Abstract
Nonacral human skin blood flow (SkBF) is determined by the balance between α-adrenergic vasoconstriction and active vasodilation. In separate studies, we used pharmacological agents to selectively block either α1- or α2-adrenoceptors to study the potential role of each receptor subtype in the control of SkBF during exercise. α1-adrenergic blockade (prazosin) increased resting SkBF but did not alter its control during exercise. Results from a subsequent α2-blockade (yohimbine) study suggest that α2-receptors mediate the relative vasoconstriction in the skin during the sympathetic activation accompanying the first few minutes of exercise. However, this vasoconstriction is overridden by active vasodilation as core temperature increases further. Both studies confirm the idea that the functional limit to increasing SkBF during prolonged exercise is due to an alteration in active vasodilation rather than vasoconstriction.
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