The effects of hyperthermia and hypoxia on ventilation during low-intensity steady-state exercise

Abstract

This study assessed whether the elevated sensitivity of ventilation to hypoxia during exercise is accounted for by an elevation of esophageal temperature (Tes). Eleven males volunteered for two exercise sessions on an underwater, head-out cycle ergometer at a steady-state rate of oxygen consumption (V̇o2) of ∼0.87 l/min (SD 0.07). In one exercise session, 31.5°C (SD 1.4) water held Tesat a normothermic level of ∼37.1°C, and in the other exercise session, water at 38.2°C (SD 0.1) maintained a hyperthermic Tesof ∼38.5°C. After a 30-min rest and 20-min warm-up, exercising participants inhaled air for 10 min [Euoxia 1 (E1)], an isocapnic hypoxic gas mixture with 12% O2in N2(H1) for the next 10 min and air again [Euoxia 2 (E2)] for the last 10 min. A significant increase in V̇Eduring all hyperthermia conditions (0.01< P < 0.048) was evident; however, during hyperthermic hypoxia, there was a disproportionate and significant ( P = 0.017) increase in V̇Erelative to normothermic hypoxia. This was the main explanation for a significant esophageal temperature and gas type interaction ( P = 0.012) for V̇E. Significant effects of hyperthermia, isocapnic hypoxia, and their positive interaction remained evident after removing the influence of V̇o2on V̇E. Serum lactate and potassium concentrations, as well as hemoglobin oxygen saturation, were each not significantly different between normothermic and hyperthermic-hypoxic conditions. In conclusion, the elevated sensitivity of exercise ventilation to hypoxia during exertion appears to be modulated by elevations in esophageal temperature, potentially because of a temperature-mediated stimulation of the peripheral chemoreceptors.