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1 Health, Leisure, and Exercise Science, Appalachian State University, Boone, North Carolina, United States
2 Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado, United States
3 Applied Physiology & Kinesiology, University of Florida, Gainesville, Florida, United States
4 Geriatric Research, Education and, VA Medical Center, Gainesville, Florida, United States
5 Dept. of Physiology, University of Florida, Gainesville,, Florida, United States; Applied Physiology & Kinesiology, University of Florida, Gainesville, Florida, United States
* To whom correspondence should be addressed. E-mail: quindryjc{at}appstate.edu.
Successive bouts of endurance exercise are associated with both increased cardiac levels of heat shock protein -72 (HSP-72) and improved cardioprotection against ischemia-reperfusion (IR) induced cardiac cell death. Although overexpression of HSP-72 has been shown to be cardioprotective in transgenic animals, it is unclear whether increased levels of HSP-72 are essential for exercise-induced cardioprotection against IR-mediated cell death. Purpose: We tested the hypothesis that exercise-induced increases in myocardial levels of HSP-72 are required to achieve exercise-mediated protection against IR-induced cardiac cell death. Methods: To test this postulate, we investigated the effect of preventing the exercise induced increase in cardiac HSP-72 on myocardial infarction and apoptosis following 50 min of in vivo ischemia and 120 min reperfusion. Adult male rats remained sedentary or performed successive bouts of endurance exercise in cold (8°C) or warm (22°C) environments. Results: Compared to sedentary control animals, exercise in a warm environment significantly increased myocardial HSP-72 content. In contrast, exercise in the cold environment prevented the exercise-induced increase in myocardial HSP-72 levels. Following in vivo myocardial IR, infarct size was reduced in both exercised groups compared to sedentary animals. Further, compared to sedentary rats, IR-induced myocardial apoptosis (as indicated by TUNEL positive nuclei and caspase-3 activity) was attenuated in both groups of exercised animals. Conclusion: Therefore, although HSP-72 has cardioprotective properties, our results reveal that increased myocardial levels of HSP-72 (above control) are not essential for exercise-induced protection against IR-induced myocardial infarction and apoptosis.
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