Objective: To assess the effects of acute exposure to simulated high altitude on baroreflex control of mean cerebral blood flow velocity (MCFV).
Patients and methods: We compared beat-to-beat changes in RR interval, arterial blood pressure, mean MCFV (by transcranial Doppler velocimetry in the middle cerebral artery), end-tidal CO2, oxygen saturation and respiration in 19 healthy subjects at baseline (Albuquerque, 1779 m), after acute exposure to simulated high altitude in a hypobaric chamber (barometric pressure as at 5000 m) and during oxygen administration (to achieve 100% oxygen saturation) at the same barometric pressure (HOX). Baroreflex control on each signal was assessed by univariate and bivariate power spectral analysis performed on time series obtained during controlled (15 breaths/min) breathing, before and during baroreflex modulation induced by 0.1-Hz sinusoidal neck suction.
Results: At baseline, neck suction was able to induce a clear increase in low-frequency power in MCFV (P<0.001) as well as in RR and blood pressure. At high altitude, MCFV, as well as RR and blood pressure, was still able to respond to neck suction (all P<0.001), compared to controlled breathing alone, despite marked decreases in end-tidal CO2 and oxygen saturation at high altitude. A similar response was obtained at HOX. Phase delay analysis excluded a passive transmission of low-frequency oscillations from arterial pressure to cerebral circulation.
Conclusions: During acute exposure to high altitude, cerebral blood flow is still modulated by the autonomic nervous system through the baroreflex, whose sensitivity is not affected by changes in CO2 and oxygen saturation levels.