This study assessed if the elevated sensitivity of ventilation to hypoxia during exercise is accounted for by an elevation of esophageal temperature (T_es). Eleven males volunteered for 2 exercise sessions on an underwater, head-out cycle ergometer at a steady-state rate of oxygen consumption (VO₂) of ~0.87 L·min^-1 (SD 0.07). In one exercise session 31.5°C (1.4) water held T_es at a normothermic level of ~37.1°C and in the other exercise session water at 38.2°C (0.1) water maintained a hyperthermic T_es of ~38.5°C. Following 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 % O₂ in N₂ (H1) for the next 10 min and air again (Euoxia 2 (E2)) for the last 10 min. A significant increase in V_E during 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 V_E relative to normothermic hypoxia. This was the main explanation for a significant esophageal temperature and gas type interaction (P = 0.012) for V_E. Significant effects of hyperthermia, isocapnic hypoxic and their positive interaction remained evident after removing the influence of VO₂ on V_E. Serum lactate and potassium concentrations, as well as hemoglobin oxygen saturation, were each not significantly different between normothermia 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 due to a temperature mediated stimulation of the peripheral chemoreceptors.