Cutaneous vasodilation at simulated high altitude: Impacts on human thermoregulation and vasoconstrictor function

Abstract

During acute altitude exposure, humans maintain higher skin temperature and lower core body temperature. However, the role of cutaneous vascular regulation in these thermoregulatory differences is unclear. Therefore, the purpose of these studies was to investigate the impact of altitude exposure on reflex control of skin blood flow and core temperature during cold exposure. In Chapter IV, the effects of hypoxia and hypocapnia on cutaneous vasoconstriction during mild cold exposure were investigated. We found that hypoxia stimulates cutaneous vasodilation in men whereas skin blood flow is unaltered in women. However, during whole body cooling skin blood flow is upward shifted in both sexes. The development of hypocapnia does not affect the vascular response to hypoxia in either sex, but reduces the magnitude of cutaneous vasoconstriction during cold exposure by 50% in women. In Chapter V, we studied the timecourse of α-adrenergic blockade by yohimbine in the cutaneous circulation and how the duration of cold exposure modulates cotransmitter-mediated vasoconstriction during cold stress. We found that yohimbine produces functional α-adrenergic blockade within 30 minutes of initial delivery and completely abolishes reflex cutaneous vasoconstriction during mild cold stress. This latter finding was surprising, and an additional protocol demonstrated that cotransmitter-mediated vasoconstriction only participates in the vascular response to cold stress when the exposure is more prolonged. In Chapter VI, the effects of hypoxia on cutaneous vasoconstrictor mechanisms and core cooling rate were tested during more prolonged and severe cold stress. In contrast to our findings during brief cold exposure, we showed that cutaneous vasoconstriction during prolonged cold stress is potentiated by hypoxia and abolishes hypoxic vasodilation. Moreover, increased cotransmitter-mediated vasoconstriction appears to account for this response. Hypoxia had no effect on core cooling rate during severe cold exposure. The selective potentiation of cotransmitter-mediated vasoconstriction observed during hypoxia in Chapter VI provided the basis for Chapter VII. This study was designed to test the effect of hypoxia on cutaneous vascular responsiveness to peripherally stimulated sympathetic vasoconstriction. The results demonstrated that α-adrenergic vasoconstrictor transduction is not affected by hypoxia, and that stimulation of adrenergic nerves with tyramine does not elicit cotransmitter-mediated vasoconstriction in skin.