Ischemic heart disease is one of the main causes of morbidity and mortality worldwide. Physical exercise is an effective lifestyle intervention to reduce the risk factors for cardiovascular disease and also to improve cardiac function and survival in patients with ischemic heart disease. Among the strategies that contribute to reduce heart damages during ischemia and reperfusion, regular physical exercise is efficient both in rodent experimental models and in humans. However, the cellular and molecular mechanisms of the cardioprotective effects of exercise remain unclear. During ischemia and reperfusion, mitochondria are crucial players in cell death, but also in cell survival. Although exercise training can influence mitochondrial function, the consequences on heart sensitivity to ischemic insults remain elusive. In this review, we describe the effects of physical activity on cardiac mitochondria and their potential key role in exercise-induced cardioprotection against ischemia-reperfusion damage. Based on recent scientific data, we discuss the role of different pathways that might help to explain why mitochondria are a key target of exercise-induced cardioprotection.
Keywords: Ischemia-reperfusion; Metabolism; Mitochondria; Oxidative stress; Physical activity.
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