Altered mitochondrial regulation in quadriceps muscles of patients with COPD

Naimi, Ashley I.; Bourbeau, Jean; Perrault, Hélène; Baril, Jacinthe; Wright-Paradis, Cynthia; Rossi, Antônio; Taivassalo, Tanja; Sheel, A. William; Rabøl, Rasmus; Dela, Flemming; Boushel, Robert

doi:10.1111/j.1475-097x.2010.00988.x

Cited by 35 publications

(54 citation statements)

References 53 publications

(171 reference statements)

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“…Our findings of a reduced maximal mitochondrial respiration to complex I compared to healthy age-matched controls are consistent with previous studies in COPD patients and, interestingly, also in sedentary individuals' lower limb muscle [3,27]. Our data are in line with PICARD et al [3], showing a significantly lower maximal respiration per unit of fibre weight involving complex I (V9max) in patients with COPD compared to fibres from healthy subjects.…”

Section: Discussionsupporting

confidence: 93%

High-intensity knee extensor training restores skeletal muscle function in COPD patients

et al. 2012

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Improving reduced skeletal muscle function is important for optimising exercise tolerance and quality of life in chronic obstructive pulmonary disease (COPD) patients. By applying high-intensity training to a small muscle group, we hypothesised a normalisation of muscle function.Seven patients with COPD performed 6 weeks (3 days?week -1 ) of high-intensity interval aerobic knee extensor exercise training. Five age-matched healthy individuals served as a reference group. Muscle oxygen uptake and mitochondrial respiration of the vastus lateralis muscle were measured before and after the 6-week training programme. Initial peak work and maximal mitochondrial respiration were reduced in COPD patients and improved significantly after the training programme. Peak power and maximal mitochondrial respiration in vastus lateralis muscle increased to the level of the control subjects and were mainly mediated via improved complex I respiration. Furthermore, when normalised to citrate synthase activity, no difference in maximal respiration was found either after the intervention or compared to controls, suggesting normal functioning mitochondrial complexes.The present study shows that high-intensity training of a restricted muscle group is highly effective in restoring skeletal muscle function in COPD patients.

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Section: Discussionsupporting

confidence: 93%

High-intensity knee extensor training restores skeletal muscle function in COPD patients

et al. 2012

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“…When compared with healthy control subjects, mitochondrial density and mitochondrial function are reduced in the lower limb muscle of patients with COPD (175,176,179,(181)(182)(183). In addition to this, the presence of specific mitochondrial impairments in COPD may affect energy conversion efficiency and selected respiratory chain complexes.…”

Section: Mitochondrial Function Of Limb Muscle In Copd and Bioenergeticsmentioning

confidence: 99%

“…In patients with COPD, chronically altered oxygen transport (351,352) and impaired oxygen use (176,(181)(182)(183)353) facilitate limb muscle oxidative stress (201,217,226,227,229,354) leading to nitroso-redox imbalance (355)(356)(357) and explaining post-transcriptional alterations (inhibition of S-nitrosylation) contributing to limb muscle dysfunction (201). Hypoxemia may also potentiate the inflammatory response (358), providing an additional mechanism linking hypoxia to specific cellular responses predisposing to muscle atrophy.…”

Section: Mechanisms Of Limb Muscle Dysfunction In Copdmentioning

confidence: 99%

An Official American Thoracic Society/European Respiratory Society Statement: Update on Limb Muscle Dysfunction in Chronic Obstructive Pulmonary Disease

Maltais¹,

Decramer²,

Casaburi³

et al. 2014

Am J Respir Crit Care Med

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885

1,033

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“…Previous studies show that muscle mitochondrial function is altered in patients with COPD (31,118,133,164), and that CS induces rapid depolarization of mitochondrial membrane potential in human pulmonary and bronchial epithelial cells with loss of cellular ATP (163,177). As a damage control mechanism, mitophagy may be activated in response to CS exposure.…”

Section: Figmentioning

confidence: 99%

Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

Nakahira

Cloonan

Mizumura

et al. 2014

Antioxidants & Redox Signaling

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Significance: Autophagy is a fundamental cellular process that functions in the turnover of subcellular organelles and protein. Activation of autophagy may represent a cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles. Selective forms of autophagy can maintain organelle populations or remove aggregated proteins. Autophagy can increase survival during nutrient deficiency and play a multifunctional role in host defense, by promoting pathogen clearance and modulating innate and adaptive immune responses. Recent Advances: Autophagy has been described as an inducible response to oxidative stress. Once believed to represent a random process, recent studies have defined selective mechanisms for cargo assimilation into autophagosomes. Such mechanisms may provide for protein aggregate detoxification and mitochondrial homeostasis during oxidative stress. Although long studied as a cellular phenomenon, recent advances implicate autophagy as a component of human diseases. Altered autophagy phenotypes have been observed in various human diseases, including lung diseases such as chronic obstructive lung disease, cystic fibrosis, pulmonary hypertension, and idiopathic pulmonary fibrosis. Critical Issues: Although autophagy can represent a pro-survival process, in particular, during nutrient starvation, its role in disease pathogenesis may be multifunctional and complex. The relationship of autophagy to programmed cell death pathways is incompletely defined and varies with model system. Future Directions: Activation or inhibition of autophagy may be used to alter the progression of human diseases. Further resolution of the mechanisms by which autophagy impacts the initiation and progression of diseases may lead to the development of therapeutics specifically targeting this pathway. Antioxid. Redox Signal. 20,

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Altered mitochondrial regulation in quadriceps muscles of patients with COPD

Cited by 35 publications

References 53 publications

High-intensity knee extensor training restores skeletal muscle function in COPD patients

High-intensity knee extensor training restores skeletal muscle function in COPD patients

An Official American Thoracic Society/European Respiratory Society Statement: Update on Limb Muscle Dysfunction in Chronic Obstructive Pulmonary Disease

Autophagy: A Crucial Moderator of Redox Balance, Inflammation, and Apoptosis in Lung Disease

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