Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80 degrees C dry bulb (80 D) and 100 degrees C dry bulb (100 D) temperatures until subjective discomfort, and in 80 degrees C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1 degrees C at 80 D, 1.9 degrees C at 100 D and 3.2 degrees C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E2 and serum thromboxane B2 levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods.
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PMID:Haemodynamic and hormonal responses to heat exposure in a Finnish sauna bath. 275 81

The plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) response of men, eumenorrheic women, and amenorrheic women (n = 6) to 1 h of rest or to a bicycle ergometer test [20 min at 30% maximum O2 uptake (VO2max), 20 min at 60% VO2max, and at 90% VO2max to exhaustion] was studied in both normal (22 degrees C) and cold (5 degrees C) environments. beta-EP and beta-LPH was measured by radioimmunoassay in venous samples collected every 20 min during rest or after each exercise bout. Exhaustive exercise at ambient temperature (Ta) 22 degrees C induced significant increases in plasma beta-EP and beta-LPH in all subjects as did work at 60% VO2max in amenorrheic and eumenorrheic women. During work at Ta 5 degrees C, the relative increase in beta-EP and beta-LPH was suppressed in eumenorrheic women and completely prevented in amenorrheic women. Although significant lowering of beta-EP and beta-LPH was observed in men and eumenorrheic women during rest at 5 degrees C, amenorrheic women maintained precold exposure levels. These findings suggest that plasma beta-EP and beta-LPH may reflect a thermoregulatory response to heat load. There appears to be a sexual dimorphism in exercise- and cold-induced release of beta-EP and beta-LPH and amenorrhea may be accompanied by alterations in these responses.
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PMID:Exercise- and cold-induced changes in plasma beta-endorphin and beta-lipotropin in men and women. 295 62

Beta-endorphin (beta-End) and adrenocorticotrophic hormone (ACTH) were determined in the peripheral blood of 14 human volunteers exercising on a bicycle ergometer. After 1 h of submaximal work below anaerobic threshold (AT), defined as the 4 mmol X l-1 lactic acid level in arteriolar blood (Kindermann 1979; Mader 1980), beta-End and ACTH levels did not change from control conditions. Eleven of the same 14 subjects performed an uninterrupted graded exercise test on the same bicycle ergometer until exhaustion. This time beta-End and ACTH levels increased concomitantly with exercise of high intensity: at each moment, during and after this maximal test, a highly significant correlation (P less than 0.0001) was noted between the levels of beta-End and ACTH. The peak values of these hormones were reached within 10 min after stopping maximal exercise, and coincided with lactic acid peak levels. A rise in lactic acid levels above the anaerobic threshold always preceded the exercise-induced rise in beta-End and ACTH. Within the population tested, two subgroups could be distinguished: one comprising individuals whose hormonal response nearly coincided with the rise in lactic acid (rapid responders) and a second group composed of subjects whose normal response appeared delayed with respect to the lactic acid rise (slow responders). These results support the view that beta-End and ACTH are secreted in equimolar quantities into the blood circulation in response to exercise, and suggest that metabolic changes of anaerobiosis play a key role in the regulation of stress-hormone release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin and ACTH levels in peripheral blood during and after aerobic and anaerobic exercise. 300 76

The kinetics of alpha-MSH secretion induced by prolonged TRH infusion were studied using perfused frog neurointermediate lobe (NIL). During a 2 h administration of TRH (10(-8) M), the secretion rate of alpha-MSH displayed two phases. During the first phase, secretion of alpha-MSH increased rapidly reaching a maximum within 20 min and then, despite continued TRH infusion, this secretion slowly declined. The second phase was characterized as plateau of elevated release (relative to basal secretion); within this second phase there was often a small peak of released alpha-MSH occurring at about 100 min. Exposure of NIL to another TRH (10(-8) M) pulse 90 min later induced a normal stimulation of alpha-MSH secretion, thus demonstrating the viability of tissue in perifusion. Continuous infusion of cycloheximide (10(-5) M) during a 5 h period totally inhibited the biosynthetic activity of NIL but did not influence TRH-induced alpha-MSH secretion. In particular, cycloheximide had no effect on the second phase of the response to prolonged infusion of TRH. Similarly, during continuous infusion of the monovalent carboxylic ionophore monensin (10(-6) M), the biphasic response to prolonged infusion of TRH (10(-8) M) was still observed. Administration of a short pulse of TRH (10(-7) M) during the declining part of the first phase or during the second phase of prolonged TRH (10(-8) M) infusion induced a significant enhancement of alpha-MSH stimulation. From these results we conclude that prolonged TRH infusion causes alpha-MSH release in a biphasic manner; attenuation of the secretory response to continuous TRH administration does not result from exhaustion of the releasable pool of alpha-MSH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biphasic effect of thyrotropin-releasing factor (TRH) on alpha-melanotropin secretion from frog intermediate lobe in vitro. 310 17

A 32-year-old male (Mr. A.), monitored during an 8-d heat acclimation (HA) investigation, unexpectedly exhibited heat intolerance and heat exhaustion. Thirteen other males completed HA without indications of either heat intolerance or heat exhaustion. Because Mr. A. responded normally to HA on days 1-4, the intervention of an unknown host factor on days 5-8 was suggested. Mr. A.'s heat exhaustion episode (day 8) was apparently forewarned by loss of body weight and increased delta HR, delta Tsk (days 5-8) and delta Tre (days 7-8) during daily 90-min trials. His symptoms indicated classical salt depletion heat exhaustion, but the calculated salt deficit (less than 0.1 g NaCl.kg-1 body weight) was mild. Post-heat exhaustion serum enzyme levels were either normal (ALT, AST) or acutely elevated (CPK). Blood beta-endorphin and cortisol levels were six times and two times greater than control values, respectively. This case report is unique because clinical/physiological measurements and blood analyses were performed before, during, and after heat intolerance and heat exhaustion.
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PMID:Heat intolerance, heat exhaustion monitored: a case report. 335 82

The aim of the present investigation was to compare the changes in plasma estradiol (E2), progesterone (P), luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), androstenedione (delta 4-A), dehydroepiandrosterone sulfate (DHEA-S), adrenocorticotropic hormone (ACTH), and prolactin (PRL) in standardized tests (15-min consecutive work loads of 60%, 70%, 80% VO2 max to exhaustion) in 13 eumenorrheic untrained (UT) and 8 highly trained women (MR). Blood was obtained 15 and 2 min before exercise and at the end of each work load or each 15 min period. The results showed a significant increase (0.05 greater than P less than 0.001, two-way ANOVA) in plasma E2 P, T delta 4-A, PRL, and ACTH both in UT and MR irrespective of the phase of the menstrual cycle. DHEA S levels increased significantly in the MR, but not in the UT, PRL and ACTH increased linearly with exercise in MR and nonlinearly in UT. In the latter group, only the 80% VO2 max work load was able to elicit significant increments in the plasma levels of these hormones. In the MR plasma T and delta 4-A levels increased relatively more pronounced (P less than 0.05) at comparable work loads and exercise times than in the UT. LH levels decreased with exercise both in the UT and MR, whereas FSH levels remained unchanged (MR) or decreased (UT). These findings suggest that during exercise the ovarian hormones are increased by more unspecific mechanisms such as a decreased metabolic clearance rate, whereas in the MR, adrenal secretion of androgens is enhanced.
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PMID:Multiple hormonal responses to physical exercise in eumenorrheic trained and untrained women. 342 89

Serum beta-endorphin levels during a graded exercise test to exhaustion. Med. Sci. Sports Exerc., Vol. 19, No. 2, pp. 78-82, 1987. Nine untrained college age males completed a graded exercise protocol to maximal capacity on a bicycle ergometer to determine if there was a relationship between intensity of exercise and serum beta-endorphin (beta-EP) levels. Subjects fasted for 12 h and abstained from physical activity at least 24 h prior to testing. Subjects completed the Multiple Affect Adjective Check List prior to and following exercise to ascertain if psychological state would be associated with beta-EP levels. The initial workload was 150 kilopond meters and was increased 150 kilopond meters every 3 min until VO2max or leg fatigue occurred. Expired gases were continuously analyzed, and a venous blood sample was drawn from an indwelling catheter during the final 30 s of each stage and 5-min post-exercise. beta-EP levels were determined from serum using a radioimmunoassay technique and corrected for cross-reactivity with beta-lipotropin using affinity chromatography. Resting beta-EP levels were 25.3 +/- 4.1 pg X ml-1 and did not demonstrate significant changes during any stage of exercise. A correlation analysis (r = 0.30) revealed no significant relationship between exercise intensity and beta-EP levels. Following exercise, beta-EP levels were significantly increased compared to resting values (38.8 +/- 4.8 pg X ml-1). In addition, psychological state was unaffected by exercise despite significant increases in recovery beta-EP levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum beta-endorphin levels during a graded exercise test to exhaustion. 357 52

After 30 min rest in the lying position, 12 healthy male volunteers (average age 22 years) received, in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg iv followed by a continuous infusion of 10 mg/hr). Thereafter they rested for a further 30 min in the recumbent position and for 15 min sitting on a bicycle ergometer; they then exercised to exhaustion. At rest plasma levels of adrenocorticotropin (ACTH), cortisol, and aldosterone increased during infusion of naloxone, while body temperature decreased. During exercise the difference in plasma ACTH between naloxone and saline periods was abolished, while the differences in plasma cortisol and aldosterone lost statistical significance. Intra-arterial pressure, heart rate, ventilation, O2 uptake, and CO2 output were continuously monitored throughout the experiment and were not affected by naloxone. This was also the case for several hormonal and biochemical measurements, including those of plasma renin, angiotensin II, norepinephrine, 13,14-dihydro-15-keto-prostaglandin F2 alpha, glucose and lactate, and serum insulin and growth hormone. Exercise performance was not changed by naloxone. In conclusion (1) during exhaustive graded exercise of short duration opioidergic inhibition of the pituitary-adrenocortical axis is probably not sustained, (2) apart from the latter mechanism, the present study does not support the hypothesis that endogenous opioids are involved in various hemodynamic, respiratory, and hormonal responses to this type of exercise.
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PMID:The nature of opioid involvement in the hemodynamic respiratory and humoral responses to exercise. 404 6

Adrenocorticotropic hormone (ACTH) levels were compared before and after submaximal and exhaustive isotonic exercise in six normally active college students (3 men and 3 women). Each subject participated in three experiments conducted at the same morning hour. Venous plasma was obtained before and immediately after 20-min runs at 65 and 80% of maximal O2 consumption (VO2 max) and after a run of gradually increasing work intensity which resulted in exhaustion (100% VO2 max) in 12.6 +/- 1.3 min. ACTH (mean +/- SE) was 48 +/- 15, 57 +/- 12, and 61 +/- 11 pg/ml before the 65, 80, and 100% VO2 max runs, and increased to 61 +/- 15 (NS), 128 +/- 18 (P less than 0.05), and 292 +/- 72 (P less than 0.05) pg/ml, respectively. Plasma glucose, growth hormone, cortisol, and lactic acid concentrations increased in a similar fashion. Cortisol and ACTH levels were significantly correlated at the higher levels of exertion: r = 0.18 (NS) for the 65% VO2 max run, r = 0.65 (P less than 0.05) for the 80% VO2 max run, and r = 0.64 (P less than 0.05) for the run to exhaustion. Both the change in ACTH with exercise and its postrun concentration were significantly related to the change in plasma lactic acid (r = 0.65, P less than 0.05) and the postrun plasma lactic acid (r = 0.64, P less than 0.05). We conclude that exercise-induced increases in plasma ACTH and their correlation with circulating cortisol depend on the intensity of isotonic exercise. Our observations also suggest that plasma lactic acid may influence ACTH release during exercise.
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PMID:Plasma adrenocorticotropin and cortisol responses to submaximal and exhaustive exercise. 631 51

The present study examined whether benzodiazepine (BZ) intake alters performance and selected hormonal and metabolic variables during submaximal exercise. Seven triathletes completed two cycling trials at 85% maximum O2 uptake starting 3 h after an ingestion of either a placebo (PLA) of gelatin or BZ (1.5 mg lorazepam) and continuing until exhaustion, according to a double-blind randomized protocol. Blood samples were collected at rest; 5, 10, and 15 min; and exhaustion for dopamine (DA), norepinephrine (NE), epinephrine (Epi), adrenocorticotropic hormone (ACTH), cortisol (CORT), insulin (INS), free fatty acid, blood glucose, and lactate (La) determinations. Time of cycling was not significantly changed after BZ or PLA administration (22.9 +/- 2.5 vs. 23.5 +/- 3.8 min, respectively). A decrease in CORT and an increase in INS (P < 0.05) were observed with BZ before cycling. In comparison with rest, exercise resulted in a decrease in INS and an increase in all the other variables investigated (P < 0.001), but DA, NE, Epi, ACTH, CORT, La, and free fatty acid were significantly less elevated under BZ (P < 0.05). No change was found in glucose and INS levels between the two treatments at the end of the test. There was a strong correlation under both PLA and BZ conditions between DA, NE, Epi, and ACTH and also between Epi and La levels. From these data, BZ intake did appear to alter metabolism but did not influence performance during intense submaximal exercise.
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PMID:Performance and metabolic effects of benzodiazepine during submaximal exercise. 800 35


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