α₁-Adrenergic blockade does not alter control of skin blood flow during exercise

Human skin blood flow (SkBF) is controlled by both an α-adrenergic vasoconstrictor system and an active vasodilator system. During upright dynamic exercise, SkBF increases linearly with increasing body core temperature (T(c)) until higher (i.e., >38°C) T(c)s, beyond which little further increase in SkBF occurs. To examine the role of the two efferent control arms in this attenuated SkBF rise, we tested nine men (aged 25-53 yr) with and without (placebo) orally administered prazosin HCl (an α₁-adrenergic antagonist) during 1 h of moderate cycle exercise (100 W) in a warm (36°C, 45% relative humidity) environment. Blockade of reflex vasoconstriction was verified via a cold challenge. During exercise, mean arterial pressure (MAP, brachial auscultation) was significantly lower (P < 0.03) and heart rate significantly higher (P < 0.02) during the prazosin trials; plasma catecholamine concentrations were unaffected. Neither esophageal temperature (T(es)) nor mean skin temperature was affected by the drug during exercise. Forearm vascular conductance (FVC) was calculated from forearm blood flow (FBF, venous occlusion plethysmography) and MAP (FVC = FBF/MAP). FVC plotted as a function of time or T(es) resulted in coincident response patterns for the placebo and prazosin treatments, reaching a plateau at a T(es) of about 38°C. The responses of the older men were not selectively altered by prazosin treatment, indicating that the lower FBF responses previously seen in older subjects during exercise in the heat does not appear to be the result of an increased α₁-adrenergic tone. The attenuation of SkBF at high T(c)s is not an α₁-adrenergically mediated constrictor response but, rather, may be related to an alteration in active vasodilation.