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

During strenuous exercise (i.e. 70% maximal O2 consumption) there is a progressive shift from muscle glycogen to blood glucose oxidation with increasing duration of exercise. By maintaining blood glucose concentration and the rate of carbohydrate oxidation necessary to exercise strenuously, carbohydrate consumption throughout exercise delays fatigue by 30-60 min in endurance-trained subjects. This requires exogenous glucose supplementation at rates in excess of 1 gram/min (i.e., 16 mg/kg/min) as evidenced by the observation that intravenous glucose infusion at this rate is required to maintain blood glucose at 5 mM. Exogenous glucose must be infused at a rate of 2.6 gram/min (i.e., 37 mg/kg/min), which is similar to the total rate of carbohydrate oxidation, in order to maintain blood glucose at 10 mM after 2 h of exercise. However, carbohydrate supplementation during intense exercise does not spare muscle glycogen utilization in people. This suggests that over the course of 2-4 hours of exercise at 70% VO2max, muscle glycogen and blood glucose contribute equally to total carbohydrate oxidation. Furthermore, during the latter stages of prolonged exercise, exogenous blood glucose supplementation may be capable of supplying almost all of the carbohydrate requirements of exercise at intensities up to 70% VO2max.
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PMID:Carbohydrate feeding during exercise. 148 49

We studied plasma ammonia and exercise tolerance in six patients with McArdle's disease (myophosphorylase deficiency, type V glycogenosis) during incremental cycle ergometry. Tests were performed either in the postabsorptive state or after supplementation with branched-chain amino and 2-oxoacids and glucose. Glucose and branched-chain 2-oxoacid combined increased total work performed from control 49 +/- 22 to 80 +/- 36 kJ (P less than 0.05). Glucose alone also improved total work performed from 49 +/- 22 to 64 +/- 33 kJ (P less than 0.05). Branched-chain 2-oxoacids alone had a variable effect, and branched-chain amino acids were of no benefit. Correlations between plasma ammonia and heart rate for individual patients were r = 0.99, P less than 0.01; r = 0.95, P less than 0.01; r = 0.84, P less than 0.01; r = 0.76, P less than 0.01; r = 0.73, P less than 0.01; and r = 0.63, P less than 0.05 and between ammonia and perceived exertion for all patients combined was r = 0.70, P less than 0.0001. In two patients, correlation of ammonia with heart rate at a power output of 60 W was r = 0.91, P less than 0.001 and at 40 W was r = 0.77, P less than 0.001. We conclude that ammonia is either a mediator or a marker of the metabolic events leading to fatigue.
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PMID:Relationship between ammonia, heart rate, and exertion in McArdle's disease. 153 42

Muscle glycogen and plasma glucose are oxidized by skeletal muscle to supply the carbohydrate energy needed to exercise strenuously for several hours (i.e., 70% maximal O2 consumption). With increasing exercise duration there is a progressive shift from muscle glycogen to blood glucose. Blood glucose concentration declines to hypoglycemic levels (i.e., 2.5 mmol/L) in well-trained cyclists after approximately h of exercise and this appears to cause muscle fatigue by reducing the contribution of blood glucose to oxidative metabolism. Carbohydrate feeding throughout exercise delays fatigue by 30-60 min, apparently by maintaining blood glucose concentration and the rate of carbohydrate oxidation necessary to exercise strenuously. Carbohydrate feedings do not spare muscle glycogen utilization. Very little muscle glycogen is used for energy during the 3-4-h period of prolonged exercise when fed carbohydrate, suggesting that blood glucose is the predominant carbohydrate source. At this time, exogenous glucose disposal exceeds 1 g/min (i.e., 16 mg.kg-1.min-1) as evidenced by the observation that intravenous glucose infusion at this rate is required to maintain blood glucose at 5 mmol/L. However, at this time these cyclist cannot exercise more intensely than 74% of maximal O2 consumption, suggesting a limit to the rate at which blood glucose can be used for energy. It is important to realize that carbohydrate supplementation during exercise delays fatigue by 30-60 min, but does not prevent fatigue. In conclusion, fatigue during prolonged strenuous exercise is often due to inadequate carbohydrate oxidation. This is partly a result of hypoglycemia, which limits carbohydrate oxidation and causes muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carbohydrate supplementation during exercise. 154 49

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

We investigated the effect of dichloroacetate (DCA) on tension generation and carbohydrate metabolism of the rat diaphragm in vitro. Isolated diaphragms were placed in individual organ chambers and were hooked to force-displacement transducers. Net lactate production and glucose and lactate oxidation were measured in vitro. Diaphragmatic fatigue was precipitated by in vivo endotoxemic shock, by in vitro hypoxia, or by in vitro repetitive tetanic stimulation. In diaphragms isolated from endotoxemic rats, DCA increased tension generation by 30 and 20% at stimulation frequencies of 20 and 100 Hz, respectively. Associated with changes in mechanical performance, DCA reduced net lactate production by 53% after 60 min of incubation and increased glucose oxidation 54% but had no effect on lactate oxidation. During in vitro hypoxia, DCA reduced net diaphragmatic lactate production by 30% and increased glucose oxidation by 45% but did not attenuate hypoxic fatigue. DCA had no effect on tension generation during repetitive tetanic stimulation. We conclude that DCA improves in vitro diaphragmatic fatigue due to endotoxicosis but not due to hypoxia or repetitive stimulation.
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PMID:Effect of dichloroacetate on mechanical performance and metabolism of compromised diaphragm muscle. 156 69

A group of newly diagnosed patients with non-insulin-dependent (type 2) diabetes mellitus (n = 133) were divided into two groups according to the symptoms of diabetes mellitus at diagnosis; a group (26 men and 17 women) with hyperglycaemic symptoms (polydipsia, polyuria, weight loss and tiredness) and a group (44 men and 46 women) without such symptoms. At the time of diagnosis, symptomatic patients tended to be leaner (P = NS), and they were more hyperglycaemic (P less than 0.001-0.06) and had lower insulin responses to an oral glucose load (P less than 0.01-0.05) than asymptomatic patients, but after 5 years no difference in these respects was found. No significant differences in the frequency of islet-cell antibodies or cardiovascular diseases were found between the two diabetic groups. At the 5-year examination, the initially symptomatic patients were receiving pharmacological treatment for hyperglycaemia more often than asymptomatic patients. No consistent differences in clinical characteristics and 5-year outcome were observed between those diabetic patients who were diagnosed on the basis of hyperglycaemic symptoms and those who were diagnosed for other reasons. In conclusion, in middle-aged patients with newly diagnosed diabetes mellitus classified as non-insulin-dependent, diabetic symptoms at diagnosis did not predict the 5-year outcome of the patients in terms of metabolic control or cardiovascular events.
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PMID:Hyperglycaemic symptoms before diagnosis of non-insulin-dependent (type 2) diabetes mellitus in relation to 5-year outcome. 158 65

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

Intense exercise (i.e.; above 60% VO2max) can be maintained for prolonged periods provided sufficient carbohydrate is available for energy and the heat generated from muscle metabolism does not cause excessive hyperthermia and/or dehydration due to sweating. It is clear that people should ingest carbohydrate during prolonged exercise (i.e.; longer than 1-2 h), which causes fatigue because of an inadequate supply of blood glucose and that fluids should also be ingested in an attempt to offset dehydration and reduce hyperthermia. Ingestion of approximately 30-60 g of carbohydrate (i.e.; glucose, sucrose, or starch) during each hour of exercise will generally be sufficient to maintain blood glucose oxidation late in exercise and delay fatigue. Since the average rates of gastric emptying and intestinal absorption can reach 1 l.h-1 for water and solutions containing up to 8% carbohydrate, exercising people can be supplemented with both carbohydrate and fluids at relatively high rates (over 60 g.h-1 of carbohydrate and 1 l.h-1 of fluid). Therefore, when sweat rate is not high (i.e.; less than 1 l.h-1), the addition of carbohydrate to fluids, and vice versa, does not prevent adequate supplementation of each, especially if large volumes are consumed to keep the stomach somewhat full and thus increase gastric emptying. Therefore, in most situations there are no trade-offs between fluid and carbohydrate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carbohydrate and fluid ingestion during exercise: are there trade-offs? 160 39

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

A total of 930 patients have been evaluated for safety in a programme of clinical trials for lisinopril-hydrochlorothiazide combination treatment. Combination therapy with these two agents is generally well tolerated. In clinical trials, adverse experiences in patients treated with a lisinopril-hydrochlorothiazide combination were dizziness (7.5%), headache (5.2%), cough (3.9%), fatigue (3.7%), orthostatic effects (3.2%), diarrhoea (2.5%), nausea (2.2%) and upper respiratory tract infection (2.2%). Withdrawals from treatment have been relatively infrequent comprising dizziness (0.8%), headache (0.3%), cough (0.6%), fatigue (0.4%), diarrhoea (0.2%), orthostatic effects and nausea (0.1% each). The most common laboratory adverse experiences in patients on therapy with the lisinopril-hydrochlorothiazide combination are: increases in serum glucose, triglycerides, uric acid, serum creatinine, blood urea nitrogen and blood urea; and decreases in serum potassium. However, in individual controlled studies, the addition of lisinopril to treatment with hydrochlorothiazide results in attenuation of some of the potentially adverse metabolic affects of the diuretic. Adverse experiences in the patients treated for periods of 50 weeks or more, the elderly and the renally impaired are similar to those seen in the total population. Overall the available data indicate that a fixed dose combination of lisinopril-hydrochlorothiazide is a well-tolerated therapeutic option in patients with mild-to-moderate hypertension.
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PMID:Review of international safety data for lisinopril-hydrochlorothiazide combination treatment. 166 80


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