Impaired regenerative capacity contributes to skeletal muscle dysfunction in chronic obstructive pulmonary disease

Abstract

Locomotor skeletal muscle dysfunction is a relevant comorbidity of chronic obstructive pulmonary disease (COPD) and is strongly associated with worse clinical outcomes including higher mortality. Over the last decades, a large body of literature helped characterize the process, defining the disruptive muscle phenotype caused by COPD which involves reduction in muscle mass, force-generation capacity, fatigue-tolerance, and regenerative potential following injury. A major limitation in the field has been the scarcity of well-calibrated animal models to conduct mechanistic research based on loss- and gain-of-function studies. This article provides an overall description of the process, the tools available to mechanistically investigate it, and the potential role of mitochondrially-driven metabolic signals on the regulation muscle regeneration after injury in COPD. Finally, a description of future avenues to further expand on the area is proposed based on very recent evidence involving mitochondrial metabolic cues affecting myogenesis.

20 years of neuromuscular electrical stimulation in COPD

“…Other potential contributors to limb muscle dysfunction in COPD are inflammation, malnutrition, oxidative stress and hypoxaemia [ 8 ] ( figure 1 ). Limb muscle atrophy, weakness [ 9 ] and poor oxidative capacity [ 10 ] are independent predictors of morbidity, mortality and increased healthcare resource utilisation in COPD [ 11 ]. Neuromuscular electrical stimulation (NMES) was first proposed in 2002 for limb muscle dysfunction in COPD.…”