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

The ergogenic potential of drugs used by athletes to enhance performance is reviewed, and areas of involvement for pharmacists interested in the problem of drug abuse in athletics are described. Athletes use drugs for therapeutic and recreational purposes, as supposed ergogenic aids, and to mask the presence of other drugs during testing. Because many athletes train for competition and not for health, they may view the risk-to-benefit ratio of ergogenic drugs as favorable and may begin using them at an early age. Alcohol is the drug most commonly used by student athletes. Although alcohol has no ergogenic benefit, it is viewed as a caloric source and an anxiolytic. Amphetamines do not prevent exhaustion but may mask fatigue, which can have dangerous consequences. Anabolic steroids appear to increase strength but frequently cause adverse reactions, primarily involving the hepatic and endocrine systems. Beta-blocking agents have been shown to reduce anxiety, hand tremor, and heart rate in precision sports like archery, but susceptible persons may experience serious adverse effects. Caffeine improves the efficiency of fuel use and reduces fatigue; its use has been banned by several athletic organizations. Neither cocaine nor marijuana causes any increase in strength. Secretion of human growth hormone may be stimulated by a variety of agents, but evidence that any subsequent increases in size and weight occur is lacking. Other substances tried by athletes include vitamins and minerals, naloxone, albuterol, and human recombinant erythropoietin. Opportunities in sports pharmacy exists in the areas of information retrieval and interpretation, drug testing, legislation to reclassify drugs, education, and research.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abuse of drugs used to enhance athletic performance. 268 62

Subjective feeling of fatigue was quantified before and 20 days after elective uncomplicated abdominal surgery in 16 otherwise-healthy patients and compared with changes in heart rate and various hormonal and substrate responses to a 10-minute bicycle exercise (65% of preoperative maximal work capacity) preoperatively and postoperatively. Postoperatively, fatigue increased (p less than 0.001) from 3.0 +/- 0.5 to 5.3 +/- 0.5 arbitrary units (mean +/- SEM). Heart rate, plasma catecholamines, and serum growth hormone, lactate, alanine, and glycerol values always increased, whereas serum insulin values decreased in response to exercise (p less than 0.01). During exercise, only heart rate (p less than 0.01) and lactate (p less than 0.05) values were higher postoperatively compared with preoperatively. Increase in fatigue postoperatively correlated significantly to increase in heart rate (p less than 0.01) and correlated positively, but not significantly, to increase in plasma levels of noradrenaline (p = 0.08), growth hormone (p = 0.09), and alanine (p = 0.08) during exercise, but not to increase in serum lactate values (p greater than 0.8). Thus, after uncomplicated surgery, there was increased fatigue and amplified metabolic and cardiovascular response to a given absolute work load. These findings are similar to those observed during detraining and suggest a therapeutic role of exercise in the treatment of postoperative fatigue.
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PMID:Fatigue and cardiac and endocrine metabolic response to exercise after abdominal surgery. 291 3

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.
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PMID:Endocrine myopathies. 306 2

Whether or not the pineal gland has a significant physiological role in humans is not known. There has nevertheless been speculation about the potential therapeutic use of melatonin (in view of its hypnotic and possible zeitgeber properties) in conditions such as insomnia and jet lag, and in shift-workers. Our work concerns the effects of melatonin administration in humans and the interactions between melatonin and other circadian variables. Chronic (one month), timed (1700 h), low-dose (2 mg daily) melatonin administration to normal subjects without environmental control consistently increased evening fatigue and slightly modified the 24 h prolactin rhythm without effect on cortisol, growth hormone, luteinizing hormone, thyroxine, testosterone or self-rated mood. In five out of 11 subjects the endogenous melatonin rhythm was advanced by one to three hours. During fractional desynchronization of circadian rhythms by increasing imposed 'day' length (26-29 h, 24 days, 500 lux), 5 mg melatonin per os at lights-out in two subjects resulted in better entrainment of the fatigue rhythm to the zeitgeber than in five out of six control subjects, without major consistent effects on other measured circadian variables. Using a new radioimmunoassay for 6-hydroxymelatonin sulphate (aMT6s), the major melatonin metabolite, we have shown that the urinary aMT6s rhythm is closely correlated to that of melatonin in plasma and is completely suppressed by an acute dose of atenolol (100 mg per os), a peripheral beta-adrenergic antagonist. During fractional desynchronization by increasing imposed 'day' length in one subject and decreasing imposed 'day' length in two subjects, the urinary aMT6s rhythm behaved similarly to that of core temperature. The results suggest that fatigue (or alertness) may be entrained by melatonin, but whether critical performance rhythms can be suitably manipulated remains to be clarified. It is likely that melatonin production is linked to the so-called 'strong' circadian oscillator.
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PMID:Some effects of melatonin and the control of its secretion in humans. 383 18

Six Holstein cows were sampled hourly for 24 h for plasma concentrations of hormones and metabolites. Cows were sampled at about 2 wk prepartum, at 3 wk postpartum, during a ketonemia induced by feed restriction to 54% of ad libitum intake, and after a recovery period. They were fed long alfalfa hay postpartum. The onset of lactation caused concentrations of growth hormone, glucagon, acetoacetate, beta-hydroxybutyrate, and total amino acids of plasma to increase and those of glucose and insulin to decrease. Feed restriction exacerbated changes at 3 wk postpartum except for total amino acids and glucagon, which both decreased to prepartal concentrations. Resumption of ad libitum feeding caused most hormones and metabolites to return to prepartum concentrations. Diurnal variations in response to feeding twice daily were most evident for growth hormone, free fatty acids, and total amino acids. The 3-wk postpartum and ketonemic periods gave the greatest responses to feeding. Molar ratios of insulin to glucagon and insulin to growth hormone tended to decrease at 3 wk postpartum and decreased further in ketonemia, demonstrating hormonal adaptations to decreased energy intake during lactation. Lactation ketosis results from more than severe energy deficit.
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PMID:Glucagon, insulin, growth hormone, and some blood metabolites during energy restriction ketonemia of lactating cows. 388 31

The objective was to determine the effect of daily s.c. injection of bovine growth hormone (bGH) on nitrogen and energy balance in six Hereford heifers. In addition, effects on urinary excretion of 3-methylhistidine and hydroxyproline and on serum mineral concentrations were monitored. A single reversal design was used with two 14-d injection periods of placebo or bGH (29.2 IU/d). Measurements were made on d 8-14 of each period. Injection of bGH did not alter apparent digestibility of dry matter, energy or nitrogen, nor urinary excretion of 3-methylhistidine or hydroxyproline. Serum concentrations of calcium, phosphorus and magnesium were normal with bGH treatment. Nitrogen retention was higher and urinary nitrogen excretion was lower when the heifers were injected with bGH than with the placebo demonstrating an effect of bGH on postabsorptive metabolism of nitrogen. Total energy balance was not altered by treatment. Energy retained as protein was higher after bGH treatment than after the placebo, implying decreased energy retained as fat and demonstrating a role for GH in altering energy partition in growing animals. Total heat production was not altered by treatment indicating no change in the gross efficiency of metabolizable energy use with bGH treatment.
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PMID:Effect of bovine growth hormone administration on metabolism of growing Hereford heifers: dietary digestibility, energy and nitrogen balance. 394 54

The endogenous opioids seem likely to be assigned a significant role in the integrated hormonal and metabolic response to exercise. This article reviews the present evidence on exercise and the endogenous opioids, and examines their involvement in a number of widely disparate physiological processes. In considering the role of individual opioid peptides, it is important to remember that many of the tools and techniques now used are still relatively crude. Most studies have demonstrated that serum concentrations of endogenous opioids, in particular beta-endorphin and beta-lipotrophin, increase in response to both acute exercise and training programmes. Elevated serum beta-endorphin concentrations induced by exercise have been linked to several psychological and physiological changes, including mood state changes and 'exercise-induced euphoria', altered pain perception, menstrual disturbances in female athletes, and the stress responses of numerous hormones (growth hormone, ACTH, prolactin, catecholamines and cortisol). Many reports have described a role for the endorphin response as seen during exercise and have used the opioid receptor antagonist, naloxone, to investigate and verify the degree of involvement of the opioids. However, whether the observed increases in peripheral endorphin concentrations are sufficient to cause immediate mood changes, create menstrual cycle dysfunction or alter pain perception is still not resolved. A relatively new implication for the endorphins and associated changes with exercise is in ventilatory regulation. A number of studies have suggested that endogenous opioids depress ventilation and may, therefore, play a role in ventilatory regulation by carbon dioxide, hypoxia and exercise. It may also be possible that during exercise, the perception of fatigue is modulated by an increase of endogenous opioids.
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PMID:Endorphins and exercise. 609 Dec 17

The effects of intravenous infusion of the nonselective alpha-adrenergic antagonist phentolamine or of the selective alpha 2-adrenergic antagonist yohimbine on growth hormone (GH), prolactin (PRL) and cortisol secretion during insulin-induced hypoglycemia were studied in 11 healthy young men. The GH response was blunted following each antagonist used, PRL secretion was higher after yohimbine and diminished after phentolamine when compared to controls. The plasma cortisol response was not influenced by either compound. In another series of experiments no effect of an oral administration of prazosin, a selective alpha 1-adrenergic antagonist, on the secretion of GH, PRL and cortisol was found in any of 7 subjects. Prazosin inhibited blood pressure increase during hypoglycemia and induced slight drowsiness and fatigue in the subjects. It is concluded that in man alpha-adrenergic stimulation of GH secretion during hypoglycemia is transmitted via alpha 2-receptors, PRL secretion is mediated via alpha 1-receptors, whereas inhibition of PRL release is mediated via alpha 2-receptors. In this experiment no effect of alpha 1- or alpha 2-blockade on cortisol response to hypoglycemia was seen.
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PMID:Role of alpha 1- and alpha 2-adrenergic receptors in the growth hormone and prolactin response to insulin-induced hypoglycemia in man. 609 32

Carbohydrate and lipid metabolism at rest and after 1 h submaximal physical exercise in cold weather (between -1 and -6 C) were studied in ten healthy male subjects treated in a randomized double-blind fashion for 2 days with either placebo, the non-selective beta-adrenoceptor antagonist with high ISA pindolol (10 mg), or the cardioselective drug atenolol (100 mg). Four subjects, on both atenolol and pindolol, complained of muscular fatigue during exercise on beta blockade; four other subjects perceived some fatigue. There were no significant differences in blood glucose or insulin levels between treatments and placebo period. Post-exercise growth hormone levels increased on placebo (p less than 0.01), on pindolol (p less than 0.01), and on atenolol (p less than 0.05), but the alteration was more prominent on pindolol than on placebo (p less than 0.05). The plasma free fatty acid concentrations increased during exercise on placebo and pindolol (p less than 0.05) and on atenolol (p less than 0.01). Serum triglyceride concentrations decreased significantly during exercise on placebo or pindolol (p less than 0.01). Triglyceride levels before exercise were significantly higher on beta blockade than on placebo (p less than 0.05). The metabolic parameters taken before and after exercise did not explain the muscle fatigue experienced by many subjects during exercise.
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PMID:Effect of the short-term beta-adrenoceptor blockade on exercise metabolism in cold weather. 614 7

Beta-blockade is known to induce muscle fatigue and tendency to hypoglycaemia during prolonged exercise. In addition, beta-blocking agents influence the secretion of many hormones, which regulate glucose. We have investigated the effects of a beta 1-selective (metoprolol) and a non-selective (propranolol) beta-blocking agent on muscle glycogenolysis, blood glucose and lactate levels, plasma levels of free fatty acids and on secretion of insulin, growth hormone, glucagon and cortisol during physical exercise in a double blind cross-over study in seven healthy male volunteers. They participated in three bicycle ergometer tests each lasting for 30 minutes under treatment of placebo (C), metoprolol (M) or propranolol (P). A biopsy was obtained from the vastus lateralis muscle before and immediately after the exercise for muscle glycogen assay. The glycogen concentration after exercise tended to be lower in C than in M or P experiment. The blood glucose level decreased during P and at 30 min there was a significant difference between P and C. The blood lactate was significantly lower before exercise during P than C or M. The increase of blood lactate during exercise, however, was not inhibited by P. Both beta-blocking agents counteracted the increase of FFA during exercise. There was a marked increase of growth hormone secretion during beta-blockade. The secretion of glucagon and cortisol were slightly increased by P and M, but the plasma insulin level was not affected by beta-blockade.
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PMID:Modification of the metabolic and hormonal response to physical exercise by beta-blocking agents. 675 73


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