Abstract
This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO 2 (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 PET CO2 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.
Original language | English (US) |
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Pages (from-to) | 976-981 |
Number of pages | 6 |
Journal | Journal of applied physiology |
Volume | 104 |
Issue number | 4 |
DOIs | |
State | Published - Apr 2008 |
Keywords
- Brain blood flow
- Hypercapnia
- Hyperthermia
- Hypocapnia
ASJC Scopus subject areas
- Physiology
- Physiology (medical)