity and physical fitness are closely related in that physical fitness is mainly, although not entirely, determined by physical activity patterns over recent weeks or months. Genetic contributions to fitness are important but probably account for less of the variation observed in fitness than is due to environmental factors, principally physical activity (14). For most individuals, increases in physical activity produce increases in physical fitness, although the amount of adaptation in fitness to a standard exercise dose varies widely and is under genetic control. Thus, at one level the topic of this report reverts to the oft-considered question of the relative importance of nature versus nurture. Consensus has perhaps never been achieved in response to this nature-nurture issue in other contexts, but we will attempt to delimit and define the question addressed in this report so that many, if not most, can find some concepts or issues with which they can agree.

We considered the general case of health-related behaviors and health-related fitness as they relate to health outcomes (Fig. 1). Several examples, but not an exhaustive list, of health-related behaviors are shown on the left side of the figure. These behaviors, singly or in concert, are important determinants of the several components of health-related fitness listed in the middle of the figure. The fitness variables are important determinants of various health outcomes, and several specific biological mechanisms have been elucidated to confirm the causal relation of fitness variables to health. Just as for cardiorespiratory fitness, all of the fitness variables have genetic components but also are strongly influenced by environmental factors. For example, the blood lipid profile has a genetic component, but diet is of great importance. For most of these associations a critical issue is the genetic-environmental interactions that determine specific fitness levels. That is, a diet high in sodium may be especially important in hypertension risk in those with a genetic proclivity for salt sensitivity. Note also that for nonfatal health outcomes, there often may be a feedback loop whereby an outcome may influence one or more health behaviors.

Interrelationships between health behaviors, various types of fitness, and health outcomes. Numerous health behaviors influence, singly or in concert, several different components of fitness—which in turn affect various health outcomes. Genetic, social, and environmental factors influence behaviors, fitness, and outcomes. Health outcomes can also influence behaviors.

The material presented in this review is used to address three specific questions:

1) Is there a dose-response relation between physical activity and health outcomes?

2) Is there a dose-response relation between cardiorespiratory fitness and health outcomes?

3) If both physical activity and cardiorespiratory fitness have a dose-response relation to health outcomes, is there a difference in the outcome gradient across categories for the two exposures, and is it possible to determine from the available data which exposure is more important for health?


We first defined the exposure and outcome variables and delimited the scope of our review. We use the basic terminology presented by Howley in the introductory paper in this supplement, with some additional, more detailed specifications of some of the terms.

Exposure variables.

Exposure variables for this report are physical activity and physical fitness. Physical activity in this report refers to either leisure-time physical activity or occupational activity, and we will not attempt to distinguish between these subtypes of activity. The physical fitness component addressed here is cardiorespiratory fitness, which was determined in the studies reviewed for this report by submaximal or maximal exercise tests of work performance rather than measured maximal oxygen uptake. These work performance tests, at least the maximal tests, correlate highly with measured maximal oxygen uptake (55,56).

Outcome variables.

Health variables constitute the outcome variables for this report. We agree with the general definitions of health summarized by Howley, and that health is a multidimensional characteristic. Health is a diffuse and perhaps even an elusive concept and often presents a challenge to health researchers. We chose not to select various clinical measures, such as lipids, blood pressure, or body composition as outcomes, because these variables will be topics of other reports in this supplement. We also did not select one of the global definitions of health that includes physical, social, and psychological dimensions, such as those presented by Howley. These broad definitions are useful in philosophical considerations of health in broad terms, but they typically have not been used as outcome measures in research on physical activity or fitness. Therefore, we chose to examine the dose-response association of activity and fitness on major physical health outcomes, which is where there are sufficient studies. Specifically, we selected two types of health measures as the outcome variables for this report:

1) morbidity from major chronic diseases such as coronary heart disease (CHD), stroke, combined cardiovascular disease, or cancer, and

2) cardiovascular disease (CVD), cancer, or all-cause mortality.

We did not include diabetes, hypertension, or other chronic diseases as outcomes for this report. The tables, especially Table 2, are already large, and we thought that we had enough data to address our questions without including nonfatal disease outcomes. We made one exception to this delimitation. We included one study in Table 4 on functional limitation as the outcome because we otherwise had only eight articles for this table, and several of them were relatively small.

Table 2
Table 2:
Physical activity and morbidity and mortality.
Table 2A
Table 2A:
Table 2B
Table 2B:
Table 2C
Table 2C:
Table 2D
Table 2D:
Table 2E
Table 2E:
Table 2F
Table 2F:
Table 2
Table 2:
G. Continued
Table 2
Table 2:
H. Continued
Table 4
Table 4:
Summary of 9 studies with assessments of both physical activity and fitness on the does-response relation to health outcomes.
Table 4
Table 4:

Identifying source material.

Our objective was to identify articles in the peer-reviewed literature that included data on at least one of the outcomes and on three or more levels of one or both of the exposure variables. To address questions 1 and 2, we reviewed studies that included assessments of either physical activity or cardiorespiratory fitness. Studies used to address question 3 were required to have data on both activity and fitness. Because there are many studies with physical activity and because these studies have been thoroughly reviewed recently (51,54,69), we restricted our review of studies to articles published in 1990 or later. Table 1 includes a summary of how material was selected for review.

Table 1
Table 1:
Process for identifying material included in review. Performed PubMed computer search using keywords related to physical activity (physical activity, exercise, exertion), physical fitness (fitness, exercise tolerance, exercise test), and health outcomes (morbidity, mortality). Restricted the search from 1990 to August 25, 2000. (Because of the limited numbers of papers, search for physical fitness includes papers from the 1980s.) Computer search identified papers with at least one of the exposures (activity or fitness) and at least one of the health outcomes, and the initial search results were:

Critical analysis of articles.

At least two, and often all three, authors read each of the 67 articles on the final list. We summarized results in tabular form, with one table for each of the questions addressed in this report. Each table includes information on characteristics of the study population, method of assessing physical activity or fitness, information on confounding variables, and summary of study outcomes with an emphasis on the dose-response gradient. We used the evidence-based approach for rating the quality of the evidence discovered and summarized in the review. There are no randomized controlled clinical trials of either physical activity or fitness and the outcomes considered here, and thus the quality of evidence is Category C for each question we addressed.


Separate tables are presented for the dose-response associations of physical activity, fitness, or both exposures to the outcomes of morbidity and mortality.

Physical activity dose-response.

Table 2 includes a summary of the evidence from 49 studies on the dose-response relation of physical activity to health outcomes. A majority of these papers have mortality as an outcome (CHD, CVD, stroke, site-specific cancer, or all-cause mortality); however, some studies include data on nonfatal chronic disease outcomes. Due to the large number of studies reviewed here with various health outcomes, vastly different approaches to assessing physical activity, and other methodological differences, it is not possible to accurately quantify a general dose-response gradient for physical activity. Nonetheless, and although there are exceptions (15,46,64), most studies show a general inverse dose-response gradient across physical activity categories for most health outcomes. The shape of the dose-response curves differ, but many of them show an asymptote, which suggests a threshold for benefits. Figure 2 shows point estimates for all-cause mortality by categories of activity for women (7 studies) and men (11 studies), respectively. In general, the point estimates for activity categories are more variable in women than in men, with one study in women (48) even showing nonsignificantly higher mortality in the more active women.

Dose-response for all-cause mortality across categories of physical activity in men (11 studies) and women (7 studies). Relative risks are shown for categories of physical activity. Note that the referent category in some studies is the least active group and for other studies is the most active group; 95% confidence intervals are included if they were available, otherwise only the point estimates (withP-values) are given. For some studies, point estimates are given for categories of physical activity within other strata (Lee et al. (38), by strata of vigorous and nonvigorous activity; Linsted et al. (46), by age groups).

Cardiorespiratory fitness dose-response.

Table 3 includes a summary of the evidence from nine studies on cardiorespiratory fitness and mortality (CHD, CVD, or all-cause mortality). There is remarkable consistency across studies, with all showing a strong inverse gradient of mortality across fitness groups. It should be noted that five of the nine studies are from the Aerobics Center Longitudinal Study (ACLS) data; and although these are from different subgroups of the ACLS, one would expect to find similar results in these different analyses. The reports from the ACLS are the only ones to include women, and it appears that the association between fitness and mortality is similar in women and in men. Data are somewhat sparse, but the pattern of results is similar in normotensive and hypertensive men, and within different age groups.

Table 3
Table 3:
Summary of studies on the dose-response relation of cardiorespiratory fitness to morbidity and mortality.
Table 3
Table 3:

Three of the studies included data on change in fitness from one examination to a second examination, with subsequent follow-up for mortality. Results from these studies are consistent with those from studies in which fitness was assessed only at baseline and study participants followed for mortality. Men who made greater improvements in fitness had greater reductions in mortality than was observed in men with little or no change in fitness.

The magnitude of reduction in mortality across fitness groups is substantial. Essentially all analyses show at least a 50% lower mortality rate in the high fit as compared with the low fit individuals. In some studies, the difference in mortality rates between the most and least fit individuals was on the order of three- to four-fold (10,13), and the difference was even greater in the report by Ekelund et al. (16).

Activity and fitness dose-response.

Table 4 includes a summary of the evidence from nine studies that include both exposures of cardiorespiratory fitness and physical activity in relation to health outcomes. All studies show an inverse gradient across fitness categories for the various health outcomes, and most show an inverse gradient across physical activity categories. In general, the gradients are steeper for fitness than for activity. For example, the report by Arraiz et al. (4) shows RRs for all-cause mortality across three fitness groups of 2.7, 1.6, and 1.0 for the most fit; and RRs for all-cause mortality across activity groups in this study were 1.5, 1.0, 1.5, and 1.0 for the most active. A similar pattern was noted in the ACLS for women (11). None of the reports summarized in Table 4 include data from a multivariable model in which activity and fitness were both included. We included one report in Table 4 that had an outcome measure different from other studies in this review. Huang et al. (30) evaluated the relation of activity and fitness to the prevalence of functional limitations. These data show an inverse gradient across both activity and fitness groups in both men and women, and the gradients are steeper for fitness than for activity.

Aerobics Center Longitudinal Study.

As shown in Table 4, there are only nine published reports from prospective studies meeting our inclusion criteria in which both physical activity and cardiorespiratory fitness have been assessed. Four of the studies summarized in Table 4 are from our ACLS database. We have recently extended mortality surveillance in our cohort and therefore decided to perform some preliminary analyses with our data specifically in relation to addressing question 3 established for this report.

From 1970 to 1994, there were 40,391 patients aged 20—90 yr who were examined at least once at the Cooper Clinic. We selected participants for these preliminary analysis who were healthy (no history of CVD, diabetes, or cancer and had a normal ECG) and achieved at least 85% of age-predicted maximal heart rate on the treadmill test. The 8755 women and 26,764 men who met these criteria were followed from the date of their baseline examination to date of death or to December 31, 1994, for survivors. These participants contributed 96,608 woman-yr and 307,594 man-yr of follow-up, during which 146 women and 805 men died. We assigned participants to three categories of physical activity based on their responses to their activity habits during the 3 months before their baseline examination. We calculated MET hours per week using Ainsworth et al.’s physical activity compendium (2) and assigned each participant to one of three activity categories: no reported activity = sedentary; up to 19.9 MET hours per week = active, and 20 or more MET hours per week = highly active. Study participants also were assigned to fitness categories based on age-sex treadmill time distributions: low fitness = least fit 20%, moderate fitness = next 40%, and high fitness = most fit 40%, as in our published studies referenced here.

We cross-tabulated the three activity and three fitness categories and calculated all-cause death rates per 1000 person-yr of observation (Fig. 3). There was an inverse mortality gradient across both activity and fitness categories in both men and women. The highest death rates for both men and women were in the unfit-sedentary group and the lowest death rates were in the high fit-highly active group. We then submitted these data to a proportional hazards analysis, with physical activity, cardiorespiratory fitness, BMI, smoking habit, alcohol intake, and parental history of CVD included in the model. Physical activity was not associated with mortality in these analyses, but the inverse gradient across fitness groups remained, with a 50% reduction in mortality in the moderately fit women and men and a 70% reduction in the high fit individuals, when compared with those in the low fit category.

All-cause mortality rates by cardiorespiratory fitness and physical activity categories in 26,764 men (A) and 8755 women (B) participating in the Aerobics Center Longitudinal Study. Height of the bars represents the death rate per 1000 person-yr of observation. Death rates are based on 307,594 man-yr and 96,608 woman-yr of observation, and on 805 deaths in men and 146 deaths in women. Unfit participants are the least fit 20% in each age-sex group, fit are the next 40% of the fitness distribution, and high fit are the most fit 40%. Sedentary persons reported no physical activity, active individuals reported up to 19.9 MET·h-1 of physical activity per week, and high active individuals reported 20 or more MET·h-1.


The review performed for this report focused on three specific questions. Evidence statements and a rationale are provided below for each of the questions. All statements are based on Category C Evidence.

1. Is there a dose-response relation between physical activity and health outcomes?

Evidence statement.

Individuals who are regularly physically active are less likely than sedentary individuals to develop health problems. The inverse gradient of risk across activity groups is seen in different population groups and for fatal and nonfatal outcomes.


Some health outcomes are probably not associated with physical activity habits, for example, rectal cancer. There is compelling evidence that regular physical activity extends longevity and reduces risk for CHD, CVD, stroke, and colon cancer. For these outcomes, there is consistent evidence for an inverse dose-response effect across physical activity groups. Data are not sufficient to determine whether the slope of the gradient is different for different health outcomes or whether the shape of the dose-response curve is linear or curvilinear.

2. Is there a dose-response relation between cardiorespiratory fitness and health outcomes?

Evidence statement.

There is an inverse gradient across categories of cardiorespiratory fitness for risk of fatal and nonfatal health outcomes. The pattern of association between fitness and outcomes is highly consistent across studies.


There are fewer studies on cardiorespiratory fitness and health than are available on physical activity and health; however, the fitness studies are compelling in their consistency and in the steepness of the dose-response gradient across fitness groups. Studies including measures of fitness are of necessity laboratory- or clinic-based and, thus, also usually have extensive and objective data on health status and potential confounding variables, such as data from clinical chemistry analyses, blood pressure, and body composition. Most of the studies show a curvilinear dose-response association for most outcomes, with an asymptote occurring in the upper part of the fitness distribution.

3. If both physical activity and cardiorespiratory fitness have a dose-response relation to health outcomes, is there a difference in the outcome gradient across categories for the two exposures, and is it possible to determine from the available data which exposure is more important for health?

Evidence statement.

The dose-response gradient for various health outcomes is steeper across categories of cardiorespiratory fitness than across physical activity groups. In preliminary analyses from the ACLS, when activity, fitness, and possible confounding variables are included in a multivariate model, fitness remains strongly associated with mortality, and the association for activity and health is no longer significant.


As indicated in the evidence statements for questions 1 and 2, data from existing studies indicate dose-response gradients across categories of activity and fitness for multiple health outcomes. It is not possible to determine from these studies whether one of the exposure variables is more important than the other as a predictor of health. Data in Table 4 suggest that fitness is more important than activity in relation to health outcomes; however, we do not think this is a valid conclusion. Physical activity is the principal determinant of cardiorespiratory fitness, although there is a genetic component. We think that the most likely explanation for the stronger dose-response gradient for fitness shown in Table 4 is that fitness is measured objectively and physical activity is assessed in the studies reviewed here by self-report, which inevitably leads to misclassification—often substantial misclassification. With activity usually producing greater misclassification rates than are seen for fitness, it follows that data from observational studies will typically show a stronger association between fitness and health outcomes than for activity and health outcomes.


The question posed in the title of this report is the major issue. This question has received attention over the past several years, which escalated after publication of the CDC/ACSM public health recommendation for physical activity (54). The focus of that recommendation was on accumulating activity of moderate intensity, and this approach was difficult for some to reconcile with prior exercise recommendations that emphasized continuous bouts of relatively vigorous exercise. Some individuals began to talk about two principal types of physical activity—activity for health benefits and activity for improving fitness. The underlying notion for this concept was apparently that low amounts and intensities of activity might improve health (reduce risk of morbidity or mortality) but not produce any improvements in fitness. Our view is that activity cannot be designated as either for health or for fitness. We submit that any physical activity that has the capacity to change either health or fitness will change both. It may well be that there are minimum amounts and intensities that are required for any physiological or psychological adaptations to occur, that specific adaptations may be produced by specific amounts and types of activity, and that it might require a large sample size to confirm that small changes in activity are associated with small changes in both health and fitness. Nonetheless, we interpret a demonstrated dose-response relationship to mean that any change in dose will produce a known response. This leads to the conclusion that given a sufficiently large sample size, an increase in physical activity of 10 kcal·d-1 would lead to detectable increments of change in physiological and psychological variables that are affected by activity. Thus, we think that the focus should be on learning more about exercise dose-response relationships in general, rather than trying to determine whether physical activity or physical fitness is more important to health benefits.

From a public health policy perspective, it is clear that recommendations and programs should be designed to promote physical activity and not fitness. It would not make sense to encourage individuals to “become fit,” but instead we can, and should, recommend that individuals “increase activity.” We think it is likely that if sedentary persons do the latter, they will achieve the former.

Our review has limitations. We imposed the limitations of the selection criteria described earlier. These criteria limited the diseases, health conditions, and clinical outcomes considered and restricted the review to human studies. In addition, there were limitations resulting from the available literature. Current studies are limited by relatively few women and by severe limitations of racial/ethnic, socioeconomic, geographic, and other diversity characteristics.


Additional research is needed to address the issues discussed here. We do not think that it is important, or even desirable, to try to determine whether physical activity or cardiorespiratory fitness is more important for health. Fitness is developed by activity, although the magnitude of response to the exercise stimulus is genetically determined. Nonetheless, it seems likely that activity will be required to develop and maintain levels of fitness that are consistent with good health. Although we do not recommend additional research to pursue the elusive question posed in the title of this report, there are important studies that should be conducted.

1) Studies of both activity and fitness should focus on defining more precisely the shape of the dose-response curve. It is established that 30 min of moderate intensity activity on most days of the week will produce important health benefits. However, suppose that a person only participates in 15 min of moderate intensity activity per day. Will he or she receive any health benefits? Conversely, are additional health benefits expected if a person obtains 60 min of activity per day? These and other issues need further exploration in randomized controlled clinical trials.

2) It is clear that cardiorespiratory fitness, which is produced by aerobic exercise, has substantial health benefits. Musculoskeletal fitness, as developed by resistance exercise, clearly has benefits for preservation or regaining function. It is unclear whether resistance exercise training would reduce the risk of chronic diseases such as hypertension, CHD, or type 2 diabetes. Furthermore, if resistance training does affect risk of chronic disease, what is the shape of the dose-response curve? These issues need to be addressed in future research studies.

3) Although it is clear there is a dose-response relationship between both activity and fitness and several health outcomes, other outcomes need further research. Are activity and fitness inversely related to the risk of breast, prostate, and lung cancer; depression and anxiety disorders; psychotic episodes; gall bladder disease; or other health conditions that have not been studied?

We thank Melba Morrow, M.A., for editorial assistance and Stephanie Parker for secretarial support. Our research is supported in part by a grant from the National Institutes of Health AG06945.

Address for correspondence: Steven N. Blair, The Cooper Institute, 12330 Preston Road, Dallas, TX 75230; E-mail:


1. Abbott, R. D., B. L. Rodriguez, C. M. Burchfiel, and J. D. Curb. Physical activity in older middle-aged men and reduced risk of stroke: the Honolulu Heart Program. Am. J. Epidemiol. 139: 881–893, 1994.
2. Ainsworth, B. E., W. L. Haskell, A. S. Leon, et al. Compendium of physical activities: classification of energy costs of human physical activities. Med. Sci. Sports Exerc. 25: 71–80, 1993.
3. Andersen, L. B., P. Schnohr, M. Schroll, and H. O. Hein. All-cause mortality associated with physical activity during leisure time, work, sports, and cycling to work. Arch. Intern. Med. 160: 1621–1628, 2000.
4. Arraiz, G. A., D. T. Wigle, and Y. Mao. Risk assessment of physical activity and physical fitness in the Canada Health Survey Mortality Follow-up Study. J. Clin. Epidemiol. 45: 419–428, 1992.
5. Bergstrom, A., T. Moradi, P. Lindblad, O. Nyren, H. O. Adami, and A. Wolk. Occupational physical activity and renal cell cancer: a nationwide cohort study in Sweden. Int. J. Cancer 83: 186–191, 1999.
6. Bernstein, L., B. F. Henderson, R. Hanisch, J. Sullivan-Halley,and R. K. Ross. Physical exercise and reduced risk of breast cancer in young women. J. Natl. Cancer Inst. 86: 1403–1408, 1994.
7. Bijnen, F. C., C. J. Caspersen, E. J. Feskens, W. H. Saris, W. L. Mosterd, and D. Kromhout. Physical activity and 10-year mortality from cardiovascular diseases and all causes: the Zutphen Elderly Study. Arch. Intern. Med. 158: 1499–1505, 1998.
8. Bijnen, F. C., E. J. Feskens, C. J. Caspersen, N. Nagelkerke, W. L. Mosterd, and D. Kromhout. Baseline and previous physical activity in relation to mortality in elderly men: the Zutphen Elderly Study. Am. J. Epidemiol. 150: 1289–1296, 1999.
9. Blair, S. N., J. B. Kampert, H. W. Kohl III, et al. Influences of cardiorespiratory fitness and other precursors on cardiovascular disease and all-cause mortality in men and women. JAMA 276: 205–210, 1996.
10. Blair, S. N., H. W. Kohl, and C. E. Barlow. Physical fitness and all-cause mortality in hypertensive men. Ann. Med. 23: 307–312, 1991.
11. Blair, S. N., H. W. Kohl III, and C. E. Barlow. Physical activity, physical fitness, and all-cause mortality in women: do women need to be active? J. Am. Coll. Nutr. 12: 368–371, 1993.
12. Blair, S. N., H. W. Kohl III, C. E. Barlow, R. S. Paffenbarger,Jr., L. W. Gibbons, and C. A. Macera. Changes in physical fitness and all-cause mortality: a prospective study of healthy and unhealthy men. JAMA 273: 1093–1098, 1995.
13. Blair, S. N., H. W. Kohl III, R. S. Paffenbarger,Jr., D. G. Clark, K. H. Cooper, and L. W. Gibbons. Physical fitness and all-cause mortality: a prospective study of healthy men and women. JAMA 262: 2395–2401, 1989.
14. Bouchard, C., and L. Pérusse. Heredity, activity level, fitness, and health. In:Physical Activity, Fitness, and Health: International Proceedings and Consensus Statement, C. Bouchard, R. J. Shephard, and T. Stephens (Eds.). Champaign, IL: Human Kinetics, 1994, pp. 106–118.
15. Dorgan, J. F., C. Brown, M. Barrett, et al. Physical activity and risk of breast cancer in the Framingham Heart Study. Am. J. Epidemiol. 139: 662–669, 1994.
16. Ekelund, L. G., W. L. Haskell, J. L. Johnson, F. S. Whaley, M. H. Criqui, and D. S. Sheps. Physical fitness as a predictor of cardiovascular mortality in asymptomatic North American men: the Lipid Research Clinics Mortality Follow-up Study. N. Engl. J. Med. 319: 1379–1384, 1988.
17. Ellekjaer, H., J. Holmen, E. Ellekjaer, and L. Vatten. Physical activity and stroke mortality in women: ten-year follow-up of the Nord-Trondelag Health Survey, 1984–1986. Stroke 31: 14–18, 2000.
18. Erikssen, G., K. Liestol, J. Bjornholt, E. Thaulow, L. Sandvik, and J. Erikssen. Changes in physical fitness and changes in mortality. Lancet 352: 759–762, 1998.
19. Evenson, K. R., W. D. Rosamond, J. Cai, et al. Physical activity and ischemic stroke risk: the Atherosclerosis Risk in Communities Study. Stroke 30: 1333–1339, 1999.
20. Farrell, S. W., J. B. Kampert, H. W. Kohl, et al. Influences of cardiorespiratory fitness levels and other predictors on cardiovascular disease mortality in men. Med. Sci. Sports Exerc. 30: 899–905, 1998.
21. Folsom, A. R., D. K. Arnett, R. G. Hutchinson, F. Liao, L. X. Clegg, and L. S. Cooper. Physical activity and incidence of coronary heart disease in middle-aged women and men. Med. Sci. Sports Exerc. 29: 901–909, 1997.
22. Gerhardsson de Verdier, M., G. Steineck, U. Hagman, A. Rieger, and S. E. Norell. Physical activity and colon cancer: a case-referent study in Stockholm. Int. J. Cancer 46:985–989, 1990.
23. Gillum, R. F., M. E. Mussolino, and D. D. Ingram. Physical activity and stroke incidence in women and men: The NHANES I Epidemiologic Follow-up Study. Am. J. Epidemiol. 143: 860–869, 1996.
24. Haapanen, N., S. Miilunpalo, I. Vuori, P. Oja, and M. Pasanen. Characteristics of leisure time physical activity associated with decreased risk of premature all-cause and cardiovascular disease mortality in middle-aged men. Am. J. Epidemiol. 143: 870–880, 1996.
25. Haapanen, N., S. Miilunpalo, I. Vuori, P. Oja, and M. Pasanen. Association of leisure time physical activity with the risk of coronary heart disease, hypertension and diabetes in middle-aged men and women. Int. J. Epidemiol. 26: 739–747, 1997.
26. Håheim, L. L., I. Holme, I. Hjermann, and P. Leren. Risk factors of stroke incidence and mortality: A 12-year follow-up of the Oslo Study. Stroke 24: 1484–1489, 1993.
27. Hein, H. O., P. Suadicani, and F. Gyntelberg. Physical fitness or physical activity as a predictor of ischaemic heart disease? A 17-year follow-up in the Copenhagen Male Study. J. Intern Med. 232: 471–479, 1992.
28. Herman, B., P. I. M. Schmitz, A. C. M. Leyten, et al. Multivariate logistic analysis of risk factors for stroke in Tilburg, The Netherlands. Am. J. Epidemiol. 118: 514–525, 1983.
29. Hu, F. B., M. J. Stampfer, G. A. Colditz, et al. Physical activity and risk of stroke in women. JAMA 283: 2961–2967, 2000.
30. Huang, Y., C. A. Macera, S. N. Blair, P. A. Brill, H. W. Kohl III, and J. J. Kronenfeld. Physical fitness, physical activity, and functional limitation in adults aged 40 and older. Med. Sci. Sports Exerc. 30: 1430–1435, 1998.
31. Kampert, J. B., S. N. Blair, C. E. Barlow, and H. W. Kohl III. Physical activity, physical fitness, and all-cause and cancer mortality: a prospective study of men and women. Ann. Epidemiol. 6: 452–457, 1996.
32. Kaplan, G. A., W. J. Strawbridge, R. D. Cohen, and L. R. Hungerford. Natural history of leisure-time physical activity and its correlates: associations with mortality from all causes and cardiovascular disease over 28 years. Am. J. Epidemiol. 144: 793–797, 1996.
33. Kiely, D. K., P. A. Wolf, L. A. Cupples, A. S. Beiser, and W. B. Kannel. Physical activity and stroke risk: the Framingham Study. Am. J. Epidemiol. 140: 608–620, 1994.
34. Kujala, U. M., J. Kaprio, S. Sarna, and M. Koskenvuo. Relationship of leisure-time physical activity and mortality: the Finnish twin cohort. JAMA 279: 440–444, 1998.
35. Kushi, L. H., R. M. Fee, A. R. Folsom, P. J. Mink, K. E. Anderson, and T. A. Sellers. Physical activity and mortality in postmenopausal women. JAMA 277: 1287–1292, 1997.
36. Lakka, T. A., J. M. Venalainen, R. Rauramaa, R. Salonen, J. Tuomilehto, and J. T. Salonen. Relation of leisure-time physical activity and cardiorespiratory fitness to the risk of acute myocardial infarction in men. N. Engl. J. Med. 330: 1549–1554, 1994.
37. Lee, I.-M., C. H. Hennekens, K. Berger, J. E. Buring, and J. E. Manson. Exercise and risk of stroke in male physicians. Stroke 30: 1–6, 1999.
38. Lee, I.-M., C.-C. Hsieh, and R. S. Paffenbarger,Jr. Exercise intensity and longevity in men: the Harvard Alumni Health Study. JAMA 273: 1179–1184, 1995.
39. Lee, I.-M., and R. S. J. Paffenbarger. Physical activity and stroke incidence: the Harvard Alumni Health Study. Stroke 29: 2049–2054, 1998.
40. Lee, I.-M., and R. S. J. Paffenbarger. Associations of light, moderate, and vigorous intensity physical activity with longevity: the Harvard Alumni Health Study. Am. J. Epidemiol. 151: 293–299, 2000.
41. Lee, I.-M., R. S. J. Paffenbarger,and C.-C. Hsieh. Physical activity and risk of developing colorectal cancer among college alumni. J. Natl. Cancer Inst 83: 1324–1329, 1991.
42. Lee, I.-M., R. S. Paffenbarger,Jr., and C.-C. Hsieh. Physical activity and risk of prostatic cancer among college alumni. Am. J. Epidemiol. 135: 169–179, 1992.
43. Lee, I.-M., H. D. Sesso, and R. S. J. Paffenbarger. Physical activity and risk of lung cancer. Int. J. Epidemiol. 28: 620–625, 1999.
44. Levi, F., C. LA Vecchia, E. Negri, and S. Franceschi. Selected physical activities and the risk of endometrial cancer. Br. J. Cancer 67: 846–851, 1993.
45. Lie, H., R. Mundal, and J. Erikssen. Coronary risk factors and incidence of coronary death in relation to physical fitness: seven-year follow-up study of middle-aged and elderly men. Eur. Heart J. 6: 147–157, 1985.
46. Lindsted, K. D., S. Tonstad, and J. W. Kuzma. Self-report of physical activity and patterns of mortality in Seventh-Day Adventist men. J. Clin. Epidemiol. 44: 355–364, 1991.
47. Martinez, M. E., E. Giovannucci, D. Spiegelman, D. J. Hunter, W. C. Willett, and G. A. Colditz. Leisure-time physical activity, body size, and colon cancer in women: Nurses’ Health Study Research Group. J. Natl. Cancer Inst. 89: 948–955, 1997.
48. Mensink, G. B., M. Deketh, M. D. Mul, A. J. Schuit, and H. Hoffmeister. Physical activity and its association with cardiovascular risk factors and mortality. Epidemiology 7: 391–397, 1996.
49. Morgan, K., and D. Clarke. Customary physical activity and survival in later life: a study in Nottingham, UK. J. Epidemiol. Commun. Health 51: 490–493, 1997.
50. Morris, J. N., D. G. Clayton, M. G. Everitt, A. M. Semmence, and E. H. Burgess. Exercise in leisure time: Coronary attack and death rates. Br. Heart J. 63: 325–334, 1990.
51. NIH Consensus Development Panel on Physical Activity and Cardiovascular Health. NIH Consensus Conference: physical activity and cardiovascular health. JAMA 276:241–246, 1996.
52. Oliveria, S. A., H. W. Kohl III, D. Trichopoulos, and S. N. Blair. The association between cardiorespiratory fitness and prostate cancer. Med. Sci. Sports Exerc. 28: 97–104, 1996.
53. Paffenbarger, R. S. J., and I.-M. Lee. A natural history of athleticism, health and longevity. J. Sports Sci. 16: S31–S45, 1998.
54. Pate, R. R., M. Pratt, S. N. Blair, et al. Physical activity and public health: a recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA 273: 402–407, 1995.
55. Pollock, M. L., R. L. Bohannon, K. H. Cooper, et al. A comparative analysis of 4 protocols for maximal treadmill stress testing. Am. Heart J. 92: 39–46, 1976.
56. Pollock, M. L., C. Foster, D. Schmidt, C. Hellman, A. C. Linnerud, and A. Ward. Comparative analysis of physiologic responses to three different maximal graded exercise test protocols in healthy women. Am. Heart J. 103: 363–373, 1982.
57. Rockhill, B., W. C. Willett, D. J. Hunter, J. E. Manson, S. E. Hankinson, and G. A. Colditz. A prospective study of recreational physical activity and breast cancer risk. Arch. Intern. Med. 159: 2290–2296, 1999.
58. Rodriguez, B. L., J. D. Curb, C. M. Burchfiel, et al. Physical activity and 23-year incidence of coronary heart disease morbidity and mortality among middle-aged men: the Honolulu Heart Program. Circulation 89: 2540–2544, 1994.
59. Sacco, R. L., R. Gan, B. Boden-Albala, et al. Leisure-time physical activity and ischemic stroke risk: the Northern Manhattan Stroke Study. Stroke 29: 380–387, 1998.
60. Sandvik, L., J. Erikssen, E. Thaulow, G. Erikssen, R. Mundal, and K. Rodahl. Physical fitness as a predictor of mortality among healthy, middle-aged Norwegian men. N. Engl. J. Med. 328: 533–537, 1993.
61. Shaper, A. G., and G. Wannamethee. Physical activity and ischaemic heart disease in middle-aged British men. Br. Heart J. 66: 384–394, 1991.
62. Shu, X. O., M. C. Hatch, W. Zheng, Y. T. Gao, and L. A. Brinton. Physical activity and risk of endometrial cancer. Epidemiology 4: 342–349, 1993.
63. Sobolski, J., M. Kornitzer, G. de Backer, et al. Protection against ischemic heart disease in the Belgian Physical Fitness Study: physical fitness rather than physical activity? Am. J. Epidemiol. 125:601–610, 1987.
64. Srivastava, A., and N. Kreiger. Relation of physical activity to risk of testicular cancer. Am. J. Epidemiol. 151: 78–87, 2000.
65. Sturgeon, S. R., L. A. Brinton, M. L. Berman, et al. Past and present physical activity and endometrial cancer risk. Br. J. Cancer 68: 584–589, 1993.
66. Tang, R., J. Y. Wang, S. K. Lo, and L. L. Hsieh. Physical activity, water intake and risk of colorectal cancer in Taiwan: a hospital-based case-control study. Int. J. Cancer 82: 484–489, 1999.
67. Thune, I., and E. Lund. Physical activity and risk of colorectal cancer in men and women. Br. J. Cancer 73: 1134–1140, 1996.
68. Thune, I., and E. Lund. The influence of physical activity on lung-cancer risk: a prospective study of 81,516 men and women. Int. J. Cancer 70: 57–62, 1997.
69. U.S. Department of Health and Human Services. Physical Activity and Health: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, S/N 017-023-00196-5, 1996.
70. Verloop, J., M. A. Rookus, K. Van Der Kooy, and F. E. Van Leeuwen. Physical activity and breast cancer risk in women aged 20–54 years. J. Natl. Cancer Inst. 92:128–135, 2000.
71. Villeneuve, P. J., H. I. Morrison, C. L. Craig, and D. E. Schaubel. Physical activity, physical fitness, and risk of dying. Epidemiology 9: 626–631, 1998.
72. Wannamethee, S. G., A. G. Shaper, and M. Walker. Changes in physical activity, mortality, and incidence of coronary heart disease in older men. Lancet 351: 1603–1608, 1998.
73. Weller, I., and P. Corey. The impact of excluding non-leisure energy expenditure on the relation between physical activity and mortality in women. Epidemiology 9: 632–635, 1998.
74. White, E., E. J. Jacobs, and J. R. Daling. Physical activity in relation to colon cancer in middle-aged men and women. Am. J. Epidemiol. 144: 42–50, 1996.


© 2001 Lippincott Williams & Wilkins, Inc.