Diaphragm strength in chronic obstructive pulmonary disease.

Polkey, Michael I.; Kyroussis, D; Hamnegärd, C H; Mills, Gary H.; Green, Malcolm; Moxham, John

doi:10.1164/ajrccm.154.5.8912741

Cited by 240 publications

(170 citation statements)

References 22 publications

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“…Although this level of respiratory muscle dysfunction may not be clinically relevant at rest, it could have significant clinical implications under certain circumstances, such as during an exacerbation or physical exercise. Importantly, our observations were consistent with previous reports, where in vivo respiratory muscle and diaphragm strength were also shown to be compromised [14,21,22]. In keeping with this, it has recently been proposed [23] that in severe COPD, several molecular mechanisms contribute to the aetiology of this respiratory muscle dysfunction, such as myosin loss [10,11], sarcomeric injury [24], oxidative stress [14] and alterations in cross-bridge cycling kinetics [8], resulting in reduced diaphragm isometric force.…”

Section: Discussionsupporting

confidence: 92%

Oxidised proteins and superoxide anion production in the diaphragm of severe COPD patients

Marín‐Corral

Minguella²,

Ramírez-Sarmiento³

et al. 2009

European Respiratory Journal

113

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In the diaphragms of chronic obstructive pulmonary disease (COPD) patients, the nature of oxidatively modified proteins and superoxide anion production were explored.Diaphragm specimens were obtained through thoracotomy because of localised lung lesions in COPD patients (16 severe and eight moderate) and 10 control subjects. Lung and respiratory muscle functions were evaluated. Oxidised proteins were identified using immunoblotting and mass spectrometry. Protein and activity levels of the identified proteins were determined using immunoblotting and activity assays. Lucigenin-derived chemiluminescence signals in a luminometer were used to determine superoxide anion levels in muscle compartments (mitochondria, membrane and cytosol) using selective inhibitors.In severe COPD patients compared with controls, respiratory muscle function was impaired; creatine kinase, carbonic anhydrase III, actin and myosin were oxidised; myosin carbonylation levels were increased five-fold; creatine kinase content and activity and myosin protein were reduced; superoxide anion levels were increased in both mitochondria and membrane compartments; and the percentage of superoxide anion inhibition achieved by rotenone was significantly greater.In severe COPD patients, oxidation of diaphragm proteins involved in energy production and contractile performance is likely to partially contribute to the documented respiratory muscle dysfunction. Furthermore, generation of the superoxide anion was increased in the diaphragms of these patients.

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Section: Discussionsupporting

confidence: 92%

Oxidised proteins and superoxide anion production in the diaphragm of severe COPD patients

Marín‐Corral

Minguella²,

Ramírez-Sarmiento³

et al. 2009

European Respiratory Journal

113

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“…An index of inspiratory muscle strength was obtained by measuring Poes and Pdi during a maximal sniff [16].…”

Section: Data Acquisitionmentioning

confidence: 99%

Respiratory muscle activity in patients with COPD walking to exhaustion with and without pressure support

Kyroussis¹,

Polkey²,

Hamnegärd³

et al. 2000

Eur Respir J

115

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The function of the diaphragm and other respiratory muscles during exercise in chronic obstructive pulmonary disease (COPD) remains controversial and few data exist regarding respiratory muscle pressure generation in this situation.The inspiratory pressure/time products of the oesophageal and transdiaphragmatic pressure, and the expiratory gastric pressure/time product during exhaustive treadmill walking in 12 patients with severe COPD are reported. The effect of noninvasive positive pressure ventilation during treadmill exercise was also examined in a subgroup of patients (n=6).During free walking, the inspiratory pressure/time products rose early in the walk and then remained level until the patients were forced to stop because of intolerable dyspnoea. In contrast, the expiratory gastric pressure/time product increased progressively throughout the walk. When patients walked the same distance assisted by noninvasive positive pressure ventilation, a substantial reduction was observed in the inspiratory and expiratory pressure/time products throughout the walk. When patients walked with positive pressure ventilation for as long as they could, the pressure/time products observed at exercise cessation were lower than those observed during exercise cessation after free walking.It is concluded that, in severe chronic obstructive pulmonary disease, inspiratory muscle pressure generation does not increase to meet the demands imposed by exhaustive exercise, whereas expiratory muscle pressure generation rises progressively. Inspiratory pressure support was shown to substantially unload all components of the respiratory muscle pump. Eur Respir J 2000; 15: 649±655.

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“…25,26 During exercise it has been shown that diaphragm work is increased in COPD and COPD patients use a larger proportion of the maximal inspiratory pressure (PI max) than healthy subjects. This pattern of breathing is closely related to the dyspnea sensation during exercise and might potentially induce respiratory muscle fatigue.…”

Section: 10mentioning

confidence: 99%

“…This pattern of breathing is closely related to the dyspnea sensation during exercise and might potentially induce respiratory muscle fatigue. 4,25,26 In an experiment, a meta-analysis including 32 random controlled trials on the effects of inspiratory muscle training (IMT) in COPD patients were performed. 27 In this study the effect size of each individual study was calculated by the difference between the means of the experimental and the control groups before and after the intervention divided by the average population standard deviation.…”

Section: 10mentioning

confidence: 99%

Recent Advances in Pulmonary Rehabilitation for Patients with COPD

Shioya¹,

Iwakura²,

Kawagoshi³

et al. 2017

Pulm Res Respir Med Open J

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Pulmonary rehabilitation (PR) is a non-pharmacologic therapy that has emerged as a standard of care for patients with chronic obstructive pulmonary disease (COPD). It is a comprehensive, multidisciplinary, patient-centered intervention that includes patient assessment, exercise training, self-management education, and psychosocial support. PR is usually given in inpatient, outpatient, community-based or home-based setting lasting 8-12 weeks. Positive outcomes from PR include increased exercise tolerance, reduced dyspnea and anxiety, increased selfefficacy, and improvement in health-related quality of life (QoL). Hospital admissions after exacerbations of COPD are also reduced with this intervention. The positive outcomes associated with PR are realized without demonstrable improvements in lung function. This paradox is explained by the fact that PR identifies and treats the systemic effects of the disease. This intervention should be considered in patients who remain symptomatic or have decreased functional status despite optimal medical management. Physical activity in patients with COPD is dependent on many factors, including physiologic, behavioral, social, environmental, and cultural factors. A strong inverse association between daily physical activity and dynamic hyperinflation, which correlates strongly with exertional dyspnea in COPD. Changing physical activity behavior inpatients with COPD needs an interdisciplinary approach, bringing together respiratory medicine, rehabilitation sciences, social sciences, and behavioral sciences. There is a need for more education and learning opportunities for primary care physicians, nurse practitioners, and all allied health care professionals about the process and benefits of PR. There is also a need for the sustainability and the safety of PR in the future study.

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Diaphragm strength in chronic obstructive pulmonary disease.

Cited by 240 publications

References 22 publications

Oxidised proteins and superoxide anion production in the diaphragm of severe COPD patients

Oxidised proteins and superoxide anion production in the diaphragm of severe COPD patients

Respiratory muscle activity in patients with COPD walking to exhaustion with and without pressure support

Recent Advances in Pulmonary Rehabilitation for Patients with COPD

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