Numerous studies have demonstrated an association between a lifestyle, including frequent moderate to vigorous physical activity and a reduced incidence of CHD. The benefits of exercise have been documented in both men and women, and can exceed a 50% lower risk of CHD. In this study, despite the relationships between predominately sports-related physical activity and a less atherogenic cardiovascular risk factor profile, physical activity was unrelated to the presence and extent of calcified subclinical atherosclerosis.
Part of the reduction in CHD risk associated with exercise is produced by favorable effects on cardiovascular risk factors. This can be summarized as a favorable effect on the insulin-resistant phenotype, including the specific components of obesity (2,9,14,19), blood pressure (2,17,19,30), fibrinogen (15,17), HDL cholesterol (2,9,14,19,30), small dense LDL cholesterol (9), diabetes mellitus, and insulin resistance (14,30). Our data confirms these benefits within a relatively healthy, middle-aged population, including reductions in blood pressure, fibrinogen, serum insulin levels, obesity, and increased HDL cholesterol.
Prior studies have established that coronary artery calcification, a validated surrogate for the presence and extent of coronary atherosclerosis (25), is related to multiple cardiovascular risk factors (32). In particular, LDL cholesterol is one of the most important variables related to the presence (29) and progression (5,26) of coronary calcium. In contrast, a relationship between LDL cholesterol and physical activity has not been consistently demonstrated by these observational and cross-sectional studies (2,9) or in randomized trials (33). This suggests that exercise may exert a differential effect on the presence and extent of calcified versus noncalcified atherosclerosis, in part mediated through its limited effect on LDL cholesterol.
This study assessed physical activity and coronary calcification in a cross-sectional manner. Longitudinal data are needed to definitively exclude an effect of physical activity on calcified atherosclerosis. However, individuals tend to maintain relatively stable exercise habits (31), and the Baecke questionnaire has demonstrated reproducibility over time (23).
Obesity and diabetes mellitus are growing problems within the spectrum of coronary disease risk. Physical activity has a strong, inverse correlation with body mass index (2,9,14,19) and insulin resistance (14,30). Thus, the promotion of regular physical exercise achieves greater importance to lower the cardiovascular risk attributed to these risk factors. Our data from a middle-aged, relatively active cohort confirm these correlations and suggest caution is required when using anatomic screening tests acting as a “litmus test” in the evaluation and treatment of coronary risk factors. EBCT is a controversial test promulgated on its ability to detect patients at risk for CHD and to motivate behavioral change. However, because of the absence of a relationship between coronary calcification and physical activity, physical activity is an important cardiovascular risk variable that should not be overlooked in a patient with low, age-adjusted levels of coronary calcium. Sedentary lifestyle patterns should be discouraged in light of clear relationships seen in this and other studies between physical inactivity, obesity, insulin resistance, and CHD risk (8).
Physical activity, particularly high-intensity exercise in sports-related activities, promotes a healthy cardiovascular risk profile, including lower body mass index and insulin resistance but is unrelated to coronary calcification. This suggests that the risk reduction associated with physical activity is mediated by factors other than retarding the development of calcified atherosclerosis. Simple clinical advice for adherence to AHA recommendations for physical activity is prudent for the maintenance of ideal body weight and an optimal cardiovascular risk factor profile, although it may not affect calcified atherosclerosis.
This study was funded by Walter Reed Army Medical Center.
This work was presented in part at the 50th Scientific Session of the American College of Cardiology, Orlando FL, March 2001.
The opinions or assertions herein are the private views of the authors and are not to be construed as reflecting the views of the Department of the Army or the Department of Defense.
Conflict of interest: None of the authors of this manuscript has a financial interest in this work. The results of this study do not constitute endorsement of any product by the authors or ACSM.
Address for correspondence: Allen J. Taylor, M.D., LTC MC USA, Director, Cardiovascular Research, Cardiology Service, Walter Reed Army Medical Center, 6900 Georgia Ave., NW, Building 2, Room 4A, Washington DC, 20307-5001; E-mail: email@example.com.
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