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Derek P. Spangler, Ben Allen, Xiao Yang, & Bruce H. Friedman Mind-Body Laboratory INTRODUCTION Autonomic responses have been shown to vary with estrogen levels across the menstrual cycle. Compared to the luteal phase (less estrogen), the follicular phase tends to be associated with : -Reductions in heart rate and sympathetic nerve activity -Increases in vagal activity and cardiovagal baroreceptor gain Less attention has been given to how cardiovascular (CV) responses are modified during menses, when estrogen levels are at their lowest. This study will test whether vagal outflow and baroreceptor regulation are significantly reduced during menses. Hormonal contraceptive (HC) users’ reduced negative affect during menses may be related to the influence of increased levels of estrogen on autonomic functioning. The present study will test whether increased sympathetic reactivity to mental stress during menstruation is attenuated for those taking HC. Understanding menstrual cycle-related effects on CV measures may improve their reliability so that Type 2 errors may be reduced in psychophysiological research. Presented at the 52 nd annual meeting of the Society for Psychophysiological Research (SPR) in New Orleans LA, Sept. 2012 Cardiovascular Responses to Stress during Menstruation__ Subjects -87 Women -Age: M = 19.37 (SD = 2.659) Self-report measures: Menstruating vs. Non-menstruating, Day in menstrual cycle, Hormonal contraceptive use (Yes or No) CV measures: -IBI (derived from ECG) -Blood pressure (radial artery cuff)= α-adrenergic activation -High-frequency heart rate variability (HF HRV) = vagal activation -Low-frequency HRV = baroreceptor regulation Procedure: CV measures assessed during three 10-min periods: Vanilla baseline Spatial n-back task (working memory stressor) Recovery Analyses: 2 (Menstruating: yes, no) X 2 (Birth control: yes, no) Between-Subjects MANOVA to test individual main effects and the interaction between menstrual status and HC use on CV measures. DISCUSSION RESULTS METHOD Longer IBIs and increased HRV likely indicates higher vagal activation during menses. Larger values of LF HRV for menstruating women suggest that menstruation is associated with more effective cardiovagal baroreceptor regulation. These results are inconsistent with the relatively low levels of estrogen during menses. The simultaneous low levels of progesterone during this time may explain menstruating women’s increased physiological regulatory capacity. Alternatively, these differences could have resulted from the reduction of negative somatic symptoms from premenstrual to menstrual phase. The moderational hypothesis was supported, suggesting that HC reduces stress reactivity during menstruation. This relation is likely driven by HC’s up-regulating effect on estrogen throughout the menstrual cycle. Menstruating women showed a larger average IBI during baseline, F(1, 82) = 4.00, p =.049, and during the n-back, F(1, 82) = 4.65, p =.03. LF HRV was marginally increased among menstruating women during baseline, F(1, 82) = 2.63, p =.10, and during task F(1, 82) = 3.07, p =.08. HF HRV trended toward relatively increased levels for menstruating women but were non-significant. An interaction was found between menstrual status and HC use in predicting diastolic blood pressure (DBP) during the n- back, F(1, 69) = 2.93, p =.09. -Heightened DBP for menstruating women who do not take HCs but no difference in DBP between menstrual groups for women taking birth control. Interaction of Menstruation & HC on DBP Birth control No birth control mmHg
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