Central motor command activates sympathetic outflow to the cutaneous circulation in humans.

Abstract

1. The aim of this study was to provide direct evidence that sympathetic outflow to the skin in humans is governed by central neural mechanisms. 2. Microneurographic measurements of skin sympathetic nerve activity (SNA) from the peroneal nerve was performed in nine subjects during: (1) static hand grip at 10, 20 and 30% maximal voluntary contraction (MVC); and (2) attempted static hand grip during partial neuromuscular blockade produced by injection of vecuronium. 3. Two minutes of static hand grip at 20 and 30% MVC (force output, 9-6 + 0X2 and 14A4 + 0.3 kg, respectively) evoked significant increases in skin SNA that were graded to the intensity of the exercise. Static hand grip at 10% MVC (force output, 4-8 + 0.1 kg) caused a small but insignificant increase in skin SNA. 4. During vecuronium-induced neuromuscular blockade, subjects failed to maintain a force output equivalent to the output produced during 10% MVC before vecuronium (force output: 1st min, 4-4 + 0-6 kg; 2nd min, 21 + 0 4 kg), in spite of maximal effort being applied. This attempted hand grip exercise consistently evoked considerable increases in skin SNA that did not significantly differ from the responses produced by hand grip at 30% MVC; total skin SNA increased by 246 + 93% during 2 min of attempted hand grip and increased by 243 + 77% during 2 min of static hand grip at 30% MVC (means+ S.E.M., P < 0 05). These increases in skin SNA were not due to activation of resting muscles because measurements of surface electromyography showed no activity in resting forearm muscles during static or attempted hand grip exercise. 5. This study provides direct neurophysiological evidence that central motor command can activate sympathetic outflow. During static hand grip, central motor command is the primary mechanism that stimulates sympathetic outflow to skin.

Autonomic Adjustments to Exercise in Humans

“…4). In contrast, skin SNA increases at the immediate onset of isometric handgrip and leg extension exercise (267,344,358,359,384). The increase in skin SNA at exercise onset appears proportional to the exercise intensity and remains elevated throughout exercise (267,283,344,358,359).…”

Sympathetic activation in exercise is not dependent on muscle acidosis. Direct evidence from studies in metabolic myopathies.

“…However, the time course of the MSNA response to exercise with a sympathetic activation occurring ‫ف‬ 45 s after onset of exercise closely resembles that characteristic of a chemoreflex (8,13,14,27). In contrast, sympathetic responses caused by a mechanoreflex (32) or central command (8,33) occur at the onset of exercise. Furthermore, the sustained MSNA and pressor response during post-handgrip ischemia, which we demonstrated in the McArdle patient, clearly indicates that the increase in MSNA during exercise in McArdle patients is caused by a chemoreflex unrelated to muscle acidity.…”

Determinants of skin sympathetic nerve responses to isometric exercise

“…Our data combined with previous research suggest the central command is likely the major stimulant of SSNA responses. A number of approaches such as neuromuscular blockade (27), visualization (11), transcortical magnetic stimulation of the motor cortex (23), and electrical stimulation of the mesencephalic locomotor region (5) have suggested the importance of central command in skin sympathetic responses to exercise. These data coupled with SSNA responses occurring early in exercise and the lack during postexercise muscle ischemia indicate that activation of muscle metaboreceptors is less important in this response (18).…”

“…This exercise-induced increase in skin sympathetic nerve activity (SSNA) is controlled by the engagement of central command and activation of muscle mechanoreceptors, and it may be controlled, under very specific conditions, by activation of muscle metaboreceptors (11). Unlike muscle sympathetic nerve activity, the precise determinants of exercise-induced increases in SSNA are equivocal.Previous studies indicate that the exercise-induced increases in SSNA are intensity dependent to ϳ45% of maximal voluntary contraction (MVC) and that level of effort modulates SSNA responses to isometric exercise (27,28). Seals (20) observed another determinant to exercise-induced increases in SSNA by demonstrating that the level of fatigue may be a prime factor regardless of exercise intensity.…”

“…Previous studies indicate that the exercise-induced increases in SSNA are intensity dependent to ϳ45% of maximal voluntary contraction (MVC) and that level of effort modulates SSNA responses to isometric exercise (27,28). Seals (20) observed another determinant to exercise-induced increases in SSNA by demonstrating that the level of fatigue may be a prime factor regardless of exercise intensity.…”