Mechanisms of exercise-induced cardioprotection

Abstract

Myocardial ischemia-reperfusion (IR) injury can cause ventricular cell death and is a major pathological event leading to morbidity and mortality in those with coronary artery disease. Interestingly, as few as five bouts of exercise on consecutive days can rapidly produce a cardiac phenotype that resists IR-induced myocardial injury. This review summarizes the development of exercise-induced cardioprotection and the mechanisms responsible for this important adaptive response.

FIGURE 1.

Relationship between duration of ischemia and the level of IR-induced cardiac injury

FIGURE 2.

Cellular events leading to ischemia-reperfusion injury in the heart ROS, reactive oxygen species.

FIGURE 3.

As few as 5 consecutive days of exercise can provide significant protection against IR-induced myocardial infarction Data are from Ref. .

FIGURE 4.

A list of proposed mediators of exercise-induced cardioprotection See text for details.

FIGURE 5.

Illustration of several exercise-induced mitochondrial alterations that promote cardioprotection against IR injury Exercise increases mitochondrial levels of the important antioxidant enzyme superoxide dismutase 2 (SOD2). Exercise training could also increase the expression of mitochondrial ATP-sensitive potassium channels along with other mitochondrial proteins that could contribute to cardioprotection. MAO-A, monoamine oxidase; SIRT3, sirtuin 3; MitoK_ATP, mitochondrial potassium ATP-sensitive channel.