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

Abstract

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 (Tc; 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 (MCAvmean; transcranial Doppler), partial pressure of end-tidal carbon dioxide (PETCO2), 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 Tc, unrelated to hydration status. Without LBNP, decreases in PETCO2 accounted fully for reductions in MCAvmean across all Tc. With LBNP at heat tolerance (+1.5 or +2.0°C), PETCO2 accounted for 69 ± 25% of the change in MCAvmean. The HYPO condition did not affect MCAvmean 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 MCAvmean 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 Tc are matched, mild hypohydration does not influence cerebrovascular or cardiovascular responses to LBNP, even when stressed by a combination of hyperthermia and LBNP.