Stimulation of skin sympathetic nerve discharge by central command. Differential control of sympathetic outflow to skin and skeletal muscle during static exercise.

Abstract

Microneurographic measurements of muscle sympathetic nerve activity (SNA) have suggested that, during static exercise, central command is much less important than skeletal muscle afferents in causing sympathetic neural activation. The possibility remains, however, that the sympathetic discharge produced by central commandis targeted mainly to tissues other than skeletal muscle. To examine this possibility, we recorded SNA with microelectrodes placed selectively in skin, as well as in muscle, nerve fascicles of the peroneal nerve during static handgrip maneuvers designed to separate the effects of central command from those of muscle afferents. To study the relative effects of cutaneous sympathetic activation on sudomotor versus vasomotor function, we simultaneously estimated changes in skin blood flow (laser Doppler velocimetry) and in sudomotor (electrodermal) activation in the region of skin innervated by the impaled nerve fascicle. Two minutes of static handgrip at 10%, 20%, and 30% of maximal voluntary contraction caused large and intensity-dependent increases in skin SNA. These increases in SNAimmediately preceded the onset of muscle tension, accelerated progressively during sustained handgrip, and resolved promptly with the cessation of motor effort. The handgrip-induced increases in skin SNA were not maintained when handgrip was followed by arrest of the forearm circulation, a maneuver that maintains the stimulation of chemically sensitive muscle afferents while eliminating theinfluences of central command and mechanically sensitive muscle afferents. During normothermia, static handgrip at 30% maximal voluntary contraction caused sustained increases in skin SNA (+400±83%, mean±SEM, p <0.05) and in electrodermal activity (+276±56%, p <0.05) but only transient increases in estimated skin vascular resistance (+ 11+2%, p<0.05). When skin temperature was increased or decreased to a new stable baseline level, subsequent increases in skin SNA during handgrip were accompanied by sustained but directionally opposite changes in estimated skin vascular resistance, with exercise-induced vasodilation during hyperthermia but exercise-induced vasoconstriction during hypothermia. From these observations, we conclude the following: 1) static exercise markedly increases sympathetic outflow to skin as well as to skeletal muscle; 2) the increases in skin SNA, unlike muscle SNA, appear to be caused mainly by central command rather than by muscle afferent reflexes; and 3) this cutaneous sympathetic activation appears to be targeted both to sweat glands and to vascular smooth muscle, with the relative targeting being temperature dependent. These findings provide neurophysiological evidencein humans to support the hypothesis that central command can be a potent stimulus to sympathetic outflow, and they emphasize the marked heterogeneity in the regulation of regional sympathetic discharge during exercise by central neural and peripheral reflex mechanisms. (Circulation Research 1991;69:228-238) A ctivation of the sympathetic ...

Control of Skin Sympathetic Nerve Activity During Intermittent Static Handgrip Exercise

“…7 Central command refers to a signal emanating from the rostral brain that projects to autonomic circuits in the brainstem and is part of the generalized activation of motor and sympathetic neurons at the onset of exercise. 7 Several of our observations support a role of central command in initiating the SSNA response to exercise.…”

“…3 SSNA is less tightly linked to baroreflex control but responds to central neural stimuli and arousal. 7 Previous studies suggest that SSNA is increased by central command and by input from mechanoreceptors but not from metabolically sensitive skeletal muscle afferents. 7,8 In addition, whereas MSNA typically rises in a time-dependent fashion and after the onset of exercise, 9,10 it has been suggested that SSNA may increase immediately before the onset of muscle contraction.…”

“…7 Previous studies suggest that SSNA is increased by central command and by input from mechanoreceptors but not from metabolically sensitive skeletal muscle afferents. 7,8 In addition, whereas MSNA typically rises in a time-dependent fashion and after the onset of exercise, 9,10 it has been suggested that SSNA may increase immediately before the onset of muscle contraction. 7 However, in recent studies performed in our laboratory, exerciseinduced increases of SSNA consistently followed the onset of muscle contraction.…”

“…7,8 In addition, whereas MSNA typically rises in a time-dependent fashion and after the onset of exercise, 9,10 it has been suggested that SSNA may increase immediately before the onset of muscle contraction. 7 However, in recent studies performed in our laboratory, exerciseinduced increases of SSNA consistently followed the onset of muscle contraction. 11,12 Furthermore, during prolonged rhythmic handgrip exercise in heart failure, SSNA rose and remained elevated during posthandgrip circulatory arrest (PHG-CA).…”

Pooling in Chronic Orthostatic Intolerance

“…I have previously attributed high P v in high P v POTS to a defective venoarterial reflex 19 and a related increased flow to the lower extremities due to the effects of gravity and the failure of venoarterial reflex-mediated vasoconstriction when upright. 20,21 Current data still suggest abnormal vasoregulation. However, I demonstrated increased supine resting resistance during venous hypertension, which suggests that vasoconstriction does occur during venous hypertension.…”