AIMS: This study investigated whether acute hyperoxia improves electrical muscle activity in active chronic obstructive pulmonary disease (COPD) patients with mild hypoxemia (rest PaO(2) = 9.1 +/- 0.4 kPa). METHODS: Two identical incremental exercise tests were performed by nine patients while breathing either air or 30% oxygen. Pulmonary gas exchanges, venous concentrations of lactate and pyruvate, and the electromyographic signal of the quadriceps muscle (vastus lateralis and vastus medialis) were sampled each minute. RESULTS: Peak working capacity increased significantly in hyperoxia (94.4 +/- 5.2W) compared with normoxia (85.4 +/- 5.8W, P < 0.01). During hyperoxic exercise and for a given work load, oxygen uptake was increased (P < 0.001) and ventilation decreased (P < 0.05). Lactate concentration was significantly decreased (P < 0.01) at isowork level and during recovery (respectively - 26% and at least - 15%). In the quadriceps muscle, M-wave amplitude (P < 0.05), root mean square (P < 0.01) and root mean square/oxygen uptake ratio (P < 0.001) were significantly increased during hyperoxic exercise compared with room air. Although median frequency values did not differ between conditions, the median frequency was significantly decreased for higher exercise intensity in hyperoxic condition. These modifications reflected better aerobic metabolism, later emergence of muscle fatigue, and greater muscle excitability and activation for the same level of exercise under hyperoxic condition. CONCLUSION: These data suggest that the acute addition of oxygen in active COPD patients improves their muscle electrical activity during dynamic exercise. Hypoxemia-induced skeletal muscle dysfunction most probably acts through mechanisms based on oxygen availability.
AIMS: This study investigated whether acute hyperoxia improves electrical muscle activity in active chronic obstructive pulmonary disease (COPD) patients with mild hypoxemia (rest PaO(2) = 9.1 +/- 0.4 kPa). METHODS: Two identical incremental exercise tests were performed by nine patients while breathing either air or 30% oxygen. Pulmonary gas exchanges, venous concentrations of lactate and pyruvate, and the electromyographic signal of the quadriceps muscle (vastus lateralis and vastus medialis) were sampled each minute. RESULTS: Peak working capacity increased significantly in hyperoxia (94.4 +/- 5.2W) compared with normoxia (85.4 +/- 5.8W, P < 0.01). During hyperoxic exercise and for a given work load, oxygen uptake was increased (P < 0.001) and ventilation decreased (P < 0.05). Lactate concentration was significantly decreased (P < 0.01) at isowork level and during recovery (respectively - 26% and at least - 15%). In the quadriceps muscle, M-wave amplitude (P < 0.05), root mean square (P < 0.01) and root mean square/oxygen uptake ratio (P < 0.001) were significantly increased during hyperoxic exercise compared with room air. Although median frequency values did not differ between conditions, the median frequency was significantly decreased for higher exercise intensity in hyperoxic condition. These modifications reflected better aerobic metabolism, later emergence of muscle fatigue, and greater muscle excitability and activation for the same level of exercise under hyperoxic condition. CONCLUSION: These data suggest that the acute addition of oxygen in active COPDpatients improves their muscle electrical activity during dynamic exercise. Hypoxemia-induced skeletal muscle dysfunction most probably acts through mechanisms based on oxygen availability.