Plasma corticotropin-releasing hormone, corticotropin, and endorphins at rest and during exercise in eumenorrheic and amenorrheic athletes

Hohtari, Hannele; Elovainio, R.; Salminen, K.; Laatikainen, Timo

doi:10.1016/s0015-0282(16)60065-1

Cited by 32 publications

(16 citation statements)

References 23 publications

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“…Peltenburg et al (1984) compararam ginastas e nadadoras pré púberes, e verificaram que os níveis de estrona, testosterona e androstenediona foram menores no grupo de ginastas, embora essas diferenças desapareceram quando próximo da puberdade. Hohtari et al (1988) verificaram que a capacidade de secreção de corticotropina e endorfinas de atletas amenorreicas após uma sessão aguda (80 a 100% do VO 2max ) em cicloergômetro não diferiu significativamente de atletas eumenorreicas, embora, nas atletas amenorreicas, a secreção de endorfina apresentou elevação na condição de repouso. Posteriormente, esse mesmo grupo de pesquisa apresentou resultados sugestivos de resposta prejudicada do eixo hipotálamo-pituitária-adrenal em atletas amenorreicas (Hohtari et al, 1991).…”

Section: Resultsunclassified

“…Vários estudos têm descrito e investigado disfunções do CM ou do comportamento de diferentes hormônios em atletas de diferentes modalidades esportivas (Friday et al, 1993;Harber et al, 1998;Hohtari et al, 1988Hohtari et al, e 1991Lindholm et al, 1993;Peltenburg et al, 1984;Pirke et al, 1990;Rickenlund et al, 2010;Waters et al, 2001Waters et al, e 2003. E embora se saiba que o exercício físico de alta intensidade contribua para irregularidades do CM (Mantoanelli et al, 2002;Stafford, 2005), a magnitude das alterações dos hormônios sexuais especificamente em atletas de elite em GR (nível Olímpico) ainda não foi descrita.…”

Section: Introductionunclassified

See 1 more Smart Citation

Desequilíbrio hormonal e disfunção menstrual em atletas de ginástica rítmica

Coelho

Simões

Lunz

2015

Revista Brasileira de Ciências do Esporte

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Section: Resultsunclassified

Section: Introductionunclassified

Desequilíbrio hormonal e disfunção menstrual em atletas de ginástica rítmica

Coelho

Simões

Lunz

2015

Revista Brasileira de Ciências do Esporte

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“…Physiological levels of plasma CRF are normally low (e.g. 5 pg ml-' in calves (Edwards & Jones, 1988); under 10pM in athletes (Hohtari et al, 1992); under 10 pg ml-' in dog (Bruhn et al, 1987)). The plasma concentrations of CRF resulting from the increase in adrenal release of CRF as a result of haemorrhage (Bruhn et al, 1987) have not been reported, but since the adrenal secretion reached only 185 pg min-' the effects on plasma CRF will have been minimal.…”

Section: Discussionmentioning

confidence: 99%

Relaxing actions of corticotropin‐releasing factor on rat resistance arteries

Shi

Richter²,

Bienert³

et al. 1993

British J Pharmacology

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1Although it well established that corticotropin-releasing factor (CRF) injected i.v. can cause hypotension and vasodilatation, there is no in vitro evidence that CRF acts as a vasodilator. We have therefore tested the hypothesis that the hypotensive effect of i.v. CRF is due to a direct vasodilator action by carrying out experiments in vitro on rat resistance arteries (i.d. 150-300ILm). 2 Initial in vivo experiments confirmed that CRF (1.5 nmol kg'1) injected i.v. caused hypotension in rats, this being partially antagonized by the CRF analogue CRF9-41.3 For the in vitro experiments, vessels were taken from the mesenteric, cerebral and femoral vascular beds, and mounted as ring preparations in an isometric myograph. The vessels were pre-contracted with one of 3 agonists (prostaglandin F2,, arginine vasopressin or noradrenaline) or with a high-potassium solution (K+). 4 With maximal concentrations of the agonists, CRF caused relaxation of mesenteric and cerebral vessels with 10nM, and near complete relaxation with 100nM. Femoral vessels preconstricted with agonists and all vessels preconstricted with K+ were less affected by CRF. In the mesenteric vessels, with sub-maximal levels of pre-constriction, CRF caused substantial relaxation at 1 nM and could cause complete relaxation at 10nM. 5 The relaxant effect of CRF on contractions of mesenteric vessels was antagonized by 100nM CRF9-41. Neither tetraethyl ammonium (30mM) nor glibenclamide (31 M) antagonized the relaxant effect of CRF. 6 The relaxant effect of CRF on mesenteric small arteries was found to be unaffected by removal of the endothelium. 7 The results indicate that CRF causes an endothelial-independent vasodilatation of rat resistance arteries under in vitro conditions at concentrations which are consistent with this being an important cause of the hypotension observed with i.v. injection of CRF.

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“…Patients with anorexia nervosa have hypercortisolism, a lack of cortisol suppression with dexamethasone, blunted ACTH responses to CRH and elevated cerebrospinal fluid levels of CRH (15)(16)(17)(18)(19)29). Amenorrheic athletes have been characterized as having plasma CRH, plasma ACTH, and urinary cortisol levels no different from those of eumenorrheic athletes (30,31). However, it has recently been shown that mean morning cortisol levels were higher in amenorrheic than in eumenorrheic athletes (32).…”

Section: Discussionmentioning

confidence: 99%

Abnormal Cortisol Secretion and Responses to Corticotropin-Releasing Hormone in Women with Hypothalamic Amenorrhea*

Biller

Federoff

Koenig

et al. 1990

The Journal of Clinical Endocrinology & Metabolism

168

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Hypothalamic amenorrhea (HA) is a common disorder associated with hypoestrogenemia and has adverse effects. The mechanism of GnRH deficiency in these women is not yet known. To investigate the role of the hypothalamic-pituitary-adrenal axis in HA, we studied 10 women [mean age, 29 +/- 7 (+/- SD) yr] with 0.5-13 yr of amenorrhea (mean, 4.3 +/- 3.7 yr) related to simple weight loss or psychological stress. We investigated cortisol and ACTH responses to a bolus of ovine CRH, 24-h plasma cortisol levels obtained every 10 min, and urinary free cortisol levels in these patients. Results were compared with those obtained in normal women during all phases of the menstrual cycle. We found that mean basal concentrations of cortisol were significantly higher (P = 0.03) in the HA patients (mean, 210 +/- 130 nmol/L) than in the normal women (100 +/- 30 nmol/L). The delta (peak - basal) cortisol was significantly lower (P = 0.004) in the HA patients than in the normal women (320 +/- 100 vs. 440 +/- 90 nmol/L, respectively). ACTH responses to CRH did not differ between HA patients and normal women. The 24-h mean cortisol was significantly higher (P = 0.006) in the HA patients than in the normal controls (280 +/- 50 and 220 +/- 50 nmol/L, respectively), due to higher cortisol levels at night. The urinary free cortisol level was significantly higher (P = 0.005) in the HA patients (230 +/- 70 nmol/day) than in normal women (150 +/- 40 nmol/day). We conclude that women with HA have a blunted cortisol response to CRH administration. In addition, they have hypercortisolism, as demonstrated by elevated 24-h mean serum cortisol levels and urinary free cortisol values. This hypothalamic-pituitary-adrenal axis activation in patients with stress or weight loss may be a mechanism in the development of amenorrhea and may relate to other potential adverse effects of HA.

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Plasma corticotropin-releasing hormone, corticotropin, and endorphins at rest and during exercise in eumenorrheic and amenorrheic athletes

Cited by 32 publications

References 23 publications

Desequilíbrio hormonal e disfunção menstrual em atletas de ginástica rítmica

Desequilíbrio hormonal e disfunção menstrual em atletas de ginástica rítmica

Relaxing actions of corticotropin‐releasing factor on rat resistance arteries

Abnormal Cortisol Secretion and Responses to Corticotropin-Releasing Hormone in Women with Hypothalamic Amenorrhea*

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