Steady-state cerebral blood flow regulation at altitude: interaction between oxygen and carbon dioxide

High-altitude ascent imposes a unique cerebrovascular challenge due to two opposing blood gas chemostimuli. Specifically, hypoxia causes cerebral vasodilation, whereas respiratory-induced hypocapnia causes vasoconstriction. The conflicting nature of these two superimposed chemostimuli presents a cha...

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Bibliographic Details
Published in:	European journal of applied physiology 2019-12, Vol.119 (11-12), p.2529-2544
Main Authors:	Lafave, Hailey C., Zouboules, Shaelynn M., James, Marina A., Purdy, Graeme M., Rees, Jordan L., Steinback, Craig D., Ondrus, Peter, Brutsaert, Tom D., Nysten, Heidi E., Nysten, Cassandra E., Hoiland, Ryan L., Sherpa, Mingma T., Day, Trevor A.
Format:	Article
Language:	eng
Subjects:	Acclimatization - physiology Adult Altitude Biomedical and Life Sciences Biomedicine Blood flow Blood Flow Velocity - physiology Blood pressure Brain - metabolism Brain - physiopathology Carbon dioxide Carbon Dioxide - metabolism Carotid artery Carotid Artery, Internal - metabolism Carotid Artery, Internal - physiopathology Cerebral blood flow Cerebrovascular Circulation - physiology Female High-altitude environments Human Physiology Humans Hypocapnia - metabolism Hypocapnia - physiopathology Hypoxia Hypoxia - metabolism Hypoxia - physiopathology Infrared spectroscopy Male Occupational Medicine/Industrial Medicine Original Article Oxygen - metabolism Oxygenation Sports Medicine Ultrasound Vasoconstriction Vasoconstriction - physiology Vasodilation Vertebrae Vertebral Artery - metabolism Vertebral Artery - physiology Young Adult
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Summary:	High-altitude ascent imposes a unique cerebrovascular challenge due to two opposing blood gas chemostimuli. Specifically, hypoxia causes cerebral vasodilation, whereas respiratory-induced hypocapnia causes vasoconstriction. The conflicting nature of these two superimposed chemostimuli presents a challenge in quantifying cerebrovascular reactivity (CVR) in chronic hypoxia. During incremental ascent to 4240 m over 7 days in the Nepal Himalaya, we aimed to (a) characterize the relationship between arterial blood gas stimuli and anterior, posterior and global (g)CBF, (b) develop a novel index to quantify cerebral blood flow (CBF) in relation to conflicting steady-state chemostimuli, and (c) assess these relationships with cerebral oxygenation (rSO 2 ). On rest days during ascent, participants underwent supine resting measures at 1045 m (baseline), 3440 m (day 3) and 4240 m (day 7). These measures included pressure of arterial (Pa)CO 2 , PaO 2 , arterial O 2 saturation (SaO 2 ; arterial blood draws), unilateral anterior, posterior and gCBF (duplex ultrasound; internal carotid artery [ICA] and vertebral artery [VA], gCBF [{ICA + VA} × 2], respectively) and rSO 2 (near-infrared spectroscopy). We developed a novel stimulus index (SI), taking into account both chemostimuli (PaCO 2 /SaO 2 ). Subsequently, CBF was indexed against the SI to assess steady-state cerebrovascular responsiveness (SS-CVR). When both competing chemostimuli are taken into account, (a) SS-CVR was significantly higher in ICA, VA and gCBF at 4240 m compared to lower altitudes, (b) delta SS-CVR with ascent (1045 m vs. 4240 m) was higher in ICA vs. VA, suggesting regional differences in CBF regulation, and (c) ICA SS-CVR was strongly and positively correlated ( r = 0.79) with rSO 2 at 4240 m.
ISSN:	1439-6319 1439-6327