Effect of hypocapnia on the sensitivity of hyperthermic hyperventilation and the cerebrovascular response in resting heated humans

Elevating core temperature at rest causes increases in minute ventilation (V_E), which leads to reductions in both arterial CO₂ partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (T_es) to reach 39°C. During heating in two separate trials, end-tidal CO₂ partial pressure decreased from the level before heating (39.4±2.0 mmHg) to the end of heating (30.5±6.3 mmHg) (P=0.005) in the Control trial. This decrease was prevented by breathing CO₂-enriched air throughout the heating such that end-tidal CO₂ partial pressure did not differ between the beginning (39.8±1.5 mmHg) and end (40.9±2.7 mmHg) of heating (P=1.00). The sensitivity of V_E to rising T_es (i.e., slope of the T_es-V_E relation) did not differ between the Control and CO₂-breathing trials (37.1±43.1 vs. 16.5±11.1 l·min^-1·°C^-1, P=0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P<0.01), despite the absence of hyperventilation-induced hypocapnia. CO₂-breathing increased MCAV relative to Control at the end of heating (P=0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest, ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia, and that most of the decrease in cerebral blood flow occurs independently of hypocapnia.

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