Exercise capacity and cytochrome oxidase activity in muscle mitochondria of COPD patients

• Published in: Respiratory medicine Vol. 104; no. 1; pp. 83 - 90
• Main Authors: D'Agostino, Bruno, Polverino, Mario, Cirino, Giuseppe, Lombardi, Assunta, Grassi, Bruno, Sullo, Nikol, Santoriello, Carlo, Polverino, Francesca, Orlotti, Donatella, Matteis, Maria, Rossi, Francesco
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01.01.2010; Elsevier; Elsevier Limited
• Subjects: Aged; Biological and medical sciences; Bronchodilator Agents - therapeutic use; Chronic obstructive pulmonary disease, asthma; Chronic obtructive pulmonary disease; Cytochrome oxidase activity; Disease; Electron Transport Complex IV - metabolism; Emphysema; Ethanolamines - therapeutic use; Exercise Test - methods; Exercise Tolerance - physiology; Family medical history; Female; Forced Expiratory Volume - physiology; Formoterol Fumarate; Hospitals; Humans; Kinetics; Long-acting β- agonists; Male; Medical sciences; Middle Aged; Mitochondria, Muscle - enzymology; Mitochondria, Muscle - physiology; Muscle, Skeletal - enzymology; Muscle, Skeletal - physiopathology; Muscular system; Musculoskeletal system; Oxidative Stress - physiology; Pilot Projects; Pneumology; Proteins; Pulmonary Disease, Chronic Obstructive - metabolism; Pulmonary Disease, Chronic Obstructive - physiopathology; Pulmonary/Respiratory; Single-Blind Method; Skeletal muscle dysfunction; Studies; Skeletal muscle dysfunction; Cytochrome oxidase activity; Long-acting β- agonists; Chronic obtructive pulmonary disease; Physical exercise; Human; Lung disease; Enzyme; Respiratory disease; Chronic disease; Cytochrome-c oxidase; Activity; β-Adrenergic receptor agonist; Striated muscle; Chronic; Mitochondria; Capacity; Dysfunction; Bronchus disease; Long-acting β-agonists; Chronic obstructive pulmonary disease; Oxidoreductases; Obstructive pulmonary disease; Pneumology
• ISSN: 0954-6111; 1532-3064; 1532-3064
• DOI: 10.1016/j.rmed.2009.07.016

Skeletal muscle dysfunction (SMD) often occurs in patients with COPD, affecting their quality of life and mitochondrion is one of the cellular organelles involved in the pathogenesis of SMD in COPD. The aim of this study was to investigate exercise capacity and mitochondria skeletal muscle oxidative processes using a pilot study, with 20 COPD patients and 10 healthy subjects, prior to and following LABA treatment. The two groups were similar for BODE (2–7) and GOLD stages (2–3), and no one was cachectic or more symptomatic. The patients were randomized according to a distribution list. The Cycle Ergometry test with tau evaluation was used to determine exercise capacity, while a skeletal muscle biopsy for cytochrome oxidase (CytOX) activity evaluation was used to determine mitochondria skeletal muscle oxidative processes. In six of the COPD treated patients the individual values of tau and CytOX activity showed inversely parallel changes with a significant relationship between the tau values and the CytOX activity. No significant differences in tau values were observed in healthy subjects. In conclusion, LABA treatment may improve skeletal muscle oxidative processes, enhancing the CytOX activity and, at least in some COPD patients, such effects could be strictly linked to the kinetic exchanges occurring at skeletal muscle level, implying an important link between the regulation of oxygen uptake, energy production and the exercise capacity of these patients. Nevertheless, further studies are required and a better understanding of the mechanism(s) underlying LABA effects might allow us to identify or unmask new therapeutic target(s) in such patients.