UMLS:C0015672 - FACTA Search

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Query: UMLS:C0015672 (fatigue)
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Exercise performance data, circulatory function and respiratory and leg muscle quality, expressed as muscle fiber composition, are reviewed and together with our own data discussed as possible limiting factors for physical performance in chronic obstructive pulmonary disease (COPD). COPD is regarded as synonymous with reduced physical performance, exaggerated breathlessness or dyspnea, muscle hypotrophy and/or wasting and, frequently, malnutrition. Impaired right ventricular circulatory function seems to be essential. The observed preponderance of fast twitch (FT), 'glycogenolytic' and capillary-poor muscle fiber type in the investigated muscles might reflect endowment, a 'hypoxic vasoconstriction'-related downregulation of the other main fiber type: the slow twitch (ST), capillary-rich, fatigue-resistant fiber, and/or selective muscle trauma to ST fibers. Ischemic heart disease (IHD) patients demonstrate a similar fiber type pattern in leg muscles. Both COPD and IHD patients have low leg muscle and plasma deposits of antioxidants such as coenzyme Q10 (CoQ10) and alpha-tocopherol. This could reflect a depressed resistance to radical induced cell trauma and/or malnutrition. The magnitude of the antioxidant reduction is less pronounced in patients rich in FT fibers indicating a ST fiber-related susceptibility to trauma. Treatment of other muscle disorders including heart muscle with, e.g., CoQ10 improves performance due to a causative enhanced antioxidant potential, reduced catabolism and/or an upregulated muscle anabolism, increased mitochondrial volume/function, etc. Such data are lacking in COPD.
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PMID:Exercise-limiting factors in respiratory distress. 151 68

Impairment of exercise tolerance is a common problem in patients with severe chronic obstructive pulmonary disease. The cause of exercise intolerance in patients with severe chronic obstructive pulmonary disease is multifactorial and includes impaired lung mechanics, fatigue of inspiratory muscles, impaired gas exchange, right ventricular dysfunction, malnutrition, occult cardiac disease, deconditioning, and psychologic problems; however, impaired lung mechanics and gas exchange abnormalities seem to be the major limiting factors. Recently, the approach to management of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease has changed because improvement in exercise tolerance has been demonstrated after pulmonary rehabilitation. Other adjunctive measures that have been shown to contribute to the observed improvement in exercise tolerance include administration of oxygen, nutritional support, cessation of smoking, and psychosocial support. The roles of ventilatory muscle endurance training, respiratory muscle rest therapy, nasally administered continuous positive airway pressure, and training of the muscles of the upper extremities are less clearly defined.
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PMID:Exercise limitation and pulmonary rehabilitation in chronic obstructive pulmonary disease. 154 79

In assessing the effectiveness of lower-limb and upper-limb nonspecific physical training, we have considered 3 objectives in this study: (1) determination of clinical and functional actual state in patients with chronic airway obstruction (CAO), before and after training; (2) determination of the tests, level of work, and duration of the session training as well as how to increase the training load throughout the training program; and (3) the "particular" upper-limb exercise training in patients with CAO. Many personal factors such as psychologic (personality, degree of patient motivation), alcohol and smoking habits, physical activity, malnutrition, as well as routine tests, at rest and maximal exercise, including the control of metabolic acidosis (lactate) and arterial blood gases (or at least of SaO2), should be considered. Exercise training has the potential to improve exercise tolerance in those who develop metabolic acidosis. The pattern of lactates during exercise represents a good criterion on the selection of patient's training. Two ergospirometric strategies, at high intensity exercise, established from the anaerobic threshold (AT) are described: (a) the above AT 45 min constant exercise (high work rate), at 60% of the difference between AT and maximum VO2 or 80% of the maximal tolerated power (MTP), and (b) the "45 min square-wave endurance exercise test" (SWEET), simulating an interval training session, established from the MTP and the AT. To the SWEET's base (% MTP from AT or aerobic training), a peak of 60 s at MTP (anaerobic training) is added every 5 min. While those 2 protocols, after 6 to 8 weeks of training, lactate and ventilation were lower for identical work rate. In addition, endurance (time in "a" and total physical work in "b") increased up to 60%. Further, maximal exercise ventilation and maximum VO2 increased after SWEET training. Roughly every 7 training sessions, a 10% to 15% reduction in heart rate (HR), during the training program, allows the patient to increase the work rate of the sessions. Evaluation of training the upper limb in patients with CAO requires measurements of MTP and maximum VO2. With the upper limb (wheelchair ergometer), Wmax, maximum VO2, and HR represent 30%, 65%, and 95%, respectively, of the lower limb (ergometer). Further, some expiratory and inspiratory accessory muscles show electromyographic fatigue at the MTP upper-limb level. This may contribute to the rationale for training respiratory muscles.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Implications of lower- and upper-limb training procedures in patients with chronic airway obstruction. 157 50

The mechanism of exertional fatigue in heart failure appears to be considerably more complex than was originally thought. Although it still seems likely that muscle underperfusion is the major culprit, the possibility that skeletal muscle changes contribute to the fatigue suggests that several new therapeutic modalities may improve exercise capacity in heart failure. If muscle atrophy due to de-conditioning or malnutrition is found to contribute to fatigue, exercise capacity in heart failure could be improved, at least in part, by exercise training or nutritional supplementation. Alternatively, agents such as anabolic steroids or growth hormone could be used to stimulate muscle hypertrophy and, thereby, help to improve the fatigue. Heart failure is a common disorder, affecting over three million Americans and many more people throughout the world. One of the most disabling problems experienced by these patients is exertional fatigue. Patients report that they are easily fatigued during normal daily activity. During maximal exercise testing, patients usually terminate exercise early due to fatigue of the legs associated with an early increase in the concentration of lactate in the blood. Traditionally, such exertional fatigue has been attributed to skeletal muscle underperfusion. Over the past five years, however, there has been increasing evidence that heart failure is associated with intrinsic skeletal muscle changes which may also contribute to the exertional fatigue. Nuclear magnetic resonance studies using 31P have demonstrated abnormal skeletal muscle metabolic responses to exercise that do not appear to be due to muscle under-perfusion. Skeletal muscle biopsy studies have demonstrated a variety of changes in patients. Anthropometric studies suggest that a generalized loss of muscle mass may occur in heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of extertional fatigue in heart failure. 210 92

Subjective fatigue was quantified before and 20 days after uncomplicated elective abdominal surgery in 12 patients and compared with changes in heart rate, enzyme activities and skeletal muscle substrates before and after bicycle exercise for 10 min at 65 per cent of patients' preoperative maximum work capacity. Fatigue increased from a mean(s.e.m.) preoperative level of 2.5(0.5) arbitrary units to 4.6(0.5) on postoperative day 20 (P less than 0.01). Body-weight, triceps skinfold thickness and arm circumference decreased postoperatively (P less than 0.02). Postoperative values of muscle enzyme activities indicative of oxidative phosphorylation capacity (citrate synthase and 3-OH-acyl coenzyme A dehydrogenase) were lower than preoperative values (P less than 0.05). Lactate dehydrogenase was unaltered and resting values of muscle glycogen and adenosine triphosphate were higher after operation (P less than 0.05). In response to exercise, heart rate, muscle glucose, glucose-6-phosphate and lactate increased (P less than 0.05), while muscle glycogen and creatine phosphate decreased (P less than 0.05). Increase in postoperative fatigue correlated with the increase in heart rate (P less than 0.05), while no significant correlations were found between fatigue and muscle parameters. Our results suggest that lack of exercise and malnutrition may be of importance in the decrease in work capacity and in fatigue after operation.
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PMID:Skeletal muscle enzyme activities and metabolic substrates during exercise in patients with postoperative fatigue. 232 98

One of the prime nutritional concerns in cancer patients is cachexia and deteriorating nutritional status. Cachexia can occur as a result of either treatment or the tumor itself. The progressive malnutrition ultimately affects performance status and organ function. Tolerance to treatment may thus be decreased, which, in turn, may adversely affect toxicity and response. In addition, the deleterious effects of malnutrition on the immune system can increase susceptibility to infection. The weakness and fatigue related to muscle wasting and changes in metabolism affect physical appearance, leading to a loss of self-esteem. Thus, the vicious cycle of cachexia severely impacts on every aspect of daily life. Providing nutritional support and effective treatment may reverse the cachexia. Studies involving caloric supplements alone have not been encouraging. Conversely, studies using megestrol acetate have shown that cancer patients gain weight and that their sense of well-being improves. However, the mechanisms of weight gain remain unknown, and further studies are needed to determine the mechanisms by which appetite is stimulated or catabolism is inhibited or both. Nursing interventions to stimulate appetite and promote greater food intake, coupled with the use of agents that alter metabolism, such as megestrol acetate, may reverse the trend of cachexia and thus provide an increased sense of well-being and improved quality of life.
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PMID:Nutritional concerns in cancer patients. 272 53

Muscle weight, protein content and contractile performance (tetanic tension, fatigue and recovery) of extensor digitorum longus and soleus were investigated in rat following systemic administration of Dexamethasone (DX), 5 mg/kg/day for ten days. These animals showed marked reduction in food intake during the course of DX treatment. As a control, a group of food restricted (FR) rats receiving equal amount of food consumed by the DX treated rats was also studied along with the saline control group, to differentiate the effect of DX on muscle from that of dietary deficiency. There was a greater degree of atrophy (reduced muscle mass and protein content) of extensor digitorum longus in DX treated rats as compared to that of the FR rats. In-situ isometric tetanic tension per gram of muscle and per unit weight of protein was similar in both the muscles in the DX treated and the FR rats. There was increased fatiguability with reduced post fatigue recovery in both the muscles of DX treated rats as compared to the FR rats. The results indicate that besides atrophy of fast twitch muscles, DX increases the fatiguability and decreases the postfatigue recovery in both fast and slow muscles.
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PMID:Fatigue and contractile responses of rat hindlimb muscles following excessive dexamethasone administration. 273 43

The influence of prolonged nutritional deprivation on the succinate dehydrogenase (SDH) activity and cross-sectional areas of individual fibers in the rat diaphragm and deep portion of the medial gastrocnemius (MGr) muscles was determined. Fatigue resistance of the diaphragm was measured by means of an in vitro nerve-muscle strip preparation. Fiber SDH activity and cross-sectional area were quantified by means of an image processing system. Diaphragm fatigue resistance was significantly improved in the nutritionally deprived (ND) group. In both muscles, nutritional deprivation resulted in a significant decrease in fiber cross-sectional area (both type I and II), type II fibers showing greater atrophy. The SDH activities of type I and II fibers in the diaphragm were not affected by nutritional deprivation. This contrasted with a significant decrease in the SDH activity of both type I and II fibers in the MGr of ND animals. An assessment of the interrelationships between fiber atrophy and fiber SDH activity revealed a greater effect of malnutrition on those diaphragm type II fibers that had the lowest relative SDH activities and the largest cross-sectional areas. By comparison, the effect of malnutrition on type I and II fibers in the MGr was nonselective with regard to fiber SDH activity. We conclude that the enhanced diaphragm fatigue resistance in the ND animals does not result from an increase in the oxidative capacity of muscle fibers and is best explained by the pattern of diaphragm muscle fiber atrophy.
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PMID:Effects of undernutrition on diaphragm fiber size, SDH activity, and fatigue resistance. 274 85

Wasting of muscle and a negative nitrogen balance are obvious effects of malnutrition, and have led to the use of anthropometric measurements and nitrogen balance for its assessment. A positive nitrogen balance and an increase in limb muscle circumference are believed to be solid indices of the beneficial effects of nutritional support. In experiments with growing rats and in young children, nitrogen retention and growth are recognized to be the desirable effects of optimal nutritional intake. This concept has been applied to malnourished adult humans (nongrowing) who have been considered potentially able to "regrow" the lost tissue. Although it is true that patients receiving long-term (greater than 6 months) home total parenteral nutrition (TPN), gain body weight and nitrogen over many months and years of observation, these processes are not seen during shorter (less than 40 days) periods of nutritional intervention given in hospital. Despite adequate intakes of nitrogen and calories, little or no significant increase in total body nitrogen is seen in a variety of patients receiving TPN in hospital over several weeks, but nutritional support does appear to improve outcome in the form of reduced complications after a period of support so short that body composition is barely altered. For example, Young and Hill showed that although amino acids and amino acids plus calories both resulted in equivalent sparing of body nitrogen, the latter was associated with quicker wound healing and fewer complications. Thus, the outcome and body composition data suggest that reversal of the adverse effects of malnutrition is not based on improvement of the traditional parameters of nutrition, such as gain in body nitrogen, or a demonstrable increase in muscle mass, or in plasma proteins. On the basis of the foregoing evidence, there are grounds for suspecting that functional abnormalities in adult humans may not be the result of simple loss of lean tissue and therefore may recover before such lean tissue is regained. This hypothesis is supported by the observation of Klidjian et al who showed that muscle force is a good measure of outcome. One of the major organ systems of the human body is the musculoskeletal system, and therefore it would seem important to determine the effect of malnutrition on that system. Previous studies of muscle function have been largely related to the examination of fatigue, myopathy, and endocrine-metabolic abnormalities. Subsequently we undertook initial studies of muscle function in very malnourished patients as outlined below.
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PMID:Rhoads lecture--1988. Bulk or bounce--the object of nutritional support. 306 74

Malnutrition may be an important complicating factor in acute and chronic lung disease. Animal studies have demonstrated significant atrophy of diaphragm muscle fibers following prolonged undernutrition resulting in a marked reduction in diaphragm muscle strength as well as alteration in other contractile and fatigue properties of the muscle. In severe chronic obstructive pulmonary disease (COPD), malnutrition is common and may, in conjunction with the influences of hyperinflation on diaphragm performance, predispose to respiratory muscle fatigue and failure. The course of progressive weight loss in patients with COPD is not known but may, in part, be related to a "hypermetabolic" state arising from an increased oxygen consumption of the respiratory muscles secondary to enhanced resistive loads and impaired mechanical efficiency of the respiratory muscles. Reports of the impact of nutritional repletion on respiratory muscle performance in critically ill patients, as well as in patients with COPD, are preliminary. Further studies are necessary to establish whether such measures impact meaningfully on both the morbidity and mortality of these patients.
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PMID:Nutrition and the respiratory muscles. 329 32

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