Many human epidemiological studies suggest that regular exercise is associated with cardiovascular benefits ( 13, 25, 31). Indeed, the incidence of myocardial infarctions is reduced in physically active individuals, and the survival rate of heart attack victims is greater in active individuals compared with sedentary people ( 13, 25). Recent experimental studies also indicate that regular endurance exercise provides myocardial protection against ischemia-reperfusion (I/R) injury ( 3, 6, 7, 9, 15, 19, 21, 29). For example, 10 wk of endurance exercise training has been shown to enhance myocardial recovery from an I/R insult, as evidenced by an enhanced recovery of left ventricle developed pressures (LVDPs) and reduced oxidative damage to the myocardium ( 9, 29). Although the exact biochemical mechanism(s) responsible for this protection is not known, it is believed that the training-induced changes in the myocardium are the cumulative result of consecutive exercise bouts over a long period (i.e., several months). This type of long-duration exercise training has been shown to elevate myocardial levels of heat shock protein (HSP) 72 and improve myocardial antioxidant defenses ( 9, 28, 29) collectively, these changes could lead to improved myocardial protection during I/R ( 9, 29). To date, the minimum duration of exercise required to protect the heart during an I/R insult is unknown. Nonetheless, two recent studies suggest that as few as 1–3 consecutive days of exercise elevates myocardial levels of HSP72 and can improve myocardial contractile performance after exposure to an in vitro model of ischemia and reoxygenation ( 21, 34).
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