Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia

• Published in: Journal of applied physiology (1985) Vol. 81; no. 5; pp. 1908 - 1910
• Main Authors: Roach, Robert C, Loeppky, Jack A, Icenogle, Milton V
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Physiological Soc 01-11-1996; American Physiological Society
• Subjects: Acute Disease; Adult; Altitude; Altitude Sickness - physiopathology; Atmosphere Exposure Chambers; Atmospheric Pressure; Biological and medical sciences; Humans; Hypoxia - physiopathology; Male; Medical sciences; Oxygen Consumption - physiology; Space life sciences; Transport. Aerospace. Diving. Altitude; Traumas. Diseases due to physical agents; Human; Acute mountain sickness; High altitude; Oxygen; Physical agent; Pathophysiology; Simulation; Environmental factor; Hypoxia; Altitude induced disorder; Trauma; Hypobarism; NASA Discipline Environmental Health; NASA Program Environmental Health; NASA Discipline Number 04-10; Non-NASA Center
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/jappl.1996.81.5.1908

Robert C.
Roach,
Jack A.
Loeppky, and
Milton V.
Icenogle
Copenhagen Muscle Research Center, Rigshospitalet, DK 2200 Copenhagen N, Denmark; The Lovelace Institutes, and Department of
Cardiology, University of New Mexico, Albuquerque, New Mexico
87108
Received 29 January 1996; accepted in final form 17 June 1996.
Roach, Robert C., Jack A. Loeppky, and Milton V. Icenogle.
Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia. J. Appl.
Physiol. 81(5): 1908-1910, 1996. Acute mountain
sickness (AMS) strikes those in the mountains who go too high too fast.
Although AMS has been long assumed to be due solely to the hypoxia of
high altitude, recent evidence suggests that hypobaria may also make a
significant contribution to the pathophysiology of AMS. We studied nine
healthy men exposed to simulated altitude, normobaric hypoxia, and
normoxic hypobaria in an environmental chamber for 9 h on separate
occasions. To simulate altitude, the barometric pressure was lowered to
432 ± 2 (SE) mmHg (simulated terrestrial altitude 4,564 m).
Normobaric hypoxia resulted from adding nitrogen to the chamber
(maintained near normobaric conditions) to match the inspired
P O 2 of the altitude exposure. By
lowering the barometric pressure and adding oxygen, we achieved
normoxic hypobaria with the same inspired
P O 2 as in our laboratory at normal
pressure. AMS symptom scores (average scores from 6 and 9 h of
exposure) were higher during simulated altitude (3.7 ± 0.8)
compared with either normobaric hypoxia (2.0 ± 0.8;
P  < 0.01) or normoxic hypobaria (0.4 ± 0.2; P  < 0.01). In conclusion,
simulated altitude induces AMS to a greater extent than does either
normobaric hypoxia or normoxic hypobaria, although normobaric hypoxia
induced some AMS.
high-altitude illness; hypobaria; barometric pressure
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Copyright © 1996 the American Physiological Society