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

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

This study was designed to determine whether insulin-dependent diabetics fatigue at a different rate than nondiabetics during anaerobic and aerobic exercise. The rate of fatigue during cycle ergometer exercise at 90 percent (anaerobic) and 60 percent (aerobic) of predicted maximum oxygen consumption in eight men who were insulin-dependent diabetics and eight nondiabetic men was determined. For the insulin-dependent diabetics, performance at 90 percent was a significantly better predictor (p less than .05) of performance at 60 percent than it was for the nondiabetics. The rate of fatigue during cycle ergometer exercise for insulin-dependent diabetics may be predictable, and this may be important in evaluating exercise tolerance for these patients.
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PMID:Fatigue rate during anaerobic and aerobic exercise in insulin-dependent diabetics and nondiabetics. 634 Jan 29

This study was undertaken to determine whether carbohydrate feeding during exercise can delay the development of fatigue. Ten trained cyclists performed two bicycle ergometer exercise tests 1 wk apart. The initial work rate required 74 +/- 2% of maximum O2 consumption (VO2 max) (range 70-79% of VO2 max). The point of fatigue was defined as the time at which the exercise intensity the subjects could maintain decreased below their initial work rate by 10% of VO2 max. During one exercise test the subjects were fed a glucose polymer solution beginning 20 min after the onset of exercise; during the other they were given a placebo. Blood glucose concentration was 20-40% higher during the exercise after carbohydrate ingestion than during the exercise without carbohydrate feeding. The exercise-induced decrease in plasma insulin was prevented by carbohydrate feeding. The respiratory exchange ratio was unchanged by the glucose feeding. Fatigue was postponed by carbohydrate feeding in 7 of the 10 subjects. This effect appeared to be mediated by prevention of hypoglycemia in only two subjects. The exercise time to fatigue for the 10 subjects averaged 134 +/- 6 min (mean +/- SE) without and 157 +/- 5 min with carbohydrate feeding (P less than 0.01).
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PMID:Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. 635 Feb 47

The thermic effect of infused glucose and insulin was measured by combining the hyperinsulinemic euglycemic clamp technique with indirect calorimetry, in 10 normal weight volunteers (group I), 7 obese subjects with normal glucose tolerance (group II), and 13 obese subjects with abnormal glucose tolerance or noninsulin-dependent diabetes mellitus before (group IIIa) and after weight loss of 10.8 +/- 0.4 kg (group IIIb). During hyperinsulinemia (760-1,100 pmol/liter), total glucose disposal from combined endogenous production and glucose infusion was 545 +/- 49, 441 +/- 70, 233 +/- 35, 231 +/- 31 mg/min and energy expenditure changed by + 0.476 +/- 0.080, +0.293 +/- 0.095, -0.114 +/- 0.063, and +0.135 +/- 0.082 kJ/min in group I, II, IIIa, and IIIb, respectively. The increased energy expenditure correlated with glucose storage (measured cost of processing the glucose: 1.33 kJ/g). In group IIIa there was no increase in energy expenditure in response to glucose and insulin infusions. After therapy (group IIIb) there was a significant recovery (P less than 0.05) of the thermic effect of infused glucose although total glucose disposal was unchanged. It is proposed that the recovered thermic effect of infused insulin/glucose is due to the different contributions of gluconeogenesis in the fasting state and during the glucose clamp before and after weight loss. In addition we hypothesize that some of the lower thermic effect of food reported in obese noninsulin-dependent diabetics may be explained by decreased energy expenditure due to a greater suppression of hepatic gluconeogenesis as well as by lower storage rate.
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PMID:Thermic effect of infused glucose and insulin in man. Decreased response with increased insulin resistance in obesity and noninsulin-dependent diabetes mellitus. 635 Mar 68

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: epidemiology, mechanisms, treatment. 636 45

In symptomatic mitral valve prolapse patients (MVP): (1) the frequency and nature of symptoms were analyzed (n = 313); (2) metabolic studies were performed (n = 20), and (3) the response to isoproterenol infusions were studied (n = 16). Chest pain is more often the initial symptom in men; palpitations are more common initially in women. Fatigue, palpitations, dyspnea and arrhythmias are more frequent in women. Chest pain and neurologic events occur with the same frequency in both sexes. Women have more symptoms than men. MVP patients have normal thyroid function tests, normal plasma cortisol, normal diurnal variation of cortisol and normal 24-hour 17-ketosteroids and 17-hydroxycortico-steroids excretion. They have a normal response to oral glucose but higher glucose and insulin levels than controls. MVP patients have increased 24-hour urinary catecholamine excretion. Isoproterenol infusions produce symptoms in a dose-related fashion in MVP patients but not in controls. Isoproterenol infusion-related symptoms included chest pain (7), extreme fatigue (6), dyspnea (6), dizziness (4), numbness (2), panic attacks (2). Isoproterenol infusions produced a greater increase in heart rate in MVP patients compared to controls. Thus, MVP patients have increased catecholamines and hyperresponse to isoproterenol infusion which indicates that their symptoms may be catecholamine related or mediated. The complex relationships of MVP symptoms are not clear; the coexistence of anxiety states and MVP is one explanation; another equally plausible explanation is that MVP may be a specific marker for the symptom complex.
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PMID:Mitral valve prolapse: a marker for anxiety or overlapping phenomenon? 636 71

To determine the possible role of altered secretion and effects of insulin in fuel homeostasis during heat exposure, the hormonal and metabolic milieu of three groups of rats were studied. The first was placed at 35 degrees C for 12 days (HE), the second was pair-fed (PF) to the first but maintained at 23 degrees C, and the third was allowed to eat ad libitum at 23 degrees C (C). Plasma insulin, glucagon, glucose, and free fatty acids (FFA), and blood lactate, pyruvate, 3-hydroxybutyrate, and individual amino acids were determined. To further characterize glucoregulation, an intraperitoneal glucose tolerance test (1 mg/g body wt) and isotopic glucose turnover (primed infusion of [3-3H]glucose) were performed. In HE rats, weight was constant for the last third of the period, and metabolic state 4 h after food removal was characterized by euglycemia but hypoinsulinemia, elevated blood pyruvate and FFA, and normal 3-hydroxybutyrate compared with C. Lowered levels of branched-chain amino acids and arginine were found. Fourteen hours after food removal glucose turnover was decreased. However, glucose intolerance accompanied by hyperinsulinemia was also found. Many of these changes were also seen in PF, including constant weight, fasting euglycemia, hypoinsulinemia, elevated FFA, and lowered valine and isoleucine. In contrast, pyruvate concentrations were normal, that of 3-hydroxybutyrate was elevated, and the decrement in glucose turnover was smaller than in HE rats. The glucose tolerance was similar to that of HE but accompanied by hypoinsulinemia. The results in HE suggest decreased energy metabolism, insulin secretion altered in a complex manner, and altered insulin action.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucoregulatory and metabolic responses to heat exposure in rats. 637 8

Adult male fatty and lean rats of Zucker strain were given access ad libitum to either a single nutritionally complete diet, or a self-selection regime with separate sources of three macronutrients, protein (casein), fat (hydrogenated coconut oil), and carbohydrate (sucrose). Animals on the single diet were fed on a powdered stock diet, and then switched to the self-selection regime. Energy intake on the self-selection regime was the same as that for the single diet condition in both fatty and lean rats. Fatty rats consumed 45% more energy than did their lean littermates. Further, fatty rats selected 47.0% of their total calories as protein, 30.1% as fat, and 22.9% as carbohydrate. The respective percentages for lean rats were 56.1, 13.0 and 30.9. In lean rats, the injection of insulin (10 U/kg) or 2-deoxy-D-glucose (500 mg/kg, 2DG) failed to increase energy intake, but increased carbohydrate intake 2 times by attenuating protein intake. Also in fatty rats, insulin did not increase energy intake, but it did increase carbohydrate by 50% by attenuating fat intake. 2DG decreased energy intake by attenuating carbohydrate and fat intakes in fatty rats. Fatty rats were slightly less hypoglycemic to insulin, but more hyperglycemic to 2DG than lean rats. These different self-selection patterns of fatty rats seemed to be associated with their endocrine, metabolic, and behavioral abnormalities.
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PMID:Feeding in response to insulin and 2-deoxy-D-glucose in Zucker rats on dietary self-selection. 638 68

A descriptive study of the psychiatric findings in 50 insulin--dependent diabetics is presented. Among the symptoms found were a marked reduction in energy level, increased fatigue and irritability, depression, and delayed psychosexual maturation. Diabetes mellitus is commonly considered to be a disease that, if properly controlled, allows the patient to lead a relatively normal life. We found, however, that these symptoms often made the patients' lives uncomfortable, reduced their functional capacity, disrupted their family life, and disturbed the adolescence of those who were affected at an early age.
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PMID:Psychiatric aspects of diabetes mellitus. 647 20


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