Experimental, epidemiologic and clinical studies have provided strong evidence that physical exercise has beneficial effects on multiple physiological variables affecting cardiovascular health (lipoprotein levels, rest blood pressure and heart rate, carbohydrate tolerance, neurohormonal activity). Regular exercise has been shown to slow the progression of cardiovascular disease and to reduce cardiovascular morbidity and mortality. More recently, exercise-induced increases in blood flow and shear stress have been observed to enhance vascular function and structure. By increasing the release of nitric oxide and prostacyclin, shear stress augments endothelium-dependent vasodilation and inhibits multiple processes involved in atherogenesis and restenosis. In this review we discuss the underlying mechanisms by which exercise-induced blood flow and shear stress exert their salutary effects on cardiovascular remodeling.