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      Adrenal, thyroid and gonadal axes are affected at high altitude

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          Abstract

          Humans cannot live at very high altitude for reasons, which are not completely understood. Since these reasons are not restricted to cardiorespiratory changes alone, changes in the endocrine system might also be involved. Therefore, hormonal changes during prolonged hypobaric hypoxia were comprehensively assessed to determine effects of altitude and hypoxia on stress, thyroid and gonadal hypothalamus–pituitary hormone axes. Twenty-one male and 19 female participants were examined repetitively during a high-altitude expedition. Cortisol, prolactin, thyroid-stimulating hormone (TSH), fT4 and fT3 and in males follicle-stimulating hormone (FSH), luteinizing hormone (LH) and total testosterone were analysed as well as parameters of hypoxemia, such as SaO 2 and paO 2 at 550 m (baseline) ( n = 40), during ascent at 4844 m ( n = 38), 6022 m ( n = 31) and 7050 m ( n = 13), at 4844 m ( n = 29) after acclimatization and after the expedition ( n = 38). Correlation analysis of hormone concentrations with oxygen parameters and with altitude revealed statistical association in most cases only with altitude. Adrenal, thyroid and gonadal axes were affected by increasing altitude. Adrenal axis and prolactin were first supressed at 4844 m and then activated with increasing altitude; thyroid and gonadal axes were directly activated or suppressed respectively with increasing altitude. Acclimatisation at 4844 m led to normalization of adrenal and gonadal but not of thyroid axes. In conclusion, acclimatization partly leads to a normalization of the adrenal, thyroid and gonadal axes at around 5000 m. However, at higher altitude, endocrine dysregulation is pronounced and might contribute to the physical degradation found at high altitude.

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          The effects of intense exercise on the female reproductive system.

          Women have become increasingly physically active in recent decades. While exercise provides substantial health benefits, intensive exercise is also associated with a unique set of risks for the female athlete. Hypothalamic dysfunction associated with strenuous exercise, and the resulting disturbance of GnRH pulsatility, can result in delayed menarche and disruption of menstrual cyclicity. Specific mechanisms triggering reproductive dysfunction may vary across athletic disciplines. An energy drain incurred by women whose energy expenditure exceeds dietary energy intake appears to be the primary factor effecting GnRH suppression in athletes engaged in sports emphasizing leanness; nutritional restriction may be an important causal factor in the hypoestrogenism observed in these athletes. A distinct hormonal profile characterized by hyperandrogenism rather than hypoestrogenism is associated with athletes engaged in sports emphasizing strength over leanness. Complications associated with suppression of GnRH include infertility and compromised bone density. Failure to attain peak bone mass and bone loss predispose hypoestrogenic athletes to osteopenia and osteoporosis. Metabolic aberrations associated with nutritional insult may be the primary factors effecting low bone density in hypoestrogenic athletes, thus diagnosis should include careful screening for abnormal eating behavior. Increasing caloric intake to offset high energy demand may be sufficient to reverse menstrual dysfunction and stimulate bone accretion. Treatment with exogenous estrogen may help to curb further bone loss in the hypoestrogenic amenorrheic athlete, but may not be sufficient to stimulate bone growth. Treatment aimed at correcting metabolic abnormalities may in fact prove more effective than that aimed at correcting estrogen deficiencies.
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            Hormonal regulation of spermatogenesis and spermiogenesis.

            Normal testicular function is dependent upon hormones acting through endocrine and paracrine pathways both in vivo and in vitro. Sertoli cells provide factors necessary for the successful progression of spermatogonia into spermatozoa. Sertoli cells have receptors for follicle stimulating hormone (FSH) and testosterone which are the main hormonal regulators of spermatogenesis. Hormones such as testosterone, FSH and luteinizing hormone (LH) are known to influence the germ cell fate. Their removal induces germ cell apoptosis. Proteins of the Bcl-2 family provide one signaling pathway which appears to be essential for male germ cell homeostasis. In addition to paracrine signals, germ cells also depend upon signals derived from Sertoli by direct membrane contact. Somatostatin is a regulatory peptide playing a role in the regulation of the proliferation of the male gametes. Activin A, follistatin and FSH play a role in germ cell maturation during the period when gonocytes resume mitosis to form the spermatogonial stem cells and differentiating germ cell populations. In vitro cultures systems have provided evidence that spermatogonia in advance stage of differentiation have specific regulatory mechanisms that control their fate. This review article provides an overview of the literature concerning the hormonal pathways regulating spermatogenesis.
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              The Effects of Insomnia and Sleep Loss on Cardiovascular Disease.

              Sleep loss has negative impacts on quality of life, mood, cognitive function, and heath. Insomnia is linked to poor mood, increased use of health care resources, decreased quality of life, and possibly cardiovascular risk factors and disease. Studies have shown increase in cortisol levels, decreased immunity, and increased markers of sympathetic activity in sleep-deprived healthy subjects and those with chronic insomnia. The literature shows subjective complaints consistent with chronic insomnia and shortened sleep can be associated with development of diabetes, hypertension, and cardiovascular disease. This article explores the relationship between insufficient sleep and insomnia with these health conditions.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                October 2018
                29 August 2018
                : 7
                : 10
                : 1081-1089
                Affiliations
                [1 ]Division of Gynaecological Endocrinology and Reproductive Medicine University Women’s Hospital, Bern University Hospital, University of Bern, Bern, Switzerland
                [2 ]University Institute of Clinical Chemistry Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
                [3 ]Laboratory of Biometry University of Thessaly, Volos, Greece
                [4 ]Division of Pneumology Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
                [5 ]Division of Intensive Care Medicine Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
                [6 ]Intensive Care Unit University Hospital, Zurich, Switzerland
                [7 ]Endocrine Research Unit Department of Internal Medicine, Mayo School of Graduate Medical Education, Centre for Translational Science Activities, Mayo Clinic, Rochester, New York, USA
                [8 ]Centre for Laboratory Medicine Cantonal Hospital, Aarau, Switzerland
                Author notes
                Correspondence should be addressed to M von Wolff: Michael.vonWolff@ 123456insel.ch

                *(M von Wolff, C T Nakas and J Pichler Hefti contributed equally to this work)

                Article
                EC180242
                10.1530/EC-18-0242
                6198189
                30352395
                b9469d59-bb3d-44ae-b740-eff10a8d4cfc
                © 2018 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 22 August 2018
                : 29 August 2018
                Categories
                Research

                cortisol,prolactin,tsh,ft3,ft4,follicle-stimulation hormone,luteinizing hormone,testosterone,altitude,hypobaric hypoxia

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