Fig. 4

A schematic outline of exercise-induced cardiac protection against an ischemia–reperfusion (I/R) injury. Cardiac myocytes are terminally differentiated and contain insufficient regenerative capacity; therefore, excessive cellular stresses caused by damaged proteins, lipids, and organelles can lead to irreversible cell damage, resulting in cell death. This unfavorable cellular condition in cardiac myocytes will be exacerbated when an I/R event concurs. In contrast, regular endurance exercise maintains the healthy cellular environment by disposing of damaged proteins and lipids and mitochondria through autophagy and mitophagy. Thus, upon an IR insult leading to cell death, exercise-trained hearts may resist I/R injuries and thus confer cardiac protection against I/R-induced myocardial infarction. EICM Exercise-induced cardiac mitophagy