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Articles in PresS, published online ahead of print October 3, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00155.2002
Submitted on March 11, 2002
Accepted on September 27, 2002
1 Department of Physical Education, University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain; The Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark
2 The Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark; Department of Exercise Science, Concordia University, Montreal, Quebec, Canada
3 The Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark
4 Department of Medicine, Section of Physiology, University of California San Diego, La Jolla, California, USA
* To whom correspondence should be addressed. E-mail: lopezcalbet{at}terra.es.
To unravel the mechanisms by which maximal oxygen uptake (VO2max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2 (hypoxia, ~5300 m.a.s.l.). With hypoxia, exercise PaO2 dropped to 31-34 mmHg and arterial O2 content (CaO2) was reduced by 35% (P < 0.001). Forty one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (PIO2) in hypoxia, while the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia (P < 0.05). Hypoxia caused a 47% decrease in VO2max (a greater fall than accountable by reduced CaO2). Peak cardiac output decreased by 17% (P < 0.01), due to equal reductions in both peak heart rate and stroke volume (P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia (P < 0.001) correlating closely with VO2max (r = 0.98, P < 0.001). Therefore three main mechanisms account for the reduction of VO2max in severe acute hypoxia: 1) reduction of PIO2; 2) impairment of pulmonary gas exchange; and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about 1/3 of the loss in VO2max.
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