Exercise training in COPD: muscle O₂transport 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 ′ mO 2 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 ′ mO 2 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 (FEV 1 ) 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 ′ mO 2 peak in both COPD (by ∼26% from 271±29 to 342±35 mL·min −1 ) and controls (by ∼32% from 418±37 to 553±41 mL·min −1 ), restoring V ′ mO 2 peak in COPD to only ∼80% of pre-training control V ′ mO 2 peak . Muscle diffusive O 2 transport increased similarly in both COPD (by ∼38% from 6.6±0.9 to 9.1±0.9 mL·min −1 ·mmHg −1 ) and controls (by ∼36% from 10.4±0.7 to 14.1±0.8 mL·min −1 ·mmHg −1 ), with the patients reaching ∼90% of pre-training control values. In contrast, muscle convective O 2 transport increased significantly only in controls (by ∼26% from 688±57 to 865±69 mL·min −1 ), leaving patients with COPD (438±45 versus 491±51 mL·min −1 ) at ∼70% of pre-training control values. While muscle diffusive O 2 transport in COPD was largely restored by exercise training, V ′ mO 2 peak remained constrained by limited plasticity in muscle convective O 2 transport.