Why is V˙o 2 max after altitude acclimatization still reduced despite normalization of arterial O2 content?

Author:

Calbet J. A. L.12,Boushel R.23,Rådegran G.2,Søndergaard H.2,Wagner P. D.4,Saltin B.2

Affiliation:

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

Abstract

Acute hypoxia (AH) reduces maximal O2 consumption (V˙o 2 max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]),V˙o 2 max remains low. To determine why, seven lowlanders were studied at V˙o 2 max(cycle ergometry) at sea level (SL), after 9–10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (Fi O2 = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by ∼15% in both AH and CH ( P < 0.05). At maximal exercise, arterial [O2] in AH was 31% lower than at SL ( P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O2extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. PulmonaryV˙o 2 max (4.1 ± 0.3 l/min at SL) fell to 2.2 ± 0.1 l/min in AH ( P < 0.05) and was only 2.4 ± 0.2 l/min in CH ( P < 0.05). These data suggest that the failure to recoverV˙o 2 max after acclimatization despite normalization of arterial [O2] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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