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

Carbohydrates are important substrates for contracting muscle during prolonged, strenuous exercise, and fatigue is often associated with muscle glycogen depletion and/or hypoglycaemia. Thus, the goals of carbohydrate nutritional strategies before, during and after exercise are to optimise the availability of muscle and liver glycogen and blood glucose, with a view to maintaining carbohydrate availability and oxidation during exercise. During heavy training, the carbohydrate requirements of athletes may be as high as 8 to 10 g/kg bodyweight or 60 to 70% of total energy intake. Ingestion of a diet high in carbohydrate should be encouraged in order to maintain carbohydrate reserves and the ability to train intensely. Ingestion of a high carbohydrate meal 3 to 4 hours prior to exercise ensures adequate carbohydrate availability and enhances exercise performance. Although hyperinsulinaemia associated with carbohydrate ingestion in the hour prior to exercise may result in some metabolic alterations during exercise, it may not necessarily impair exercise performance and may, in some cases, enhance performance. Carbohydrate ingestion during prolonged, strenuous exercise, where performance is often limited by carbohydrate availability, delays fatigue. This is due to maintenance of blood glucose levels and a high rate of carbohydrate oxidation, rather than a slowing of muscle glycogen utilisation, although liver glycogen reserves may be spared. During recovery from exercise, muscle glycogen resynthesis is critically dependent upon the ingestion of carbohydrate. Factors influencing the rate of muscle glycogen resynthesis include the timing, amount and type of carbohydrate ingested and muscle damage. Adequate carbohydrate availability before, during and after exercise will maintain carbohydrate oxidation during exercise and is associated with enhanced exercise performance.
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PMID:Carbohydrate nutrition and fatigue. 156 11

Pneumocystis carinii pneumonia (PCP) is the most frequently occurring opportunistic infection in individuals infected with the human immunodeficiency virus. Improved methods of diagnosing and treating PCP have resulted in increased survival rates. Nurses are more frequently faced with treatment of the critical care patient with PCP. Knowledge about the mechanisms and manifestations of PCP as well as its diagnosis and treatment provides a baseline for the nursing management of PCP. Nursing care for the critically ill adult patient with PCP focuses on the management of the human responses to PCP including hyperthermia, impaired gas exchange, altered respiratory function, fatigue, and altered nutrition, and on the management of the side effects of treatment including nausea, vomiting, and hypoglycemia. Effective interventions related to these patient problems can improve the quality of care and ultimately affect patient outcomes.
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PMID:Critical care management of the patient with HIV infection who has Pneumocystis carinii pneumonia. 159 14

To determine running performance and hormonal and metabolic responses during insulin-induced hypoglycemia, fed and fasted male rats (315 +/- 3 g) were infused with insulin (100 mU/ml, 1.5 ml/h) or saline (1.5 ml/h) for 60 min and then killed at rest or after running on the treadmill (21 m/min, 15% grade). Insulin-infused fed rats ran poorly during the second 10 min of a 20-min exercise test. They were capable of running a total of 43 +/- 5 min, compared with 138 +/- 6 min for saline-infused fed rats. Fasted insulin-infused rats were able to run only 12.8 +/- 0.8 min, compared with 122 +/- 15 min for fasted saline-infused rats. In fasted rats, blood glucose was 1.6 +/- 0.1 mM after 60 min of insulin infusion and 1.2 +/- 0.1 mM after running to exhaustion. Artificial increase of plasma free fatty acids had no effect on performance. Intravenous infusion of glucose at the time of fatigue produced an immediate recovery, allowing the formerly fatigued rats to run 20 min without development of fatigue. These results provide evidence that severe hypoglycemia can be a significant cause of fatigue, even if it occurs early in the course of an exercise bout.
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PMID:Insulin-induced hypoglycemia in fed and fasted exercising rats. 160 10

Classic studies conducted in the 1920s and 1930s established that the consumption of a high carbohydrate (CHO) diet before exercise and the ingestion of glucose during exercise delayed the onset of fatigue, in part by preventing the development of hypoglycaemia. For the next 30 to 40 years, however, interest in CHO ingestion during exercise waned. Indeed, it was not until the reintroduction of the muscle biopsy technique into exercise physiology in the 1960s that a series of studies on CHO utilisation during exercise appeared. Investigations by Scandinavian physiologists showed that muscle glycogen depletion during prolonged exercise coincided with the development of fatigue. Despite this finding, attempts to delay fatigue during prolonged exercise focused principally on techniques that would increase muscle glycogen storage before exercise. The possibility that CHO ingestion during exercise might also delay the development of muscle glycogen depletion and hence, at least potentially, fatigue, was not extensively investigated. This, in part, can be explained by the popular belief that water replacement to prevent dehydration and hyperthermia was of greater importance than CHO replacement during prolonged exercise. This position was strengthened by studies in the early 1970s which showed that the ingestion of CHO solutions delayed gastric emptying compared with water, and might therefore exacerbate dehydration. As a result, athletes were actively discouraged from ingesting even mildly concentrated (greater than 5 g/100ml) CHO solutions during exercise. Only in the early 1980s, when commercial interest in the sale of CHO products to athletes was aroused, did exercise physiologists again begin to study the effects of CHO ingestion during exercise. These studies soon established that CHO ingestion during prolonged exercise could delay fatigue; this finding added urgency to the search for the optimum CHO type for ingestion during exercise. Whereas in the earlier studies, estimates of CHO oxidation were made using respiratory gas exchange measurements, investigations since the early 1970s have employed stable 13C and radioactive 14C isotope techniques to determine the amount of ingested CHO that is oxidised during exercise. Most of the early interest was in glucose ingestion during exercise. These studies showed that significant quantities of ingested glucose can be oxidised during exercise. Peak rates of glucose oxidation occur approximately 75 to 90 minutes after ingestion and are unaffected by the time of glucose ingestion during exercise. Rates of oxidation also appear not to be influenced to a major extent by the use of different feeding schedules.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxidation of carbohydrate ingested during prolonged endurance exercise. 164 41

The medium-chain acyl-CoA dehydrogenase (MCAD) deficiency of mitochondrial beta oxidation has been identified in a nine-year old boy with a very bland course and easy fatigue as the main symptom. Repeated low frequency stimulation test and EMG for excluding a myasthenia gravis, and screening for urinary organic acid excretion were helpful for the diagnosis. The EMG test at the m. trapezius by stimulation of the n. accessorius showed an extreme decrease of muscle power down to 49%. After i.v. injection of Edrophonium the loss of power of 20% was still significant, so that we could exclude a myasthenia gravis, but we had found signs of a generalised defect in cell chemistry. The diagnosis could be confirmed by a positive 3-phenylpropionic acid-test and moleculargenetic proof of the Adenine to Guanine mutation at position 985 in the MCAD cDNA (G985) with the polymerase chain reaction. The incidence of this organic aciduria is probably 1:60,000 in Germany, but with more attention to this disease and diagnosis of cases with bland courses the incidence will be higher. The MCAD-defect should be considered in the differential diagnosis of patients with Reye syndrome-like encephalopathies, non-ketotic hypoglycaemia or sudden unexpected deaths in infancy.
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PMID:[Acyl coenzyme A dehydrogenase deficiency of medium-chain fatty acids in a 9-year-old boy with adymia. A rare mitochondrial cytopathy which may be more common than previously assumed]. 177 46

Although fats and protein contribute to energy demands of exercise, carbohydrate, principally glycogen, is the preferred fuel for muscular activity. Because of its limited storage, depletion of muscle glycogen has been shown to be one factor responsible for fatigue and exhaustion during prolonged exercise. Thus, dietary carbohydrate plays a key role in exercise performance and training. When the athlete's diet is low in carbohydrate, little glycogen is resynthesized between training sessions, leaving the individuals with low muscle glycogen and a state of chronic fatigue. The most sensitive period for glycogen resynthesis is within the first few hours after exercise. Optimal recovery from an exhaustive exercise bout depends on a reasonably rich carbohydrate diet soon after the exercise. Such feedings serve to replenish carbohydrate stores in both liver and muscles. Exertional hypoglycemia can occur when liver glucose output falls below the rate of muscle glucose uptake. Though this seldom occurs in well-fed and highly trained individuals, sugar feedings during long-term exercise has been shown to enhance performance. Thus, the important role of dietary carbohydrate before, during and after endurance activities is well established, whereas our understanding of the nutritional needs for protein and fat remain unclear.
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PMID:Carbohydrate for athletic training and performance. 181 89

It is well recognized that energy from CHO oxidation is required to perform prolonged strenuous (greater than 60% VO2 max) exercise. During the past 25 years, the concept has developed that muscle glycogen is the predominant source of CHO energy for strenuous exercise; as a result, the potential energy contribution of blood glucose has been somewhat overlooked. Although during the first hour of exercise at 70-75% VO2max, most of the CHO energy is derived from muscle glycogen, it is clear that the contribution of muscle glycogen decreases over time as muscle glycogen stores become depleted, and that blood glucose uptake and oxidation increase progressively to maintain CHO oxidation (Fig. 1.7). We theorize that over the course of several hours of strenuous exercise (i.e., 3-4 h), blood glucose and muscle glycogen contribute equal amounts of CHO energy, making blood glucose at least as important as muscle glycogen as a CHO source. During the latter stages of exercise, blood glucose can potentially provide all of the CHO energy needed to support exercise at 70-75% VO2max if blood glucose availability is maintained. During prolonged exercise in the fasted state, however, blood glucose concentration often decreases owing to depletion of liver glycogen stores. This relative hypoglycemia, although only occasionally severe enough to result in fatigue from neuroglucopenia, causes fatigue by limiting blood glucose (and therefore total CHO) oxidation. The primary purpose of CHO ingestion during continuous strenuous exercise is to maintain blood glucose concentration and thus CHO oxidation and exercise tolerance during the latter stages of prolonged exercise. CHO feeding throughout continuous exercise does not alter muscle glycogen use. It appears that blood glucose must be supplemented at a rate of approximately 1 g/min late in exercise. Feeding sufficient amounts of CHO 30 minutes before fatigue is as effective as ingesting CHO throughout exercise in maintaining blood glucose availability and CHO oxidation late in exercise. Most persons should not wait, however, until they are fatigued before ingesting CHO, because it appears that glucose entry into the blood does not occur rapidly enough at this time. It also may be advantageous to ingest CHO throughout intermittent or low-intensity exercise rather than toward the end of exercise because of the potential for glycogen synthesis in resting muscle fibers. Finally, CHO ingestion during prolonged strenuous exercise delays by approximately 45 minutes but does not prevent fatigue, suggesting that factors other than CHO availability eventually cause fatigue.
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PMID:Carbohydrate ingestion during prolonged exercise: effects on metabolism and performance. 193 83

Skeletal muscle, liver and heart glycogen variations, induced by swimming in thermal water (at 35 degrees C) as a model of physical exercise for clinical use, were studied. Muscle and liver glycogen moderately decreases after a 30-min period of swimming and comes near to depletion after 60 min. Heart glycogen decreases only slightly after 60 min. Blood glucose and plasma insulin decrease only after 60 min of swimming. A 30-min swim in thermal water, cooled to 25 degrees C, depletes muscle and liver glycogen and slightly decreases heart glycogen. Under these conditions, plasma insulin decreases and hypoglycemia occurs. The results seem to indicate some advantages of swimming in hot thermal water in order to prevent glycogen store depletion as the physiological prerequisite for a physical exercise of clinical interest to obtain therapeutical benefits, avoiding premature fatigue and exhaustion.
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PMID:Effect of swimming in thermal water on skeletal muscle, liver and heart glycogen. 213 67

A 31-year-old male patient with type Ia glycogen storage disease was admitted to our department complaining of general fatigue and right hypochondriac pain. He exhibited massive hepatomegaly with systemic hypoglycemia, lactic acidosis, hyperuricemia, hyperpyruvatemia and hyperlipemia. The failure of blood glucose levels to increase after a glucagon loading test, and a reduced lactate level on glucose tolerance test were also observed. Various imaging techniques suggested hepatic adenoma with hemorrhage in the tumor, which was confirmed histologically. There was a complete absence of glucose 6-phosphatase activity, as determined by an enzyme assay on resected liver specimens, which proved the case to be type Ia glycogen storage disease. We also reviewed all previously reported cases of hepatic tumor and glycogen storage diseases. We conclude that, since hepatic adenoma is not rare in this disease, and is complicated by hemorrhage, rupture and malignancy, careful follow-ups are necessary.
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PMID:A case of type Ia glycogen storage disease complicated by hepatic adenoma. 217 Feb 59

L-Glutamate and related excitatory amino acids (EAA) are firmly established as major excitatory synaptic transmitter substances in the vertebrate central nervous system. Questions which have been addressed include: How many receptors are there for the EAAs?; What ion channels and/or 'second-messenger' systems are regulated by these receptors?; What are the roles of EAAs in higher neural functions?; Are they involved in neurological disorders? EAA receptors appear not only to mediate normal synaptic transmission along excitatory pathways but also to participate in the modification of synaptic connections during development. However, overaction of receptors can also mediate neuronal degeneration and even cell death. NMDA receptor antagonists markedly attenuate neuronal necrosis. Therefore, it appears that ischemia- and hypoglycemia-associated brain damage results not from a lack of energy substrates but rather via the mediation of NMDA receptors and 'excitotoxic' mechanisms. The action of ketamine anesthesia is closely associated with a block of the NMDA receptor. Ketamine binds to a site within the lumen of the NMDA-activated channel and can become trapped there when the channel closes. Current evidence indicated that NMDA receptor antagonists will be of value for the treatment of delayed neuronal death. NMDA receptor will lead to understanding the mechanisms underlying learning and memory, the control of neuronal excitability and neuronal death.
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PMID:[Synaptic mechanisms of excitatory amino acids and NMDA receptor mediated brain excitability]. 217 10


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