HighlightsHeart failure is associated to autonomic dysfunction of cardiovascular system characterized by sympathetic hyperactivity.Exercise intervention promotes mechanisms that restores the autonomic balance.The effects of exercise training on sympathetic nerve activity in heart failure patients have not been summarized.In patients with heart failure, exercise training reduces sympathetic nerve activity compared with non-trained patients.The quality of evidence across the studies was moderate and the heterogeneity across the studies was high.

The physiological regulation of vascular function is essential for cardiovascular health and depends on adequate control of molecular mechanisms triggered by endothelial cells in response to mechanical and chemical stimuli induced by blood flow. Endothelial dysfunction is one of the major risk factors for cardiovascular disease, where an imbalance between synthesis of vasodilator and vasoconstrictor molecules is one of its main mechanisms. In this context, the shear stress is one of the most important mechanical stimuli to improve vascular function, due to endothelial mechanotransduction, triggered by stimulation of various endothelial mechanosensors, induce signaling pathways culminating in increased bioavailability of vasodilators molecules such as nitric oxide, that finally trigger the angiogenic mechanisms. These mechanisms allow providing the physiological basis for the effects of exercise on vascular health. In this review it is discussed the molecular mechanisms involved in the vascular response induced by shear stress and its impact in reversing vascular injury associated with the most prevalent cardiovascular disease in our population.