Exercise training in COPD: muscle O2 transport plasticity

Both convective oxygen (O-2) transport to, and diffusive transport within, skeletal muscle are markedly diminished in patients with COPD. However, it is unknown how these determinants of peak muscle O-2 uptake (V'(mO2)peak) respond to exercise training in patients with COPD. Therefore, the purpose of this study was to assess the plasticity of skeletal muscle O-2 transport determinants of V'(mO2)peak in patients with COPD. Adaptations to 8 weeks of single-leg knee-extensor exercise training were measured in eight patients with severe COPD (mean +/- SEM forced expiratory volume in 1 s (FEV1) 0.9 +/- 0.1 L) and eight healthy, well-matched controls. Femoral arterial and venous blood samples, and thermodilution-assessed leg blood flow were used to determine muscle O-2 transport and utilisation at maximal exercise pre- and post-training. Training increased V'(mO2)peak in both COPD (by similar to 26% from 271 +/- 29 to 342 +/- 35 mL.min(-1)) and controls (by similar to 32% from 418 +/- 37 to 553 +/- 41 mL.min(-1)), restoring V'(mO2)peak in COPD to only similar to 80% of pre-training control V'(mO2)peak. Muscle diffusive O-2 transport increased similarly in both COPD (by similar to 38% from 6.6 +/- 0.9 to 9.1 +/- 0.9 mL.min(-1).mmHg(-1)) and controls (by similar to 36% from 10.4 +/- 0.7 to 14.1 +/- 0.8 mL.min(-1).mmHg(-1)), with the patients reaching similar to 90% of pre-training control values. In contrast, muscle convective O-2 transport increased significantly only in controls (by similar to 26% from 688 +/- 57 to 865 +/- 69 mL.min(-1)), leaving patients with COPD (438 +/- 45 versus 491 +/- 51 mL.min(-1)) at similar to 70% of pre-training control values. While muscle diffusive O-2 transport in COPD was largely restored by exercise training, V'(mO2)peak remained constrained by limited plasticity in muscle convective O-2 transport.