Exercise and muscle function in COPD

3^rd International Conference on Chronic Obstructive Pulmonary Disease

July 11-12, 2016 Brisbane, Australia

Mark Olfert

West Virginia University School of Medicine, USA

Posters & Accepted Abstracts: J Pulm Respir Med

Abstract :

Exercise limitation is a hallmark of chronic lung diseases such as COPD. Th ere is evidence of systemic contributions that contribute to exercise limitation above and beyond central pulmonary dysfunction but the cellular mechanisms remain poorly understood. Th is talk will review current and new data obtain from muscle biopsies in patients with COPD in the regards to exercise function and expression of angiogenic regulators and infl ammatory molecules in skeletal muscle. Importantly, this discussion will highlight evidence obtained in a diversity of COPD patients, which include cigarette smoked induced COPD as well as the genetic variant of COPD resulting from alpha-1 antitrypsin defi cient (AATD) individuals. Further insight will be glean from data obtain in AATD individuals that have developed COPD and AATD who have not develop COPD. Th e focus of the presentation will address whether abnormalities in the muscle angiogenic response to exercise are a consequence of systemic infl ammation stemming from lung damage or if these are based on O2 transport limitation and what eff ects exercise training and or physical fi tness exhibits in this context. Th e central premise of the talk is based on observation that deregulation of several key angiogenic regulators is responsible for many of the structural and functional alterations found in skeletal muscle of patients with COPD especially those with a cachectic phenotype and that these abnormalities produce a phenotype that is unable to protect skeletal muscle from chronic infl ammation. Exercise training can help to restore and or minimize the abnormal angio-metabolic signal axis in muscle, thereby increasing muscle capillarity and improving muscle function.

Biography :

Email: imolfert@hsc.wvu.edu