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Submitted on December 19, 2002
Accepted on February 11, 2003
From the Comparative Medicine Clinical Research Center (J.K.W.), Wake Forest University Health Sciences, Winston-Salem, NC, and Department of Psychology, University of Pittsburgh, Pa.
* To whom correspondence should be addressed. E-mail: kwilliam{at}wfubmc.edu.
Objective--Exercise reduces the risk for coronary heart disease. However, the mechanisms mediating the beneficial effects of exercise remain ambiguous. In particular, it is uncertain whether exercise inhibits the development of atherosclerosis, a major pathobiologic process underlying heart disease.
Methods and Results--To address this question, adult male monkeys were fed an atherogenic diet while assigned to one of four experimental conditions for 34 months: 1) runner/no group disruption, ie, "stable" (n=19); 2) runner plus frequent social group disruption, ie, "unstable" (n=19); 3) sedentary/stable (n=15); or 4) sedentary/unstable (n=18). Neither exposure to exercise nor social group disruption significantly affected the resulting coronary artery atherosclerosis extent or lumen areas (all ANOVA values, P>0.05). When compared with sedentary individuals, exercise animals had lower resting heart rates (119.0±3 vs132.0±3 bpm, P=0.002), greater echocardiographically measured left ventricular ejection fractions (77.2±0.01% vs 73.8±0.01%, P=0.02), greater quantitative angiographically measured dilation of coronary arteries to phenylephrine (2.6±1% vs -3.7±1% change from baseline diameter, P=0.003), and a reduced cortisol response to an adrenocorticotropin challenge. These measures were not significantly affected by social condition.
Conclusions--Thus, exercise improved some measures of cardiovascular health and reduced stress responsivity but did not inhibit progression of coronary artery atherosclerosis or promote positive artery remodeling. It is concluded that exercise may exert cardioprotective effects without influencing atherosclerosis extent.
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