Exercise Preconditioning of the Myocardium

Diseases of the heart (e.g. myocardial ischaemia reperfusion injury) remain the major cause of death in the industrialized world. Therefore, developing a pragmatic countermeasure to reduce myocardial ischaemia reperfusion injury is vital. In this regard, a plethora of evidence indicates that regular exercise can protect the heart during an ischaemia reperfusion insult (i.e. cardioprotection). This review summarizes studies indicating that both short-term (i.e. 1–5 days) and long-term (i.e. weeks to months) endurance exercise provides cardioprotection. Data are presented showing that exercise duration and exercise intensity are both important factors in achieving a cardioprotective phenotype. Importantly, it appears that the exercise duration of a single exercise session should last for 60 minutes and should be performed at about 75% maximum oxygen consumption in order to achieve exercise-induced cardioprotection. Furthermore, data are presented showing that exercise-induced cardioprotection against myocardial stunning can persist for at least 9 days after the cessation of exercise training, but is lost 18 days after exercise. This review also summarizes the exercise-induced adaptations that occur to the myocardium. In particular, extrinsic changes observed in human and animal models include neural, hormonal, humoral, vascular and reduced body fat. Other anatomical and biochemical/molecular changes that have been studied as putative mechanisms in exercise-induced cardioprotection include alterations in anatomic coronary arteries, induction of myocardial heat shock proteins, increased myocardial cyclooxygenase-2 activity, elevated endoplasmic reticulum stress proteins, nitric oxide production, improved function of sarcolemmal and/or mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels and increased myocardial antioxidant capacity. However, the most compelling evidence for exerciseinduced cardioprotection is the fact that exercise training upregulates key antioxidant enzymes that have been shown to promote cardioprotection. Moreover, data are presented showing that exercise training induces cardiac mitochondrial changes that result in reduced oxidant production. In addition, recently our laboratory has shown that exercise training evokes changes in mitochondrial phenotype that are protective against apoptotic stimuli. Specifically, data are presented showing that several mitochondrial proteins are altered following repeated bouts of endurance exercise and several of these differentially expressed proteins are potential important cardioprotective mediators. Finally, in hopes of stimulating debate and future research, this review concludes with a discussion of unanswered questions related to exercise-induced cardioprotection.