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Background —Cardiorespiratory fitness is favorably associated with most modifiable coronary heart disease (CHD) risk factors. Findings are limited, however, by few data for women, persons with existing CHD, and low-risk populations. In the present study, we described cross-sectional associations between cardiorespiratory fitness and CHD risk factors in a large cohort of middle-aged men and women, of whom the majority were LDS Church members (Mormons), with and without existing CHD. Methods and Results —Comprehensive health examinations were performed on 3232 men (age 45.9±10.8 years) and 1128 women (age 43.8±12.8 years) between 1975 and 1997. Maximal treadmill exercise testing was used to categorize those with (12% of the men and 10% of the women) and those without CHD into age- and sex-specific cardiorespiratory fitness quintiles. After adjustments for age, body fat, smoking status, and family history of CHD, favorable associations were observed between fitness and most CHD risk factors among men and women, regardless of CHD status. Conclusions —These data indicate that enhanced levels of cardiorespiratory fitness may confer resistance to elevations in CHD risk factors even in a low-risk sample of middle-aged men and women. Furthermore, these findings reinforce current public health recommendations that advocate increased national levels of physical activity and cardiorespiratory fitness for primary and secondary CHD prevention.

The purpose of this study was to assess noninvasively the effects of intense aerobic training on cardiac structure and function in a group of healthy, college-age men (25 experimental and 11 control, mean age 22 years). Echocardiographic, electrocardiographic (ECG), and fitness measurements were obtained before and after a 3-month endurance training program and compared with similar measurements obtained in nonexercising subjects. The supervised training program consisted of 50-minute jogging sessions 5 days a week at 85% of maximal heart rate. Compared with the control group, echocardiography after training showed an increase in left ventricular (LV) end-diastolic dimension (p less than 0.05). LV posterobasal wall thickness, septal wall thickness and ejection fraction did not change significantly. ECG measurements revealed a decrease in resting heart rate (p less than 0.05) and an increase in R-wave voltage in leads V5 and V6 (p less than 0.01). The measured maximal oxygen consumption increased by 16% (p less than 0.001). These data indicate that intense aerobic training in college-age men results in a significant increase in resting LV end-diastolic dimension and volume. The increase in maximal stroke volume associated with exercise training may be partially explained by these changes in cardiac dimensions.

Because of the uncertainty as to the extent to which cardiac size is determined by exercise training vs genetic endowment, this study investigated familial (genetic plus common family environment) vs nonfamilial influences on cardiac size. College-age monozygotic twins (group 1, 31 sets), dizygotic twins (group 2, 10 sets), siblings of like sex (group 3, six sets), and nonrelated subjects (group 4, 15 sets) underwent echocardiographic and electrocardiographic tests, measurement of maximum oxygen uptake (VO2max), and evaluation of pulmonary and body composition; mean intrapair differences of the four groups were compared. Mean intrapair differences in cardiac size varied as much for subjects in group 1 as for those in groups 2 and 3. However, subjects in groups 1, 2, and 3 had less variation (p less than .05) than those in group 4. After the initial testing, 14 pairs of monozygotic twins, five sets of dizygotic twins, and six sets of siblings underwent 14 weeks of exercise training (both members participated) and all tests were repeated. After exercise training, subjects in group 1 still had as much intrapair variability in cardiac size as those in groups 2 and 3. The data suggest cultural familial influences are more important in determining cardiac size than nonfamilial influences or even genetic influences alone.