EXERCISE-INDUCED REDUCTION IN MYOCARDIAL INFARCT SIZE AFTER CORONARY-ARTERY OCCLUSION IN RAT

Chronic exercise (E) has been thought to be beneficial to the cardiovascular system by increasing energy production and utilization, improving myocardial contractility and increasing myocardial vascularity; whether or not any of these effects are beneficial to ischemic myocardium is uncertain. In this study, rats were forced to swim one hr/day, 5 days/wk for 5 weeks. They were sacrificed and the myocardial capillary bed was perfused with carbon black. Using a calibrated eyepiece grid, histologic sections of heart were examined to determine capillary/fiber ratios (C/F) and myocardial fiber diameter. C/F was increased by 30% in E rats [0.87 ± 0.06 (mean ± SE)(N = 4 rats)] when compared with sedentary controls (C) [0.67 ± 0.04 (N = 4 rats), P <0.05]. This training effect occurred in the absence of hypertrophy since there were no differences in ventricular weight (1.21 ± 0.04 mg in E rats vs 1.16 ± 0.03 mg in C rats) or in fiber diameter (13.0 ± 0.2 μ in E rats vs 13.1 ± 0.2 μ in C rats) in the two groups. An additional 27 E rats and 25 C rats underwent left coronary artery occlusion and were sacrificed 48 hr later. Myocardial infarct size was measured by planimetry of histologic sections of serial slices of left ventricle (LV). In the 27 E rats, 21.5 ± 1.9% of the LV was infarcted compared with 31.3 ± 2.6% in the 25 C rats (P <0.005). Thus, infarct size was reduced by 30% in E rats. In the rat, exercise results in a reduction of myocardial infarct size after coronary artery occlusion which, at least in part, may be related to increased myocardial vascularity.