Increase of sympathetic discharge to skeletal muscle but not to skin during mild lower body negative pressure in humans.

Haemodynamic studies in humans have concluded that the cutaneous circulation is regulated by cardiopulmonary baroreceptors. In contrast, neurophysiological studies have indicated that skin sympathetic outflow, unlike muscle sympathetic outflow, is unaffected by perturbations in baroreceptor activity. 2. Thus, in an attempt to resolve this discrepancy, both muscle and skin sympathetic nerve activity was recorded during unloading of mainly cardiopulmonary afferents with non-hypotensive lower body negative pressure (LBNP) performed in both normothermic and hyperthermic conditions. The function of the sympathetic activity was studied by estimations of skin blood flow (laser Doppler velocimetry), of calf blood flow (plethysmography) and of sudomotor activity (electrodermal responses). 3. A level of LBNP that caused robust increases in sympathetic outflow and vascular resistance in the skeletal muscle of the lower leg had no effect on sympathetic activity and vascular resistance in the skin of the same region in the same subjects. Both at normothermia and during hyperthermia LBNP decreased electrodermal activity. Experiments performed during sham LBNP and with skin temperature kept constant suggest that the electrodermal response was due to a decrease in skin temperature produced by the LBNP. 4. In conclusion, these findings challenge the concept that the cutaneous circulation participates importantly in the peripheral circulatory adjustments to unloading of cardiopulmonary afferents during orthostatic stress in humans. During non-hypotensive LBNP, the skeletal muscle bed accounts for all of the reflex vasoconstriction in the calf.