Effect of voluntary hypocapnic hyperventilation on the relationship between core temperature and heat loss responses in exercising humans

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.

Thermoregulatory responses to combined moderate heat stress and hypoxia

“…There has been little research into the interaction between chemoreceptors and thermoreceptors. In resting humans, hypocapnia achieved through voluntary hyperventilation reduces cutaneous blood flow elicited by moderate heat stress in nonglabrous skin and in exercising humans, hypocapnia induced by voluntary hyperventilation attenuates cutaneous vasodilatory responses by increasing the vasodilatory threshold and reducing sensitivity . In contrast, hypercapnia causes modest vasodilation in nonglabrous skin under normothermic conditions, whereas superimposed hypercapnia during passive heating does not affect cutaneous blood flow .…”

“…In resting humans, hypocapnia achieved through voluntary hyperventilation reduces cutaneous blood flow elicited by moderate heat stress in nonglabrous skin 36 and in exercising humans, hypocapnia induced by voluntary hyperventilation attenuates cutaneous vasodilatory responses by increasing the vasodilatory threshold and reducing sensitivity. 37 In contrast, hypercapnia causes modest vasodilation in nonglabrous skin under normothermic conditions, 10 whereas superimposed hypercapnia during passive heating does not affect cutaneous blood flow. 38 Overall, these findings suggest that hypocapnia might contribute to the blunted forearm cutaneous blood flow responses to heating during hypoxia, but further examination of the cutaneous vascular responses to hypoxia with and without the attendant hypocapnia would be required.…”

Effect of saddle height on skin temperature measured in different days of cycling

“…We hypothesized the effects of different knee angles and saddle height positions on skin temperature, but no differences were observed. Although changes in the saddle height can increase the neuromuscular activation of specific muscles and thus increase their heat production (Saltin et al 1970 ; Kenny et al 2003 ), these were not reflected in increased skin temperature, probably due to higher sweat rate (Buono et al 2010 ; Fujii et al 2014 ). Higher sweat rate reduces the skin temperature and this favours its thermal gradient with the core (Cuddy et al 2014 ).…”

Ventilatory response to increasing body temperature: Characteristics and effect on central fatigue

“…Because hyperthermia-induced hyperventilation causes hypocapnia, it is plausible that the greater ventilatory sensitivity to increasing body temperature causes a greater drop in PaCO2. The results from Fujii et al 31) may therefore explain, in part, the negative relationship between ventilatory sensitivity to increasing body temperature and the cutaneous vasodilatory response.…”

“…3) 13) , which is consistent with the compensation hypothesis. On the other hand, Fujii et al 31) recently examined the effect of voluntary hypocapnic hyperventilation on heat-dissipating responses and reported that hypocapnia increases the Tes threshold for cutaneous vasodilation and reduces the sensitivity of the cutaneous vasodilatory response. Because hyperthermia-induced hyperventilation causes hypocapnia, it is plausible that the greater ventilatory sensitivity to increasing body temperature causes a greater drop in PaCO2.…”