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

Endocrine and metabolic responses to resistance exercise were compared in 5 athletes self-administering (SL) anabolic steroids and 8 athletes (L) not using these compounds. Exercise consisted of 5 sets of 10 repetitions in the squat and quarter squat. Blood samples were collected before (pre) and immediately after (post) exercise, and following 30 minutes of recovery (post-30). Except for significantly lower lactate concentrations in SL (p less than 0.015) at post-30, the responses to exercise and recovery were similar in both groups. Significantly higher hematocrits (p less than 0.0001), total androgen concentrations (p less than 0.0001), and androgen/cortisol ratios (p less than 0.0001) were observed in the SL group across all time periods. Plasma androgen concentrations increased about 22% in SL following exercise, even though plasma LH concentrations were significantly lower (p less than 0.0001) than in L. Plasma ACTH and cortisol concentrations were not significantly affected. Both groups displayed similar endocrine and metabolic responses to an acute bout of resistance exercise. The higher androgen/cortisol ratios and lower plasma lactate concentrations during recovery are two potential factors which may help explain the lower subjective level of fatigue following training sessions often reported by individuals who use anabolic steroids.
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PMID:Physiological responses to resistance-exercise in athletes self-administering anabolic steroids. 196 89

To investigate the adrenostatic potential of a nonhypnotic low dose etomidate infusion, we administered 0.03 mg/kg etomidate in a bolus injection, followed by constant infusion of 0.3 mg/kg.h for 24 h to 6 patients with severe Cushing's syndrome. The dose-response relationship also was determined in 15 normal subjects. Three groups of 5 received, respectively, doses of 0.03, 0.1, and 0.3 mg/kg.h etomidate for 5 h after an initial bolus dose of 0.03 mg/kg. The response to exogenously administered ACTH [0.25 mg ACTH-(1-24)], injected after the etomidate or control infusion, was determined in all normal subjects. In the six hypercortisolemic patients, serum cortisol concentrations decreased from 1374 +/- 436 nmol/L (mean +/- SEM) to 188 +/- 91 nmol/L after 11 h of etomidate infusion and remained low until the end of the infusion. Cortisol levels returned to pretreatment concentrations by 24 h. Excretion of urinary free cortisol decreased from 1180 +/- 196 to 185 +/- 66 nmol/day. In the normal subjects, administration of etomidate led to a dose-dependent decrease in serum cortisol from about 550 to 83 nmol/L, while 11-deoxycortisol rose from low or undetectable levels up to 346 nmol/L. In response to ACTH, cortisol levels rose in inverse proportion to the etomidate dose. It was, however, significantly reduced compared to normal saline infusion even after the lowest dose. Changes in aldosterone and corticosterone concentrations were similar to those in cortisol, and 11-deoxycorticosterone changed in a pattern similar to that of 11-deoxycortisol. Two of five normal subjects reported tiredness during the highest etomidate infusion. No other side-effects were noted. We conclude that iv administered etomidate in a low nonhypnotic dose reduces serum cortisol concentrations in a dose-dependent manner in both hyper- and eucortisolemic subjects. This study suggests that etomidate at a dose of 0.1 mg/kg.h or lower may be an effective strategy for the control of severe hypercortisolemia.
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PMID:Infusion of low dose etomidate: correction of hypercortisolemia in patients with Cushing's syndrome and dose-response relationship in normal subjects. 215 85

Corticotrophin (ACTH) deficiency is an important cause of a potentially lethal form of adrenocortical failure. Difficulties can arise in making the diagnosis, especially when secretion of other pituitary trophic hormones is normal. Presenting features of seven patients with ACTH deficiency, in whom the diagnosis was difficult for a variety of reasons, are reported and discussed. Two patients had a normal cortisol response to synthetic ACTH. The possibility of ACTH deficiency should be considered in any patient presenting with weight loss, vomiting, muscular fatigue and stiffness, hyponatraemia or hypoglycaemia.
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PMID:ACTH deficiency: problems in recognition and diagnosis. 254 52

Six patients (four females, two males; aged 18-65 years), previously treated by external pituitary irradiation (2000-4000 cGY in 8-15 fractions over 10-20 days) for pituitary tumours, presented with the symptoms of excessive and inappropriate tiredness suggestive of ACTH deficiency, despite a normal peak cortisol response to an insulin tolerance test (four cases) or to a glucagon stimulation test (two cases). These six patients were found to have significantly lower mean 24 h urinary free cortisol levels (100 +/- 40 nmol; mean +/- SD) compared with the mean value of 31 normal controls (210 +/- 70.8 nmol; P less than 0.01). In addition serum cortisol profiles based on a series of four timed samples between 0900-2300 h were subnormal (mean 130 nmol/l) in comparison with profiles obtained from 12 normal controls (mean 270 nmol/l) (P less than 0.001). Glucocorticoid replacement therapy promptly abolished their symptoms. These results suggest that a discordance between ACTH secretion under basal circumstances and ACTH response to pharmacological tests may exist in patients with ACTH deficiency. We speculate that defective endogenous corticotrophin-releasing hormone (CRF) secretion, due to radiation-induced damage at hypothalamic level, is one cause of this phenomenon.
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PMID:Adrenocorticotrophin (ACTH) deficiency undetected by standard dynamic tests of the hypothalamic-pituitary-adrenal axis. 284 48

The role of the pituitary-adrenocortical system (PACS) in body adaptation abilities was studied on rats. The adaptation abilities were tested by a body working capacity (the running time in a treadmill till fatigue). The single administration of ginseng results in the increase of a working capacity up to 132%, the seven-day one up to 179%. This makes it possible to speak about two levels of adaptation, each being characterized by a specific PACS status and a degree of PACS involvement in adaptation abilities. The single administration of ginseng is accompanied by an increase in the basal level of ACTH and corticosteroids. At a 7-day administration the basal level of ACTH and corticosteroids does not change but PACS reactivity to the immobilising stress increases. The preliminary administration of 15 mg/100 g b. w. hydrocortisone, 7 days before testing of the working capacity and PACS status, causes the block in PACS function. It results in the decrease of the basal corticosteroid content in plasma and the inability of stress factor to cause the rise in the corticosteroid level. The PACS blocking results in the decrease of a working capacity in normal rats not treated with ginseng and in animals singly treated with ginseng. The PACS blocking effected the increment in a working capacity caused by a 7-day ginseng administration to a lesser extent, however, the decrease in a working capacity took place even in this case. The conclusion is made that PACS status changes with the transition of a body to a higher level of adaptation: PACS excitation occurs or the system excitability increases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of pituitary-adrenocortical system in body adaptation abilities. 285 76

ACTH 1-39 and many of its fragments enhance regeneration of rat peripheral nerve and improve motor unit reorganization. The analog of ACTH 4-9 (Org 2766), with longer-lasting activity and greater biological potency for many parameters, was evaluated for its restorative powers on neuromuscular function following denervation. Org 2766 (10 micrograms/kg/48 hr IP) was administered to rats starting 3 hr after crush denervation of the extensor digitorum longus (EDL) muscle. Contractile strength, motor unit performance under low, optimum and high frequency stimulation, and number and size distribution of motor units of the EDL stimulated through the regenerating peroneal nerve were compared to saline-treated controls. Muscles of parallel animal groups were stimulated directly in vitro. Contractile strength and motor unit performance during high frequency stimulation were significantly improved by Org 2766 treatment at both 7 and 11 days after crush denervation. Org 2766 improves motor unit reformation both qualitatively (more small motor units that are highly resistant to fatigue) and quantitatively (stronger motor units). This peptide does not affect muscle contractile components. Prolonged treatment (21 days) with Org 2766 has a negative effect on motor unit performance, indicating that it exerts its favorable effects early in regeneration and exposure to this peptide should be limited to this period.
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PMID:ACTH 4-9 analog (Org 2766) improves qualitative and quantitative aspects of motor nerve regeneration. 285 5

Water deprivation (WD) resulted in increased serum osmotic pressure (OP) and decreased body weight (WB); adrenal aldosterone content did not change. Adrenal corticosterone content tended to be elevated during early WD, indicating a stress response, but tended to decrease after seven days of WD, suggesting adrenal fatigue. During water restriction (WR), after the period of weight loss, adrenal corticosterone content and serum OP were elevated. As the birds began to gain weight, aldosterone levels did not change but adrenal corticosterone content and serum OP approached control values, suggesting that the birds were beginning to adapt to the WR. Adrenal sensitivity to ACTH was indicated by the elevated adrenal aldosterone and corticosterone content after ACTH injection.
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PMID:Adrenal responses to chronic and acute water stress in Japanese quail Coturnix japonica. 285 51

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

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

This paper assesses mechanisms that may contribute to the higher incidence of increased muscle fatigue during exercise and reduced exercise performance as observed with selective compared with non-selective beta-adrenoceptor antagonists. Published data and the results obtained in 8 healthy subjects (mean age 23 years) studied before and after acute beta-adrenoceptor blockade with pindolol (nonselective, 10 mg) and metoprolol (beta 1-receptor selective, 100 mg) suggest that the differences in the cardiovascular and respiratory effects between the 2 types of antagonists are marginal and cannot explain the discrepancies concerning exercise perception and performance. Conversely, basic differences between the 2 types of antagonists were shown in different groups of hypertensive men (mean age 32 years) studied before and after 4 weeks of treatment with pindolol (15 mg), and with metoprolol (200 mg) and acebutolol (cardioselective, 500 mg), by single crossover technique. Whereas lipolysis was similarly inhibited by both selective and non-selective antagonists, hypoglycaemia occurred only under non-selective blockade. It apparently reflects the inhibition of glycogen breakdown; concomitant rises in plasma adrenaline and ACTH probably reflect counter-regulatory mechanisms.
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PMID:beta-adrenoceptor blockade and physical activity: cardiovascular and metabolic aspects. 613 35


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