Chronic Obstructive Pulmonary Disease

Biography

Biography: Esther Barreiro

Abstract

Muscle dysfunction is a major systemic manifestation in patients with lung diseases, especially in those with chronic obstructive pulmonary disease (COPD). The difference between respiratory and limb muscle dysfunction needs to be made as the diaphragm must contract at a specific resting length, which is not the case in the limb muscles. A reduction in lower limb muscle strength (namely quadriceps weakness) and atrophy (smaller size of the muscle fibers) have important clinical implications as they are predictors of disease prognosis and mortality in COPD patients. In the last two decades, many different factors and biological mechanisms have been shown to participate in the multifactorial etiology of skeletal muscle dysfunction in COPD. Our group has extensively contributed to the understanding of part of those mechanisms such as muscle oxidative stress and inflammation, oxidation of specific key muscle proteins, systemic inflammation, proteolysis mediated by the ubiquitin-proteasome system, structural muscle alterations (myofibers and sarcomere disruptions), deficiency in key muscle proteins, nutritional abnormalities, signaling pathways of muscle atrophy, apoptosis, autophagy, epigenetics, unfolding of muscle proteins, and modifications of these molecular and cellular events in response to several therapeutic strategies such as exercise and/or muscle training and rehabilitation. The conclusions are that until effective and safer pharmacological therapies emerge, exercise and muscle training modalities, alone or in combination with nutritional support, are undoubtedly the best treatment options to improve muscle mass and function, and quality of life in COPD patients. In my talk, the most recent results shown to be involved in the pathophysiology of skeletal muscle dysfunction in patients with COPD will be shown and discussed.