Effect of Hyperoxia on Gas Exchange and Lactate Kinetics Following Exercise Onset in Nonhypoxemic COPD Patients

Abstract

The slow oxygen uptake (VO(2)) kinetics observed in COPD patients is a manifestation of skeletal muscle dysfunction of multifactorial origin. We determined whether oxygen supplementation during exercise makes the dynamic VO(2) response faster and reduces transient lactate increase. Ten patients with severe COPD (ie, mean [+/- SD] FEV(1), 31 +/- 10% predicted) and 7 healthy subjects of similar age performed four repetitions of the transition between rest and 10 min of moderate-intensity, constant-work rate exercise while breathing air or 40% oxygen in random order. Minute ventilation (VE), gas exchange, and heart rate (HR) were recorded breath-by-breath, and arterialized venous pH, PCO(2), and lactate levels were measured serially. Compared to healthy subjects, the time constants (tau) for VO(2), HR, carbon dioxide output (VCO(2)), and VE kinetic responses were significantly slower in COPD patients than in healthy subjects (70 +/- 8 vs 44 +/- 3 s, 98 +/- 14 vs 44 +/- 8 s, 86 +/- 8 vs 61 +/- 4 s, and 81 +/- 7 vs 62 +/- 4 s, respectively; p < 0.05). Hyperoxia decreased end-exercise E in the COPD group but not the healthy group. Hyperoxia did not increase the speed of VO(2) kinetics but significantly slowed VCO(2) and E response dynamics in both groups. Only small increases in lactate occurred with exercise, and this increase did not correlate with the tau for VO(2). In nonhypoxemic COPD patients performing moderate exercise, the lower ventilatory requirement induced by oxygen supplementation is not related to improved muscle function but likely stems from direct chemoreceptor inhibition.