The Impact of Acute High Altitude Exposure (3800m) And Isocapnic Hypoxia/Hyperoxia on Neurovascular Coupling in Healthy Volunteers
Authors: Leacy Jack , Burns David , Jendzjowsky Nicholas , Braun Connor , Herrington Brittney , Wilson Richard , Vermeulen Tyler , Foster Glen , Rosenberg Alexander , Anderson Garen , Rickards Caroline , Lucking Eric , O'Halloran Ken , Day Trevor 
Published: April 2020

Neurovascular coupling (NVC) is the co‐ordination of regional cerebral blood flow relative to local neuronal activity. Manipulation of arterial blood gases has a direct impact on cerebrovascular tone. Hypoxia has a vasodilatory effect whereas hypocapnia incurs vasoconstriction of cerebral vessels. The aims of this study were to determine whether acute exposure to high altitude and acute isocapnic hypoxia/hyperoxia affect the NVC response. We hypothesized that acute exposure to high‐altitude would impair NVC due to the ventilatory induced acid‐base disturbance associated with hypoxic exposure.14 healthy volunteers were assessed at baseline (1045m) and on days 2 and 9 residing at altitude (3800m). Cerebral blood velocity through the posterior cerebral artery (PCAv) was measured using transcranial Doppler ultrasound. NVC was measured as the peak and mean changes in PCAv during visual stimulation, represented as a percentage change from resting PCAv. Arterial blood was sampled from the radial artery. Ventilatory gas control was achieved via an end‐tidal forcing system. At baseline, participants were exposed to separate ventilatory challenges: room air and isocapnic hypoxia designed to mimic the O2 availability at 3800m and 5360m, respectively. On days 2 and 9 at 3800m, participants were exposed to three separate gas challenges: room air and isocapnic hyperoxia/hypoxia. The hyperoxia and hypoxia challenges were designed to mimic the O2 availability at 1045m and 5360m, respectively. NVC was assessed during each gas challenge using a 30‐sec standardized strobe light stimulus (6Hz).Exposure to high altitude elicited hypoxic‐hypocapnia, demonstrated by significant reductions in PaO2 and PaCO2 (both P<0.001). No significant changes in arterial pH were observed following acute exposure to 3800m (P=0.72) due to a compensatory renal metabolic acidosis, evidenced by significant reductions in arterial bicarbonate (P<0.001). No significant differences in peak or mean NVC response were found between baseline and days 2/9 at altitude (P=0.41, P=0.55 respectively). No significant differences were found for mean NVC response during isocapnic hypoxia or hyperoxia challenges relative to room air (P>0.16). Significant reductions were found during isocapnic hypoxia for peak NVC response at baseline and day 2 at altitude (P<0.04). However, no significant differences for peak NVC response were observed on day 9 (P=0.53).Our data illustrates that NVC remains intact following acute exposure to high altitude and during acute isocapnic manipulation of O2 availability. Future studies should examine the independent effects of CO2 manipulation and acid‐base disturbance on cerebrovascular function.Support or Funding InformationExpedition was funded by National Sciences and Engineering Research Council of Canada. In addition, Jack Leacy is a PhD trainee funded by the Department of Physiology, University College Cork