EFFECT OF SYSTEMIC YOHIMBINE ON THE CONTROL OF SKIN BLOOD-FLOW DURING LOCAL HEATING AND DYNAMIC EXERCISE

We previously demonstrated that systemic alpha(1)-adrenergic blockade (prazosin) does not alter control of nonacral human skin blood flow (SkBF) during prolonged exercise. The purpose of this investigation was to examine the effects of systemic alpha(2)-adrenergic blockade on, and thus the potential contribution of alpha(2)-adrenergic vasoconstriction (VC) to, control of SkBF during graded local heating and dynamic leg exercise. Five healthy men (aged 24-30 yr) were tested after 36 h of oral yohimbine (Y; a selective alpha(2)-antagonist) treatment, or no drug [control (C)]. The dosage of Y used caused sympathetic activation, as demonstrated by significant increases in resting heart rate (Delta = 13 beats/min; P < 0.05) and mean arterial pressure (MAP, Delta = 11 mmHg; P < 0.05). Laser Doppler flowmetry was utilized to monitor changes in forearm cutaneous vascular conductance (CVC) during graded local heating of the forearm. During stepwise local heating of the forearm at sustained (20 min) local temperatures (T-local) of 34-42 degrees C, the CVC-T-local, response curve was shifted leftward by Y [half-maximum effective dose = 39.6 +/- 0.2 vs. 40.8 +/- 0.2 degrees C; P < 0.05). On a different day, the subjects performed 45 min of semi-upright dynamic leg exercise (at 48 +/- 1% maximal oxygen consumption) in a warm (36 degrees C) environment during which forearm blood flow (FBF; venous occlusion plethysmography) was measured and forearm vascular conductance (FVC; FBF/MAP) was calculated. From the initiation of exercise, FVC increased with a constant steep slope with Y [Delta FVC/initial 0.3 degrees C change in esophageal temperature (Delta T-es) = 7.2 +/- 1.8 U) but showed a slower initial rate of increase over the first few minutes in the control tests (3.4 +/- 0.6 U; P < 0.05), resulting in a more sigmoidal-shaped curve. There were no further drug effects on FVC after this initial phase as core (esophageal) temperature (T-es) increased further and FVC rose rapidly in both conditions. Likewise, there was no drug effect on the attenuated rise in FVC at higher T-es levels. These results suggest that local warming reduces, but does not abolish, alpha(2)-adrenergic vasoconstriction (VC) and that alpha(2)-receptors mediate the relative VC of forearm skin during the sympathetic activation accompanying the first few minutes of exercise. However, this VC is overridden by active vasodilation as T-es increases further. These results also confirm the idea that the functional limit to increasing SkBF during prolonged exercise is due to an alteration in active vasodilation rather than an imposition of adrenergic VC or increased vasoconstrictor activity.