Exercise training in COPD: muscle O₂ transport plasticity

Both convective oxygen (O₂) 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 O₂ uptake (V'_mO2peak) respond to exercise training in patients with COPD. Therefore, the purpose of this study was to assess the plasticity of skeletal muscle O₂ transport determinants of V'_mO2peak 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 O₂ transport and utilisation at maximal exercise pre- and post-training.Training increased V'_mO2peak 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'_mO2peak in COPD to only ∼80% of pre-training control V'_mO2peak Muscle diffusive O₂ 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 O₂ 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 O₂ transport in COPD was largely restored by exercise training, V'_mO2peak remained constrained by limited plasticity in muscle convective O₂ transport.