OXYGEN EFFECT ON O-2 DEFICIT AND VO2 KINETICS DURING EXERCISE IN OBSTRUCTIVE PULMONARY-DISEASE

We evaluated the effect of supplemental O-2 on energy metabolism of hy poxemic humans by measuring O-2 uptake (V over dot O-2) kinetics and o ther cardiorespiratory parameters in nine male chronic obstructive pul monary disease (COPD) patients and seven age-matched control subjects (on air and on 30% O-2) at rest and during moderate cycle ergometer ex ercise. Heart rate, ventilation, V over dot O-2 CO2 output, respirator y exchange ratio, O-2 cost of work, and work efficiency were measured with a computerized metabolic cart; O-2 deficit and V over dot O-2 tim e courses were calculated. In COPD patients, 30% O-2 breathing resulte d in 1) reduction of O-2 deficit (from 488 +/- 34 ml in air to 398 +/- 27 ml in O-2; P < 0.05) and phase 2 V over dot O-2 time constant (fro m 116 +/- 13 s in air to 74 +/- 12 s in O-2; P < 0.05); 2) a smaller s teady-state increment in CO2 output than in room air (315 +/- 17 my mi n in O-2 vs. 358 +/- 27 ml/min in air; P < 0.02), which resulted in a lower exercise respiratory exchange ratio (0.75 +/- 0.02 in O-2 vs. 0. 80 +/- 0.02 in air; P < 0.02); and 3) reduced steady-state ventilation (22.6 +/- 1.0 l/min in O-2 vs. 25.4 +/- 1.1 l/min in air; P < 0.05). In conclusion, 30% O-2 breathing accelerated exercise V over dot O-2 k inetics in mildly hypoxemic COPD patients. The observed V over dot O-2 kinetics improvement with O-2 supplementation is consistent with an e nhancement of aerobic metabolism in skeletal muscles during moderate e xercise.