Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

Abstract

Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP). Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS+20mmHg LBNP (HSLBNP), while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA V mean). Cerebrovascular responses were calculated from the slope of the change in MCA V mean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide ([Formula: see text]) during rebreathing. MCA V mean was similar in HS (55±19cms(-1)) and HSLBNP (52±16cms(-1)), and both values were reduced relative to NT (66±20cms(-1)), yet the rise in MCA V mean per Torr increase in [Formula: see text] during rebreathing was similar in each condition (NT: 2.5±0.6cms(-1)Torr(-1); HS: 2.4±0.8cms(-1)Torr(-1); HSLBNP: 2.1±1.1cms(-1)Torr(-1)). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1±0.65cms(-1)mmHg(-1)100Torr(-1); HS: 2.4±0.8cms(-1)mmHg(-1)100Torr(-1); HSLBNP: 2.0±1.0cms(-1)mmHg(-1)100Torr(-1)). These data indicate that cerebrovascular reactivity is not compromised during whole-body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.