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1 Division of Physiology, Department of Life Sciences, New Mexico Highlands University, Las Vegas 87701-9000; 2 Lovelace Respiratory Research Institutes, Albuquerque 87108-5127; 3 Department of Health Promotion, Physical Activity, and Exercise, University of New Mexico, Albuquerque 87131-5686; 4 VA Hospital and Department of Cardiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131-5686; and 5 Department of Physiology, School of Medicine, University of Graz, A-8010 Graz, Austria
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We hypothesized that exercise would cause
greater severity and incidence of acute mountain sickness (AMS) in the
early hours of exposure to altitude. After passive ascent to simulated
high altitude in a decompression chamber [barometric
pressure = 429 Torr, ~4,800 m (J. B. West, J. Appl.
Physiol. 81: 1850-1854, 1996)], seven men
exercised (Ex) at 50% of their altitude-specific maximal workload four
times for 30 min in the first 6 h of a 10-h exposure. On another day
they completed the same protocol but were sedentary (Sed). Measurements
included an AMS symptom score, resting minute ventilation
(
E), pulmonary function, arterial
oxygen saturation (SaO2), fluid input,
and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak
AMS scores of 4.4 ± 1.0 and 1.3 ± 0.4 in Ex and Sed, respectively
(P < 0.01); but resting
E and
SaO2 were not different between trials.
However, SaO2 during the exercise bouts
in Ex was at 76.3 ± 1.7%, lower than during either Sed or at rest in
Ex (81.4 ± 1.8 and 82.2 ± 2.6%, respectively, P < 0.01). Fluid intake-urine volume shifted to slightly positive
values in Ex at 3-6 h (P = 0.06). The mechanism(s)
responsible for the rise in severity and incidence of AMS in Ex may be
sought in the observed exercise-induced exaggeration of arterial
hypoxemia, in the minor fluid shift, or in a combination of these factors.
fluid balance; edema; oxygen saturation; pathophysiology
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