Influence of passive hyperthermia on human ventilation during rest and isocapnic hypoxia

The purpose of this study was to examine the potential interaction of core temperature and isocapnic hypoxia on human ventilation and heart rate (HR). In 2 resting head-out water-immersion trials, 8 males first breathed air and then 12% O2 in N2 while the end-tidal partial pressure of carbon dioxide was kept 0.98 (0.66) mmHg (mean (SD)) above normothermic resting levels. The first immersion trial was with a normothermic esophageal temperature (Tes) of approximately 36.7 degrees C, and for the second trial, 1 h later, water temperature was increased to give a hyperthermic Tes of approximately 38.2 degrees C. Isocapnic hypoxia increased normothermic ventilation by 4 L.min-1 (p = 0.01) from 10.12 (1.07) to 14.20 (3.21) L.min-1, and hyperthermic ventiliation by 7 L.min-1 (p = 0.002) from 13.58 (2.58) to 20.79 (3.73) L.min-1. Ventilation increases during hyperthermia were mediated by breathing frequency and, during isocapnic hypoxia, by tidal volume. Unexpectedly, there was an absence of any hypoxic ventilatory decline that could be attributed to a hydrostatic effect of immersion. Isocapnic hypoxia increased the HR by similar amounts of approximately 10 and approximately 11 beats.min-1 in normothermia and hyperthermia, respectively. In conclusion, it appears that hyperthermia increases human ventilatory but not heart rate responses to isocapnic hypoxia.