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

^* From the Rehabilitation Clinical Trials Center, Harbor-UCLA Research and Education Institute, Torrance, CA.

Correspondence to: Richard Casaburi, PhD, MD, FCCP, Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Research and Education Institute, Building RB2, 1124 W Carson St, Torrance, CA 90502; e-mail: casaburi{at}ucla.edu

Study objectives: The slow oxygen uptake (O₂) 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 O₂ response faster and reduces transient lactate increase.

Design: Ten patients with severe COPD (ie, mean [± SD] FEV₁, 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 (E), gas exchange, and heart rate (HR) were recorded breath-by-breath, and arterialized venous pH, PCO₂, and lactate levels were measured serially.

Results: Compared to healthy subjects, the time constants () for O₂, HR, carbon dioxide output (CO₂), and E 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 O₂ kinetics but significantly slowed CO₂ and E response dynamics in both groups. Only small increases in lactate occurred with exercise, and this increase did not correlate with the for O₂.

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.

Key Words: COPD • exercise • gas exchange kinetics • lactate • muscle dysfunction • oxygen

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