Mitochondrial functional alterations in COPD locomotor muscle are independent of cachexia and fiber type shift
2014
Although prior studies have examined mitochondrial function in COPD muscle, none have compared cachectic versus non-cachectic patients, nor have they compared patients with type II shift versus those who are not shifted. Since mitochondrial dysfunction is thought to contribute to muscle atrophy in COPD, we hypothesized that mitochondrial alterations would be greater in cachectic patients. Similarly, we hypothesized that an impaired muscle oxidative capacity, an increase in mitochondrial ROS emission and an insensitivity to permeability transition would be greater in COPD patients with a shift towards greater type II fiber abundance. Strikingly, our results show that although there is a greater reduction in mitochondrial oxidative capacity in cachectic patients, both ROS emission and sensitivity to permeability transition are similar in cachectic versus non-cachectic patients. In regard to our second hypothesis, whereas there were no differences in oxidative capacity or ROS emission between COPD patients with type II fiber shift, a lower sensitivity to permeability transition was seen in COPD patients with a type II fiber shift. As such, our analysis reveals that fiber type shift per se is unlikely to account for the lower muscle oxidative capacity and increase in mitochondrial ROS emission seen in COPD muscle, but could explain the lower sensitivity to permeability transition. Overall, our results suggest that mitochondrial involvement in COPD is primarily to reduce oxidative capacity of COPD muscle, but as some changes are dissociated from a fiber type shift, these changes may constitute dysfunction even if they are not contributing to development of cachexia.
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