REDUCED ISCHEMIA AND REPERFUSION INJURY FOLLOWING EXERCISE TRAINING

We examined the effects of two exercise training modalities, i.e., low -intensity endurance and sprint running, on in vitro, isovolumic myoca rdial performance following ischemia and reperfusion. Rats ran on a tr eadmill 5 d.wk(-1) for 6 wk at the following levels: endurance; 20 m.m in(-1), 0% grade, 60 min.d(-1) and sprint; five 1-min runs at 75 m.min (-1), 15% grade interspersed with 1-min active recovery runs at 20 m.m in(-1), 15% grade. Both endurance and sprint training significantly im proved exercise tolerance relative to control (P < 0.05) on two graded exercise tests. Buffer perfused hearts of control (N = 18), endurance (N = 20), and sprint (N = 13) trained animals underwent no-flow ische mia (30 min) and reperfusion (30 min) in a Langendorff mode. During re perfusion, left ventricular developed pressure and its first derivativ e were 20% higher in sprint (P < 0.05) than either endurance or contro l hearts. Left ventricular end-diastolic pressure was lowest in sprint during reperfusion (sprint, 10 +/- 1 mm Hg vs endurance, 14 +/- 2 mm Hg; and control, 14 +/- 2 mm Hg, at 30 min reperfusion). Hearts were t hen used for biochemical studies or dissociated into single cells for measurement of contraction, cell calcium, and action potential duratio n. Single cell contractions were greatest in sprint despite similar ca lcium transients in all groups. Ischemia/reperfusion caused action pot ential prolongation in control but not trained myocytes. Hearts from s print had the greatest glyceraldehyde-3-phosphate dehydrogenase activi ty (P < 0.05) and a tendency towards increased superoxide dismutase ac tivity. These results suggest that sprinting increases myocardial resi stance to ischemia/reperfusion. This protection may he secondary to in creased myofilament calcium sensitivity and/or myocardial expression o f glyceraldehyde-3-phosphate dehydrogenase.