Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In low back pain patients the paraspinal muscles demonstrate excess fatigability. Whether the cause is "central" as could result from impaired motor unit recruitment due to poor motivation or fear of pain, or "peripheral", and caused by defects in the contractile apparatus, is unknown. Using surface electromyography in conjunction with a standardized isometric fatigue test, this study investigates the mechanisms causing paraspinal muscle dysfunction in patients with both nonsurgical and postsurgical chronic low back pain. During the fatigue test normal subjects and both patient groups exhibited electromyographic increases. These were significantly greater in both patient groups, indicating increased central drive to their muscles. These findings may suggest that patients' excess fatigue is peripheral in origin, with increased central drive arising secondary to muscle wasting or denervation, although a central activation defect has not been excluded. Impaired physical performance in low back pain patients does not seem to be caused by lack of central drive.
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PMID:Increased central drive during fatiguing contractions of the paraspinal muscles in patients with chronic low back pain. 848 53

Muscle atrophy, weakness, injury, and fatigue are inevitable and immutable concomitants of old age. Atrophy results from a gradual process of fiber denervation with loss of some fibers and atrophy of others. Fast fibers show more denervation and atrophy than slow fibers. Some fast fibers are reinnervated by axonal sprouting from slow fibers resulting in remodeling of motor units. With aging, the decreases in strength and power are greater than expected from the loss in muscle mass. Contraction-induced injury is proposed as a mechanism of the fast fiber denervation. With atrophy and weakness, human beings show a dramatic decrease in endurance and increase in fatigability with aging, but strength and endurance training slows the process.
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PMID:Muscle fatigue in old animals. Unique aspects of fatigue in elderly humans. 858 73

Patients with advanced cancer or AIDS are frequently bothered by anorexia, decreased food intake, fatigue, weight loss, muscle wasting, and a decline in functional status. Nutritional support may afford these patients a better, although not longer life. Available interventions include nutrition counseling, homemade or commercial food supplements, appetite stimulants, enteral nutrition, and parenteral nutrition. Conservative cost estimates for these interventions range from $52/month for homemade supplements to $8,400/month for home parenteral nutrition. Clinicians need to be familiar with the benefits, risks, and costs of these therapies in order to suggest appropriate options.
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PMID:Costs and benefits of nutrition support in cancer. 860 60

We investigated the effects of clenbuterol on the muscle mass, contractile properties, myosin phenotype, and bioenergetic enzyme activity in the gastrocnemius (GS)-plantaris (PL)-soleus (SO) muscle complex. Rats were sham-injected or treated with clenbuterol (2 mg.kg-1, subcutaneously) for 14 d. Clenbuterol increased (P < 0.05) body weight and muscle complex weight. Also, clenbuterol treatment resulted in an increase in total muscle force production and maximal shortening velocity (P < 0.05). No difference (P > 0.05) in relative force production (force.g-1 muscle) existed between experimental groups. However, muscle fatigue increased with clenbuterol treatment. Myosin heavy chain (MHC) composition was not altered in the GS or PL muscles, but shifted toward the fast Type II MHC in the SO. Myosin light chain (MLC) composition was not altered in any of the muscles. Clenbuterol caused a decrease in oxidative and glycolytic enzyme activity in the GS and PL, but not the SO. These data suggest that the clenbuterol-induced increase in muscle mass and maximal force generation is due to hypertrophy of both fast and slow fibers. Furthermore, these findings support the notion that beta-agonists may be beneficial in combating conditions that result in muscle wasting and dysfunction.
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PMID:Effects of clenbuterol on contractile and biochemical properties of skeletal muscle. 878 54

Studies using nuclear magnetic resonance have shown that undernutrition affects muscle performance and energetics. It is unclear to what extent underfeeding and refeeding influence the availability of muscle glycogen, net glycogenolysis, skeletal muscle wasting, and recovery. We hypothesized that muscle performance is independent of muscle size and weight, is specific to muscle type, and is unrelated to muscle glycogen concentrations. Slow- and fast-twitch muscles were studied in three groups of adult male Wistar rats: well-fed controls, hypoenergetically fed (Hypo) rats, and rats refed for 4 d after the hypoenergetic diet. Glycogen concentrations and net glycogenolysis; serum glucose, insulin, and protein concentrations; and muscle weight, protein, and cross-sectional area were studied relative to the performance of both types of muscles. Our study controlled for muscle size, weight, and type and electrolyte-micronutrient deficiency. Undernutrition affected muscle performance in five ways. First, compared with controls, fatigue increased only in the soleus muscles of Hypo rats yet the maximal relaxation rate (MRR) decreased in both the soleus and extensor digitorum longus (EDL) muscles. Second, muscle glycogen concentrations did not significantly correlate with fatigue in either the soleus or the EDL although net glycogenolysis was significantly correlated with fatigue in the soleus (r = -0.64; P > 0.01 < 0.05). Third, lower glycogen concentrations did not hinder net glycogenolysis in the EDL of Hypo rats or the soleus of refed rats. Fourth, muscle weight, size, and protein were dissociated from function. Fifth, refeeding did not restore muscle endurance; however, the MRR of the soleus normalized. In conclusion, glycogen values and muscle performance did not correlate but net glycogenolysis correlated with fatigue in the soleus. Also, there was a dissociation between muscle weight, size, and protein and muscle function during hypoenergetic feeding and refeeding.
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PMID:Effect of hypoenergetic feeding and high-carbohydrate refeeding on muscle tetanic tension, relaxation rate, and fatigue in slow- and fast-twitch muscles in rats. 925 Jan 7

The majority of patients with chronic heart failure (CHF) have a decreased exercise tolerance. It has not been well established if muscle fatigue is related to a peripheral myopathy with specific metabolic, histologic and biochemical abnormalities. CHF patients demonstrate depressed oxidative capacity and activation of anaerobic glycolysis, leading to a reduction in the energy substrates. In addition, the skeletal muscles of the lower limbs demonstrate a shift toward type IIb fibers. Many factors, such as prolonged immobilization, reduced blood flow and neuroendocrine activation, can be cited in order to explain the origin of this myopathy. Recent studies show that immobilization is not the only reason for modifications in skeletal muscle composition, since patients with disuse atrophy show an increased percentage in myosin heavy chain I, while IIb is decreased. The opposite pattern is observed in CHF. It would appear that several factors such as deconditioning, prolonged immobilization and reduced blood flow, may produce muscular atrophy. The reasons behind specific changes in fibre composition may be found in metabolic factors such as insulin resistance, TNF levels and dysfunction of the ergo-metabolo muscle receptors.
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PMID:[Skeletal musculature modifications and mechanisms of fatigue in chronic heart failure]. 928 Jul 30

The combination of abnormally low plasma cystine and glutamine levels, low natural killer (NK) cell activity, skeletal muscle wasting or muscle fatigue, and increased rates of urea production defines a complex of abnormalities that is tentatively called "low CG syndrome." These symptoms are found in patients with HIV infection, cancer, major injuries, sepsis, Crohn's disease, ulcerative colitis, chronic fatigue syndrome, and to some extent in overtrained athletes. The coincidence of these symptoms in diseases of different etiological origin suggests a causal relationship. The low NK cell activity in most cases is not life-threatening, but may be disastrous in HIV infection because it may compromise the initially stable balance between the immune system and virus, and trigger disease progression. This hypothesis is supported by the coincidence observed between the decrease of CD4+ T cells and a decrease in the plasma cystine level. In addition, recent studies revealed important clues about the role of cysteine and glutathione in the development of skeletal muscle wasting. Evidence suggests that 1) the cystine level is regulated primarily by the normal postabsorptive skeletal muscle protein catabolism, 2) the cystine level itself is a physiological regulator of nitrogen balance and body cell mass, 3) the cyst(e)ine-mediated regulatory circuit is compromised in various catabolic conditions, including old age, and 4) cysteine supplementation may be a useful therapy if combined with disease-specific treatments such as antiviral therapy in HIV infection.
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PMID:Role of cysteine and glutathione in HIV infection and other diseases associated with muscle wasting and immunological dysfunction. 936 43

We previously reported that patients with spinal muscular atrophy do not lose muscle strength over time as measured quantitatively. However, we noted that many patients with spinal muscular atrophy suffer from what they call fatigue. We wondered if we could measure fatigue during a single maximal voluntary contraction, whether fatigue might increase with time, independent of muscle strength, and whether increasing fatigue might correlate with loss of function in some patients. We measured fatigue during a single maximal voluntary contraction in a cohort of patients having spinal muscular atrophy using quantitative strength testing. We included only patients with spinal muscular atrophy aged 5 years or older, so they could follow instructions regarding muscle contraction, and who were followed for at least 2 years. Seventy-six children with spinal muscular atrophy and 24 untrained individuals, aged 5 to 57 years (mean, 16.8 years), were studied. There was no discernible abnormal fatigue in patients with spinal muscular atrophy compared to untrained controls using our methodology. Thus, spinal muscular atrophy may not be associated with fatiguability. Moreover, spinal muscular atrophy does not appear to cause progressive muscle fatigue with age or loss of function. It is possible that fatigue was undetectable by our methods. An alternative explanation is that what patients describe as fatigue may be caused by factors outside the neuromuscular system. Such factors may include chronic respiratory insufficiency with hypoventilation and carbon dioxide retention as well as chronic malnutrition and negative nitrogen balance.
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PMID:Muscle fatigue in spinal muscular atrophy. 937

Muscle catabolism is a characteristic metabolic response to sepsis, severe infection, and injury. In patients with severe and protracted sepsis, the catabolic response results in muscle wasting and fatigue, which may adversely affect the outcome in these patients. An understanding of the regulation of muscle protein breakdown during sepsis and the mechanisms involved is important from a clinical standpoint and is essential for the development of new therapeutic modalities to prevent protein loss from muscle tissue. Studies in septic patients and experimental animals have provided evidence that the myofibrillar proteins actin and myosin are particularly sensitive to the effects of sepsis. Among the factors that regulate muscle protein breakdown during sepsis, the proinflammatory cytokines tumor necrosis factor and interleukin-1, together with glucocorticoids, are the principal mediators. Intracellular protein breakdown is regulated by multiple proteolytic pathways. Among these, the energy-ubiquitin-dependent pathway accounts for a major portion of muscle protein breakdown during sepsis. The development of specific proteasome inhibitors may make it possible in the future to target the molecular mechanisms of sepsis-induced increase in muscle proteolysis. Such treatment may prove an important avenue to reduce the metabolic cost in patients with severe infection or sepsis.
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PMID:Sepsis: stimulation of energy-dependent protein breakdown resulting in protein loss in skeletal muscle. 945 37

As a potent promoter of muscle growth, clenbuterol has been proposed as a treatment for muscle wasting diseases. Thus, the effects of clenbuterol on dystrophic skeletal muscle was examined. Male dystrophic (dy/dy) mice aged 4-5 weeks were treated with clenbuterol for 3 weeks, and the isometric contractile, fatigue and histochemical properties of the slow-twitch soleus and fast-twitch plantaris muscles measured. Muscles of dystrophic animals produced lower forces, contracted more slowly and exhibited greater fatigue resistance than age-matched normal animals. Dystrophic soleus muscles also had higher proportions of type I fibres than normal mice. Clenbuterol significantly reduced the natural death rate of dystrophic mice, as 3 of 11 untreated animals died prior to completion of the 3-week experimental period, whereas none of the 9 clenbuterol-treated animals died. Clenbuterol treatment significantly increased the relative mass (P<0.001) and relative tetanic force production (P<0.01) of the soleus of dystrophic animals, most likely due to increases in protein accretion and improved regeneration. The plantaris of clenbuterol-treated dystrophic animals also exhibited higher mass (P<0.05) and higher absolute forces than untreated mice. The results from this study show that clenbuterol could be a valuable adjunct to treatments of muscle wasting diseases such as muscular dystrophy.
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PMID:Examining potential drug therapies for muscular dystrophy utilising the dy/dy mouse: I. Clenbuterol. 961 33


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