Ventilatory And Cerebrovascular Responses To Increasing Body Temperature During Exercise With Inhaling Hypercapnic Air

Abstract

Minute ventilation (VE) reportedly increases in proportion to increases in core temperature during submaximal dynamic exercise at a constant workload. This increase could induce excessive elimination of CO2 and result in a reduction in arterial PCO2 (PaCO2). Such hypocapnia could, in turn, suppress the increase in VE and induce a reduction in cerebral blood flow (CBF). We therefore hypothesized that inhaling hypercapnic air during submaximal exercise at a constant workload in the heat will augment PaCO2, leading to higher VE and mitigation of the decrease in CBF. PURPOSE: To examine the effect of inhaling hypercapnic air on ventilatory and cerebrovascular responses to increasing body temperature during exercise in the heat. METHODS: Eleven subjects exercised for ~60 min on a cycle ergometer at 50% of peak oxygen uptake with (eucapnic session; EC) and without inhaling hypercapnic air (hypocapnic session; HC). The subjects began inhaling hypercapnic air at the point end-tidal PCO2 started to decline. Esophageal temperature (Tes), skin temperature, VE, tidal volume (VT), respiratory frequency (fR), respiratory gases, middle cerebral artery mean blood velocity (MCA Vmean), heart rate, and arterial blood pressure were continuously recorded. RESULTS: During the exercise, Tes and VE increased and MCA Vmean decreased time-dependently in both sessions. Plotting VE, VT, fR, and changes in MCA Vmean (%MCA Vmean) as functions of changes in Tes from the start of the hypercapnic air inhalation (ΔTes) revealed that VE increased significantly more per 1 °C increase in ΔTes in the EC than in the HC (21.3 ± 12.5 vs. 7.5 ± 6.5 l·min−1·°C−1, P< 0.05), and this increase in VE was accompanied by an attenuated reduction in VT and by an increase in fR. %MCA Vmean declined in the HC (68.0 ± 35.4 % at ΔTes= 1.5 °C), but did not decline much in the EC (91.9 ± 12.0 % at ΔTes= 1.5 °C, P <0.05 vs. HC) (100 %MCA Vmean was the value at the start of hypercapnic air inhalation). CONCLUSIONS: These results suggest that hypocapnia induced by hyperthermic hyperventilation suppresses the ventilatory response and reduces CBF, and that inhaling hypercapnic air augments VE and attenuates the reduction in CBF. Supported by grants from COE projects, and from the Ministry of Education, Science, and Culture, Japan.