Cerebrovascular Reactivity is Increased with Acclimatization to 3,454 M Altitude

Abstract

Controversy exists regarding the effect of high-altitude exposure on cerebrovascular CO 2 reactivity (CVR). Confounding factors in previous studies include the use of different experimental approaches, ascent profiles, duration and severity of exposure and plausibly environmental factors associated with altitude exposure. One aim of the present study was to determine CVR throughout acclimatization to high altitude when controlling for these. Middle cerebral artery mean velocity (MCAv mean ) CVR was assessed during hyperventilation (hypocapnia) and CO 2 administration (hypercapnia) with background normoxia (sea level (SL)) and hypoxia (3,454 m) in nine healthy volunteers (26 ± 4 years (mean ± s.d.)) at SL, and after 30 minutes (HA0), 3 (HA3) and 22 (HA22) days of high-altitude (3,454 m) exposure. At altitude, ventilation was increased whereas MCAv mean was not altered. Hypercapnic CVR was decreased at HA0 (1.16% ± 0.16%/mm Hg, mean ± s.e.m.), whereas both hyper-and hypocapnic CVR were increased at HA3 (3.13% ± 0.18% and 2.96% ± 0.10%/mm Hg) and HA22 (3.32% ± 0.12% and 3.24% ± 0.14%/mm Hg) compared with SL (1.98% ± 0.22% and 2.38% ± 0.10%/mm Hg; Po0.01) regardless of background oxygenation. Cerebrovascular conductance (MCAv mean /mean arterial pressure) CVR was determined to account for blood pressure changes and revealed an attenuated response. Collectively our results show that hypocapnic and hypercapnic CVR are both elevated with acclimatization to high altitude.

Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress

“…(3) CVRCO 2 and high altitude. The CVRCO 2 increased with chronic hypoxic exposure, which is consistent with some previous reports (Fan et al 2010(Fan et al , 2014Lucas et al 2011;Flück et al 2015;Willie et al 2015). This is largely explained by the combined effects of reduced hydrogen buffering capacity and increased cerebral perfusion pressure (Fan et al 2014(Fan et al , 2016Willie et al 2015).…”

Specific effect of hypobaria on cerebrovascular hypercapnic responses in hypoxia

“…The present results showed a left shift in CVR sigmoid curve in HH, in line with a previous study at high altitude while breathing hyperoxic mixed gas (Fan et al, ). Many studies have evaluated the cerebrovascular reactivity to CO 2 in humans exposed to high altitude (Ainslie & Burgess, ; Fan et al, , ; Flück, Siebenmann, Keiser, Cathomen, & Lundby, ; Jansen et al, ; Jensen et al, ; Lucas et al, ; Willie et al, ). However, CVR in hypoxia remains unclear with controversial results.…”

AltitudeOmics: Resetting of Cerebrovascular CO2 Reactivity Following Acclimatization to High Altitude

“…The effect of high altitude exposure on cerebrovascular CO 2 reactivity has been examined by a number of studies (Jensen et al, 1996 ; Jansen et al, 1999 ; Ainslie and Burgess, 2008 ; Fan et al, 2010 , 2012 , 2014 ; Lucas et al, 2011 ; Villien et al, 2013 ; Rupp et al, 2014 ; Flück et al, 2015 ; Willie et al, 2015 ). More recently, studies have assessed cerebrovascular CO 2 reactivity in background hypoxia (Rupp et al, 2014 ; Flück et al, 2015 ; Willie et al, 2015 ), which has been shown to blunt the CBF response to CO 2 (McPherson et al, 1987 ; Fan et al, 2013 ; Ogoh et al, 2014 )—presumably by exhausting the dilatory response and reducing prostanoid synthesis (Leffler et al, 1986 ). Those studies have found cerebrovascular CO 2 reactivity to be either reduced (Rupp et al, 2014 ; Flück et al, 2015 ), or unchanged (Willie et al, 2015 ) following ascent to high altitude, while ventilatory responsiveness to CO 2 was enhanced.…”

“…More recently, studies have assessed cerebrovascular CO 2 reactivity in background hypoxia (Rupp et al, 2014 ; Flück et al, 2015 ; Willie et al, 2015 ), which has been shown to blunt the CBF response to CO 2 (McPherson et al, 1987 ; Fan et al, 2013 ; Ogoh et al, 2014 )—presumably by exhausting the dilatory response and reducing prostanoid synthesis (Leffler et al, 1986 ). Those studies have found cerebrovascular CO 2 reactivity to be either reduced (Rupp et al, 2014 ; Flück et al, 2015 ), or unchanged (Willie et al, 2015 ) following ascent to high altitude, while ventilatory responsiveness to CO 2 was enhanced. In contrast, studies assessing cerebrovascular CO 2 reactivity in background hyperoxia have consistently found it to be elevated with high altitude ascent (Fan et al, 2010 , 2012 , 2014 ) and prolonged exposure to hypoxia (Poulin et al, 2002 ), coinciding with enhanced ventilatory CO 2 sensitivity.…”