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Gifford 2017 J Appl Physiol (1985)

From Bioblast
Publications in the MiPMap
Gifford JR, Trinity JD, Kwon OS, Layec G, Garten RS, Park SY, Nelson AD, Richardson RS (2017) Altered skeletal muscle mitochondrial phenotype in COPD: disease versus disuse. J Appl Physiol (1985) 124:1045-53.

Β» PMID: 29357496

Gifford JR, Trinity JD, Kwon OS, Layec G, Garten RS, Park SY, Nelson AD, Richardson RS (2017) J Appl Physiol (1985)

Abstract: Patients with chronic obstructive pulmonary disease (COPD) exhibit an altered skeletal muscle mitochondrial phenotype, which often includes reduced mitochondrial density, altered respiratory function, and elevated oxidative stress. As this phenotype may be explained by the sedentary lifestyle that commonly accompanies this disease, the aim of this study was to determine if such alterations are still evident when patients with COPD are compared to controls matched for objectively-measured, physical activity (PA, accelerometery). Indices of mitochondrial density (citrate synthase, CS activity), respiratory function (respirometry in permeabilized fibers) and muscle oxidative stress (4-Hydroxynonenal Content, 4-HNE) were assessed in muscle fibers biopsied from the vastus lateralis of 9 patients with COPD and 9 PA-matched controls (CON). Despite performing similar levels of PA (CON:18{plus minus}3, COPD:20{plus minus}7 daily minutes moderate-vigorous PA; CON: 4596{plus minus}683, COPD: 4219{plus minus}763 steps per day, P>0.70), patients with COPD still exhibited several alterations in their mitochondrial phenotype, including attenuated skeletal muscle mitochondrial density (CS activity; CON 70.6{plus minus}3.8, COPD 52.7{plus minus}6.5 U/mg, P<0.05), altered mitochondrial respiration (e.g. ratio Complex I-driven State 3 to Complex II-driven State 3, CI/CII; CON: 1.20{plus minus}0.11, COPD: 0.90{plus minus}0.05, P<0.05), and oxidative stress (4-HNE; CON: 1.35{plus minus}0.19, COPD: 2.26{plus minus}0.25 relative to Ξ²-actin, P<0.05). Furthermore, CS activity (r=0.55), CI/CII (r=0.60) and 4-HNE (r=0.49) were all significantly correlated with pulmonary function, assessed as forced expiratory volume in 1 second (FEV1, P<0.05), but not PA (P>0.05). In conclusion, the altered mitochondrial phenotype in COPD is present, even in the absence of differing levels of PA, and appears to be related to the disease itself. β€’ Keywords: COPD, Mitochondrial Dysfunction, Muscle Dysfunction, Physical Activity β€’ Bioblast editor: Kandolf G


Labels: MiParea: Respiration, Patients  Pathology: COPD 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 


Coupling state: OXPHOS  Pathway: N, S, NS