| Keywords |
Hyperthermia ; Isocapnic hypoxia ; vetilation ; Heart rate ; Oxygen saturation |
| Abstract |
The purpose of this study was to examine the influence of hot environment on ventilatory and cardiovascular response to isocapnic hypoxia at rest. Six volunteers (mean (±Sd): 30 ± 8 yrs, 176 ± 1 cm, 74 ± 11 kg) underwent two separate testing sessions which were normothermic (21oC, 40% RH) and hyperthermic (50oC, 40% RH) hypoxia. Each participant breathed 12% O2 in N2 mixture while the end tidal partial pressure of carbon dioxide (PETCO2) was kept approximately 1 mmHg above normothermic resting levels. Ventilation ( E) was higher in hyperthermic condition than normothermic condition during pre-hypoxia and isocapnic hypoxia (p < .05) and there were significant increases in VE at hyperthermic group for pre-hypoxia and isocapnic hypoxia (p < .05) except the resting. For brething frequency (fR), there were significant increases in hyperthermic condition during pre-hypoxia and isocapnic hypoxia (p < .05) and also were significant increases in fR at hyperthermic group than normothermic group for pre-hypoxia and isocapnic hypoxia (p < .05). Tidal Volume (VT) was higher in hyperthermic condition than normothermic condition during pre-hypoxia and isocapnic hypoxia (p < .05) and there were significant increases in VT at hyperthermic group for pre-hypoxia (p < .05). There were significant increases in heart rate (HR) at hyperthermic condition during pre-hypoxia and isocapnic hypoxia (p < .05) but not at normothermic and also were significant increases in HR at hyperthermic group than normothermic group for pre-hypoxia and isocapnic hypoxia (p < .05). For oxygen saturation (SaO2), there were significant decreases at isocapnic hypoxia relative to the resting in hyperthermic and normothermic condition (p < .05) and there was no difference between hyperthermic and normothermic group during rest, pre-hypoxia, and isocapnic hypoxia (p > .05). In conclusion, there were effects for the change of cardiovascular responses and the increase of ventilatory responses to duplicate stimuli both hyperthermia and hypoxia. |