Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress

Abstract

This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ (PetCO₂). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PetCO₂ ∼20 Torr) and normoxic hypercapnic (increase in PetCO₂ ∼9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and PetCO₂ was used to evaluate cerebrovascular CO₂ responsiveness. Passive heat stress increased core temperature (1.1 ± 0.2°C, P < 0.001) and reduced middle cerebral artery blood velocity by 8 ± 8 cm/s ( P = 0.01), reduced CBVC by 0.09 ± 0.09 CBVC units ( P = 0.02), and decreased PetCO₂ by 3 ± 4 Torr ( P = 0.07), while mean arterial blood pressure was well maintained ( P = 0.36). The slope of the CBVC-PetCO₂ relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 ± 0.006 vs. 0.009 ± 0.004 CBVC units/Torr, P = 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PetCO₂ relationship was not different between normothermia and heat stress conditions (0.028 ± 0.020 vs. 0.023 ± 0.008 CBVC units/Torr, P = 0.31). These results indicate that cerebrovascular CO₂ responsiveness, to the prescribed steady-state changes in PetCO₂, is unchanged during passive heat stress.