Mitochondrial Antioxidant Enzymes and Endurance Exercise-induced Cardioprotection against Ischemia-Reperfusion Injury.
Coronary artery disease (CAD) is the most common cause of myocardial injuries induced by prolonged cessation of blood flow (ischemia) to cardiac myocytes due to atherosclerosis. By contrast, growing evidence has shown that a non-pharmacological strategy, endurance exercise, provides cardioprotection against ischemic myocardial injuries. Despite the prominent cardioprotective benefit; however, the exact molecular and cellular protective mechanisms remain an exciting issue. Nonetheless, given that excess production of reactive oxygen species (ROS) is a
primary mediator of cardiac injuries caused by an I/R insult, improved myocardial antioxidant capacity in response to endurance exercise has been suggested to be a key mechanism against I/R injuries, in particular, Therefore, this review will focus the role of endurance exercise-induced improvement in myocardial antioxidants in cardioprotection against I/R induced myocardial infarction.
The degree of myocardial injuries varies depending upon the duration of ischemia, but beyond 20 minutes results in irreversible myocyte damage, but a timely restoration of the obstructed blood flow (reperfusion) can ameliorate levels of cell death. Nevertheless, this salvage procedure (i.e., reperfusion by angioplasty) still contributes to significant cell death and to formation of fibrosis,
thus gradually leading to heart failure.
Despite three decades of incessant pharmacological trials to mitigate I/R-induced myocardial injuries in the clinical setting, currently, satisfactory therapy is still greatly lacking, and thus there
is an urgent need to devise potent therapeutic strategies. However, exact mechanisms responsible for exercise-induced cardioprotection against an I/R insult remain poorly understood and elusive.
Sport Exerc Med Open J. 2018; 4(1): 9-15. doi: 10.17140/SEMOJ-4-155
