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)

We studied the effects of individualised growth hormone (GH) substitution, aiming at normal insulin-like growth factor I (IGF-I) levels, on biomechanical output and surface electromyogram (EMG) of isokinetic muscle strength and endurance performance in 18 hypopituitary adults and compared with 17 matched healthy controls. The muscle function tests consisted of isokinetic contractions of the right knee extensors, from which torque and EMG were recorded. Three patients were excluded from the final analysis of the muscle function tests due to technical errors and one control subject moved from the area during the study. We found that GH-deficient adults without GH substitution were weaker and had less endurance than healthy control subjects. At the group level, plasma levels of IGF-I were normalised but generally no significant effects upon biomechanical output and EMG were found after dose titration and 6 months of a constant GH dose. However, subjects with the largest changes in IGF-I had significantly better biomechanical output and EMG compared to those with small changes in IGF-I. This finding may indicate that the net increase in IGF-I levels is critical for improvements in biomechanical output, EMG and perception of fatigue to occur.
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PMID:Growth hormone substitution titrated to obtain IGF-I levels in the physiological range in hypopituitary adults: effects upon dynamic strength, endurance and EMG. 1289 66

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

Adult growth hormone (GH) deficiency results mainly from pituitary or peri-pituitary disease and/or its treatment and is frequently accompanied by other anterior pituitary hormone deficiencies. GH deficiency (GHD) results in a number of psychological and physical symptoms and signs which in combination constitute the adult 'GHD syndrome'. The psychological symptoms include decreased energy levels, social isolation, and lack of positive well being, depressed mood and increase in anxiety. The physical symptoms and signs include abnormal body composition with reduced lean body mass, increased central adiposity, and decreased extracellular fluid volume, decreased bone mineral density with an increased risk of fracture, reduced muscle strength, reduced exercise capacity, increased LDL cholesterol and reduced insulin sensitivity. Hypopituitarism and GHD are associated with an increased standardised mortality ratio. The diagnosis of GHD is confirmed by the insulin tolerance test or alternative stimulation test in the presence of structural pituitary disease and/or additional pituitary hormone deficiencies. Replacement with synthetic growth hormone by once daily subcutaneous injection can reverse many of the symptoms and signs of growth hormone deficiency, but the long-term effects are yet to be established. Whether or not all patients with GHD should receive GH replacement remains a matter for debate: a selective approach to therapy based on psychological well being and quality of life has been adopted in many centres.
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PMID:Do all adults with growth hormone deficiency require growth hormone treatment? 1457 66

In any given population of free-living individuals 65 years of age and older, a substantial proportion (in the range of 6% to 25%) suffers from many of the elements of the syndrome of frailty. Although the syndrome is complex and still lacks a standard definition, there is a growing consensus about the signs and symptoms as well as the pattern of biological correlates that characterize this disorder. Patients who are afflicted with frailty typically exhibit loss of muscle strength, fatigue easily, are physically inactive, and have a slow-and often unsteady-gait, with an increased risk (and fear) of falling. They are likely to have a poor appetite and to have undergone a recent, unintentional loss of weight. Frail individuals are more likely than the nonfrail to experience impaired cognition and depression. They die sooner. Frailty, of course, is frequently complicated by a variety of coexistent illnesses. Among the biological correlates of frailty are sarcopenia (now readily measurable by dual-energy x-ray absorptiometry [DXA]), osteopenia (with an increased susceptibility to fracture), and activation of the inflammatory and coagulation systems, with a rise in inflammatory cytokines and several markers of coagulopathy. Age-dependent changes in a number of hormones also appear to promote the development of frailty in the elderly, particularly via their effects on muscle mass and strength, bone density, and by contributing to activation of the catabolic cytokines. In particular, serum levels of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) decline progressively during aging, and an association between reduction in the levels of these hormones and the involution of advancing age has been proposed. It is not yet known whether, in comparison with their nonfrail counterparts, frail individuals consistently manifest larger reductions in GH and IGF-1 (and other anabolic hormones). More research is needed before it will be known whether the benefits of administering GH to the frail elderly will outweigh the disadvantages. The poor appetite and weight loss that occur in many frail individuals are likely to be accompanied by a degree of visceral protein depletion (with its attendant morbidity), which can be estimated by making serial measurements of indicators of visceral protein status such as transthyretin (TTR), retinol-binding protein (RBP), and albumin. One characteristic of the frailty syndrome that distinguishes it from the effects of aging per se is the potential reversibility of many of its features. Progressive resistance training is feasible for many elderly individuals-even the oldest old-and, by increasing muscle mass and strength, can ameliorate or reverse important aspects of physical frailty. To the extent that visceral protein depletion has been caused by an inadequate intake of calories and protein, consumption of a more adequate diet can result in betterment of the frail patient's nutritional status, as determined by clinical improvement and favorable changes in TTR, RBP, and albumin.
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PMID:Frailty in the elderly: contributions of sarcopenia and visceral protein depletion. 1457 59

Octreotide long-acting release (LAR) is a somatostatin analogue designed for once monthly intramuscular injection. As with endogenous somatostatin, octreotide LAR inhibits secretion of growth hormone (GH) as well as various other peptide hormones. In the treatment of acromegaly, octreotide LAR effectively controlled the secretion of GH and insulin-like growth factor-1 (IGF-1) in about 55-70% of patients (n > 100) who had previously been treated with somatostatin analogues, a similar degree of control to that observed with subcutaneous octreotide and lanreotide slow release (SR). Progressive control of serum levels of GH and IGF-1 was achieved with octreotide LAR in clinical studies of up to 4 years' duration. In addition, primary therapy with octreotide LAR provided effective control of GH and IGF-1 secretion, particularly in patients with a pretreatment GH level <20 microg/L. The percentage of patients achieving a target serum GH level of <2-2.5 micro g/L or normal IGF-1 levels was significantly greater with octreotide LAR 10, 20 or 30 mg every 28 days than with lanreotide SR 30 mg every 7-14 days in a large (n = 125) sequential, 6-month study, but was not significantly different between treatment groups in a small, randomised, nonblind, parallel group study of previously untreated patients. The volume of pituitary tumour shrinkage achieved with octreotide LAR or lanreotide SR was also similar ( approximate, equals 33% after 24 months). Acromegaly symptoms, such as headache, increased perspiration, paraesthesia, fatigue and osteoarthralgia were improved during treatment with octreotide LAR or lanreotide SR. Overall, octreotide LAR is generally well tolerated by most patients. The incidence of gastrointestinal symptoms is about 30% but, in most cases, events are transient and mild to moderate. Gallbladder abnormalities (sediment, sludge, microlithiasis and gallstones) can occur, but only 1% have become symptomatic to date. The prevalence of biliary abnormalities did not change after switching from subcutaneous octreotide, or from lanreotide SR, to octreotide LAR. Glucose metabolism can be affected by octreotide LAR in some patients; about 15% become hyperglycaemic, usually mild in severity. In summary, octreotide LAR controls GH and IGF-1 secretion in about 55-70% of patients with acromegaly. Octreotide LAR is administered intramuscularly every 28 days, offering improved patient compliance and convenience over three-times-daily subcutaneous octreotide. Long-term therapy provides progressive control of serum GH and IGF-1 levels, and is generally well tolerated by most patients. Thus, for the medical management of acromegaly, octreotide LAR is an effective, well tolerated and convenient treatment option.
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PMID:Octreotide long-acting release (LAR): a review of its use in the management of acromegaly. 1460 59

In noise effect research often the awakening reaction is maintained to be the only important health related reaction. The main argument is that sleep represents a trophotropic phase ("energy storing"). In contrast to this awakening reactions or lying awake belong to the ergotropic phase ("energy consuming"). Frequent or long awakening reactions endanger therefore the necessary recovery in sleep and, in the long-run, health. Findings derived from arousal and stress hormone research make possible a new access to the noise induced nightly health risk. An arousal is a short change in sleeping condition, raising the organism from a lower level of excitation to a higher one. Arousals have the function to prevent life-threatening influences or events through activation of compensation mechanisms. Frequent occurrences of arousal triggered by nocturnal noise leads to a deformation of the circadian rhythm. Additionally, the deep sleep phases in the first part of the night are normally associated with a minimum of cortisol and a maximum of growth hormone concentrations. These circadian rhythms of sleep and neuroendocrine regulation are necessary for the physical as well as for the psychic recovery of the sleeper. Noise exposure during sleep which causes frequent arousal leads to decreased performance capacity, drowsiness and tiredness during the day. Long-term disturbances of the described circadian rhythms have a deteriorating effect on health, even when noise induced awakenings are avoided.
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PMID:Stress hormones and sleep disturbances - electrophysiological and hormonal aspects. 1507 May 28

For more than 30 years, growth hormone (GH) has been observed to be preferentially secreted during deep, slow-wave sleep (SWS). However, the mechanisms that underlie this robust relationship that links anabolic processes in the body with behavioral rest and decreased cerebral metabolism remain to be elucidated. Current evidence indicates that GH secretion during the beginning of sleep appears to be primarily regulated by GH-releasing hormone (GHRH) stimulation occurring during a period of relative somatostatin withdrawal, which also is associated with elevated levels of circulating ghrelin. Apparently, two populations of GHRH neurons need to be simultaneously active to stimulate, in a coordinated fashion, SWS and pituitary GH release. Pharmacological interventions that are capable of increasing the duration and/or the intensity of SWS such as oral administration of gamma-hydroxybutyrate (GHB), also increase the rate of GH release. Because the normal negative feedback exerted by GH on central GHRH is inoperative in patients with GH deficiency, it is possible that the decreased energy levels and fatigue often reported by GH-deficient adults partly reflect an alteration in sleep-wake regulation. Preliminary data from a sleep study of adults with GH deficiency using wrist actigraphy for 6 nights at home and polysomnography in the laboratory indeed show decreased total sleep time and increased sleep fragmentation in GH-deficient patients as compared with normal controls.
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PMID:Reciprocal interactions between the GH axis and sleep. 1513 71

Erythropoietin (EPO) is a hematopoietic growth hormone that regulates survival, proliferation, and differentiation of erythroid progenitor cells. A reduction in tissue oxygenation stimulates EPO production, through a complex feedback mechanism. Patients with cancer-related anemia have an inadequate EPO response that is further impaired by cancer treatments such as chemotherapy. Cancer-related anemia substantially impairs patient functioning and may contribute to poor treatment outcomes. A significant number of studies demonstrates that treatment of anemia in cancer patients using recombinant human EPO (rHuEPO, epoetin alfa) significantly increases haemoglobin (Hb) levels, reduces transfusion requirements, and improves quality of life, particularly by relieving fatigue. Recent data also show that epoetin alfa therapy may improve cognitive function in patients receiving chemotherapy. In addition, the correction of anemia may prolong survival by enhancing tumor oxygenation, thus increasing tumor sensitivity to chemotherapy or radiation. The indicated dose of epoetin alfa is 150-300 IU/kg three times per week, but it is commonly dosed at 40,000-60,000 IU once weekly based on trial data and extensive clinical use. Determining the timing of initiation of epoetin alfa is a clinical judgement; however, data suggest that patient functioning declines and the risk of transfusion increases when the Hb level falls under 12 g/dL.
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PMID:Treatment of cancer-related anemia with epoetin alfa: a review. 1532 36

Some of the physiological changes associated with the taper and their relationship with athletic performance are now known. Since the 1980s a number of studies have examined various physiological responses associated with the cardiorespiratory, metabolic, hormonal, neuromuscular and immunological systems during the pre-event taper across a number of sports. Changes in the cardiorespiratory system may include an increase in maximal oxygen uptake, but this is not a necessary prerequisite for taper-induced gains in performance. Oxygen uptake at a given submaximal exercise intensity can decrease during the taper, but this response is more likely to occur in less-skilled athletes. Resting, maximal and submaximal heart rates do not change, unless athletes show clear signs of overreaching before the taper. Blood pressure, cardiac dimensions and ventilatory function are generally stable, but submaximal ventilation may decrease. Possible haematological changes include increased blood and red cell volume, haemoglobin, haematocrit, reticulocytes and haptoglobin, and decreased red cell distribution width. These changes in the taper suggest a positive balance between haemolysis and erythropoiesis, likely to contribute to performance gains. Metabolic changes during the taper include: a reduced daily energy expenditure; slightly reduced or stable respiratory exchange ratio; increased peak blood lactate concentration; and decreased or unchanged blood lactate at submaximal intensities. Blood ammonia concentrations show inconsistent trends, muscle glycogen concentration increases progressively and calcium retention mechanisms seem to be triggered during the taper. Reduced blood creatine kinase concentrations suggest recovery from training stress and muscle damage, but other biochemical markers of training stress and performance capacity are largely unaffected by the taper. Hormonal markers such as testosterone, cortisol, testosterone : cortisol ratio, 24-hour urinary cortisol : cortisone ratio, plasma and urinary catecholamines, growth hormone and insulin-like growth factor-1 are sometimes affected and changes can correlate with changes in an athlete's performance capacity. From a neuromuscular perspective, the taper usually results in markedly increased muscular strength and power, often associated with performance gains at the muscular and whole body level. Oxidative enzyme activities can increase, along with positive changes in single muscle fibre size, metabolic properties and contractile properties. Limited research on the influence of the taper on athletes' immune status indicates that small changes in immune cells, immunoglobulins and cytokines are unlikely to compromise overall immunological protection. The pre-event taper may also be characterised by psychological changes in the athlete, including a reduction in total mood disturbance and somatic complaints, improved somatic relaxation and self-assessed physical conditioning scores, reduced perception of effort and improved quality of sleep. These changes are often associated with improved post-taper performances. Mathematical models indicate that the physiological changes associated with the taper are the result of a restoration of previously impaired physiological capacities (fatigue and adaptation model), and the capacity to tolerate training and respond effectively to training undertaken during the taper (variable dose-response model). Finally, it is important to note that some or all of the described physiological and psychological changes associated with the taper occur simultaneously, which underpins the integrative nature of relationships between these changes and performance enhancement.
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PMID:Physiological changes associated with the pre-event taper in athletes. 1548 4

The aim of the present study was to investigate acute hormonal and neuromuscular responses and recovery in strength athletes versus nonathletes during heavy resistance exercise performed with the forced and maximum repetitions training protocol. Eight male strength athletes (SA) with several years of continuous resistance training experience and 8 physically active but non-strength athletes (NA) volunteered as subjects. The experimental design comprised two loading sessions: maximum repetitions (MR) and forced repetitions (FR). MR included 12-RM squats for 4 sets with a 2-min recovery between sets. In FR the initial load was higher than in MR so that the subject could lift approximately 8 repetitions by himself and 4 additional repetitions with assistance. Before and after the loading protocols, blood samples were drawn to determine serum testosterone, free testosterone, cortisol and growth hormone concentrations, and blood lactate. Maximal voluntary isometric force and EMG activity of the leg extensors was measured before and after the loading as well as 24 and 48 hrs after the loading. The concentrations of the hormones measured increased significantly (p < .01-.001) after both loadings in both groups. The responses tended to be higher in FR than the MR loading and the increases of testosterone concentrations were significantly (p < .01) greater in both loadings in SA than in NA. Both loading protocols in both groups also led to neuromuscular fatigue observable with significant acute decreases in isometric strength by 32-52% (p < .001) and in maximal iEMG (p < .05-01) associated with large increases in blood lactate. These data suggest that, at least in experienced strength athletes, the forced-repetition protocol is a viable alternative to the more traditional maximum-repetition protocol and may even be a superior approach.
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PMID:Acute hormonal responses to heavy resistance exercise in strength athletes versus nonathletes. 1550 91


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