Abstract
Background: The prevalence of sarcopenia is high in advanced COPD. Although in muscle atrophy an imbalance between anabolism and catabolism is evident, data on regulation of muscle protein turnover in COPD is conflicting. Therefore, we studied molecular signatures of protein turnover in a large, well-phenotyped cohort.
Methods: Quadriceps muscle biopsies were obtained from 91 COPD patients and 14 healthy control subjects (C), recruited in Maastricht (NLD) and Golnik (SLV). Sarcopenia was assessed by DEXA. Protein and mRNA levels of regulatory constituents of muscle maintenance were analyzed.
Results: Patients were clustered by sarcopenia (Yes: S (N=39); No: NS (N=52)). Muscle maintenance regulatory constituents are depicted in Table 1.
Conclusion: Protein synthesis signalling is increased despite reduced AKT activity in sarcopenic COPD patients. Autophagy appears induced, while ubiquitin-proteasome system regulation is unaltered. This impaired coordination of protein synthesis and proteolytic signalling, despite activation of myogenesis, may contribute to muscle loss in COPD.
- Copyright ©the authors 2016
