No effect of skin temperature on human ventilation response to hypercapnia during light exercise with a normothermic core temperature

Hyperthermia potentiates the influence of CO₂ on pulmonary ventilation (\( \dot{V}_{\text{E}} \)). It remains to be resolved how skin and core temperatures contribute to the elevated exercise ventilation response to CO₂. This study was conducted to assess the influences of mean skin temperature (\( \overline{T}_{\text{SK}} \)) and end-tidal PCO₂ (P_ETCO₂) on \( \dot{V}_{\text{E}} \) during submaximal exercise with a normothermic esophageal temperature (T _ES). Five males and three females who were 1.76 ± 0.11 m tall (mean ± SD), 75.8 ± 15.6 kg in weight and 22.0 ± 2.2 years of age performed three 1 h exercise trials in a climatic chamber with the relative humidity (RH) held at 31.5 ± 9.5% and the ambient temperature (T _AMB) maintained at one of 25, 30, or 35°C. In each trial, the volunteer breathed eucapnic air for 5 min during a rest period and subsequently cycle ergometer exercised at 50 W until T _ES stabilized at ~37.1 ± 0.4°C. Once T _ES stabilized in each trial, the volunteer breathed hypercapnic air twice for ~5 min with P_ETCO₂ elevated by approximately +4 or +7.5 mmHg. The significantly (P < 0.05) different increases of P_ETCO₂ of +4.20 ± 0.49 and +7.40 ± 0.51 mmHg gave proportionately larger increases in \( \dot{V}_{\text{E}} \) of 10.9 ± 3.6 and 15.2 ± 3.6 L min⁻¹ (P = 0.001). This hypercapnia-induced hyperventilation was uninfluenced by varying the \( \overline{T}_{\text{SK}} \) to three significantly different levels (P < 0.001) of 33.2 ± 1.2°C, to 34.5 ± 0.8°C to 36.4 ± 0.5°C. In conclusion, the results support that skin temperature between ~33 and ~36°C has neither effect on pulmonary ventilation nor on hypercapnia-induced hyperventilation during a light exercise with a normothermic core temperature.