Abstract

In patients with chronic obstructive pulmonary disease (COPD), exercise training-induced improvements in peak O2 uptake (V̇O2peak) are reliant on adaptations beyond the lungs, particularly in skeletal muscle. Muscle V̇O2peak is determined by the integration of convective and diffusive O2 transport, which are markedly diminished in COPD. It remains to be determined how these components of O2 transport respond to exercise training and if their adaptation is compromised in COPD. PURPOSE: To test the hypothesis that exercise training improvements in muscle convective and diffusive O2 transport, and therefore V̇O2peak, would not be attenuated in patients with COPD compared to matched controls. METHODS: Metabolic and vascular adaptations to single leg knee extensor exercise (KE) training (1 h, 3 times a week for 8 weeks) were compared between 8 patients with severe COPD (FEV1±SE=0.9±0.1 L, 30% of predicted) and 8 controls matched for age and physical activity. Femoral arterial and venous blood samples, in conjunction with thermodilution, were used to determine muscle O2 transport and utilization at peak KE. RESULTS: Training increased muscle convective O2 transport in the controls (0.69±0.07 vs. 0.80±0.10 l/min, p<0.05), but not in the patients with COPD (0.44±0.06 vs. 0.49±0.08 l/min, p>0.05). Muscle diffusive O2 transport was increased with training in both the patients (6.6±0.8 vs. 9.1±0.1.2 ml/min/mmHg) and controls (10.4±0.9 vs. 13.3±0.9 ml/min/mmHg) (each p<0.05), which equated to an 86% training response in the patients relative to the controls. Training increased V̇O2peak in the patients with COPD (0.27±0.04 vs. 0.34±0.05 l/min) and controls (0.42±0.05 vs. 0.58±0.07 l/min) and peak work rate in the patients (12±2 vs. 16±2 W) and controls (24±4 vs. 36±4 W) (each p<0.05), which equated to a 44% (V̇O2peak) and 33% (peak work rate) training response in the patients relative to the controls. CONCLUSION: These findings document limited plasticity in convective O2 transport to the muscle, but relatively conserved plasticity in muscle diffusive O2 transport with exercise training in COPD. Thus, despite a near restoration of muscle diffusive O2 transport, the improvements in muscle V̇O2peak and peak work rate in patients with COPD were constrained by the limited plasticity in convective O2 transport.

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