We hypothesize that structural changes in the lung affect regenerative capacity, dependent on COPD phenotype.
Ex-smoking COPD patients (n=54) with FEV1 30-80% predicted underwent a 12-week aerobic- and muscle strengthening intervention. For all subjects, data were collected through clinical examinations, HRCT, lung function, physical capacity, symptom questionnaires, and blood samples. The cohort was phenotyped and subdivided by a theoretical baseline threshold of 320µm airspace radius (rAiDA) measured by Airway Dimension Assessment (AiDA) to indicate a more emphysematous lung.
Recruitment is ongoing. After intervention, 30 subjects (55%) with baseline rAiDA320µm had stable or at least 5% decrease of airspace radius and 91% had increased FEV1 (>5%). Of those with an rAiDA>320µm, 85% had stable or decreased airspace and 85% had increased FEV1. In addition, a pilot proteomic analysis on serum (n=5) revealed increased concentrations of proteins related to regeneration, inflammation, and ECM remodeling, e.g. hepatocyte growth factor (36%), IL-10 (46%) and decorin (25%), but a decrease in fibroblast growth factor 2 (21%) after the intervention.
Our preliminary findings indicate that exercise had measurable effects in both subgroups of AiDA and seem to activate signaling pathways related to both remodeling and inflammation.
The implications of this project are significant for enhancing our understanding of how exercise affects lung regeneration in COPD patients. The study's focus on biomarkers and phenotypic differences can in the future help tailor exercise interventions based on the individual needs and lung characteristics of COPD patients, leading to more personalized and effective treatment plans.
Exercise
Regeneration