Affiliation:
1. Laboratory for Exercise and Environmental Physiology, 8888 University Dr., School of Kinesiology, Simon Fraser University, Burnaby, BC V5A 1S6, Canada.
Abstract
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% O2in N2while 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 ~36.7 °C, and for the second trial, 1 h later, water temperature was increased to give a hyperthermic Tesof ~38.2 °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 ~10 and ~11 beats·min–1in normothermia and hyperthermia, respectively. In conclusion, it appears that hyperthermia increases human ventilatory but not heart rate responses to isocapnic hypoxia.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Nutrition and Dietetics,Physiology,General Medicine,Endocrinology, Diabetes and Metabolism
Cited by
13 articles.
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