Markers of inflammation and disuse in vastus lateralis of chronic obstructive pulmonary disease patients

Crul, Tim; Spruit, M A; Gayan‐Ramirez, Ghislaine; Quarck, Rozenn; Gosselink, Rik; Troosters, Thierry; Pitta, Fábio; Decramer, Marc

doi:10.1111/j.1365-2362.2007.01867.x

Cited by 105 publications

(111 citation statements)

References 36 publications

(46 reference statements)

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“…Quadriceps strength often decreases during hospitalization for a COPD exacerbation (241,273,274). The reduction in quadriceps force during hospitalization is significantly correlated to a smaller improvement in walking time 1 month after discharge (273).…”

Section: Limb Muscle Function and Exacerbation Of 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

850

1,033

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Section: Limb Muscle Function and Exacerbation Of 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

850

1,033

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“…1). Other studies have compared IGF-I and MyoD expression between COPD patients and healthy age-matched subjects [20] and found that the expression of these two anabolic markers were reduced in hospitalised and clinically stable COPD patients compared to healthy controls. A study by CRUL et al [20] suggested that diminished physical activity may be the main mechanism accounting for decreased muscle IGF-I and MyoD levels in COPD.…”

Section: Baseline Muscle Remodelling Markersmentioning

confidence: 99%

“…Other studies have compared IGF-I and MyoD expression between COPD patients and healthy age-matched subjects [20] and found that the expression of these two anabolic markers were reduced in hospitalised and clinically stable COPD patients compared to healthy controls. A study by CRUL et al [20] suggested that diminished physical activity may be the main mechanism accounting for decreased muscle IGF-I and MyoD levels in COPD. In support of this notion, physical inactivity has been shown to be associated with decreased IGF-I mRNA levels and alterations in the MyoD/myogenin expression ratio in a mouse muscle-disuse model [21,22].…”

Section: Baseline Muscle Remodelling Markersmentioning

confidence: 99%

Effect of pulmonary rehabilitation on muscle remodelling in cachectic patients with COPD

Vogiatzis¹,

Simoes²,

Stratakos³

et al. 2010

European Respiratory Journal

142

177

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It is known that non-cachectic patients with chronic obstructive pulmonary disease (COPD) respond well to pulmonary rehabilitation, but whether cachectic COPD patients are capable of adaptive responses is both important and unknown.10 cachectic and 19 non-cachectic COPD patients undertook high-intensity cycling training, at the same relative intensity, for 45 min?day -1 , 3 days?week -1 for 10 weeks. Before and after rehabilitation vastus lateralis muscle biopsies were analysed morphologically and for the expression of muscle remodelling factors (insulin-like growth factor (IGF)-I, myogenic differentiation factor D (MyoD), tumour necrosis factor (TNF)-a, nuclear factor (NF)-kB and myostatin) and key components of ubiquitin-mediated proteolytic systems (muscle ring finger protein (MURF)-1 and Atrogin-1).Rehabilitation improved peak work-rate and the 6-min walk distance similarly in non-cachectic (18¡3% and 42¡13 m, respectively) and cachectic (16¡2% and 53¡16 m, respectively) patients, but quality of life only improved in non-cachectic COPD. Mean muscle fibre cross-sectional area increased in both groups, but significantly less in cachectic (7¡2%) than in non-cachectic (11¡2%) patients. Both groups equally decreased the proportion of type IIb fibres and increased muscle capillary/fibre ratio. IGF-I mRNA expression increased in both groups, but IGF-I protein levels increased more in non-cachectic COPD. MyoD was upregulated, whereas myostatin was downregulated at the mRNA and protein level only in non-cachectic patients. Whilst rehabilitation had no effect on TNF-a expression, it decreased the activation of the transcription factor NF-kB in both groups by the same amount. Atrogin-1 and MURF-1 expression were increased in cachectic COPD, but it was decreased in non-cachectic patients.Cachectic COPD patients partially retain the capacity for peripheral muscle remodelling in response to rehabilitation and are able to increase exercise capacity as much as those without cachexia, even if they exhibit both quantitative and qualitative differences in the type of muscle fibre remodelling in response to exercise training.

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“…We studied the expression of IL-6, IL-8, TNF-in vastus lateralis of patients with stable disease and during exacerbations at the protein level and mRNA-level. 40 For the latter RT-PCR was used. We found that TNF-expression was below the detection limit.…”

Section: Muscle Weakness In Copd Patientsmentioning

confidence: 99%

Pulmonary rehabilitation 2007: From bench to practice and back

Decramer

2008

CIM

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COPD is a disease that is not confined to the airways and the lungs, but also produces systemic consequences. Muscle weakness is one of these. It is produced by a multitude of factors including deconditioning, systemic inflammation, oxidative stress, nutritional imbalance, reduced anabolic status, systemic corticosteroids, hypoxemia, hypercapnia, electrolyte disturbances, cardiac failure. The most important factors appear to be inactivity and systemic inflammation. Inactivity was shown to be present in patients with COPD from early in the course of the disease on. Systemic inflammation was shown to be predominantly present during COPD exacerbations. IL-6 has the propensity to reduce muscle function in experimental animals. At present there is no evidence of local production of cytokines in the muscle in patients with COPD. Muscle weakness is also important in the clinical course of the disease as it is associated with exercise intolerance, reduced quality of life, enhanced utilization of health care resources and reduced survival.Rehabilitation is the best treatment for muscle weakness and deconditioning in patients with COPD. Indeed, it is the intervention with the largest effect on health status and exercise capacity in these patients. Several factors that may enhance the effects of rehabilitation have been studied. These include: growth hormone/ IGF-I, anabolic steroids, clenbuterol, creatine, anti-cytokine treatment, erythropoietin, oxygen, non-invasive mechanical ventilation and electrical stimulation. Recently, the potential of protease-inhibitors in reversing deconditioning-induced muscle dysfunction was demonstrated. Adjuncts are potentially particularly useful in patients who do not respond to a rehabilitation programme. Analysis of large d-bases demonstrated that about one third of the patients does not respond to rehabilitation. A follow-up study suggests that decline in exercise capacity after a rehabilitation programme is particularly present in these patients and not in the patients with a clear initial response. A better understanding of the factors controlling the response to rehabilitation, may lead to significant advances in this field.

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Markers of inflammation and disuse in vastus lateralis of chronic obstructive pulmonary disease patients

Cited by 105 publications

References 36 publications

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

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

Effect of pulmonary rehabilitation on muscle remodelling in cachectic patients with COPD

Pulmonary rehabilitation 2007: From bench to practice and back

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