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 PnormalCO2 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 PnormalCO2, 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. Abstract 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 (PnormalCO2 = ∼4 mmHg), we investigated arterialized PnormalCO2, 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 PnormalCO2 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 < 0.001), which remained elevated by 0.021 (0.011–0.031; P < 0.001) 6 days after HDTBR. Arterialized pH returned to pre‐HDTBR levels 13 days after BR with a change of –0.001 (–0.009 to 0.007; P = 0.991). Compared to pre‐HDTBR, cerebrovascular reactivity during and after HDTBR did not change. Baseline ventilation, ventilatory recruitment threshold and the slope of the ventilatory response were similar between pre‐HDTBR and all other time points. Taken together, these data suggest that the mildly increased ambient PnormalCO2 combined with 30 days of strict 6° HDTBR did not change arterialized PnormalCO2 levels. Therefore, the experimental conditions were not sufficient to elicit a detectable physiological response.

OBJECTIVETo determine whether the combination of a cephalad fluid shift induced by headdown tilt (HDT) bed rest and chronic exposure to mild hypercapnia for 30 days will alter sleep architecture and circadian rhythm, contributing to characteristics of Spaceflight Associated Neuro‐ocular Syndrome (SANS).METHODSAfter 14 days of ambulatory normocapnic familiarization with the facility and baseline data collection (BDC), eleven subjects (5 female) breathed mild, ambient hypercapnia (0.5% CO2) throughout 30 days of 6° HDT at the German Aerospace Center (DLR): envihab facility. Following HDT, subjects were monitored for an additional 14 days of ambulatory, normocapnic recovery (R). Overnight polysomnography (PSG) was measured using a type‐2 sleep monitoring system, and the PSG was scored by a Polysomnographic Technologist to assess sleep duration, staging, latency, and arousals. Circadian rhythm was assessed by monitoring 24‐hour core body temperature with rectal temperature probes. Arterial PCO2 levels were estimated from transcutaneous PCO2 monitoring throughout sleep. Retinal thickness was measured via optical coherence tomography (OCT); those with increased thickness >50μ in the nasal quadrant were classified as RET+, those <50μ were classified as RET‐. After one night of familiarization with the instrumentation, measurements were collected at six different time points (one BDC, three HDT, and two R).RESULTSWhen comparing RET+ to RET‐, subjects had: significantly less total sleep time (TST) in BDC (345 ± 25 min vs 401 ± 23 min, p < 0.05), HDT4 (303 ± 64 min vs 375 ± 20 min, p < 0.05), HDT28 (344 ± 59 min vs 407 ± 32 min, p < 0.05), and R+4 (344 ± 68 min vs 421 ± 21 min, p < 0.05); significantly less stage 2 (N2) sleep in HDT4 (157 ± 43 min vs 220 ± 9 min, p < 0.05), HDT28 (198 ± 32 min vs 256 ± 21 min, p < 0.05), and R+4 (187 ± 74 min vs 271 ± 32, p < 0.05); significantly more wake after sleep onset (WASO) in HDT4 (147 ± 85 min vs 57 ± 27 min, p < 0.05) and R+4 (134 ± 106 min vs 41 ± 12 min, p < 0.05); and a significantly reduced core body temperature amplitude at BDC (0.3 ± 0.1 deg vs 0.5 ± 0.1 deg, p < 0.05), HDT4 (0.2 ± 0.1 deg vs 0.4 ± 0.1 deg, p < 0.05), HDT28 (0.3 ± 0.1 deg vs 0.4 ± 0.1 deg, p < 0.05), and R+10 (0.3 ± 0.0 deg vs 0.4 ± 0.1 deg, p < 0.05).CONCLUSIONSPrior to and throughout the experimental conditions, when compared to RET‐, RET+ subjects were “short” sleepers and in general had less N2 sleep, greater WASO, and had a lower amplitude of core body temperature. We conclude that insufficient sleep may predispose certain individuals to the development of retinal thickening, a finding of SANS. Objective PSG may be a potential variable to consider when determining astronaut spaceflight duration.Support or Funding InformationNASA Human Research Program NNJ14ZSA001NThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.