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The Effects of Acute High Altitude Exposure and Arterial Blood Gas Manipulation on Neurovascular Coupling in Healthy Humans
Author(s) -
Leacy Jack,
Burns David,
Jendzjowsky Nicholas,
Braun Connor,
Herrington Brittney,
Wilson Richard,
Vermeulen Tyler,
Rosenberg Alexander,
Anderson Garen,
Rickards Caroline,
Lucking Eric,
Foster Glen,
O'Halloran Ken,
Day Trevor
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.03530
Subject(s) - effects of high altitude on humans , medicine , transcranial doppler , arterial blood , hyperoxia , anesthesia , neurovascular bundle , cerebral blood flow , cardiology , middle cerebral artery , basilar artery , hypoxia (environmental) , ischemia , chemistry , oxygen , anatomy , lung , organic chemistry
Neurovascular coupling (NVC) is the temporal and spatial link between local neuronal activity and regional cerebral blood flow. High altitude elicits several vasoactive stimuli, which alter cerebrovascular tone through changes in arterial blood gases (ABGs). Previous work from our group has found NVC to remain intact during ascent to high altitude. However, given the incremental nature of the ascent profile, NVC was determined in individuals that were fully acclimatized. This study aimed to assess the effects of 1) rapid ascent to and residence at high altitude (pre vs. post acclimatisation) and 2) the isolated and combined effects of ABG manipulation on NVC response magnitude. We hypothesized that acute exposure to high altitude would impair NVC. 12 healthy participants (5 female) were recruited for this expedition. Arterial blood draws from the radial artery and NVC were measured at baseline (1045m) and on days 2 and 9 at altitude (3800m). End‐tidal gas challenges were used to elicit the isolated and combined effects of blood gas manipulation, specifically isocapnic‐hypoxia and hyperoxia gas challenges. Cerebral blood velocity was measured through the posterior cerebral artery (PCAv) using transcranial Doppler ultrasound. NVC was measured as the peak (Δpeak) and mean (Δmean) changes in PCAv during intermittent visual stimulation (VS). In addition, NVC was quantified as the change in total area under the curve (ΔtAUC) during VS. Lastly, the NVC waveform was compartmentalised into three distinct temporal regions (0‐10, 11‐20‐ and 20‐30‐seconds post‐stimulus onset) to assess mechanistic involvement during the NVC response. Immediate and chronic exposure to high altitude elicited hypoxic‐hypocapnia, evidenced by reductions in both PaO 2 and PaCO 2 (P<0.001). However, arterial pH was unchanged following acute exposure to high‐altitude (P=0.72) due to reductions in arterial bicarbonate (P< 0.001), indicative of a compensatory renal metabolic acidosis. No significant differences were observed for Δpeak, Δmean, ΔtAUC NVC response between baseline and days 2 and/or 9 at altitude (P>0.05). Moreover, neither the independent effects of hypoxia and hypocapnia, nor combined hypoxic‐hypocapnia affected Δpeak, Δmean or ΔtAUC NVC response (P >0.05). Finally, no significant differences in the magnitude of the haemodynamic response across temporal regions of the NVC response were observed during acute and sustained exposure to high altitude (P>0.05) and/or isolated and combined manipulation of ABGs (P>0.05). Our results reveal remarkable stability of the NVC response magnitude during pronounced physiological stressor associated with rapid ascent and residence at high altitude.