Response to Electrostimulation Is Impaired in Muscle Cells from Patients with Chronic Obstructive Pulmonary Disease

• Published in: Cells (Basel, Switzerland) Switzerland), 2021-11, Vol.10 (11), p.3002
• Main Authors: Catteau, Matthias, Passerieux, Emilie, Blervaque, Léo, Gouzi, Farés, Ayoub, Bronia, Hayot, Maurice, Pomiès, Pascal
• Format: Article
• Language: English
• Subjects: Adaptation; Antibodies; Antioxidants; Antioxidants - metabolism; Atrophy; Biomarkers - metabolism; Biopsy; Biosynthesis; Case-Control Studies; Cell culture; Cell Differentiation; Chronic obstructive pulmonary disease; Contraction; COPD; differentiation; Electric Stimulation Therapy; Endurance; EPS; Exercise; Fatty acids; Female; Glucose; Human health and pathology; Humans; INK4a protein; Kinases; Life Sciences; Lipid Peroxidation; Lung diseases; Male; Metabolism; Microscopy; Middle Aged; Mitochondria; Muscle Cells - pathology; Muscle contraction; Muscle Fibers, Skeletal - pathology; muscle weakness; Musculoskeletal system; MyoD protein; Myotubes; Obstructive lung disease; Organelle Biogenesis; Oxidative Stress; p16 Protein; Physical fitness; Protein biosynthesis; Protein synthesis; Proteins; Proteolysis; Pulmonary Disease, Chronic Obstructive - pathology; Pulmonary Disease, Chronic Obstructive - therapy; Pulmonology and respiratory tract; satellite cells; Skeletal muscle; Strength training; Superoxide dismutase; Tissues and Organs; TOR protein; Values
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells10113002

Among the comorbidities associated with chronic obstructive pulmonary disease (COPD), skeletal muscle weakness and atrophy are known to affect patient survival rate. In addition to muscle deconditioning, various systemic and intrinsic factors have been implicated in COPD muscle dysfunction but an impaired COPD muscle adaptation to contraction has never been extensively studied. We submitted cultured myotubes from nine healthy subjects and nine patients with COPD to an endurance-type protocol of electrical pulse stimulation (EPS). EPS induced a decrease in the diameter, covered surface and expression of MHC1 in COPD myotubes. Although the expression of protein degradation markers was not affected, expression of the protein synthesis marker mTOR was not induced in COPD compared to healthy myotubes after EPS. The expression of the differentiation markers p16 and p21 was impaired, while expression of Myf5 and MyoD tended to be affected in COPD muscle cells in response to EPS. The expression of mitochondrial biogenesis markers PGC1α and MFN2 was affected and expression of TFAM and COX1 tended to be reduced in COPD compared to healthy myotubes upon EPS. Lipid peroxidation was increased and the expression of the antioxidant enzymes SOD2 and GPx4 was affected in COPD compared to healthy myotubes in response to EPS. Thus, we provide evidence of an impaired response of COPD muscle cells to contraction, which might be involved in the muscle weakness observed in patients with COPD.