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Sleep
Original research
Effects of moderate alcohol consumption and hypobaric hypoxia: implications for passengers’ sleep, oxygen saturation and heart rate on long-haul flights
  1. Rabea Antonia Trammer1,
  2. Daniel Rooney1,
  3. Sibylle Benderoth1,
  4. Martin Wittkowski1,
  5. Juergen Wenzel1,
  6. Eva-Maria Elmenhorst1,2
  1. 1 Department of Sleep and Human Factors Research, Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany
  2. 2 Institute of Occupational, Social and Environmental Medicine, Medical Faculty, RWTH Aachen University, Aachen, Germany
  1. Correspondence to PD Dr. Eva-Maria Elmenhorst, Department of Sleep and Human Factors Research, Institute of Aerospace Medicine, German Aerospace Center, Cologne, Nordrhein-Westfalen, Germany; eva-maria.elmenhorst{at}dlr.de

Abstract

Background Passengers on long-haul flights frequently consume alcohol. Inflight sleep exacerbates the fall in blood oxygen saturation (SpO2) caused by the decreased oxygen partial pressure in the cabin. We investigated the combined influence of alcohol and hypobaric hypoxia on sleep, SpO2 and heart rate.

Methods Two groups of healthy individuals spent either two nights with a 4-hour sleep opportunity (00:00–04:00 hours) in the sleep laboratory (n=23; 53 m above sea level) or in the altitude chamber (n=17; 753 hPa corresponding to 2438 m above sea level, hypobaric condition). Participants consumed alcohol before one of the nights (mean±SE blood alcohol concentration 0.043±0.003%). The order of the nights was counterbalanced. Two 8-hour recovery nights (23:00–07:00 hours) were scheduled between conditions. Polysomnography, SpO2 and heart rate were recorded.

Results The combined exposure to alcohol and hypobaric condition decreased SpO2 to a median (25th/75th percentile) of 85.32% (82.86/85.93) and increased heart rate to a median (25th/75th percentile) of 87.73 bpm (85.89/93.86) during sleep compared with 88.07% (86.50/88.49) and 72.90 bpm (70.90/78.17), respectively, in the non-alcohol hypobaric condition, 94.97% (94.59/95.33) and 76.97 bpm (65.17/79.52), respectively, in the alcohol condition and 95.88% (95.72/96.36) and 63.74 bpm (55.55/70.98), respectively, in the non-alcohol condition of the sleep laboratory group (all p<0.0001). Under the combined exposure SpO2 was 201.18 min (188.08/214.42) below the clinical hypoxia threshold of 90% SpO2 compared with 173.28 min (133.25/199.03) in the hypobaric condition and 0 min (0/0) in both sleep laboratory conditions. Deep sleep (N3) was reduced to 46.50 min (39.00/57.00) under the combined exposure compared with both sleep laboratory conditions (alcohol: 84.00 min (62.25/92.75); non-alcohol: 67.50 min (58.50/87.75); both p<0.003).

Conclusions The combination of alcohol and inflight hypobaric hypoxia reduced sleep quality, challenged the cardiovascular system and led to extended duration of hypoxaemia (SpO2 <90%).

  • Altitude
  • Polysomnography
  • Sleep
  • Aviation
  • Hypoxia
  • Hypoxemia

Data availability statement

Data are available upon reasonable request. Data will be made available by the corresponding author upon reasonable request.

https://doi.org/10.1136/thorax-2023-220998

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    Data availability statement

    Data are available upon reasonable request. Data will be made available by the corresponding author upon reasonable request.

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    Footnotes

    • Contributors RAT: Conceptualization, formal analysis, writing - original draft, writing - review and editing. DR: Conceptualization, methodology, investigation, writing - review and editing. SB: Conceptualization, investigation, writing - review and editing. MW: Conceptualization, methodology, investigation, writing - review and editing. JW: Conceptualization, methodology, investigation, writing - review and editing. E-ME: Conceptualization, methodology, investigation, writing - review and editing, supervision, project administration, funding acquisition, guarantor.

    • Funding DLR Aeronautics Program (institutional funding; grant number: not applicable).

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.