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

Abstract

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• C. During heating, minute ventilation (V E ) 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 inV E from the normoxic level was small (20-29%) and unchanged during heating. When P ET,CO 2 was restored to eucapnic levels,V E was unchanged, but MCAV mean was partly restored to the level seen prior to heating (28.1% restoration at T oes 37.6• C and 38.1% restoration at T oes 38.0 • 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 (∼20%) and unaffected by increasing core temperature. Moreover, hypocapnia induced by hyperthermic hyperventilation reduces cerebral blood flow but not ventilatory responses.

Effect of hypohydration on hyperthermic hyperpnea and cutaneous vasodilation during exercise in men

“…In that study, however, core temperature (oral temperature) was substantially higher in the dehydration trial than rehydration trials (37.69 vs. 37.07°C at 12 h after entering the hot environment). Because elevations in core temperature increase V E at rest (18,19), as it does during exercise, the increased V E seen in the dehydration trial could have been caused by the greater increase in core temperature rather than the increased P osm . Consistent with that idea, before Ex2 in the present study, V E did not significantly differ between the FR Values are means Ϯ SD.…”

“…We therefore suggest that hypohydration is not a factor for hyperthermic hyperpnea and that other factor(s) could be involved. Although it has been proposed that hyperthermic hyperpnea may be associated with increased sensitivity of peripheral chemoreceptors induced by hyperthermia (53), Fujii et al (18) suggested that the increased sensitivity of peripheral chemoreceptors is not the dominant factor for hyperthermic hyperpnea. Another possible factor that could contribute to hyperthermic hyperpnea is the increase in core temperature, itself (53).…”

“…If hyperthermic hyperpnea is induced by thermoregulatory drive in exercising humans, we suggest that thermoregulatory drive (increase in ventilation) overrides chemoregulation (e.g., arterial CO 2 pressure) in hyperthermic exercising humans. On the other hand, evidence suggests that reducing arterial CO 2 pressure through hyperthemic hyperpnea reduces blood flow to the brain (18,41), so that the overridden chemoregulation could threaten brain circulatory homeostasis. Clearly, hierarchical ordering of homeostasis in hyperthermic exercising humans is complex, and additional studies will be required to conclusively determine whether hyperthermic hyperpnea is a thermoregulatory response.…”

Ventilatory response to increasing body temperature: Characteristics and effect on central fatigue

“…Hyperventilation induced by increases in body temperature leads to excessive elimination of CO2 and a decrease of arterial PCO2 (PaCO2) both at rest and during prolonged exercise 3,5,6,10,11,[16][17][18] (Fig. 1C).…”

“…1C). Given that changes in PaCO2 influence V ・ E via chemoreceptors, and that there is a positive linear relationship between V ・ E and PaCO2 19,20) , it seems likely that this hypocapnia suppresses the increase in V ・ E. To investigate the effect of hypocapnia on hyperthermia-induced hyperventilation, we examined the ventilatory response to increasing body temperature in subjects breathing CO2-enriched air to maintain PaCO2 at the eucapnic level at rest 17) and during exercise 14) . We found that V ・ E is unchanged at rest, but that during prolonged exercise at 50% of V ・ O2peak the ventilatory sensitivity to increasing body temperature is 2-3 times greater in CO2-enriched air than in room air (hypocapnic condition) ( Table 1), and that this augmentation is caused by increases in tidal volume and respiratory frequency.…”