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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten adults and ten children exercised maximal voluntary tooth clenching until pains appeared in the jaw muscles, i.e. the muscle pain threshold of tooth clenching was determined. Subsequently, the subjects were instructed to exercise tooth clenching until they were forced to stop because of intolerable pains and exhaustion of the contracting muscles, i.e. the muscle pain tolerance of tooth clenching was recorded, and during these bouts of clenching the pain tolerance of tooth clenching was recorded, and during these bouts of clenching the pain threshold was also determined. In adults, determination of the pain tolerance decreased the pain threshold by 19%, and in children it either decreased the pain threshold by 20% or increased it by 56%. It is proposed to introduce the muscle pain tolerance of tooth clenching as an adjunct in the clinical examination of cases of facial pains presumed to originate from the jaw muscles, but the test should be interpreted with caution.
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PMID:Influence of muscle pain tolerance on muscle pain threshold in experimental tooth clenching in man. 28 68

The purpose of this study was to evaluate changes in muscle soreness and serum enzyme activity following consecutive drop jumps. Seven male subjects (mean age 30.6 years) performed drop jumps from a 80-cm box height every 7 s until exhaustion (mean = 114 drop jumps). A questionnaire was used to assess muscle soreness (0 = no pain, 7 = unbearable painful) both pre- and post-exercise (0, 12, 24, 36 and 48 h, and 3, 4 and 5 days after the exercise). Blood samples were also taken from three subjects at each of these times. For the other four subjects, blood samples were taken pre-exercise and 0, 12 and 36 h and 5 days post-exercise only. Although there was large inter-subject variability in the development of muscle soreness, all the subjects reported muscle soreness in their lower extremity muscles, especially in the quadriceps femoris. Muscle soreness developed significantly (P less than 0.01) over time, its peak (mean +/- S.E. = 3.7 +/- 0.7) occurring 12-48 h post-exercise. Serum enzyme activity changed significantly over time (P less than 0.05), but the changes were small. Not one subject showed a large increase in creatine kinase, and the average increase was less than 1.3 times as much as the pre-exercise level throughout the period of study. These results suggest that the muscle damage that occurs after drop jumping is not associated with a large release of muscle enzymes into the blood, and muscle soreness is not necessarily related to enzyme elevation following drop jumps.
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PMID:Muscle soreness and serum enzyme activity following consecutive drop jumps. 189 57

A 67-year-old Japanese housewife, who had been attended the out patient department of medicine, Fukuoka Dental College (FDC) Hospital for paroxysmal atrial fibrillation, was admitted to FDC Hospital because of high fever, exhaustion, anorexia, myalgia and mild stupor. Her ECG finding revealed atrial fibrillation and roentgenologic examination of the chest showed diffuse opacities in the left lung field (S10) without pleural effusion. As she had told her physician that her pet parakeet had been dead recently, she was diagnosed immediately as psittacosis. She was instantly treated with minocycline orally and deslanoside intravenously. Laboratory findings on admission disclosed the following results: Complement-fixing antibodies against Chlamydia psittaci were 1:64, and liver dysfunction (GOT 253, GPT 86, LDH 846) was shown. The white blood cell count was 4,700 associated with shift to the left, C-reactive protein was 6 plus and the erythrocyte sedimentation rate was 109 mm in 1 hour. The course in the hospital was satisfactory and after 38 hospital days she was discharged with complete recovery from the psittacosis. It is emphasized the importance of that the question about the history of contact with psittacine birds or other avian species is essential to diagnose psittacosis.
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PMID:[A case of psittacosis]. 213 52

Metabolic fatigue is a characteristic muscle response to intense exercise that has outstripped the rate of ATP replacement. The accumulation of metabolic by-products, namely hydrogen ions and diprotonated phosphate, interferes with actin-myosin interaction, effectively preserving muscle ATP levels by preventing further ATP hydrolysis. Muscle force and metabolite concentrations return to normal in about 5 minutes. Less intense exercise causes a more subtle, non-metabolic fatigue due to a still-undefined disturbance of excitation-contraction coupling, which can last for several hours. In this type of fatigue, greater effort is required to generate submaximal forces. Endurance exercise is mainly limited by the size of muscle glycogen stores and how efficiently they are used. Endurance training permits an athlete to work aerobically at high rates, consuming a mixture of lipid and carbohydrate fuels. When muscle glycogen is used up, exercise can only continue at the relatively low rate supportable by lipid metabolism. Anaerobic exercise is also limited by subjective factors such as dyspnoea and muscle pain, which have objective determinants. Extremely prolonged exercise can lead to general collapse because of dehydration, hyperthermia, or hypoglycaemia. None of these factors explains the phenomenon of asthenia, a subjective sense of exhaustion that produces no objective impairment of physical performance. The metabolic myopathies are experiments of nature that promise to shed new light on the biochemical basis of muscle fatigue. This will require quantitative studies of the kind provided by topical magnetic resonance spectroscopy, correlating physiology and metabolism in vivo.
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PMID:Muscle metabolism during fatigue and work. 226 24

It has been suggested in the lay literature that static stretching and/or warm-up will prevent the occurrence of Delayed-Onset Muscle Soreness (DOMS). The primary purpose of this study was to determine the effects of static stretching and/or warm-up on the level of pain associated with DOMS. Sixty-two healthy male and female volunteers were randomly assigned to four groups: (a) subjects who statically stretched the quadriceps muscle group before a step, (b) subjects who only performed a stepping warm-up, (c) subjects who both stretched and performed a stepping warm-up prior to a step test, and (d) subjects who only performed a step test. The step test (Asmussen, 1956) required subjects to do concentric work with their right leg and eccentric work with their left leg to voluntary exhaustion. Subjects rated their muscle soreness on a ratio scale from zero to six at 24-hour intervals for 5 days following the step test. A 4x2x2 ANOVA with repeated measures on legs and Duncan's New Multiple Range post-hoc test found no difference in peak muscle soreness among the groups doing the step test or for gender (p greater than .05). There was the expected significant difference in peak muscle soreness between eccentrically and concentrically worked legs, with the eccentrically worked leg experiencing greater muscle soreness. We concluded that static stretching and/or warm-up does not prevent DOMS resulting from exhaustive exercise.
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PMID:The effects of static stretching and warm-up on prevention of delayed-onset muscle soreness. 248 63

This study was undertaken in an attempt to determine the maximal oxygen uptake in a small muscle group by measuring directly the oxygen expenditure of the forearm. Five healthy medical students volunteered. The subjects' maximal forearm work capacity was determined on a spring-loaded hand ergometer. Exercise was continued until exhaustion by pain or fatigue. Two weeks later intra-arterial and intravenous catheters were placed in the dominant arm. Blood samples for measurement of oxygen concentration were collected via the catheters. Forearm blood flow was measured by means of the indicator dilution technique. Oxygen uptake was determined according to the Fick principle. The forearm oxygen uptake attained at maximal work loads was a mean of 201 (SD +/- 56) mumol.min-1.100 ml-1. It was impossible at maximal exercise to discern a plateau of the oxygen uptake curve in relation to work output. It is suggested that a plateau in the oxygen uptake curve is not a useful criterion for maximal oxygen uptake in a small muscle group. Skeletal muscle may have an unused capacity for oxygen consumption even at maximal exercise intensity where muscle work cannot be continued due to muscle pain and fatigue.
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PMID:Forearm oxygen uptake during maximal forearm dynamic exercise. 275 71

The myalgic encephalomyelitis syndrome has been described over the past 40 years as a relapsing illness occurring mainly in young females, with the cardinal symptoms of muscle pain and exhaustion. This paper reviews recent studies on the syndrome in the United Kingdom, United States and New Zealand. The possible pathogenesis of the syndrome is discussed, as is the difficulty of managing such patients where no certain aetiology is present. It is suggested that the syndrome should be described as the myalgic exhaustion syndrome.
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PMID:The myalgic encephalomyelitis syndrome. 285 13

Clinical and biochemical findings in skeletal muscle in 11 patients with chronic fatigue myalgia syndromes of unknown aetiology are reported. All patients had severe asthenia for from one to 10 years with greatly limited exercise capacity and protracted exhaustion after minor exercise. Diffuse myalgia was prominent and was exacerbated for hours to days after exercise. Assay of skeletal muscle carnitine, phosphorylase, all glycolytic enzymes and the mitochondrial marker enzymes monoamine oxidase, isocitrate dehydrogenase and cytochrome oxidase were normal. These findings lend no support to the presence of a major defect in muscle intermediary energy pathways in this syndrome.
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PMID:Chronic fatigue and myalgia syndrome: mitochondrial and glycolytic studies in skeletal muscle. 303 60

Myalgic Encephalomyelitis or post-viral fatigue syndrome is a common disorder, which has been known previously under a variety of different names, i.e., Iceland disease or Royal Free disease. It may occur in epidemics or sporadically. The cause is unknown, with patients complaining of exhaustion, fatigue, muscle aches and pains, and invariable psychiatric symptoms such as emotional lability, poor memory/concentration, and depression. Present-day research points to the cause as a metabolic disorder secondary to persistent viral infection.
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PMID:Postviral fatigue syndrome. 306 94

Patients with late effects of poliomyelitis, i.e., PPS, are being seen at an ever increasing frequency by general physicians, neurologists, and orthopedists. An appropriate time interval for the onset of late manifestations has elapsed since the major epidemics of poliomyelitis in the 1940s and 1950s. Post-polio neurological manifestations primarily include new weakness, atrophy, muscle pain, and fasciculations. Fortunately, the weakness is of a very slow, progressive nature. Abnormal laboratory studies include routine EMG, demonstrating chronic denervation; SFEMG, demonstrating increased fiber density, increased jitter, and blocking; and muscle biopsy most often revealing fiber-type grouping of chronic denervation and small isolated angular (or angulated) fibers and group atrophy in some series, both suggestive of active denervation. Unfortunately, both EMG and muscle biopsy studies suffer from a lack of specificity as they do not appear to distinguish asymptomatic from symptomatic (new weakness, PPMA) patients with prior poliomyelitis. Although the cause of PPMA is unknown, electrophysiological (SFEMG) and muscle biopsy studies suggest that the process involves a loss or dropout of axon terminals of reinnervated motor units. The axons terminal dropout could be due to dysfunction in the cell soma, the axon, or the terminals themselves. Whether motor neuron exhaustion, a persistent viral infection, or immune-mediated mechanisms play a role in the pathogenesis of the late weakness is unclear at present and will require further investigation. Treatment at this time is of a supportive nature. A major controversy involves the role of strengthening exercises in these patients since experimental animal studies suggest that excessive exercise of denervated muscles leads to increased weakness. Clearly, a better understanding of PPS and PPMA will allow more effective management of these patients' problems and might also provide insight into other motor neuron and neuromuscular junction diseases.
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PMID:Neurological manifestations of the post-polio syndrome. 331 37


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