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

Heat and cold stress influence cerebral blood flow (CBF) regulatory factors (e.g., arterial CO partial pressure). However, it is unclear whether the CBF response to a CO stimulus (i.e., cerebrovascular-CO responsiveness) is maintained under different thermal conditions. This study aimed to compare cerebrovascular-CO responsiveness between normothermia, passive heat, and cold stress conditions. Sixteen participants (8 females; 25 ± 7 yr) completed two experimental sessions (randomized) comprising normothermic and either passive heat or cold stress conditions. Middle and posterior cerebral artery velocity (MCA, PCA) were measured during rest, hypercapnia (5% CO inhalation), and hypocapnia (voluntary hyperventilation to an end-tidal CO of 30 mmHg). The linear slope of the cerebral blood velocity (CB) response to changing end-tidal CO was calculated to measure cerebrovascular-CO responsiveness, and cerebrovascular conductance (CVC) was used to examine responsiveness independent of blood pressure. CB-CVC-CO responsiveness to hypocapnia was greater during heat stress compared with cold stress (MCA: +0.05 ± 0.08 cm/s/mmHg/mmHg, = 0.04; PCA: +0.02 ± 0.02 cm/s/mmHg/mmHg, = 0.002). CB-CO responsiveness to hypercapnia decreased during heat stress (MCA: -0.67 ± 0.89 cm/s/mmHg, = 0.02; PCA: -0.64 ± 0.62 cm/s/mmHg; = 0.01) and increased during cold stress (MCA: +0.98 ± 1.33 cm/s/mmHg, = 0.03; PCA: +1.00 ± 0.82 cm/s/mmHg; = 0.01) compared with normothermia. However, CB-CVC-CO responsiveness to hypercapnia was not different between thermal conditions ( > 0.08). Overall, passive heat, but not cold, stress challenges the 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). This study demonstrates that thermoregulatory-driven perfusion pressure changes, from either cold or heat stress, impact cerebrovascular responsiveness to hypercapnia. Compared with cold stress, heat stress poses a greater challenge to the maintenance of cerebral perfusion during hypocapnia, challenging cerebrovascular reserve capacity while increasing cerebrovascular-CO responsiveness. This likely exacerbates cerebral hypoperfusion during heat stress since hyperthermia-induced hyperventilation results in hypocapnia. No regional differences in middle and posterior cerebral artery responsiveness were found with thermal stress.