Characterising the protective vasodilatory effects of hypobaric hypoxia on the neurovascular coupling response.

Abstract

Neurovascular coupling (NVC) is the link between local neuronal activity and regional cerebral blood flow. High altitude (HA) ascent induces acute hypoxic vasodilation of the cerebral vasculature, with associated changes in CO₂ and acid-base status. We aimed to characterise the effects of (a) acute removal of the HA-induced vasodilation and (b) rapid ascent to and residency at HA on NVC responses. In twelve healthy participants (7 M/5F), arterial blood gases and NVC were measured at baseline (1130 m) and on days two (<24 h at HA) and nine (post-acclimatisation) at 3800 m. Acute gas challenges were performed using end-tidal forcing, with (a) normoxia and isocapnic hypoxia at 1130 m and (b) poikilocapnic hypoxia and isocapnic hyperoxia on days two and nine at 3800 m. Posterior cerebral artery velocity (PCAv) was measured using transcranial Doppler ultrasound in each condition and time-point. NVC was assessed via a standardized 30 s intermittent strobe light visual stimulus (VS), and quantified as the peak and mean change from baseline in PCAv. No significant differences were observed for any NVC metric across all conditions and time points. Our results reveal remarkable stability of the NVC response following (a) acute removal of HA-induced hypoxic vasodilation and (b) rapid ascent to and residency at 3800 m.