Study objectives: 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.
Design: 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.
Results: 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).
Conclusion: 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.