Cortisol: Rise and Fall depending on many factors

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    Cortisol: Rise and Fall depending on many factors


    I found this to be a great article so I figured I would share it. It is basically saying that although a morning workout will increase cortisol levels during that workout, it will keep cortisol levels lower throughout the day.

    The largest cortisol peak seems to be that with the mid day meal and it is reduced by working out in the morning.

    A similar nighttime meal (to the one in the afternoon) will yield less of a cortisol response as well an evening workout. Very interesting how cortisol responses with identical meals or workouts, varies with time of day .





    Feedback from meal-related peaks determines diurnal changes in cortisol response to exercise

    G Brandenberger, M Follenius and B Hietter

    Diurnal variations in cortisol response to exercise and their relation to the events of the day were assessed by comparing daily cortisol patterns on the control day and on days when exercise was performed at different times. A remarkable midday cortisol peak coincided with the noon meal, but cortisol levels were irregularly affected by an identical meal in the evening. However, the exercise produced equal increases when performed during quiescent periods (i.e. without any secretory peaks at 1000, 1430, 1700, and 2130 h), but peak levels for exercise at 2130 h were significantly lower because of the lower basal levels in the evening. When the same exercise was performed at 1300 h (i.e. coinciding with the postprandial peak), only a brief leveling-off interrupted the decline in cortisol levels. The meal-related evening peak, if any, provoked a similar decrease in response to exercise performed at 2000 h. Similarly, the midday peak itself was reduced by a prior exercise-induced cortisol rise. These results show that the daily cortisol pattern results from the interactions between the meal-related peaks, especially the major midday cortisol peak, and the exercise- induced increases, both of which inhibit the response to subsequent stimulation. The identical responses to exercise at the different quiescent periods tested, despite a general downward trend in basal cortisol levels, establish the primacy of such feedback mechanisms over those responsible for the circadian rhythm.

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    LMD,
    Is there a quick and dirty relationship between HCG and cortisol?
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    The effect of prolactin, human chorionic gonadotropin, insulin and insulin-like growth factor 1 on adrenal steroidogenesis in isolated guinea-pig adrenal cells.

    * O'Connell Y,
    * McKenna TJ,
    * Cunningham SK.

    Department of Endocrinology, St Vincent's Hospital, Dublin, Ireland.

    The controlling mechanism for adrenal androgen production has not been elucidated. The presence of receptors for prolactin, human chorionic gonadotropin (hCG), insulin and insulin-like growth factor 1 (IGF-1) in the adrenal cortex raises the possibility of their involvement in the control of adrenal steroidogenesis. This study was undertaken to investigate the effects of prolactin, hCG, insulin and IGF-1 in the presence and absence of ACTH on cortisol and androgen production using isolated guinea-pig adrenal cells. hCG 10(-7) and 10(-6) M significantly increased cortisol (P < 0.05) production. hCG 10(-6) M significantly increased androstenedione (A4) (P < 0.05) production. In the presence of ACTH, 10(-12) M, hCG 10(-6) M significantly increased the cortisol (P < 0.01) and A4 (P < 0.01) responses. Although the mean cortisol and A4 response to ACTH 10(-9) M was reduced in the presence of hCG 10(-6) M, this was not statistically significant. Prolactin 10(-8) M increased cortisol (P < 0.01), A4, and dehydroepiandrosterone (P < 0.05) production. In the presence of ACTH 10(-12) M, prolactin 10(-8) M increased the cortisol and A4 (P < 0.05) responses. However, the maximally ACTH-stimulated cortisol and A4 responses were not significantly altered in the presence of prolactin 10(-8) M. Insulin 10(-11)-10(-8) M and IGF-1 10(-10)-10(-7) M resulted in no significant increase in cortisol, A4 or dehydroepiandrosterone production. This study suggests that prolactin and hCG could play a role in modulation of adrenal steroidogenesis, particularly when ACTH levels are low. However, there was no evidence that prolactin or hCG is the specific cortical androgen stimulating hormone.








    Here is a study on women:


    Ovarian and adrenal steroid production: regulatory role of LH/HCG
    T. Piltonen1, R. Koivunen1, L. Morin-Papunen1, A. Ruokonen2, I.T. Huhtaniemi3 and J.S. Tapanainen1,4

    1 Departments of Obstetrics and Gynaecology, and 2 Clinical Chemistry, Oulu University Hospital, Oulu and 3 Department of Physiology, University of Turku, Turku, Finland

    BACKGROUND: The contribution of the adrenal glands to the total circulating steroid pool in women is not well known. There is evidence that human adrenals express the LH receptor gene and that LH may affect adrenal androgen secretion. METHODS: HCG stimulation tests (a single dose of 5000 IU i.m.) were performed in women at reproductive age (group 1, n = 6, age 21–39 years) before and after treatment with a GnRH agonist for 3 weeks, and in oophorectomized post-menopausal women (group 2, n = 6, 47–59 years) during and after estrogen replacement therapy (ERT). RESULTS: HCG did not stimulate the secretion of cortisol, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulphate (DHEAS) in group 2. In contrast, in group 1, the basal concentrations of serum 17-hydroxyprogesterone (17-OHP), androstenedione, testosterone and estradiol (E2) were stimulated significantly (17-OHP 105%, androstenedione 31%, testosterone 20%, E2 136%) by HCG, and the treatment with GnRH agonist decreased the responses. The basal serum concentrations of these steroids were significantly lower in oophorectomized women (17-OHP 57%, androstenedione 46%, testosterone 25%), and HCG did not increase these levels. It can be approximated that the ovarian contribution to the circulating levels of 17-OHP, androstenedione and testosterone is 25–30%, and that the adrenals are the primary source of cortisol, DHEA and DHEAS. CONCLUSION: LH/HCG does not have a major role in the regulation of adrenal steroid synthesis in endocrinologically healthy women.
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    Thanks, that bonked one of my theories. I'll study up some more. Good things!

    I wish the second study had used lower dosage and more than one administration. I must spread the love before I can rep you!
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