There is a substantial and persuasive body of evidence linking sedentary living habits with cardiovascular disease. Studies from all three branches of medical science-clinical/pathologic, epidemiologic, and experimental-collectively support a conclusion that the association between inactivity and increased cardiovascular disease risk is causal(2). Clinical/pathologic reports indicate more coronary artery disease observed at autopsy in sedentary persons when compared with those who are more active (8), and endurance athletes have greater coronary artery dilating capacity than sedentary control subjects(6). Epidemiologic studies on physical activity and cardiovascular disease meet classical criteria for determining causality including consistency, strong exposure-response gradient, repeatability, specificity, assessment of exposure before endpoints, and control of confounding variables (10). Furthermore, two studies published in 1993 show reductions in mortality in initially sedentary men who started a physical activity program (1,9). There are no randomized clinical trials of physical activity with cardiovascular disease mortality as the outcome. Such studies are not likely to be undertaken due to logistical complexity and cost. However, meta-analyses of randomized studies in cardiac rehabilitation show reduced mortality in exercising men compared with sedentary control subjects. Recent randomized trials in humans show less coronary artery disease progression and more regression in participants who exercise than in those who do not (11). Animal studies also support this finding (7). Numerous well-controlled experiments support the value of physical activity in modifying cardiovascular disease risk factors such as abnormal lipid profile, hypertension, carbohydrate intolerance, and abdominal obesity (4). The weight of this accumulated evidence has led groups such as the American Heart Association and U.S. Public Health Service to declare physical inactivity a risk factor for cardiovascular disease and other problems and to label it as a major public health problem that demands attention(5,12).
There is a possible problem with identifying physical inactivity as a cause of cardiovascular disease in women. Most available studies include only men, and the studies that include women show inconsistent results. In a 1987 review, of 14 studies on physical inactivity and cardiovascular disease in women, 10 showed no association (10). There is, however, a flaw in many of these studies. Assessment of physical activity is difficult, and most questionnaires used in epidemiologic studies were developed by men and used with men. Studies with women typically applied these same questionnaires, which tend to focus on sports and other vigorous leisure-time activity. However, during the period that these studies were performed(1950s-1970s), many women were homemakers and may have obtained much of their physical activity via housework and childcare. These activities were not assessed in studies on sedentary habits and cardiovascular disease in women. Thus, the failure of some studies to show an association between inactivity and disease may be due to misclassification on the exposure variable.
A recent report on physical activity, physical fitness, and mortality in women addresses the inadequate assessment of activity. A group of 10,224 men and 3,120 women were followed for mortality outcome for 8 yr after both physical activity and fitness were measured as part of a general health examination. Physical activity was assessed by self-report on a medical history, and fitness was determined by a maximal exercise test on a treadmill. Although self-reported activity is a subjective measure, physical fitness was measured by an objective laboratory test. Age-adjusted death rates in this study showed a steep inverse gradient across low, moderate, and high physical fitness categories, with comparable findings for women and men. Death rates per 10,000 person-years of follow-up across the fitness groups were 64, 26, and 20 for men and 40, 16, and 7 for women. When death rates were compared across low, moderate, and high categories of self-reported physical activity, different patterns emerged for the two sexes. The rates per 10,000 for men were 46, 40, and 27, a significant inverse gradient; for women no trend was seen with rates of 23, 18, and 24. The primary determinant of physical fitness is the habitual activity pattern. The similarity of results for fitness in both men and women suggests that the more active (and fit) women received comparable benefits to men. Lack of association between inactivity and mortality in women is likely due to an inadequate measurement of physical activity (3).
In summary, sedentary habits are probably as hazardous for women as they are for men. Many other risk factors appear to have the same impact in the two sexes, and there is no reason to believe that physical inactivity is different. The inconsistent results in the literature regarding physical inactivity and cardiovascular disease in women are likely due to misclassification resulting from inadequate assessment measures.
1. Blair, S. N. 1993 C. H. McCloy Research Lecture: physical activity, physical fitness, and health. Res. Q. Exerc. Sport
2. Blair, S. N. Physical activity, fitness, and coronary heart disease. 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. 579-590.
3. Blair, S. N., H. W. Kohl, and C. E. Barlow. Physical activity, physical fitness, and all-cause mortality in women: do women need to be active? J. Am. Coll. Nutr.
4. Bouchard, C., R. J. Shephard, and T. Stephens, (Eds.).Physical Activity, Fitness, and Health
. Champaign, IL: Human Kinetics, 1994.
5. Fletcher, G. F., S. N. Blair, J. Blumenthal, et al. AHA Statement on Exercise: benefits and recommendations for physical activity programs for all Americans. Circulation
6. Haskell, W. L., C. Sims, J. Myll, W. M. Bortz, F. G. St. Goar, and E. Alderman. Coronary artery size and dilating capacity in ultradistance runners. Circulation
7. Kramsch, D. M., A. J. Aspen, B. M. Abramowitz, T. Kreimendahl, and W. B. Hood. Reduction of coronary atherosclerosis by moderate conditioning exercise in monkeys on an atherogenic diet. N. Engl. J. Med.
8. Morris, J. N. and M. D. Crawford. Coronary heart disease and physical activity of work: evidence of a national necropsy survey.Br. Med. J.
9. Paffenbarger, R. S., Jr., R. T. Hyde, A. L. Wing, I-M. Lee, D. L. Jung, and J. B. Kampert. The association of changes in physical-activity level and other lifestyle characteristics with mortality among men. N. Engl. J. Med.
10. Powell, K. E., P. D. Thompson, C. Caspersen, and J. S. Kendrick. Physical activity and the incidence of coronary heart disease.Ann. Rev. Pub. Health
11. Schuler, G. S., R. Hambrecht, G. Schlierf, et al. Regular physical exercise and low-fat diet: effects on progression or coronary artery disease. Circulation
12. U.S. Public Health Service. Healthy People 2000: National Health Promotion and Disease Prevention Objectives
. Washington, DC: DHHS, 1991.
Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors
Nanette K. Wenger: Preventive Coronary Interventions for Women
Udho Thadani: Hypertension and Cardiovascular Disease Risk in Women
Steven N. Blair: Physical Inactivity and Cardiovascular Disease Risk in Women
Ronald T. Burkman: Oral Contraceptive Use and Coronary and Cardiovascular Risk
Margo A. Denke: Lipids, Estrogen Status, and Coronary Heart Disease Risk in Women
Caren Solomon: Diabetes Mellitus and Risk of Cardiovascular Disease in Women
Murray Freedman: Postmenopausal Hormone Replacement Therapy and Cardiovascular Disease Risk
This mongraph is based on the proceedings of an ACSM Roundtable entitled“Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors,” held June 21-22, 1994, in Indianapolis, Indiana.
The Exercise and Cardiovascular Disease Risk in Women: Interaction with Selected Endocrine Factors Roundtable was funded through a grant from Wyeth-Ayerst Laboratories.