Do alterations in intramuscular extracellular matrix protein levels disrupt the normal process of muscle remodelling in response to exercise training in patients with COPD?

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Background: A growing body of evidence demonstrates that in ageing, altered intramuscular extracellular matrix protein (ECM) composition profoundly hinders the capacity for muscle adaptation in response to exercise training (ET). We evaluated the pattern of ECM expression in response to ET between healthy young participants and patients with COPD. Methods: Vastus lateralis muscle biopsies from 29 patients (mean±SD FEV1: 43±16% predicted) and 14 healthy subjects were analysed before and after an interval ET programme for myofibre distribution and size, whereas a selection of ECM molecules was quantified using ELISA. Results: Compared to healthy participants, patients exhinited a lower capacity to increase myofibre type I distribution (by 4.7±3.4 % versus 1.3±2.2 %) and mean fibre cross-sectional area (by 13.6±3.2 % versus 9.1±1.9 %). ET induced a diverse pattern of protein levels between the two cohorts in ECMs regulating tissue structure and fibrotic remodelling [Collagen (COL 1 & 4)], exerkine myogenesis (SPARC), necroapoptotic response (Tenacin, TNC), adherence to muscle-cell precursors (Fibronectin, FN) and tissue stability (Biglycan, BGN) (Figure 1). Conclusion: Attenuated ET-induced myofibre adaptation in COPD could be associated with disregulated levels of intramuscular ECM composition and their role on muscle fibre regeneration. erj;66/suppl_69/PA4748/F1 F1 F1

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