Níveis de beta-endorfina em resposta ao exercício e no sobretreinamento: [revisão] / Levels of beta-endorphin in response to exercise and overtraining: [review]

O sobretreinamento (ST) é um fenômeno esportivo complexo e multifatorial; e atualmente não existe nenhum marcador independente que possa diagnosticá-lo. Interessantemente, alguns sintomas do ST apresentam relação com os efeitos da b-endorfina (b-end1-31). Alguns de seus efeitos são importantes para o treinamento, como analgesia, maior tolerância ao lactato e euforia do exercício. Esses efeitos podem ser revertidos por destreinamento ou por ST, ocasionando diminuição no desempenho, redução da tolerância à carga e depressão. O exercício físico é o principal estímulo da b-end1-31, pois sua secreção é volume/intensidade dependente, tanto para exercícios aeróbios quanto anaeróbios. No entanto, o treinamento excessivo pode diminuir suas concentrações, alterando assim seus efeitos benéficos para o treinamento. Portanto, a b-end1-31 poderia ser utilizada como um marcador adicional de ST, principalmente porque seus efeitos apresentam extensa relação com os sintomas do ST.

Overtraining (OT) is a complex and multifactorial sport phenomenon, and there is no independent marker that can diagnose OT. Interestingly, some symptoms of OT are related to b-endorphin (b-end1-31) effects. Some of its effects, such as analgesia, increasing lactate tolerance, and exercise-induced euphoria, are important for training. These effects can be reverted by detraining or OT, which may cause decrease in performance, reduced load tolerance, and depression. The main stimulus for b-end1-31 secretion is to exercise because its secretion is volume/intensity dependent for both aerobic and anaerobic exercise. Excess training, however, may reduce b-end1-31 concentrations, thus altering its beneficial effects. Therefore, b-end1-31 could be used as an additional OT marker, mainly because its effects are strongly related to OT symptoms.

Plasma met-enkephalin, beta-endorphin and leu-enkephalin levels in human hepatic encephalopathy

To address the role of the opioid system in the pathogenesis of hepatic encephalopathy [HE] we measured plasma met- enkephalin, beta -endorphin and leu- enkephalin in patients with different grades of HE compared to control subjects and patients with cirrhosis. Plasma met- enkephalin levels were significantly higher in patients with cirrhosis and all grades of HE than controls. Plasma beta levels were similar in the 3 groups. Plasma leu- enkephalin levels were significantly higher -endorphin in HE grades II, III and IV than in controls, patients with cirrhosis and HE grade I patients. Our results support data on the involvement of met- enkephalin and leu- enkephalin in the pathogenesis of HE and provide a rationale for the use of opioid receptor antagonists in the treatment of HE

Stress in hearing and balance in Meniere's disease.

Stress is an unavoidable every-day phenomenon. Physiological coping with stress depends on the appropriate release of stress hormones as well as their alleviation at the termination of the stress. Despite quite a body of research indicating that stress affects inner ear function, this concept has found little application in otolaryngology. Today's evidence clearly indicates that the inner ear is equipped to detect stress hormones and some of these hormones have been shown to affect the inner ear function. Major stress control pathways shown to affect the inner ear include several third order axes, the hypothalamus-pituitary-adrenal axis, the hypothalamus-pituitary-thyroid axis and the hypothalamus-pituitary-gonadal axis whose functioning are interactive and inter-dependent. Less well-studied are the second order hypothalamus-pituitary control axis and its interaction with other hormones. To explore these we carried out a retrospective study on a series of Ménière's patients who had undergone a neurotomy of the vestibular nerve in the dept of ORL at the Hopital Nord, Marseille. Ménière's patients were particularly appropriate for this study since stress has long been recognised as a factor associated with the triggering of the symptoms of this pathology. Patients with acoustic neuroma and facial spasm were taken as a control population. We investigated the level of a battery of stress hormones including prolactin beta-endorphin and growth hormone. The blood sample was taken on the morning before surgery. The most striking observation was the presence of hyperprolactinemia in 30% of the Ménière patients (more than 20 microg/l) with confirmation of prolactinoma in 6 patients. The level of beta-endorphin could also be elevated. Horner, K.C., Guieu, R., Magnan, J., Chays, A. and Cazal, Y. Neuropysychopharmacology, (2001) 26:135-138. These observations suggest that neuroendocrinological feedback pathways controlling stress can be disturbed in Ménière's patients and depression of hypothalamic dopaminergic inhibition of prolactin secretion might be implicated. A further study on non-operated Ménière's patients presenting hyperprolactinemia and on dopamine agonist treatment, is needed in order to assess the role of stress in Ménière's patients. Progress in this domain could open the door towards integration of the stress concept into clinical management of various inner ear disorders.

Effect of propofol on perception of pain in mice: study on the mechanism of action

Propofol is an intravenous anesthetic used clinically. The latencies of pain threshold of different subhypnotic doses [12.5, 25 and 50 mg kg-1] of propofol administrated intraperitoneally [ip] into mice were measured by using hot plate method technique. The possible mechanism of pain control by propofol was also investigated through blocking beta- endorphin receptors and measuring serum level of beta-endorphin. Morphine [1.5 mg kg-1, ip] was used as reference of reduction of pain sensation. The results showed that propofol in doses of 25 and 50 mg kg-1 increased significantly the latency of pain threshold, but the lower dose [12.5 mg kg-1] failed to produce any significant change. This indicated that propofol reduced pain sensation and this effect is dose-dependent. It was also observed that propofol prevents hyperalgesia produced by prostaglandin [PGE2] [0.5 mg kg-1, ip]. For investigating the mechanism of action of propofol, pretreatment with naloxone [1.0 mg kg-1, ip] abolished significantly the antinociceptive action of propofol. Furthermore, serum level of beta- endorphin was increased significantly after propofol injection particularly at the peak time of propofol action. Serum level of corticosterone was also increased significantly at the time of beta- endorphin release

methodological approach to beta-endorphin assay in biological samples

In this study, a methodological approach to B-endorphin in biological fluids [seminal plasma, blood plasma and serum] was done. Measurement of beta-endorphin was performed by immunoassay method [immunoradiometric assay [IRMA] and radioimmunoassay [RIA]], either directly or proceeded by extraction procedures, e.g. Sep Pak [C18], affinity columns of sepharose particles and HPLC. A recovery study of B-endorphin was done to assess the binding effect of endogenous proteins in test samples on assay performance. It can be concluded that measurement of B-endorphin in peripheral blood samples [plasma and serum] can be performed by a direct immunoradiometric assay without extraction methods. As regards the measurement of B-endorphin in seminal plasma by IRMA and RIA, it must be proceeded by acidification of the sample, boiling and extraction by Sep Pak [C18] cartridges

Beta-endorphin, ACTH, and cortisol secretion in man during standardized oral surgical stress and effect of diazepam.

An experiment was conducted to evaluate the responses of plasma stress hormones (beta-endorphin, ACTH and cortisol) to third molar surgery, and the effect of diazepam pretreatment on these responses. Eleven patients who required surgical removal of two lower impacted molars (left and right) were studied. The results showed that plasma beta-endorphin, ACTH and cortisol levels were increased significantly during surgery and decreased to baseline levels 30 minutes after completion of the operation in nonsedated patients. When diazepam was premedicated intravenously, elevations of ACTH and cortisol were abolished. Plasma beta-endorphin was still increased but significantly blocked by diazepam pretreatment.