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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate thigh muscle strength and endurance in patients with COPD compared with healthy controls. Forty-two patients (26 women; 16 men) with moderate to severe COPD and 53 (29 women; 24 men) age-matched healthy controls participated in the study. The subjects were tested for maximum voluntary contractions (MVC), endurance and fatigue of the thigh muscles on an isokinetic dynamometer (KinCom). Endurance was expressed as the number of attained repetitions of knee extension and muscle fatigue as a fatigue index (FI). MVC in knee extension was 17% lower in female patients (P=0.017) but no difference was found in male patients (P=0.56) compared to controls. MVC in knee flexion was lower both in female (51%) (P<0.001) and male patients (40%) (P<0.001) compared to controls. Both female and male patients had significantly lower muscle endurance compared to controls. Female patients had a higher FI (22.5%) than female controls (10%) (P=0.001) while no difference was found regarding FI between male patients (15%) and male controls (10%) (P=0.103). The level of self-reported everyday physical activity did not differ between groups. The results showed impaired skeletal muscle function in COPD, except for MVC in knee extension in male patients. Female patients seemed to be more prone to decrease in thigh muscle function. More focus on improving muscle strength and muscle endurance should be considered when designing pulmonary rehabilitation programs. Patients with preserved level of physical activity can be included in exercise programs and gender-related differences should be taken into account.
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PMID:Thigh muscle strength and endurance in patients with COPD compared with healthy controls. 1633 14

We briefly review the evidence for a hypothesis, which links the ventilatory response to heavy intensity, sustained exercise-to-exercise performance limitation in health. A key step in this linkage is a respiratory muscle fatigue-induced metaboreflex, which increases sympathetic vasoconstrictor outflow, causing reduced blood flow to locomotor muscles and locomotor muscle fatigue. In turn, the limb fatigue comprises an important dual contribution to both peripheral and central fatigue mechanisms, which contribute to limiting exercise performance. Clinical implications for respiratory limitations to exercise in patients with chronic obstructive lung disease (COPD) and chronic heart failure (CHF) are discussed and key unresolved problems are outlined.
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PMID:Consequences of exercise-induced respiratory muscle work. 1678 Dec

The function of respiratory muscles, and mainly inspiratory muscles, is impaired in COPD patients. Most of these impairments are essentially due to pulmonary hyperinflation that puts these muscles in a disadvantageous situation. The main consequence of this dysfunction is respiratory muscle fatigue that may cause shortness of breath, exertion intolerance, and hypoventilation with onset of hypercapnic respiratory failure. This function may be measured at the pulmonary function laboratory by means of unspecific (spirometry, pulmonary volumes) or specific tests (maxim respiratory pressures [MIP - M], transdiaphragmatic pressure, tension-time index of the diaphragm, electromyography, or endura tests). Therapy should aim at improving hyperinflation with bronchodilator therapy, improving muscular strength with rehabilitation, and in severe cases muscle rest with mechanical ventilation. Peripheral muscle dysfunction is a common complication in moderate-severe COPD, and it may be the result of chronic inactivity, hypoxemia, electrolytic impairments, under nutrition, steroids, oxidative stress, and systemic inflammation. Besides, it may contribute to patients' quality of life worsening, disability, and even an increase in morbimortality. It may tested by impedanciometry, muscle strength tests (dynamometry), imaging tests, and even muscle biopsy in research studies. Peripheral muscle dysfunction is potentially manageable with rehabilitation, nutritional supplementation, and anabolic drugs. However, therapeutic success is often incomplete, so that further studies with new therapeutic strategies are needed.
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PMID:[Clinical consequences of muscle dysfunction in chronic obstructive pulmonary disease]. 1676 33

There is increasing evidence that systemic inflammation plays an important role in the pathogenesis of COPD. Inflammatory markers show relationships with exercise performance, health related quality of life and breathlessness. These are important clinical outcomes in the management of COPD. Even more so is the consideration that systemic inflammation in COPD may be directly associated with mortality and deterioration of disease. Long-term exercise training clearly has beneficial properties in healthy subjects, whether the same is true in COPD remains to be seen. This review discusses aspects of the anti-inflammatory effects of exercise in relation to patients with COPD. There is intriguing evidence that the exercise-induced cytokine response differs in COPD patients compared with healthy subjects. We consider the role of IL-6 in the manifestation of fatigue in COPD and consider the implications of raised CRP- and TNF-alpha. Early data suggests beneficial effects of polyunsaturated fatty acid PUFA supplementation and exercise training in combination with appropriate nutritional support may yield rewarding therapeutic benefits. This review raises the hypothesis that physical training in COPD is associated with immunological changes that may confer anti-inflammatory benefits and in part, explain changes seen after pulmonary rehabilitation in COPD patients.
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PMID:Exercise and the inflammatory response in chronic obstructive pulmonary disease (COPD)--Does training confer anti-inflammatory properties in COPD? 1701 May 29

The chronic respiratory questionnaire, available as an interviewer and a self-administered instrument, includes 20 items across four domains: dyspnea (5 items), fatigue (4 items), emotional function (7 items), and mastery (4 items). When completing this instrument, patients rate their experience on a 7-point scale ranging from 1 (maximum impairment) to 7 (no impairment). The Chronic Respiratory Questionnaire has demonstrated excellent measurement properties for both discriminative and evaluative purposes and served as a model in numerous methodological studies in chronic airflow limitation and patients with chronic obstructive pulmonary disease. We performed a systematic review of the literature on the chronic respiratory questionnaire to summarize the key qualities of the chronic respiratory questionnaire and to appraise the work regarding the minimal important difference of the chronic respiratory questionnaire. This paper includes a revision of our initial definition of the minimal important difference and a methodological framework for using anchor based approaches to establish the minimal important difference pioneered by Jaeschke and colleagues. Other approaches to evaluate the minimal important difference include distribution-based methods and panel-based methods. Investigators have used all of these approaches to establish the minimal important difference for the chronic respiratory questionnaire and the results are in general agreement with the minimal important difference of 0.5 for the mean domain scores of the chronic respiratory questionnaire. As a result of this literature review and discussion at the workshop, we established several research objectives. These objectives include the exploration of presentation of quality of life information and prospective anchor-based approaches.
COPD 2005 Mar
PMID:Measurement properties and interpretability of the Chronic respiratory disease questionnaire (CRQ). 1713 67

COPD exacerbations often lead to a downward spiral of physical activity. To compensate for the discomfort brought on by exertional dyspnea and the accompanying fatigue, patients with COPD will settle into a sedentary lifestyle that deconditions their bodies, serves to further aggravate breathlessness, and results in a further downward adjustment of physical activity. Progression of COPD imposes profound limitation on activities of daily living and gives rise to anxiety and depression. The distressing symptoms of breathlessness and the perception of these abnormalities by the patient lead to a reduction in health-related quality of life. The clinician's therapeutic interventions have to address these symptom and activity limitations with the goal of improving the patient's quality of life.
COPD 2007 Sep
PMID:How are you doing? What are you doing? Differing perspectives in the assessment of individuals with COPD. 1772 76

Inspiratory muscle weakness in patients with COPD is of major clinical relevance. For instance, maximum inspiratory pressure generation is an independent determinant of survival in severe COPD. Traditionally, inspiratory muscle weakness has been ascribed to hyperinflation-induced diaphragm shortening. However, more recently, invasive evaluation of diaphragm contractile function, structure, and biochemistry demonstrated that cellular and molecular alterations occur, of which several can be considered pathologic of nature. Whereas the fiber type shift towards oxidative type I fibers in COPD diaphragm is regarded beneficial, rendering the overloaded diaphragm more resistant to fatigue, the reduction of diaphragm fiber force generation in vitro likely contributes to diaphragm weakness. The reduced diaphragm force generation at single fiber level is associated with loss of myosin content in these fibers. Moreover, the diaphragm in COPD is exposed to oxidative stress and sarcomeric injury. This review postulates that the oxidative stress and sarcomeric injury activate proteolytic machinery, leading to contractile protein wasting and, consequently, loss of force generating capacity of diaphragm fibers in patients with COPD. Interestingly, several of these presumed pathologic alterations are already present early in the course of the disease (GOLD I/II), although these patients appear not limited in their daily life activities. Treatment of diaphragm dysfunction in COPD is complex since its etiology is unclear, but recent findings indicate the ubiquitin-proteasome pathway as a prime target to attenuate diaphragm wasting in COPD.
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PMID:Diaphragm adaptations in patients with COPD. 1821 29

Transplantation may imply severe biopsychosocial impairments. In order to know the quality of life of patients one year after transplantation, 58 subjects were compared to three different groups of patients (stabilized and acute COPD patients, and lung cancer patients in a surgery unit). Patients filled in two questionnaires: EORTC QLQ-C30 (quality of life) and HAD (anxiety and depression). The quality of life dimensions with inter-group differences were physical, role, emotional and cognitive functioning, global health status, and a number of symptoms (fatigue, dyspnea, insomnia and appetite loss). There were differences in depression, and but not in anxiety. Transplant and surgical patients showed better quality of life and affective status than chronic pulmonary patients. Discriminant analysis showed that the transplant group was the best described group. We conclude that patients, one year after transplantation, show similar quality of life as asymptomatic hospitalised patients, somewhat better than chronic patients in a stabilized stage of the disease, and much better than severe chronic patients.
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PMID:[Quality of life in transplant patients, compared to other stressful health situations in pulmonary patients]. 1841 89

Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO(2)). Acute metabolic acidosis was induced by administration of ammonium chloride (NH(4)Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33.2 +/- 11.5 years; FEV(1) 108.3 +/- 16.2% predicted), 14 asthma patients (5 male; age 48.1 +/- 16.1 years; FEV(1) 101.6 +/- 15.3% predicted), and 15 moderate to severe COPD patients (9 male; age 62.8 +/- 6.8 years; FEV(1) 50.0 +/- 11.8% predicted). An acute metabolic acidemia of BE -3.1 mmol x L(-1) was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference -0.1 kPa x sec x L(-1) [95%-CI: -0.1 - -0.02]. In COPD patients PaCO(2) was significantly lowered during metabolic acidemia (mean difference -1.73 mmHg [-3.0 - -0.08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure.
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PMID:Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemia. 1962 91

Skeletal muscle dysfunction contributes to exercise limitation in COPD. In this study cigarette smoke exposure was hypothesized to increase expression of the inflammatory cytokine, TNF-alpha, thereby suppressing PGC-1alpha, and hence affecting down stream molecules that regulate oxygen transport and muscle function. Furthermore, we hypothesized that highly vascularized oxidative skeletal muscle would be more susceptible to cigarette smoke than less well-vascularized glycolytic muscle. To test these hypotheses, mice were exposed to cigarette smoke daily for 8 or 16 weeks, resulting in 157% (8 weeks) and 174% (16 weeks) increases in serum TNF-alpha. Separately, TNF-alpha administered to C2C12 myoblasts was found to dose-dependently reduce PGC-1alpha mRNA. In the smoke-exposed mice, PGC-1alpha mRNA was decreased, by 48% in soleus and 23% in EDL. The vascular PGC-1alpha target molecule, VEGF, was also down-regulated, but only in the soleus, which exhibited capillary regression and an oxidative to glycolytic fiber type transition. The apoptosis PGC-1alpha target genes, atrogin-1 and MuRF1, were up-regulated, and to a greater extent in the soleus than EDL. Citrate synthase (soleus-19%, EDL-17%) and beta-hydroxyacyl CoA dehydrogenase (beta-HAD) (soleus-22%, EDL-19%) decreased similarly in both muscle types. There was loss of body and gastrocnemius complex mass, with rapid soleus but not EDL fatigue and diminished exercise endurance. These data suggest that in response to smoke exposure, TNF-alpha-mediated down-regulation of PGC-1alpha may be a key step leading to vascular and myocyte dysfunction, effects that are more evident in oxidative than glycolytic skeletal muscles.
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PMID:TNF-alpha-mediated reduction in PGC-1alpha may impair skeletal muscle function after cigarette smoke exposure. 1985 10


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