Independent and interactive effects of incremental heat strain, orthostatic stress, and mild hypohydration on cerebral perfusion

The purpose of this study was to identify the dose-dependent effects of heat strain and orthostasis [via lower body negative pressure (LBNP)], with and without mild hypohydration, on systemic function and cerebral perfusion. Eleven men (means ± SD: 27 ± 7 y; body mass 77 ± 6 kg), resting supine in a water-perfused suit, underwent progressive passive heating [0.5°C increments in core temperature (T_c; esophageal to +2.0°C)] while euhydrated (EUH) or hypohydrated (HYPO; 1.5–2% body mass deficit). At each thermal state, mean cerebral artery blood velocity (MCAv_mean; transcranial Doppler), partial pressure of end-tidal carbon dioxide (PET_CO2), heart rate (HR) and mean arterial blood pressure (MAP; photoplethysmography) were measured continuously during LBNP (0, −15, −30, and −45 mmHg). Four subjects became intolerant before +2.0°C T_c, unrelated to hydration status. Without LBNP, decreases in PET_CO2 accounted fully for reductions in MCAv_mean across all T_c. With LBNP at heat tolerance (+1.5 or +2.0°C), PET_CO2 accounted for 69 ± 25% of the change in MCAv_mean. The HYPO condition did not affect MCAv_mean or any cardiovascular variables during combined LBNP and passive heat stress (all P > 0.13). These findings indicate that hypocapnia accounted fully for the reduction in MCAv_mean when passively heat stressed in the absence of LBNP and for two-thirds of the reduction when at heat tolerance combined with LBNP. Furthermore, when elevations in T_c are matched, mild hypohydration does not influence cerebrovascular or cardiovascular responses to LBNP, even when stressed by a combination of hyperthermia and LBNP.