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

Abstract

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 (V̇_MO_2peak) 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 V̇_MO_2peak 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 V̇_MO_2peak 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 V̇_MO_2peak in COPD to only ∼80% of pre-training control V̇_MO_2peak. 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, V̇_MO_2peak remained constrained by limited plasticity in muscle convective O₂ transport.