Exercise Training in Chronic Obstructive Pulmonary Disease: Muscle O2 Transport Plasticity.

Both convective O2 transport to, and diffusive transport within, skeletal muscle are markedly diminished in patients with chronic obstructive pulmonary disease (COPD). However, it is unknown how these determinants of peak muscle O2 uptake (V̇MO2peak) 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 V̇MO2peak in patients with COPD.Adaptations to 8 weeks of single-leg knee-extensor exercise training were measured in 8 patients with severe COPD (forced expiratory volume in 1 s (FEV1)±sem=0.9±0.1 l) and 8 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 V̇MO2peak 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 V̇MO2peak in COPD to only ∼80% of pre-training control V̇MO2peak Muscle diffusive O2 transport increased similarly in both COPD (by ∼38% from 6.6±0.9 to 9.1±0.9 mL·min·mmHg-1) and controls (by ∼36% from 10.4±0.7 to 14.1±0.8 mL·min·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, V̇MO2peak remained constrained by limited plasticity in muscle convective O2 transport. ©The authors 2021. For reproduction rights and permissions contact permissions@ersnet.org.