Impaired muscle mitochondrial density and/or function: a COPD-specific mitochondropathy or simply deconditioning?

Chronic obstructive pulmonary disease (COPD) is a pulmonary disease with some systemic consequences. Skeletal muscle dysfunction is one of the earliest systemic manifestations of COPD in some patients, and contributes to limited exercise capacity and poor health outcomes. The aetiology of skeletal muscle abnormalities in COPD is not fully understood, but probably represents a combination of deconditioning, muscle atrophy and nutritional deficiencies. Studies have shown that skeletal muscle from patients with COPD displays other abnormalities including increased oxidative stress, muscle fibre apoptosis and mitochondrial dysfunction. Indeed, reduced mitochondrial density and function are recognised as important components of skeletal muscle dysfunction in COPD, and reduced oxidative capacity at a skeletal muscle level is likely to contribute to exercise limitation in this population. Mitochondrial density and function are potential therapeutic targets in COPD, but it remains uncertain whether impaired mitochondrial density and/or function are attributable to ageing, inactivity and deconditioning, a COPD-specific “mitochondropathy”, or a combination of these factors. However, endurance exercise training is known to increase mitochondrial density and function in healthy volunteers, whether determined by, for example, measurements of maximal activities of mitochondrial enzymes or oxygen consumption and adenosine triphosphate production rates in …