title: Exercise capacity and cytochrome oxidase activity in muscle mitochondria of COPD patients.
abstract: 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.
authors.affiliation: Dip. di Medicina Sperimentale, Sez. di Farmacologia, Facoltà di Medicina e Chirurgia, Seconda Università di Napoli, Italy. bruno.dagostino@unina2.it
authors.forename: Bruno
authors.initials: B
authors.lastname: D'Agostino
authors.forename: Mario
authors.initials: M
authors.lastname: Polverino
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Cirino
authors.forename: Assunta
authors.initials: A
authors.lastname: Lombardi
authors.forename: Bruno
authors.initials: B
authors.lastname: Grassi
authors.forename: Nikol
authors.initials: N
authors.lastname: Sullo
authors.forename: Carlo
authors.initials: C
authors.lastname: Santoriello
authors.forename: Francesca
authors.initials: F
authors.lastname: Polverino
authors.forename: Donatella
authors.initials: D
authors.lastname: Orlotti
authors.forename: Maria
authors.initials: M
authors.lastname: Matteis
authors.forename: Francesco
authors.initials: F
authors.lastname: Rossi
mesh_terms: D000368:Aged; D001993:Bronchodilator Agents / Q000627:therapeutic use; D003576:Electron Transport Complex IV / Q000378:metabolism*; D004983:Ethanolamines / Q000627:therapeutic use; D005080:Exercise Test / Q000379:methods; D017079:Exercise Tolerance / Q000502:physiology*; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D000068759:Formoterol Fumarate; D006801:Humans; D008297:Male; D008875:Middle Aged; D008931:Mitochondria, Muscle / Q000201:enzymology / Q000502:physiology*; D018482:Muscle, Skeletal / Q000201:enzymology / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology; D010865:Pilot Projects; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism / Q000503:physiopathology*; D016037:Single-Blind Method
chemical_list: D001993:Bronchodilator Agents; D004983:Ethanolamines; D003576:Electron Transport Complex IV; D000068759:Formoterol Fumarate