The 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 males (Mean ±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, oesophageal to +2.0°C)] whilst 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 (P_ETCO₂), heart rate (HR) and mean arterial blood pressure (MAP, photoplethysmography) were measured continuously during LBNP (0, -15, -30, -45 mm Hg). Four subjects became intolerant before +2.0°C T_c, unrelated to hydration status. Without LBNP, decreases in P_ETCO₂ accounted fully for reductions in MCAv_mean across all T_c. With LBNP at heat tolerance (+1.5°C or +2.0°C), P_ETCO₂ 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. Further, 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.

http://ift.tt/2AUZpu5