We evaluated the effect of supplemental O2 on energy metabolism of hypoxemic humans by measuring O2 uptake (VO2) kinetics and other cardiorespiratory parameters in nine male chronic obstructive pulmonary disease (COPD) patients and seven age-matched control subjects (on air and on 30% O2) at rest and during moderate cycle ergometer exercise. Heart rate, ventilation, VO2, CO2 output, respiratory exchange ratio, O2 cost of work, and work efficiency were measured with a computerized metabolic cart; O2 deficit and VO2 time courses were calculated. In COPD patients, 30% O2 breathing resulted in (1) reduction of O2 deficit (from 488 +/- 34 ml in air to 398 +/- 27 ml in O2; p < 0.05) and phase 2 VO2 time constant (from 116 +/- 13 s in air to 74 +/- 12 s in O2; p < 0.05); (2) a smaller steady-state increment in CO2 output than in room air (315 +/- 17 ml/min in O2 versus 358 +/- 27 ml/min in air; p < 0.02), which resulted in a lower exercise respiratory exchange ratio (0.75 +/- 0.02 in O2 versus 0.80 +/- 0.02 in air; p < 0.02); and (3) reduced steady-state ventilation (22.6 +/- 1.0 l/min in O2 versus 25.4 +/- 1.1 l/min in air; p < 0.05). In conclusion, 30% O2 breathing accelerated exercise VO2 kinetics in mildly hypoxemic COPD patients. The observed VO2 kinetics improvement with O2 supplementation is consistent with an enhancement of aerobic metabolism in skeletal muscles during moderate exercise.

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