Augmented sympathetic activity does not attenuate cerebral vasomotor reactivity to hypercapnia during heat stress

Abstract

Recent work identified that augmented sympathetic activity, via lower body negative pressure (LBNP) induced central hypovolemia, attenuates cerebral vascodilation to hypercapnia during normothermic conditions. If a similar response occurs in individuals with elevated internal temperature remains unknown. This study tested the hypothesis that, relative to normothermic conditions, heat stress would attenuate cerebral vasodilation during hypercapnia and that this response would be further attenuated when LBNP is superimposed upon the heat stress. In 10 healthy individuals (9 men) cerebral vasodilation was assessed as the increase in cerebral vascular conductance (CVC) during 3, 6, 9, 12, and 15 Torr elevations in end‐tidal carbon dioxide (PETCO2) during the following conditions: normothermia, control heat stress (Δ 1.5 ± 0.2°C), and heat stress + 20 mm Hg (Δ 1.6 ± 0.2°C). Due to logistical reasons the normothermic trial was always performed first followed by control heat stress, then heat stress + LBNP. In all thermal conditions CVC increased in a hypercapnic dependent fashion (main effect of PETCO2: P < 0.01). However, contrary to our hypothesis the CVC response to elevations in PETCO2 were similar during the three thermal conditions (main effect of thermal condition: P >; 0.45). These data suggest that CVMR is not influenced be elevated sympathetic activity induced by control heat stress and heat stress + LBNP.