Exposure to passive heat and cold stress differentially modulates cerebrovascular-CO₂ responsiveness

Heat and cold stress influence cerebral blood flow (CBF) regulatory factors (e.g., arterial CO₂ partial pressure). However, it is unclear whether the CBF response to a CO₂ stimulus (i.e., cerebrovascular-CO₂ responsiveness) is maintained under different thermal conditions. This study aimed to compare cerebrovascular-CO₂ responsiveness between normothermia, passive heat and cold stress conditions. Sixteen participants (8 female; 25 ± 7 yrs) completed two experimental sessions (randomised) comprising of normothermic and either passive heat or cold stress conditions. Middle and posterior cerebral artery velocity (MCAv, PCAv) was measured during rest, hypercapnia (5% CO₂ inhalation) and hypocapnia (voluntary hyperventilation to an end-tidal CO₂ of 30 mmHg). The linear slope of the cerebral blood velocity (CBv) response to changing end-tidal CO₂ was calculated to measure cerebrovascular-CO₂ responsiveness, and cerebrovascular conductance (CVC) was used to examine responsiveness independent of blood pressure. CBv-CVC-CO₂ responsiveness to hypocapnia was greater during heat stress compared to cold stress (MCA: +0.05 ± 0.08 cm/s/mmHg/mmHg, p=0.04; PCA: +0.02 ± 0.02 cm/s/mmHg/mmHg, p=0.002). CBv-CO₂ responsiveness to hypercapnia decreased during heat stress (MCA: -0.67 ± 0.89 cm/s/mmHg, p=0.02; PCA: -0.64 ± 0.62 cm/s/mmHg; p=0.01) and increased during cold stress (MCA: +0.98 ± 1.33 cm/s/mmHg, p=0.03; PCA: +1.00 ± 0.82 cm/s/mmHg; p=0.01) compared to normothermia. However, CBv-CVC-CO₂ responsiveness to hypercapnia was not different between thermal conditions (p>0.08). Overall, passive heat, but not cold, stress challenges maintenance of cerebral perfusion. A greater cerebrovascular responsiveness to hypocapnia during heat stress likely reduces an already impaired cerebrovascular reserve capacity and may contribute to adverse events (e.g., syncope).