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

¹Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, ²Department of Internal Medicine; University of Texas Southwestern Medical Center at Dallas, Dallas, and ³Department of Kinesiology, University of Texas at Arlington, Arlington, Texas

Submitted 28 September 2007 ; accepted in final form 17 January 2008

This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ (PET_CO2). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PET_CO2 20 Torr) and normoxic hypercapnic (increase in PET_CO2 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 PET_CO2 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-PET_CO2 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-PET_CO2 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 PET_CO2, is unchanged during passive heat stress.

brain blood flow; hyperthermia; hypocapnia; hypercapnia

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