Mending injured endothelium in chronic heart failure: a new target for exercise training

Abstract

The recognition that poor cardiac performance is not the sole determinant of exercise intolerance in CHF patients has altered the target of exercise training. Endothelial dysfunction impairs exercise-induced vasodilation, thereby limiting oxygen supply to working muscles and increasing ventricular afterload. Since the 1990s, it has become clear that partial correction of this maladaptive reaction is a premise for the success of exercise training. Growing evidence indicates that increased NO bioavailability and reduction in oxidative stress result from regular physical activity. However, the basic concept of endothelial dysfunction has shifted from a pure "damage model" to a more dynamic process in which endothelial repair fails to keep pace with local injury. Indeed, recent evidence indicates that endothelial progenitor cells (EPC) and circulating angiogenic cells (CAC) contribute substantially to preservation of a structurally and functionally intact endothelium. In chronic heart failure, however, these endogenous repair mechanisms appear to be disrupted. In this review, we aim to give an overview on what is currently known about the influence of physical exercise on recruitment of EPC and activation of CAC in this particular patient group.