Increased vasopressin and adrenocorticotropin responses to stress in the midluteal phase of the menstrual cycle.

Accumulating evidence indicates that gonadal steroids modulate functioning of the hypothalamic-pituitary-adrenal (HPA) axis, which has been closely linked to the pathophysiology of anxiety and depression. However, the effect of the natural menstrual cycle on HPA axis responsivity to stress has not been clearly described. In nine healthy women, metabolic and hormonal responses to treadmill exercise stress during the early follicular phase of the menstrual cycle, when gonadal steroid levels are low, were compared with responses in the midluteal phase of the cycle, when both progesterone and estrogen levels are relatively high. Exercise intensity was gradually increased over 20 min to reach 90% of each subject's maximal oxygen consumption during the final 5 min of exercise. Basal plasma lactate, glucose, ACTH, vasopressin, oxytocin, and cortisol levels were similar in the two cycle phases. However, in response to exercise stress, women in the midluteal phase had enhanced ACTH (P < 0.0001), vasopressin (P < 0.01), and glucose (P < 0.001) secretion. These findings suggest that relatively low levels of gonadal steroids during the early follicular phase of the menstrual cycle provide protection from the impact of stress on the HPA axis.

[1]  H. Vaudry,et al.  Vasopressin stimulates cortisol secretion from human adrenocortical tissue through activation of V1 receptors. , 1993, The Journal of clinical endocrinology and metabolism.

[2]  M. Ferin,et al.  A 5‐Day Estradiol Therapy, in Amounts Reproducing Concentrations of the Early‐Mid Follicular Phase, Prevents the Activation of the Hypothalamo‐Pituitary‐Adrenal Axis by Interleukin‐1α in the Ovariectomized Rhesus Monkey , 1995, Journal of neuroendocrinology.

[3]  N. Barden,et al.  Estrogen-induced decrease of glucocorticoid receptor messenger ribonucleic acid concentration in rat anterior pituitary gland. , 1987, Molecular endocrinology.

[4]  W. Kraemer,et al.  Adrenal activation and the prolactin response to exercise in eumenorrheic and amenorrheic runners. , 1991, Journal of applied physiology.

[5]  S. Porges,et al.  Responses to Laboratory Psychosocial Stress in Postpartum Women , 2001, Psychosomatic medicine.

[6]  M. Ferin,et al.  Stimulatory effects of interleukin-induced activation of the hypothalamo-pituitary-adrenal axis on gonadotropin secretion in ovariectomized monkeys replaced with estradiol. , 1994, Endocrinology.

[7]  N. Barden,et al.  Hormonal regulation of type II glucocorticoid receptor messenger ribonucleic acid in rat brain. , 1991, Endocrinology.

[8]  P. Chiodera,et al.  Oxytocin reduces metyrapone-induced ACTH secretion in human subjects , 1987, Brain Research.

[9]  Bruce S. McEwen,et al.  INDUCTION OF CORTICOTROPIN-RELEASING HORMONE GENE EXPRESSION BY GLUCOCORTICOIDS: IMPLICATION FOR UNDERSTANDING THE STATES OF FEAR AND ANXIETY AND ALLOSTATIC LOAD , 1998, Psychoneuroendocrinology.

[10]  F. Goodwin,et al.  Clinical and biochemical manifestations of depression. Relation to the neurobiology of stress (1) , 1988, The New England journal of medicine.

[11]  J. Lavoie,et al.  Menstrual cycle phase dissociation of blood glucose homeostasis during exercise. , 1987, Journal of applied physiology.

[12]  B. Andersch,et al.  Premenstrual complaints. I: Prevalence of premenstrual symptoms in a Swedish urban population , 1986 .

[13]  R. Mogg,et al.  Oxytocin as Part of Stress Responses , 1990 .

[14]  M. Altemus,et al.  Preliminary research on plasma oxytocin in normal cycling women: investigating emotion and interpersonal distress. , 1999, Psychiatry.

[15]  N. Barden,et al.  Antidepressants regulate glucocorticoid receptor messenger RNA concentrations in primary neuronal cultures. , 1989, Brain research. Molecular brain research.

[16]  P. Deuster,et al.  Hormonal and metabolic responses to exercise across time of day and menstrual cycle phase. , 1997, Journal of applied physiology.

[17]  J. Amico,et al.  Gonadal steroid modulation of oxytocin and vasopressin gene expression in the hypothalamus of the osmotically stimulated rat. , 1993, Endocrinology.

[18]  S. Hayashi,et al.  Implications of estrogen‐dependent brain organization for gender differences in hypothalamo‐pituitary‐adrenal regulation , 1995, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[19]  T. Dinan,et al.  d‐Fenfluramine/prolactin response throughout the menstrual cycle: evidence for an oestrogen‐induced alteration , 1991, Clinical endocrinology.

[20]  A. Leshner,et al.  Menstrual cycle status and adrenocortical reactivity to pyschological stress , 1976, Psychoneuroendocrinology.

[21]  C. Kirschbaum,et al.  Short-term estradiol treatment enhances pituitary-adrenal axis and sympathetic responses to psychosocial stress in healthy young men. , 1996, The Journal of clinical endocrinology and metabolism.

[22]  A Luger,et al.  Acute hypothalamic-pituitary-adrenal responses to the stress of treadmill exercise. Physiologic adaptations to physical training. , 1987, The New England journal of medicine.

[23]  A. Bonen,et al.  Effects of menstrual cycle on metabolic responses to exercise. , 1983, Journal of applied physiology: respiratory, environmental and exercise physiology.

[24]  F. Goodwin,et al.  Clinical and biochemical manifestations of depression. Relation to the neurobiology of stress (2) , 1988, The New England journal of medicine.

[25]  J. Amico,et al.  BREAST STIMULATION IN CYCLING WOMEN, PREGNANT WOMEN AND A WOMAN WITH INDUCED LACTATION: PATTERN OF RELEASE OF OXYTOCIN, PROLACTIN AND LUTEINIZING HORMONE , 1986, Clinical endocrinology.

[26]  E. D. de Kloet,et al.  The influence of ovarian steroids on hypothalamic-pituitary-adrenal regulation in the female rat. , 1995, The Journal of endocrinology.

[27]  L. Bernstein,et al.  Behavioral stress responses in premenopausal and postmenopausal women and the effects of estrogen , 1993 .

[28]  M. Esler,et al.  Journal of Clinical Endocrinology and Metabolism Printed in U.S.A. Copyright © 1999 by The Endocrine Society Estrogen Supplementation Attenuates Glucocorticoid and Catecholamine Responses to Mental Stress in , 2022 .

[29]  B. Kudielka,et al.  Impact of gender, menstrual cycle phase, and oral contraceptives on the activity of the hypothalamus-pituitary-adrenal axis. , 1999, Psychosomatic medicine.

[30]  D. Rubinow,et al.  Prospective assessment of menstrually related mood disorders. , 1984, The American journal of psychiatry.

[31]  R. Harrison,et al.  Progesterone enhances glucocorticoid dissociation from the AtT-20 cell glucocorticoid receptor. , 1980, Endocrinology.

[32]  F. Antoni.  Vasopressinergic Control of Pituitary Adrenocorticotropin Secretion Comes of Age , 1993, Frontiers in Neuroendocrinology.

[33]  R. DeFronzo,et al.  Menstrual cyclicity has a profound effect on glucose homeostasis. , 1989, Fertility and sterility.

[34]  J. Bertrand,et al.  Demonstration of an antiglucocorticoid action of progesterone on the corticosterone inhibition of beta-endorphin release by rat anterior pituitary in primary culture. , 1984, Endocrinology.

[35]  G. Chrousos,et al.  The concepts of stress and stress system disorders. Overview of physical and behavioral homeostasis. , 1992, JAMA.

[36]  E. Love,et al.  The epidemiology of premenstrual symptoms in a population-based sample of 2650 urban women: attributable risk and risk factors. , 1992, Journal of clinical epidemiology.

[37]  D. Murphy,et al.  Abnormalities in the regulation of vasopressin and corticotropin releasing factor secretion in obsessive-compulsive disorder. , 1992, Archives of general psychiatry.

[38]  D. Goldstein,et al.  Plasma and urinary catecholamines during the human ovulatory cycle. , 1983, American journal of obstetrics and gynecology.

[39]  D. Murphy,et al.  Effect of menstrual cycle phase on neuroendocrine and behavioral responses to the serotonin agonist m-chlorophenylpiperazine in women with premenstrual syndrome and controls. , 1997, The Journal of clinical endocrinology and metabolism.

[40]  R. Handa,et al.  Estrogen-Induced Alterations in the Regulation of Mineralocorticoid and Glucocorticoid Receptor Messenger RNA Expression in the Female Rat Anterior Pituitary Gland and Brain , 1993, Molecular and Cellular Neuroscience.

[41]  P. Eneroth,et al.  Psychoneuroendocrine stress responses and mood as related to the menstrual cycle. , 1985, Psychosomatic medicine.

[42]  R. Handa,et al.  Chronic estrogen-induced alterations in adrenocorticotropin and corticosterone secretion, and glucocorticoid receptor-mediated functions in female rats. , 1992, Endocrinology.

[43]  R. Boileau,et al.  Cortisol Levels during Prolonged Exercise: The Influence of Menstrual Phase and Menstrual Status , 1992, International Journal of Sports Medicine.

[44]  B. Nicklas,et al.  The Menstrual Cycle and Exercise: Performance, Muscle Glycogen, and Substrate Responses , 1989, International journal of sports medicine.

[45]  M. Demitrack,et al.  CSF oxytocin in anorexia nervosa and bulimia nervosa: clinical and pathophysiologic considerations. , 1990, The American journal of psychiatry.

[46]  G. Goodwin,et al.  Blunting of neuroendocrine responses to infusion of L-tryptophan in women with perimenstrual mood change , 1991, Psychological Medicine.

[47]  R. Rose,et al.  Cortisol and Growth Hormone Responses to Psychological Stress during the Menstrual Cycle , 1977, Psychosomatic medicine.

[48]  M. Ferin,et al.  Stress and the menstrual cycle: short- and long-term response to a five-day endotoxin challenge during the luteal phase in the rhesus monkey. , 1999, The Journal of clinical endocrinology and metabolism.

[49]  E. Frank,et al.  Late luteal phase dysphoric disorder in young women. , 1990, The American journal of psychiatry.

[50]  R. Jarrett,et al.  Changes in oral glucose tolerance during the menstrual cycle. , 1968, British medical journal.

[51]  S. Lightman,et al.  Psychological stress of exposure to uncontrollable noise increases plasma oxytocin in high emotionality women , 1990, Psychoneuroendocrinology.

[52]  G. Chrousos,et al.  Hormonal and metabolic responses of untrained, moderately trained, and highly trained men to three exercise intensities. , 1989, Metabolism: clinical and experimental.

[53]  E. Young,et al.  Sex differences in response to exogenous corticosterone: a rat model of hypercortisolemia. , 1996, Molecular psychiatry.

[54]  S. R. Johnson.  The epidemiology and social impact of premenstrual symptoms. , 1987, Clinical obstetrics and gynecology.

[55]  M. Rotondi,et al.  Inhibitory effect of exogenous oxytocin on ACTH and cortisol secretion during labour. , 1999, Clinical and experimental obstetrics & gynecology.

[56]  K. Light,et al.  Dysregulation of cardiovascular and neuroendocrine responses to stress in premenstrual dysphoric disorder , 1998, Psychiatry Research.

[57]  J. Cacioppo,et al.  Postmenopausal Hormone Replacement: Effects on Autonomic, Neuroendocrine, and Immune Reactivity to Brief Psychological Stressors , 1998, Psychosomatic medicine.

[58]  R. Handa,et al.  Androgen regulation of adrenocorticotropin and corticosterone secretion in the male rat following novelty and foot shock stressors , 1994, Physiology & Behavior.

[59]  N. Holbrook,et al.  Physiological functions of glucocorticoids in stress and their relation to pharmacological actions. , 1984, Endocrine reviews.

[60]  L. Fisher,et al.  Glucocorticoid suppression of the sympathetic nervous system and adrenal medulla. , 1986, Life Science.

[61]  N. Kruyt,et al.  Cortisol, 17α-OH-progesterone and androgen responses to a standardized ACTH-stimulation in different stages of the normal menstrual cycle , 1982 .

[62]  M. Ferrini,et al.  Estradiol abolishes autologous down regulation of glucocorticoid receptors in brain. , 1995, Life sciences.

[63]  V. Viau,et al.  Variations in the hypothalamic-pituitary-adrenal response to stress during the estrous cycle in the rat. , 1991, Endocrinology.

[64]  M. Altemus,et al.  Suppression of hypothalmic-pituitary-adrenal axis responses to stress in lactating women. , 1995, The Journal of clinical endocrinology and metabolism.