ABSTRACT
Two thermolytic thermoregulatory responses, cutaneous vasodilation and sweating, begin when core temperature reaches a critical threshold, after which response magnitudes increase linearly with increasing core temperature; thus the slope indicates response sensitivity. We evaluated the influence of hypocapnia induced by voluntary hyperventilation on the core temperature threshold and sensitivity of thermoregulatory responses. Ten healthy males performed 15 min of cycling at 117 W (29.5°C, 50% RH) under three breathing conditions: 1) spontaneous ventilation, 2) voluntary normocapnic hyperventilation, and 3) voluntary hypocapnic hyperventilation. In the hypocapnic hyperventilation trial, end-tidal CO2 pressure was reduced throughout the exercise, whereas it was maintained around the normocapnic level in the other two trials. Cutaneous vascular conductances at the forearm and forehead were evaluated as laser-Doppler signal/mean arterial blood pressure, and the forearm sweat rate was measured using the ventilated capsule method. Esophageal temperature threshold was higher for the increase in cutaneous vascular conductance in the hypocapnic than normocapnic hyperventilation trial at the forearm (36.88 ± 0.36 vs. 36.68 ± 0.34°C, P < 0.05) and forehead (36.89 ± 0.31 vs. 36.75 ± 0.31°C, P < 0.05). The slope relating esophageal temperature to cutaneous vascular conductance was decreased in the hypocapnic than normocapnic hyperventilation trial at the forearm (302 ± 177 vs. 420 ± 178% baseline/°C, P < 0.05) and forehead (236 ± 164 vs. 358 ± 221% baseline/°C, P < 0.05). Neither the threshold nor the slope for the forearm sweat rate differed significantly between the hypocapnic or normocapnic hyperventilation trials. These findings indicate that in exercising humans, hypocapnia induced by voluntary hyperventilation does not influence sweating, but it attenuates the cutaneous vasodilatory response by increasing its threshold and reducing its sensitivity.
