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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). To date, the minimum duration of exercise required to protect the heart during an I/R insult is unknown. 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). 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). 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). 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). 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). Many human epidemiological studies suggest that regular exercise is associated with cardiovascular benefits ( 13, 25, 31). These data indicate that 3–5 consecutive days of exercise improves myocardial contractile performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses. Furthermore, exercise (3 and 5 days) increased ( P < 0.05) myocardial glutathione levels and manganese superoxide dismutase activity. Both heat stress and exercise resulted in an increase ( P < 0.05) in the relative levels of left ventricular heat shock protein 72 (HSP72). No differences existed between heat-stressed and exercise groups in LVDP, +dP/d t, and −dP/d t at any time during ischemia or reperfusion. Compared with control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher ( P < 0.05) left ventricular developed pressure (LVDP), maximum rate of left venticular pressure development (+dP/d t), and maximum rate of left ventricular pressure decline (−dP/d t) at all measurement periods during both ischemia and reperfusion. Coronary occlusion was maintained for 30-min followed by a 30-min period of reperfusion. Twenty-four hours after heat stress or exercise, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of four experimental groups: 1) control, 2) 3 consecutive days of treadmill exercise, 3) 5 consecutive days of treadmill exercise (60 min/day at 60–70%V˙ o 2 max), and 4) whole body heat stress (15 min at 42☌). These experiments examined the independent effects of short-term exercise and heat stress on myocardial responses during in vivo ischemia-reperfusion (I/R).