Sympathetic nervous system and muscle: A two way interaction in health and disease

This review deals with the several mechanisms that control the fine balance between muscle energy expenditure and neurally mediated vascular responses during exercise. During exercise the SNS is activated as an opposing mechanism to the endothelium – derived vasodilatation in order to preserve hemodynamic balance (and teleologically protect against inadequate perfusion of vital organs like the heart and the brain). The activation of SNS is finely modulated (functional sympatholysis) to maintain blood pressure and tissue oxygen delivery. Overall, the neural control of vascular tone during exercise has two components: central command and muscle reflex. The latter consists of a reflex, which arises from stimulation of mechanically sensitive (driven by mechanical forces) and metabolically sensitive (driven by changes in the biochemical milieu) afferent nerve endings within the exercising muscle. Together these systems are integrated and regulate SNS tone. In heart failure the abnormal muscle causes an enhanced muscle reflex to exercise, which further promotes an excessive ventilatory response subjectively perceived as breathlessness (the “muscle hypothesis”). It has been proposed that chronic overactivity of the muscle reflex may be responsible for the chronic sympathetic activation seen in HF state. In early hypertension the basal sympathetic tone is increased. It has been hypothesized that the rise in the sympathetic tone of the kidney contributes to a resetting of the renal BP-natriuresis relationship to higher levels of BP. This theory integrates the classic Guyton model (pressurenatriuresis relationship) with the central regulating role of the SNS. Some preliminary data show that muscle perfusion is abnormal in hypertension (due possibly to rarefaction), and this may be accompanied by alterations of the muscle reflex and sympathetic tone response during exercise. The mechanisms of this altered response are speculative. A close relationship exists between intensity of exercise and several cardiopulmonary physiologic mechanisms. The sympathetic nervous system (SNS) plays an important role in regulating blood flow and oxygen supply to active skeletal muscles. This review will discuss the several mechanisms that control the fine balance between muscle energy expenditure and neurally mediated vascular responses during exercise. In the first part, the mechanisms of skeletal vascular responses to sympathetic nervous activation will be presented. In the second part, observations regarding the origin of neural stimulus elicited by muscle activity will be reported. In the third part, data regarding the derangement of these mechanisms in AÚÙËÚȷ΋ Y¤ÚÙ·ÛË 16, 1: 11 20, 2007