Purpose of review: The focus of this review is on translation of putative mechanisms of altered energy metabolism and muscle maintenance in cachexia to clinical comparative and intervention studies on chronic obstructive pulmonary disease (COPD).
Recent findings: Pulmonary cachexia is a well recognized feature of COPD, but its cause is poorly understood. Recent studies have shed new light on the molecular mechanisms that underlie cachexia in this disorder. In addition to muscle wasting, COPD patients also suffer from so-called loss of peripheral 'muscle oxidative phenotype', rendering these muscles less energy efficient and more prone to oxidative stress, which may in turn augment loss of muscle mass.
Summary: Recent translational approaches have clearly advanced our understanding of the pathophysiology of cachexia in COPD. Although this complex clinical syndrome may clearly benefit from multidimensional interventions, for a tailored therapeutic approach based on distinct wasting and pulmonary phenotypes, more mechanistic knowledge on abnormal regulation of energy balance and muscle maintenance in COPD cachexia is needed.