Deficient muscle regeneration potential in sarcopenic COPD patients: Role of satellite cells

Abstract

Sarcopenia is a major comorbidity in chronic obstructive pulmonary (COPD). Whether deficient muscle repair mechanisms and regeneration exist in the vastus lateralis (VL) of sarcopenic COPD remains debatable. In the VL of control subjects and severe COPD patients with/without sarcopenia, satellite cells (SCs) were identified (immunofluorescence, specific antibodies, anti‐Pax‐7, and anti‐Myf‐5): activated (Pax‐7+/Myf‐5+), quiescent/regenerative potential (Pax‐7+/Myf‐5‐), and total SCs, nuclear activation (terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling [TUNEL]), and muscle fiber type (morphometry and slow‐ and fast‐twitch, and hybrid fibers), muscle damage (hematoxylin‐eosin staining), muscle regeneration markers (Pax‐7, Myf‐5, myogenin, and MyoD), and myostatin levels were identified. Compared to controls, in VL of sarcopenic COPD patients, myostatin content, activated SCs, hybrid fiber proportions, TUNEL‐positive cells, internal nuclei, and muscle damage significantly increased, while quadriceps muscle strength, numbers of Pax‐7+/Myf‐5‐ and slow‐ and fast‐twitch, and hybrid myofiber areas decreased. In the VL of sarcopenic and nonsarcopenic patients, TUNEL‐positive cells were greater, whereas muscle regeneration marker expression was lower than in controls. In VL of severe COPD patients regardless of the sarcopenia level, the muscle regeneration process is triggered as identified by SC activation and increased internal nuclei. Nonetheless, a lower regenerative potential along with significant alterations in muscle phenotype and damage, and increased myostatin were prominently seen in sarcopenic COPD.

Exercise Training-Induced Extracellular Matrix Protein Adaptation in Locomotor Muscles: A Systematic Review

“…All studies demonstrated that repetitive bouts of exercise over time (training) promotes changes in muscle architecture, capillarisation and myogenesis in younger and older participants, consistent with other studies [ 4 , 13 , 17 , 54 , 58 ]. Despite the variability regarding participant sex, age and exercise type/duration, muscle remodelling was accompanied by ECM adaptation.…”

“…Myostatin regulates myogenesis and inhibits muscle mass by maintaining satellite cell quiescence. Recently, the group of Barreiro demonstrated that sarcopenic muscle from COPD patients is characterised by increased levels of myostatin compared to non-sarcopenic controls [ 58 ]. However, the levels of decorin and fibronectin in sarcopenic muscle after exercise training is not known.…”

“…The importance of exercise training conditioning muscle has long been recognised for its therapeutic effect in healthy adults and counteracting muscle wasting [ 2 , 58 ]. Recently, advances have supported better understanding of the potential of exercise training for maintaining muscle mass, strength and function during ageing.…”

Do Redox Balance and Inflammatory Events Take Place in Mild Bronchiectasis? A Hint to Clinical Implications

“…Nutritional evaluation included the assessment of body mass index (BMI) and determination of fat-free mass index (FFMI) using bioelectrical impedance [ 13 , 17 , 28 , 29 , 30 ]. Blood analytical parameters (systemic inflammatory cells and markers) were also obtained in all participants.…”

“…Blood analytical parameters (systemic inflammatory cells and markers) were also obtained in all participants. Lung function parameters were determined in all study subjects following standard procedures [ 13 , 17 , 28 , 29 , 30 ]. Exercise capacity was assessed through the 6-min walking distance following previous methodologies [ 31 ].…”