Baroreflex-induced sympathetic activation does not alter cerebrovascular CO₂ responsiveness in humans

We investigated the effect of baroreflex-induced sympathetic activation, produced by lower body negative pressure (LBNP) at -40 mmHg, on cerebrovascular responsiveness to hyper- and hypocapnia in healthy humans. Transcranial Doppler ultrasound was used to measure blood flow velocity (CFV) in the middle cerebral artery during variations in end-tidal carbon dioxide pressure (P_ET,_CO2) of +10, +5, 0, -5, and -10 mmHg relative to eupnoea. The slopes of the linear relationships between P_ET,_CO2 and CFV were computed separately for hyper- and hypocapnia during the LBNP and no-LBNP conditions. LBNP decreased pulse pressure, but did not change mean arterial pressure. LBNP evoked an increase in ventilation that resulted in a 9 ± 2 mmHg decrease in P_ET,_CO2, which was corrected by CO₂ supplementation of the inspired air. LBNP did not affect cerebrovascular CO₂ response slopes during steady-state hypercapnia (3.14 ± 0.24 vs. 2.96 ± 0.26 cm s^-1 mmHg^-1 or hypocapnia (1.31 ± 0.18 vs. 1.32 ± 0.19 cm s^-1 mmHg^-1), or the CFV responses to voluntary apnoea (+51 ± 19 vs. +50 ± 18%). Thus, cerebrovascular CO₂ responsiveness was not altered by baroreflex-induced sympathetic activation. Our data challenge the concept that sympathetic activation restrains cerebrovascular responses to alterations in CO₂ pressure.