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Reduced ischemia and reperfusion injury following exercise training

1997; Lippincott Williams & Wilkins; Volume: 29; Issue: 4 Linguagem: Inglês

10.1097/00005768-199704000-00013

1530-0315

Joseph R. Libonati, John P. Gaughan, Colleen Hefner, Andrew J. Gow, A. M. Paolone, Steven R. Houser,

Cardiac Arrest and Resuscitation

We examined the effects of two exercise training modalities, i.e., low-intensity endurance and sprint running, on in vitro, isovolumic myocardial performance following ischemia and reperfusion. Rats ran on a treadmill 5 d.wk-1 for 6 wk at the following levels: endurance; 20 m.min-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.min-1, 15% grade. Both endurance and sprint training significantly improved 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 ischemia (20 min) and reperfusion (30 min) in a Langendorff mode. During reperfusion, left ventricular developed pressure and its first derivative were 20% higher in sprint (P < 0.05) than either endurance or control 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 then used for biochemical studies or dissociated into single cells for measurement of contraction, cell calcium, and action potential duration. Single cell contractions were greatest in sprint despite similar calcium transients in all groups. Ischemia/reperfusion caused action potential prolongation in control but not trained myocytes. Hearts from sprint had the greatest glyceraldehyde-3-phosphate dehydrogenase activity (P < 0.05) and a tendency towards increased superoxide dismutase activity. These results suggest that sprinting increases myocardial resistance to ischemia/reperfusion. This protection may be secondary to increased myofilament calcium sensitivity and/or myocardial expression of glyceraldehyde-3-phosphate dehydrogenase.