857.8 - Sleep Disturbance and Sympathetic Reactivity in Menopausal Women

Chowdhury Tasnova Tahsin (University of Minnesota), Nisha Panigrahy (University of Minnesota), William Stokes (University of Minnesota), Miguel Anselmo (University of Minnesota), Aline Glazos (University of Minnesota), Emma Lee (University of Minnesota), Cavan Reilly (University of Minnesota), Marnie Vanden Noven (Belmont University), Jason Carter (Montana State University), Manda Keller-Ross (University of Minnesota, University of Minnesota)

Introduction: Cardiovascular disease (CVD) is the leading cause of death in women. Sleep disturbances (DS), such as insomnia or frequent nocturnal awakenings, may increase the risk of CVD. Prior work suggests that autonomic blood pressure (BP) dysregulation in postmenopausal women may exaggerate risk of hypertension (HTN) and CVD. In addition, individuals with greater BP and sympathetic neural responses to stressors, such as a cold pressor test (CPT), demonstrate future risk for HTN development. Further, when exposed to 24-hour sleep deprivation, older women, but not older men, demonstrate greater sympathetic activity. It is unknown, however, if women who experience DS demonstrate a greater sympathetic reactivity to a CPT. The purpose of this study was to determine if postmenopausal women with DS exhibit sympathetic reactivity to a CPT compared to women without DS.

Methods: Eighteen women (62±1yrs old; mean±SE) participated in two study visits. Visit 1: Informed consent and medical and health questionnaires. Visit 2: DS was assessed by the Menopause-Specific Quality of Life questionnaire. Participants were classified as having disturbed sleep (DS; n=10) or non-disturbed sleep (NDS; n=8) based on a scale of 1 indicating ‘none’ and 2-8 being how bothersome it is. The study was conducted in the morning after overnight fast and abstinence of alcohol, caffeine, and exercise. Muscle sympathetic nerve activity (MSNA) was measured from the peroneal nerve using microneurography. Heart rate (HR) via 3-lead electrocardiography, MSNA, and beat-to-beat BP using a non-invasive finger cuff were measured during a 10-min quiet rest and a two-min CPT of the left hand.

Results: Menopause onset ranged from 40-57yrs (50±1yrs). Body mass index was similar between groups (DS=25±1kg/m2, NDS=24±2kg/m2, p=0.53). MSNA burst incidence (bursts/100 heart beats, hb) increased throughout the CPT (time effect, plt;0.01), but increases were not significantly different between DS (Δ19±6b/100hb; 95% CI [7,31]) and NDS (Δ11±6b/100hb; 95% CI [-2,24]) (time*group, p=0.36) groups. Systolic BP, Diastolic BP and HR increased similarly (pgt;0.05) during the CPT for both groups. Sleep difficulty score was correlated with resting diastolic BP (r=0.43, p=0.03) and trended to correlate with the age of menopause (r= -0.37, p=0.05).

Conclusion: These findings suggest that women with DS do not demonstrate greater sympathetic reactivity to a CPT, however, we did observe that DS was linked to greater diastolic BP at rest and appeared to be more bothersome for women who completed menopause at an earlier age. These findings suggest a pathway by which disrupted sleep may contribute to the future development of HTN and CVD in postmenopausal women.

NIH 1 K01 AG064038-01A1 (MLKR), UMN Grant-in-Aid (MLKR), NIH National Center for Advancing Translational Science, grant UL1TR002494, Womens Health Research Seed Grant, University of Minnesota, American Physiological Society Research Career Enhancement Award