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Physiological and functional failure in chronic obstructive pulmonary disease, congestive heart failure and cancer: a debilitating intersection of sarcopenia, cachexia and breathlessness.
Dudgeon, D, Baracos, VE
Current opinion in supportive and palliative care. 2016;(3):236-41
Abstract
PURPOSE OF REVIEW Loss of skeletal muscle mass and cachexia are important manifestations of chronic obstructive pulmonary disease and have been associated with breathlessness, functional limitation and poor prognosis. A number of other life-limiting illnesses, including cancer and chronic heart failure as well as acute conditions seen in ICU such as sepsis, are characteristically associated with cachexia and sarcopenia. These conditions may have respiratory muscle atrophy of sufficient magnitude to contribute to the development of breathlessness and associated functional limitation. The purpose of this review is to summarize findings related to a direct role for severe respiratory muscle wasting in the etiology of breathlessness in advanced, life limiting illness. RECENT FINDINGS Localized wasting of respiratory muscles appears to be part of systemic wasting of skeletal muscles, driven by deconditioning, nutritional insufficiencies and inflammation, and because of disease-specific factors (tumor factors and exacerbations), anabolic insufficiency, autonomic dysfunction, drugs (such as corticosteroids and chemotherapy agents), mechanical ventilation and comorbidities. Marked morphological and biochemical abnormalities have been noted in diaphragm muscle biopsies. SUMMARY Older patients with multiple comorbidities associated with muscle loss and cachexia are likely to be at elevated risk of respiratory muscle atrophy and functional loss, because of the presence of multiple, interacting etiologic factors.
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Respiratory and Limb Muscle Dysfunction in COPD.
Barreiro, E, Gea, J
COPD. 2015;(4):413-26
Abstract
In the next decade, Chronic Obstructive Pulmonary Disease (COPD) will be a major leading cause of death worldwide. Impaired muscle function and mass are common systemic manifestations in COPD patients and negatively influence survival. Respiratory and limb muscles are usually affected in these patients, thus contributing to poor exercise tolerance and reduced quality of life (QoL). Muscles from the lower limbs are more severely affected than those of the upper limbs and the respiratory muscles. Several epidemiological features of COPD muscle dysfunction are being reviewed. Moreover, the most relevant etiologic factors and biological mechanisms contributing to impaired muscle function and mass loss in respiratory and limb muscles of COPD patients are also being discussed. Currently available therapeutic strategies such as different modalities of exercise training, neuromuscular electrical and magnetic stimulation, respiratory muscle training, pharmacological interventions, nutritional support, and lung volume reduction surgery are also being reviewed, all applied to COPD patients. We claim that body composition and quadriceps muscle strength should be routinely explored in COPD patients in clinical settings, even at early stages of their disease. Despite the progress achieved over the last decade in the description of this relevant systemic manifestation in COPD, much remains to be investigated. Further elucidation of the molecular mechanisms involved in muscle dysfunction, muscle mass loss and poor anabolism will help design novel therapeutic targets. Exercise and muscle training, alone or in combination with nutritional support, is undoubtedly the best treatment option to improve muscle mass and function and QoL in COPD patients.
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[Peripheral muscle dysfunction in chronic obstructive pulmonary disease].
Roca, M, Mihăescu, T
Pneumologia (Bucharest, Romania). 2012;(3):178-82
Abstract
Although primarily a disease of the lungs, Chronic Obstructive Pulmonary Disease (COPD) associates systemic manifestations and comorbidities. The skeletal muscles function is restricted in COPD, because of decreased endurance and strength. Skeletal muscle weakness has a great clinical importance in COPD, as it is recognized to contribute independently to poor health status, reduced quality of life and increased mortality. The purpose of this paper is to describe the current knowledge of the structural and functional abnormalities of skeletal muscles in COPD and the possible physiopathologic determination of these dysfunctions. The understanding of these abnormalities is essential in development of new therapeutic strategies to combat muscle dysfunction in COPD, including the pulmonary rehabilitation programs.
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Muscle fibre type shifting in the vastus lateralis of patients with COPD is associated with disease severity: a systematic review and meta-analysis.
Gosker, HR, Zeegers, MP, Wouters, EF, Schols, AM
Thorax. 2007;(11):944-9
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Abstract
BACKGROUND Skeletal muscle dysfunction is a common feature in chronic obstructive pulmonary disease (COPD) which is associated with intrinsic muscular abnormalities. One of the most consistently reported alterations is a shift from fibre type I to II in the vastus lateralis of these patients. Surprisingly, the relationship between this shift and the severity and phenotype of COPD remains unclear. A study was conducted to determine whether vastus lateralis muscle fibre type proportions are associated with COPD disease severity and to provide reference values for the proportions of fibre types in the vastus lateralis in COPD. METHODS A systematic review and a meta-analysis were conducted in which muscle fibre type data and markers of disease severity were collected from the literature. RESULTS The forced expiratory volume in 1 s (FEV(1)), the ratio of FEV(1) to forced vital capacity (FVC) and body mass index were positively associated with the proportion of type I fibres in COPD. A proportion of 51% for vastus lateralis fibre type I and 13% for fibre type IIX were calculated from the combined data as normal values for patients with typical GOLD stage 3-4 COPD aged 60-70 years. Based on these reference values, a proportion of fibre type I <27% and of fibre type IIX >29% were defined as pathologically abnormal. CONCLUSIONS This review sheds new light on the relationship between skeletal muscle abnormalities and important hallmarks of the disease in severe COPD, and identifies absence of data in GOLD stages 1-2. This review also provides reference values on fibre type composition for diagnostic purposes in COPD.
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Inspiratory muscle strength in chronic obstructive pulmonary disease.
Larson, JL, Covey, MK, Corbridge, S
AACN clinical issues. 2002;(2):320-32
Abstract
Chronic obstructive pulmonary disease is associated with a functional weakness of the inspiratory muscles. Multiple factors contribute to the decline in functional strength including hyperinflation of the chest, deterioration in nutritional status, and the indirect effects of an exacerbation. The decreased inspiratory muscle strength contributes to sensations of dyspnea and places individuals at risk for respiratory muscle fatigue. The worsening dyspnea causes individuals to reduce their physical activities and ultimately become physically deconditioned. Maximal inspiratory pressure is commonly used to measure functional strength of the inspiratory muscles, and interventions to minimize the extent of decline include inspiratory muscle training, aerobic exercise training, nutritional supplementation, and methods to prevent exacerbations. In the critical care unit, multiple comorbid conditions contribute to further decline in inspiratory muscle strength, making it important to assess respiratory muscle function regularly.
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Respiratory muscles in chronic obstructive pulmonary disease and asthma.
Barbarito, N, Ceriana, P, Nava, S
Minerva anestesiologica. 2001;(9):653-8
Abstract
Chronic obstructive pulmonary disease (COPD) and asthma are characterized by airflow obstruction and significant increase of respiratory muscle workload, with concrete risk of ventilatory pump failure. Respiratory muscles, the main component of this pump, undergo structural and functional changes during the course of these diseases. Aim of the present paper is to analyze modifications of respiratory muscles in COPD and asthma. An analysis of the most important controlled clinical studies released during the past years was carried out. The patients suffered from chronic obstructive pulmonary disease and asthma. In COPD, respiratory muscles have to cope with an increased load, an intrinsic weakness and a mechanical disadvantage, especially in the diaphragmatic length-force relationship; in patients with acute asthma, the main features are a massive hyperinflation and a persistent inspiratory muscle activity during expiration. Modifications of respiratory muscles deserve great consideration not only for the complete comprehension of the underlying physiopathologic aspects of these diseases, but also for the optimal clinical management: a reduced pulmonary hyperinflation in COPD place the respiratory muscles in a better position of the force-length curve while great care must be payed to the metabolic and nutritional aspects. During asthmatic crisis respiratory muscles are subjected to a sort of intense training but anyway persistence of bronchospasm in most severe attacks can lead to exhaustion of the ventilatory pump and need of mechanical ventilatory support.