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1 Applied Physiology and Kinesiology, University of Florida, Gainesville, Fl, USA
* To whom correspondence should be addressed. E-mail: spowers{at}hhp.ufl.edu.
The calcium-activated protease calpain has been shown to play a deleterious role in the heart during ischemia-reperfusion (IR). We tested the hypothesis that exercise training would minimize IR-induced calpain activation and provide cardioprotection against IR-induced injury. Hearts from adult male rats were isolated in a working heart preparation and myocardial injury was induced with 25 minutes of global ischemia followed by 45 minutes of reperfusion. In sedentary control rats, IR significantly increased calpain activity and impaired cardiac performance (cardiac work during reperfusion = 24% of baseline). Compared to sedentary animals, exercise training prevented the IR-induced rise in calpain activity and improved cardiac work (recovery = 80% of baseline). Similar to exercise, pharmacological inhibition of calpain activity resulted in comparable cardioprotection against IR injury (recovery = 86% of baseline). The exercise-induced protection against IR-induced calpain activation was not due to altered myocardial protein levels of calpain or calpastatin. However, exercise training was associated with increased myocardial antioxidant enzyme activity (Mn-superoxide dismutase, catalase) and a reduction in oxidative stress. Importantly, exercise training also prevented the IR-induced degradation of the calcium ATPase (SERCA2a). These findings suggest that increases in endogenous antioxidants may diminish the free radical mediated damage and/or degradation of calcium handling proteins (such as SERCA2a), typically observed following IR. In conclusion, these results support the concept that calpain activation is an important component of IR-induced injury and that exercise training provides cardioprotection against IR injury, at least in part, by attenuating IR-induced calpain activation.
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