Dysfunction of the respiratory and of peripheral skeletal muscles is known to occur in patients with severe COPD. The underlying mechanisms of muscle dysfunction in COPD are not well understood. Skeletal muscles generate ROS at rest and ROS production increases during contractile activity. Oxidative stress occurs in skeletal muscle during skeletal muscle fatigue and sepsis-induced muscle dysfunction, accompanied by an increased load imposed on the diaphragm in patients with severe COPD (148). This may be due to hypoxia, impaired mitochondrial metabolism, and increased cyto-chrome C oxidase activity in skeletal muscle in patients with COPD (148-150). Engelen and coworkers have found reduced muscle glutamate (a precursor of glutathione) levels associated with increased muscle glycolytic metabolism in patients with severe COPD (151). Lowered levels of glutamate were associated with decreased GSH levels, suggesting that oxidant/antioxidant imbalance is involved in skeletal muscle dysfunction in patients with COPD. A causal relationship between abnormally low muscle redox potential at rest and the alterations of protein metabolism observed in patients with emphysema has been suggested. This is supported by Rabinovich, who showed decreased muscle redox capacity probably due to lower ability to synthesize GSH during endurance training in patients with COPD (148). Recently, Agusti et al. (152) have shown that apoptotic pathways may be involved in skeletal muscle atrophy in patients with COPD. However, it remains to be determined whether oxidative stress plays a central role in mediating muscle mass wasting/apoptosis, particularly in susceptible subsets of patients with COPD.
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