Chronic Obstructive Pulmonary Disease

Biography

Biography: Mark Olfert

Abstract

Exercise limitation is a hallmark of chronic lung diseases, such as COPD. There is evidence of systemic contributions that contribute to exercise limitation above and beyond central pulmonary dysfunction, but the cellular mechanisms remain poorly understood. This talk will review currentl and new data obtain from muscle biopsys in patients with COPD in the regards to exercise function and expression of angiogenic regulators and inflammatory molecules in skeletla 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 deficient (AATD) individuals. Further insight will be glean from data obtain in AATD individuals that have developed COPD and AATD who have not develop COPD. The focus of the presentation will address whether abnormalities in the muscle angiogenic response to exercise are a consequence of systemic inflammation stemming from lung damage, or if these are based on O2 transport limitation, and what effect exercise training and/or physical fitness exhibits in this context. The 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 inflammation. Exercise training can help to restore and/or minimize the abnormal angio-metabo signal axis in muscle, thereby increasing muscle capillarity and improving muscle function.