Exercise-induced cardioprotection: From endogenous to exogenous mechanisms

Acute myocardial infarction (AMI) remains the leading form of cardiovascular morbidity and mortality, while exercise is a preventative and therapeutic countermeasure. The collective benefits of exercise on the heart are called cardioprotection. Exercise-induced cardioprotection encompasses four broad areas: 1) cardiovascular disease (CVD) risk factor improvement, 2) anatomical remodeling of the heart, 3) improved cardiac physiologic function, and 4) mechanisms of exercise preconditioning.

With respect to the latter area of cardioprotection, research indicates that a few days of moderate intensity aerobic exercise preconditions the heart against cardiac dysrhythmias, ventricular pump dysfunction, and tissue death. The short duration protective timeframe, hours to days after exercise, indicates that the mechanisms are biochemical in nature. Protective mechanisms within exercised hearts include endogenous antioxidant enzymes, better regulation of cytosolic Ca²⁺, and more efficient bioenergetics. However, a formative body of work conducted over the last decade indicates that additional exogenous mechanisms may be receptor mediated, presumably providing cardioprotection via circulating factors. Preliminary findings indicate that tissue-to-tissue cross talk involves cardioprotective paracrine factors derived from muscle or autocrine factors originating from the heart itself. This protection is termed exogenous (or remote) cardiac preconditioning, and appears to include δ-opioid receptors, IL-6 receptors, and perhaps other surface receptors on exercised cardiac tissue.

The current review outlines existing knowledge on exercise and factors of cardiac preconditioning, and highlights the avenues for next-step scientific advances to understanding treatments against AMI.