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1 Department of Physical Education, University of Las Palmas de Gran Canaria, 35017 Las Palmas de Gran Canaria, Spain; 2 The Copenhagen Muscle Research Centre, Rigshospitalet, 2200 Copenhagen N, Denmark; 3 Department of Exercise Science, Concordia University, Montreal, Quebec, Canada H4B 1R6; and 4 Department of Medicine, Section of Physiology, University of California San Diego, La Jolla, California 92093
To unravel the mechanisms by which maximal
oxygen uptake (
O2 max) 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, ~5,300 m above sea level). 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, whereas 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
O2 max (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
O2 max
(r = 0.98, P < 0.001). Therefore,
three main mechanisms account for the reduction of
O2 max 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 one-third of the loss in
O2 max.
cardiac output; fatigue; performance; cardiovascular physiology
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