Mechanisms underlying hemodynamic and neuroendocrine stress reactivity at different phases of the menstrual cycle

Authors

  • Jennifer L. Gordon,

    1. Department of Psychiatry, University of North Carolina at Chapel Hill, North Carolina, USA
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  • Susan S. Girdler

    Corresponding author
    1. Department of Psychiatry, University of North Carolina at Chapel Hill, North Carolina, USA
    • Address correspondence to: Susan S. Girdler, Ph.D., Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, CB# 7160, 101 Manning Drive, Chapel Hill, NC 27599-3366, USA. E-mail: Susan_Girdler@med.unc.edu

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  • This research was supported by NIH grant RO1-DA013705, CTSA grant UL1RR025747, and NIH grant T32-MH093315. Dr. Gordon is also the recipient of a postdoctoral fellowship of the Fonds de la Recherche en Santé du Québec (FRSQ).

Abstract

This study examined the association of menstrual cycle phase with stress reactivity as well as the hormonal and neuroendocrine mechanisms contributing to cycle effects. Fifty-seven women underwent a modified Trier Social Stress Test during the early follicular, late follicular, and luteal phases of the menstrual cycle. Greater increases in cardiac index (CI) and greater decreases in vascular resistance index (VRI) during speech were observed in the luteal phase relative to other phases, while greater increases in epinephrine (EPI) was observed during the late follicular and luteal phases compared to the early follicular phase. Luteal phase estradiol predicted luteal EPI reactivity but not CI or VRI reactivity, while luteal phase EPI reactivity predicted luteal phase CI and VRI reactivity. Thus, cycle-related changes in EPI reactivity may be a stronger determinant of cycle effects on hemodynamic reactivity than sex hormones per se.

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