Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that the immune-endocrine communication plays an important role in development and progression of multiple sclerosis (MS). Interferon beta (IFN beta-1b) treatment is the therapy of choice in patients suffering from relapsing remitting or secondary chronic progressive multiple sclerosis. While typical adverse events of IFN beta-1b treatment such as flu-like symptoms or fatigue are well studied, little is known about the acute changes in the immune and neuroendocrine system. Therefore, we analyzed the short-term effects of IFN beta-1b on cortisol, epinephrine, norepinephrine, prolactin and growth hormone (GH) plasma levels before and 4, 8 and 24 h after IFN beta-1b administration in healthy subjects. Moreover, we determined heart rate, blood pressure, body temperature, leukocyte and lymphocyte subsets and plasma levels of interleukin (IL)-1 beta, IL-6, IL-10 and tumor necrosis factor (TNF)-alpha. IFN beta-1b led to an increase in body temperature and heart rate, and in parallel, elevated cortisol, prolactin and GH plasma levels at 4 and 8 h after IFN beta-1b injection. There were no significant alterations in blood pressure, norepinephrine or epinephrine plasma levels. Simultaneously, IFN beta-1b injection led to an immediate granulocytosis while concomitantly decreasing peripheral lymphocytes, especially natural killer (NK) cells. At the same time, IL-6, IL-10 and TNF-alpha plasma levels showed an overall increase. Overall, cytokine administration exerts strong stimulatory effects on the hypothalamic-pituitary-adrenal (HPA)-axis that may contribute to the side effects of IFN beta-1b therapy and affect the efficacy of IFN beta-1b treatment.
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PMID:Acute interferon beta-1b administration alters hypothalamic-pituitary-adrenal axis activity, plasma cytokines and leukocyte distribution in healthy subjects. 1238 50

A 68-year-old man presented with general fatigue, increasing adynamia, weakness, vertigo and recurrent syncope. Six weeks earlier the diagnosis of a macroprolactinoma had been established based on a greatly elevated prolactin concentration (161 170 micro U/l) and MR-evidence of a 3.5 cm measuring pituitary mass. The patient had been started on cabergoline (1.5 mg weekly). Orthostatic hypotension due to the dopamine agonist was considered very likely and carbergoline therapy was stopped. However, there was no relief of the symptoms and further syncopes followed. Testing of blood pressure and heart rate regulation, selective testing of postganglionic cardiac neurons with [ 123 J] metaiodobenzylguanidine scintigraphy provided evidence of grossly impaired neurogenic cardiovascular regulation due to failure of postganglionic efferent sympathetic activity. This is characteristic for pure autonomic failure. The patient was treated symptomatically with high fluid intake, compression stockings, fludrohydrocortisone (0.1 mg o.d.s.), piroxicam (20 mg o.d.s.) and etilephrin (10 mg q.d.s.), which enabled him to cope with daily activities without syncope. This case shows that vertigo in a patient with macroprolactinoma is not always related to drug therapy but may be related to other causes.
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PMID:Autonomic failure mimicing dopamine agonist induced vertigo in a patient with macroprolactinoma. 1239 37

We evaluated the results of medical treatment for male prolactinomas. We encountered eight patients with male prolactinomas. The age was 25 to 54 years old (mean 43 years) and the chief clinical symptoms were visual acuity/field defect in three patients, pituitary apoplexy in one patient, disturbance of ejection in one patient, generalized convulsion in one patient, headache in one patient and general fatigue in one patient. The serum prolactin level was 279 to 7,360 ng/ml (mean 2,832 ng/ml). The tumors in all patients were large with a mean diameter of 34.9 mm (range, 21 to 43 mm). In only one patient, the operation was performed due to pituitary apoplexy. All the patients were treated by medication, with bromocriptine being used in seven patients and terguride in one. The follow-up period was 0.8 to 13 years (mean 5.9 years) and, in all patients, the medical treatment was continued. The tumor decreased in size in all patients and the serum prolactin level at the last follow-up observation was 0.5 to 70.5 ng/ml (mean 26.9 ng/ml). All the neurological symptoms disappeared in the early stage of treatment. As for the complications of medical treatment; in one patient, orthostatic hypotension occurred during the initial administration of bromocriptine and one patient suffered CSF leakage two months after the administration of bromocriptine, so the repair of the sella floor by transsphenoidal surgery was necessary. The medical treatment for male prolactinomas is effective for a long term and should be the primary treatment for the male prolactinomas. In conclusion, patients can maintain a good quality of life for a long time by using dopamine agonists.
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PMID:[Results of treatment for male prolactinomas]. 1249 80

Sleep remains an important enigma in neurobiology; it has a robust adaptive value yet its function remains elusive. Changes in sleep are hallmarks of the acute phase response to infectious challenge. The molecular regulation of these responses involves a cytokine cascade within brain, including interleukin-1 and tumor necrosis factor, and several other substances such as growth hormone releasing hormone, prolactin, nitric oxide and nuclear factor kappaB. These substances are also involved in the regulation of normal spontaneous sleep. Fatigue and sleep disturbances are common in cancer patients and in those receiving cytokine therapy. Regardless, the role of sleep in cancer is relatively uninvestigated.
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PMID:Sleep in host defense. 1261 85

Chronic Fatigue Syndrome (CFS) is a clinical condition characterized by a persistent or relapsing debilitating fatigue at rest, lasting more than 6 months, and made worse by exercise. At the present moment, there are three potential etiopathogenic factors: immunologic, viral and neuroendocrine. The purpose of our study was to evaluate possible alterations of the hypothalamic-pituitary-adrenal (HPA) axis in our CFS patients by studying the circadian rhythms of prolactin (PRL), thyrotropic hormone (TSH), adrenocorticotropic hormone (ACTH), and cortisol (CS). A total of 36 patients were enrolled according to the Centers for Disease Control and Prevention case-definition criteria. Twenty healthy subjects were included as controls. Blood samples were taken every 4 hours during a single 24-hour period. We performed a fluorometric enzyme immunoassay with serum PRL, cortisol and TSH, and an immunoradiometric assay with plasma ACTH. The circadian rhythms of PRL, TSH, ACTH and CS were statistically significant in both CFS and control groups. At 24:00 and 04:00 hrs the CFS patients showed lower ACTH levels than healthy subjects (p < 0.001); the PRL levels were higher at 04.00 h in CFS patients than in healthy subjects.
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PMID:Chronic fatigue syndrome: circadian rhythm and hypothalamic-pituitary-adrenal (HPA) axis impairment. 1262 84

We have studied 12 recreationally active men to measure their responses to exercise in the heat and relate these to measures of hypothalamic function explored with a buspirone [5-hydroxytryptamine 1A (5-HT(1A)) agonist, dopaminergic D(2) antagonist] neuroendocrine challenge, with and without pretreatment with pindolol (5-HT(1A) antagonist). Pindolol treatment allowed the serotonergic and non-serotonergic components of prolactin release to be distinguished. Subjects exercised at 73 (5)% maximal rate of oxygen uptake (VO(2max)) until volitional fatigue at 35 degrees C (relative humidity, 30%). On another two occasions they underwent a buspirone challenge [0.5 mg (kg body mass)(-1)], once with, and once without, pindolol [0.5 mg (kg body mass)(-1)] pretreatment and the circulating plasma concentrations of prolactin were measured for the next 2.5 h. Rectal temperature increased throughout exercise, whilst mean skin temperature remained constant. There was a wide inter-subject variation in prolactin response to the neuroendocrine challenges. The proportion of the prolactin response to buspirone attributable to a non-serotonergic component (most likely dopaminergic) correlated both with exercise duration (r=0.657, P=0.028), rectal temperature at fatigue (r=0.623, P=0.041) and the rate of temperature rise (r=-0.669, P=0.024). Our results suggest that high activity of the dopaminergic pathways in the hypothalamus is a predictor of exercise tolerance in the heat.
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PMID:Responses to exercise in the heat related to measures of hypothalamic serotonergic and dopaminergic function. 1268 6

Pituitary hormones have an important role during exercise yet relatively little is known about the stimulus for their release. Body temperature progressively increases during prolonged steady-state exercise in the heat and we have investigated the role that this may play in the release of prolactin, growth hormone and cortisol (as an indicator of adrenocorticotropic hormone) into the circulation. Fit young male subjects exercised at 73% V(O2,max) until volitional fatigue at 20 degrees C and at 35 degrees C (30% relative humidity at both temperatures). Rectal temperature and mean skin temperature were monitored and blood samples analysed for lactate, glucose, cortisol, growth hormone and prolactin concentrations. During the first 20 min, core temperature rose continuously and to a similar extent at both temperatures, while mean skin temperature was approximately 4 degrees C lower during exercise in the cool. Blood glucose concentration was essentially constant throughout the period of exercise while lactate concentration increased in the first 10 min and then remained constant with very similar changes in the two exercise conditions. Prolactin and growth hormone concentrations both increased during the exercise period while the concentration of cortisol declined slightly before rising slightly over the 40 min period. Prolactin release was significantly greater when exercise was carried out in the heat while there was no difference in the release of growth hormone or cortisol in the two conditions. When plotted as a function of rectal temperature, growth hormone concentration showed a linear relationship which was the same at ambient temperatures of 35 degrees C and 20 degrees C. Prolactin concentration had a curvilinear relationship with rectal temperature and this differed markedly at the two ambient temperatures. Cortisol concentration showed no dependence on any measure of body temperature. Our results are consistent with some aspect of body temperature being a stimulus for growth hormone and prolactin secretion; however, the precise mechanism clearly differs between the two hormones and we suggest that skin temperature modulates prolactin release, but does not affect the release of growth hormone.
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PMID:Ambient temperature and the pituitary hormone responses to exercise in humans. 1295 63

Increased body temperature is thought to be an important component of the higher perception of exertion that is a feature of fatigue during exercise in the heat but a causal relationship has yet to be demonstrated. We have investigated the effect of passive heating on the perception of exertion during a standard bout of exercise and also assessed the effect of cooling the head on compensating for the increased body temperature on the feelings of exertion. Ten male subjects performed a 14-min cycling exercise [average power approximately 63% of maximum power output ( W(max))] at an ambient temperature of 35 degrees C at resting rectal temperature [mean (SD): 37.49 (0.27) degrees C; control (CON) trial] on one occasion, and after sitting in a sauna to raise rectal temperature [mean (SD): 38.95(0.13) degrees C; sauna (SAU) trial]. During the exercise, subjects reported their ratings of overall perceived exertion (RPE), perceived exertion of the legs (RPE(legs)) and thermal comfort (TC). A blood sample was collected by the end of the exercise for determination of plasma glucose, lactate and prolactin and haematocrit. RPE values were significantly elevated after passive heating [mean (SE): 14.5 (0.7) units in CON and 17.2 (0.5) units in SAU, at the end of exercise; P<0.001] as were the RPE(legs) ( P<0.01), while ratings of TC were similar in CON and SAU trials. Passive heating increased blood glucose ( P<0.05) but had no effect on lactate at the end of the exercise. Plasma prolactin was markedly elevated as a result of the sauna exposure [mean (SE): 1598 (152) versus 225 (31) mU l(-1) in SAU and CON trials, respectively; P<0.001]. Six of the subjects repeated the two trials but with the face cooled during exercise (trials CON(FAN) and SAU(FAN)) that was achieved by combining face fanning and spraying the face with a mist of cooled water. Face cooling decreased RPE values after sauna to a point that no differences between the two conditions existed. RPE(legs) scores and heart rate, however, remained higher in SAU(FAN) compared with CON(FAN) ( P<0.05). We conclude that hyperthermia is a causative element of the increased perception of exertion during submaximal exercise in the heat and that the effect of increased core temperature on the feelings of exertion is modulated by face cooling.
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PMID:The effect of passive heating and face cooling on perceived exertion during exercise in the heat. 1464 27

The purpose of this study was to determine the effect of carbohydrate ingestion before and during intense constant load cycling to volitional fatigue on surface electromyographic (sEMG) activity from the vastus lateralis (VL) and vastus medialis (VM) muscles. After 24-h diet and training control, 8 well-trained subjects (maximal O(2 )uptake (VO(2max )) 66+/- 2 ml. kg-1. min-1; mean plusmn; SD) ingested 8 ml. kg-1 of either a 6.4% carbohydrate-electrolyte (CHO) or a placebo (PLA) solution immediately before, followed by 2 ml. kg-1 of the same solution every 15 min while cycling to exhaustion at 84+/- 1% of VO(2max.) Exercise time to fatigue was 13% longer with CHO ingestion compared to PLA (58:54+/- 8:48 vs. 51: 18 +/- 5:54 min:s, NS). VO(2 ) (4.22 +/- 0.11 vs. 4.20 +/- 0.14 L. min-1 ), heart rate (172 +/- 4 vs. 176 +/- 4 beats. min-1), ratings of perceived effort (18 +/- 0.1 vs. 19+/- 0.1), and rates of carbohydrate oxidation (314 +/- 28 vs. 324 +/- 26 ?mol. kg-1. min -1) were similar for both PLA and CHO at exhaustion. There was no main treatment effect of CHO ingestion on blood glucose or lactate concentrations, nor plasma prolactin levels either during exercise or at fatigue. However, CHO ingestion attenuated the rise in EMG root mean square (RMS) activity during the latter stages (>45 min) of exercise and at the point of exhaustion for both VM (0.325 +/- 0.010 vs. 0.403 +/- 0.020 mV; =p.006) and VL (0.298+/- 0.011 vs. 0.370 +/- 0.007 mV; p =.0004). We conclude that in well-trained subjects, the ingestion of carbohydrate attenuated the increase in surface electromyographic activity during intense, constant load cycling leading to exhaustion in approximately 1 h. The precise mechanism(s) underlying this effect cannot be attributed to alterations in CHO availability but, instead, may be linked to changes in afferent sensory input.
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PMID:Reduced neuromuscular activity with carbohydrate ingestion during constant load cycling. 1511 90

The purpose of the experiment was to examine whether selective serotonin (5-HT) re-uptake transporter blockade by paroxetine has any effect on perceived effort (RPE) during exercise or the time to reach volitional fatigue and on the prolactin and cortisol responses during prolonged exercise performed in a warm environment. Eight healthy males performed two cycle rides to exhaustion in a warm (32 degrees C) environment at 60% of maximum oxygen uptake. Paroxetine (20 mg) or placebo was administered 5 h before exercise trials in a randomised double blind fashion. Time to exhaustion was not significantly influenced by administration of paroxetine: median (range) time to exhaustion was 93.3 (76.2-175.0) min on the placebo trial and 92.5 (66.0-151.0) min on the paroxetine trial. Rectal temperature was higher at rest and throughout exercise on the paroxetine trial. The serum concentrations of prolactin and cortisol were determined throughout exercise as peripheral markers of central 5-HT activity. RPE increased over time but was not influenced by paroxetine administration. Prolactin and cortisol levels increased over time but paroxetine administration did not influence the hormone responses during exercise. In conclusion, acute administration of paroxetine failed to alter RPE, exercise capacity or the response of the determined peripheral hormone markers of central 5-HT activity during prolonged exercise in a warm environment.
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PMID:Paroxetine administration failed [corrected] to influence human exercise capacity, perceived effort or hormone responses during prolonged exercise in a warm environment. 1532 6


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