Unchanged cerebrovascular CO2 reactivity and hypercapnic ventilatory response during strict head‐down tilt bed rest in a mild hypercapnic environment

Key points Carbon dioxide levels are mildly elevated on the International Space Station and it is unknown whether this chronic exposure causes physiological changes to astronauts. We combined ∼4 mmHg ambient PCO2 with the strict head‐down tilt bed rest model of spaceflight and this led to the develo...

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Veröffentlicht in:The Journal of physiology 2020-06, Vol.598 (12), p.2491-2505
Hauptverfasser: Laurie, Steven S., Christian, Kate, Kysar, Jacob, Lee, Stuart M.C., Lovering, Andrew T., Macias, Brandon R., Moestl, Stefan, Sies, Wolfram, Mulder, Edwin, Young, Millennia, Stenger, Michael B.
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Sprache:eng
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Zusammenfassung:Key points Carbon dioxide levels are mildly elevated on the International Space Station and it is unknown whether this chronic exposure causes physiological changes to astronauts. We combined ∼4 mmHg ambient PCO2 with the strict head‐down tilt bed rest model of spaceflight and this led to the development of optic disc oedema in one‐half of the subjects. We demonstrate no change in arterialized PCO2, cerebrovascular reactivity to CO2 or the hypercapnic ventilatory response. Our data suggest that the mild hypercapnic environment does not contribute to the development of spaceflight associated neuro‐ocular syndrome. Chronically elevated carbon dioxide (CO2) levels can occur in confined spaces such as the International Space Station. Using the spaceflight analogue 30 days of strict 6° head‐down tilt bed rest (HDTBR) in a mild hypercapnic environment (PCO2 = ∼4 mmHg), we investigated arterialized PCO2, cerebrovascular reactivity and the hypercapnic ventilatory response in 11 healthy subjects (five females) before, on days 1, 9, 15 and 30 of bed rest (BR), and 6 and 13 days after HDTBR. During all HDTBR time points, arterialized PCO2 was not significantly different from the pre‐HDTBR measured in the 6° HDT posture, with a mean (95% confidence interval) increase of 1.2 mmHg (–0.2 to 2.5 mmHg, P = 0.122) on day 30 of HDTBR. Respiratory acidosis was never detected, although a mild metabolic alkalosis developed on day 30 of HDTBR by a mean (95% confidence interval) pH change of 0.032 (0.022–0.043; P 
ISSN:0022-3751
1469-7793
DOI:10.1113/JP279383