Exercise and the coronary circulation-alterations and adaptations in coronary artery disease

Coronary vasorelaxation depends on nitric oxide (NO) bioavailability, which is a function of endothelial nitric oxide synthase-derived NO production and NO inactivation by reactive oxygen species. This fine-tuned balance is disrupted in coronary artery disease (CAD). The impairment of NO production in conjunction with excessive oxidative stress promotes the loss of endothelial cells by apoptosis, leads to a further aggravation of endothelial dysfunction and triggers myocardial ischemia in CAD. In healthy individuals, increased release of NO from the vasculature in response to exercise training results from changes in endothelial nitric oxide synthase expression, phosphorylation, and conformation. However, exercise training has assumed a role in cardiac rehabilitation of patients with CAD, as well, because it reduces mortality and increases myocardial perfusion. This has been largely attributed to exercise training-mediated correction of coronary endothelial dysfunction in CAD. Indeed, regular physical activity restores the balance between NO production and NO inactivation by reactive oxygen species in CAD, thereby enhancing the vasodilatory capacity in different vascular beds. Because endothelial dysfunction has been identified as a predictor of cardiovascular events, the partial reversal of endothelial dysfunction secondary to exercise training might be the most likely mechanism responsible for the exercise training-induced reduction in cardiovascular morbidity and mortality in patients with CAD.