Reduced Muscle Redox Capacity after Endurance Training in Patients with Chronic Obstructive Pulmonary Disease

Abstract

The present study was undertaken to test whether endurance training in patients with COPD, along with enhancement of muscle bioenergetics, decreases muscle redox capacity as a result of recurrent episodes of cell hypoxia induced by high intensity exercise sessions. Seventeen patients with COPD (FEV(1), 38 +/- 4% pred; PaO2), 69 +/- 2.7 mm Hg; PaCO2, 42 +/- 1.7 mm Hg) and five age-matched control subjects (C) were studied pretraining and post-training. Reduced (GSH) and oxidized (GSSG) glutathione, lipid peroxidation, and gamma-glutamyl cysteine synthase heavy subunit chain mRNA expression (gammaGCS-HS mRNA) were measured in the vastus lateralis. Pretraining redox status at rest and after moderate (40% Wpeak) constant-work rate exercise were similar between groups. After training (DeltaWpeak, 27 +/- 7% and 37 +/- 18%, COPD and C, respectively) (p < 0.05 each), GSSG levels increased only in patients with COPD (from 0.7 +/- 0.08 to 1.0 +/- 0.15 nmol/ mg protein, p < 0.05) with maintenance of GSH levels, whereas GSH markedly increased in C (from 4.6 +/- 1.03 to 8.7 +/- 0.41 nmol/ mg protein, p < 0.01). Post-training gammaGCS-HS mRNA levels increased after submaximal exercise in patients with COPD. No evidence of lipid peroxidation was observed. We conclude that although endurance training increased muscle redox potential in healthy subjects, patients with COPD showed a reduced ability to adapt to endurance training reflected in lower capacity to synthesize GSH.

Incapacity, Handicap, and Oxidative Stress Markers of Male Smokers With and Without COPD

“…72 Oxidative stress is known as a major cause of myopathy in subjects with COPD. 67,73 The present paper supports this hypothesis, since the COPD group, when compared with the non-COPD group, has a lower glutathione level (Fig. 1B).…”

Possible mechanisms underlying the development of cachexia in COPD

“…Thus, ROS and/or RNS may play a role in cachexia as molecules capable of incurring tissue damage. However, these authors [46] found that cachectic patients were able to increase their exercise capacity after training, and by relatively the same amount as noncachectic patients and normal subjects. In this context, it should not be forgotten that ROS can also serve as signalling molecules in the process of adaptation to exercise.…”

“…Furthermore, exercise training appears to accentuate oxidative stress in COPD [46]. Thus, ROS and/or RNS may play a role in cachexia as molecules capable of incurring tissue damage.…”

Skeletal muscle dysfunction and oxidative stress in patients with chronic obstructive lung disease

“…Therefore, exercise training in COPD patients would be expected to upregulate antioxidant capacity and oxidative capacity in active tissues. However, to date, investigators have found that COPD patients exhibit only a minor increase or even a decrease in muscle antioxidant potential following exercise training 79,80) , although there is a lack of data about the relationship between exercise training and muscular antioxidant capacity in COPD patients. Even though endurance exercise training is performed as part of pulmonary rehabilitation, it could cause oxidative stress in patients with severe COPD 81,82) .…”