Effects of chemoreflexes on hyperthermic hyperventilation and cerebral blood velocity in resting heated humans.

We tested the hypothesis that hyperthermic hyperventilation in part reflects enhanced chemoreceptor ventilatory O(2) drive, and that the resultant hypocapnia attenuates ventilatory responses and/or middle cerebral artery mean blood velocity (MCAV(mean)) in resting humans. Eleven healthy subjects were passively heated for 50-80 min, causing oesophageal temperature (T(oes)) to increase by 1.6 degrees C. During heating, minute ventilation increased (P < 0.05), while end-tidal CO(2) pressure (P(ET,CO(2))) and MCAV(mean) declined. A hyperoxia test in which three breaths of hyperoxic air were inspired was performed once before heating and three times during the heating. When we observed hypocapnia (P(ET,CO(2)) below 40 mmHg), P(ET,CO(2)) was restored to the eucapnic level by adding 100% CO(2) to the inspired air immediately before the last two tests. Minute ventilation was significantly reduced by hyperoxia, and that reduction gradually increased with increasing T(oes). However, the percentage decrease in from the normoxic level was small (20-29%) and unchanged during heating. When P(ET,CO(2)) was restored to eucapnic levels, was unchanged, but MCAV(mean) was partly restored to the level seen prior to heating (28.1% restoration at T(oes) 37.6 degrees C and 38.1% restoration at T(oes) 38.0 degrees C). These findings suggest that although hyperthermia increases chemoreceptor ventilatory O(2) drive in resting humans, the relative contribution of the chemoreceptor ventilatory O(2) drive to hyperthermic hyperventilation is small ( approximately 20%) and unaffected by increasing core temperature. Moreover, hypocapnia induced by hyperthermic hyperventilation reduces cerebral blood flow but not ventilatory responses.