Endurance exercise training is known to promote beneficial adaptations to numerous tissues including the heart. Indeed, endurance exercise training results in a cardioprotective phenotype that resists injury during an ischemia-reperfusion (IR) insult. Because IR-induced cardiac injury is due, in part, to increased production of radicals and other reactive oxygen species, many studies have explored the impact of exercise training on myocardial antioxidant capacity. Unfortunately, the literature describing the effects of exercise on the cardiac antioxidant capacity is widely inconsistent. Nonetheless, a growing body of evidence indicates that regular bouts of endurance exercise promote an increase in the expression of both superoxide dismutase 1 and 2 in cardiac mitochondria. Moreover, emerging evidence suggests that exercise also increases accessory antioxidant enzymes in the heart. Importantly, robust evidence indicates that as few as five consecutive days of endurance exercise training results in a cardiac phenotype that resists IR-induced arrhythmias, myocardial stunning, and infarction. Further, mechanistic studies indicate that exercise-induced increases in mitochondrial superoxide dismutase 2 play a key role in this adaptation. Future studies are required to provide a complete picture regarding the cellular adaptations that are responsible for exercise-induced cardioprotection.