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Exercise-induced protection against myocardial apoptosis and necrosis: MnSOD, calcium-handling proteins, and calpain

Joel P. French^*,,1,2, Karyn L. Hamilton^,1, John C. Quindry^*,||, Youngil Lee^*, Patrick A. Upchurch^* and Scott K. Powers^*,

^* Department of Applied Physiology and Kinesiology, Center for Exercise Science, and

Department of Physiology and Physiological Genomics, University of Florida, Gainesville, Florida, USA;

Department of Medicine, Cardiology Division, University of Minnesota, Minneapolis, Minnesota, USA;

Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado, USA; and

^|| Department of Health, Leisure, and Exercise Science, Appalachian State University, Boone, North Carolina, USA

²Correspondence: University of Minnesota Department of Medicine, Cardiology Division, MMC 508 Mayo, 420 Delaware St. SE, Minneapolis, MN 55455, USA. E-mail: frenc147{at}umn.edu

Exercise provides protection against myocardial ischemia-reperfusion (IR) injury. Understanding the mechanisms of this protection may lead to new interventions for the prevention and/or treatment of heart disease. Although presently these mechanisms are not well understood, reports suggest that manganese superoxide dismutase (MnSOD) and calpain may be critical mediators of this protection. We hypothesized that an exercise-induced increase in MnSOD would provide cardioprotection by attenuating IR-induced oxidative modification to critical Ca²⁺-handling proteins, thereby decreasing calpain-mediated cleavage of these and other proteins attenuating cardiomyocyte death. After IR, myocardial apoptosis and infarct size were significantly reduced in hearts of exercised animals compared with sedentary controls. In addition, exercise prevented IR-induced calpain activation as well as the oxidative modification and calpain-mediated degradation of myocardial Ca²⁺-handling proteins (L-type Ca²⁺ channels, phospholamban, and sarcoplasmic/endoplasmic reticulum calcium ATPase). Further, IR-induced activation of proapoptotic proteins was attenuated in exercised animals. Importantly, prevention of the exercise-induced increase in MnSOD activity via antisense oligonucleotides greatly attenuated the cardioprotection conferred by exercise. These results suggest that MnSOD provides cardioprotection by attenuating IR-induced oxidation and calpain-mediated degradation of myocardial Ca²⁺-handling proteins, thereby preventing myocardial apoptosis and necrosis.—French, J. P., Hamilton, K. L., Quindry, J. C., Lee, Y., Upchurch, P. A., Powers, S. K. Exercise-induced protection against myocardial apoptosis and necrosis: MnSOD, calcium-handling proteins, and calpain.

Key Words: ischemia • reperfusion • antioxidant

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