EFFECTS OF EXERCISE TRAINING ON VASCULAR FUNCTION AND MYOCARDIAL PERFUSION

Abstract

It has long been unclear how exercise training improves myocardial perfusion in patients with stable CAD. Regression of coronary atherosclerosis and collateral formation have been favorite theories; however, angiographic techniques have so far failed to document any significant increase in coronary collaterals at rest. Although net regression of stenotic lesions may be achieved in high-intensity exercise training, it is unlikely that it causes the significant improvement in myocardial perfusion that is seen much earlier than plaque regression. The novel tools to examine coronary endothelial function in vivo and in vitro have now made it clear that exercise training enhances myocardial perfusion by increasing both eNOS and ecSOD expression, which attenuates the premature breakdown of NO by ROS. These increases in local NO production and half-life improve endothelium-dependent vasodilation in response to flow or acetylcholine. These functional changes will occur rather rapidly after the initiation of an exercise training program, although no studies are available on their precise time course. Anatomic changes, such as augmentation of the capillary bed and slowing of the progression of coronary atherosclerosis, may require more extended periods of training (Fig. 4). Recently, first reports about a possible association between endothelial dysfunction and the frequency of clinical events has been documented. Further prospective studies are needed to establish whether endothelial dysfunction is just an indicator of plaque instability or an independent prognostic marker. If it turns out to be the latter, exercise training may be promoted from a symptomatic intervention to a preventive strategy with long-term prognostic benefits.