Exercise training in COPD: muscle O transport plasticity.

Both convective oxygen (O) 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 uptake (') respond to exercise training in patients with COPD. Therefore, the purpose of this study was to assess the plasticity of skeletal muscle O transport determinants of ' 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) 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 transport and utilisation at maximal exercise pre- and post-training.Training increased ' in both COPD (by ∼26% from 271±29 to 342±35 mL·min) and controls (by ∼32% from 418±37 to 553±41 mL·min), restoring ' in COPD to only ∼80% of pre-training control ' Muscle diffusive O transport increased similarly in both COPD (by ∼38% from 6.6±0.9 to 9.1±0.9 mL·min·mmHg) and controls (by ∼36% from 10.4±0.7 to 14.1±0.8 mL·min·mmHg), with the patients reaching ∼90% of pre-training control values. In contrast, muscle convective O transport increased significantly only in controls (by ∼26% from 688±57 to 865±69 mL·min), leaving patients with COPD (438±45 491±51 mL·min) at ∼70% of pre-training control values.While muscle diffusive O transport in COPD was largely restored by exercise training, ' remained constrained by limited plasticity in muscle convective O transport.