Tahsin Chowdhury Tasnova, Anselmo Miguel, Lee Emma, Stokes William, Fonkoue Ida T, Vanden Noven Marnie L, Carter Jason R, Keller-Ross Manda L
Division of Rehabilitation Science, Medical School, University of Minnesota, Minneapolis, Minnesota, United States.
Division of Physical Therapy, Medical School, University of Minnesota, Minneapolis, Minnesota, United States.
Am J Physiol Heart Circ Physiol. 2024 Mar 1;326(3):H752-H759. doi: 10.1152/ajpheart.00724.2023. Epub 2024 Jan 12.
Sleep disturbance, one of the most common menopausal symptoms, contributes to autonomic dysfunction and is linked to hypertension and cardiovascular risk. Longitudinal studies suggest that hyperreactivity of blood pressure (BP) to a stressor can predict the future development of hypertension. It remains unknown if postmenopausal females who experience sleep disturbance (SDG) demonstrate greater hemodynamic and sympathetic neural hyperreactivity to a stressor. We hypothesized that postmenopausal females with reported sleep disturbance would exhibit increased hemodynamic and sympathetic reactivity to a stressor compared with postmenopausal females without sleep disturbance (non-SDG). Fifty-five postmenopausal females (age, 62 ± 4 yr old; SDG, = 36; non-SDG; = 19) completed two study visits. The Menopause-Specific Quality of Life Questionnaire (MENQOL) was used to assess the presence of sleep disturbance (MENQOL sleep scale, ≥2 units). Beat-to-beat BP (finger plethysmography), heart rate (HR; electrocardiogram), and muscle sympathetic nerve activity (MSNA; microneurography; SDG, = 25; non-SDG, = 15) were continuously measured during a 10-min baseline and 2-min stressor (cold pressor test; CPT) in both groups. Menopause age and body mass index were similar between groups ( > 0.05). There were no differences between resting BP, HR, or MSNA ( > 0.05). HR and BP reactivity were not different between SDG and non-SDG ( > 0.05). In contrast, MSNA reactivity had a more rapid increase in the first 30 s of the CPT in the SDG (burst incidence, Δ10.2 ± 14.8 bursts/100 hb) compared with the non-SDG (burst incidence, Δ4.0 ± 14.8 bursts/100 hb, time × group, = 0.011). Our results demonstrate a more rapid sympathetic neural reactivity to a CPT in postmenopausal females with perceived sleep disturbance, a finding that aligns with and advances recent evidence that sleep disturbance is associated with sympathetic neural hyperactivity in postmenopausal females. This is the first study to demonstrate that muscle sympathetic nerve activity (MSNA) to a cold pressor test is augmented in postmenopausal females with perceived sleep disturbance. The more rapid increase in MSNA reactivity during the cold pressor test in the sleep disturbance group was present despite similar increases in the perceived pain levels between groups. Baseline MSNA burst incidence and burst frequency, as well as blood pressure and heart rate, were similar between the sleep disturbance and nonsleep disturbance groups.
睡眠障碍是最常见的更年期症状之一，会导致自主神经功能紊乱，并与高血压和心血管风险相关。纵向研究表明，血压（BP）对应激源的高反应性可预测高血压的未来发展。经历睡眠障碍（SDG）的绝经后女性对应激源是否表现出更大的血流动力学和交感神经高反应性仍不清楚。我们假设，与没有睡眠障碍的绝经后女性（非SDG）相比，报告有睡眠障碍的绝经后女性对应激源会表现出血流动力学和交感反应性增加。55名绝经后女性（年龄62±4岁；SDG组n = 36；非SDG组n = 19）完成了两次研究访视。使用更年期特异性生活质量问卷（MENQOL）评估睡眠障碍的存在情况（MENQOL睡眠量表，≥2分）。在两组的10分钟基线期和2分钟应激源期（冷加压试验；CPT）期间，连续测量逐搏血压（手指体积描记法）、心率（HR；心电图）和肌肉交感神经活动（MSNA；微神经ography；SDG组n = 25；非SDG组n = 15）。两组间的绝经年龄和体重指数相似（P>0.05）。静息血压、心率或MSNA之间无差异（P>0.05）。SDG组和非SDG组之间的HR和BP反应性无差异（P>0.05）。相比之下，与非SDG组（爆发发生率，Δ4.0±14.8次爆发/100次心跳）相比，SDG组在CPT的前30秒内MSNA反应性增加更快（爆发发生率，Δ10.2±14.8次爆发/100次心跳，时间×组，P = 0.011）。我们的结果表明，有睡眠障碍的绝经后女性对CPT的交感神经反应性更快，这一发现与最近关于睡眠障碍与绝经后女性交感神经活动亢进相关的证据一致，并进一步证实了该证据。这是第一项证明有睡眠障碍的绝经后女性对冷加压试验的肌肉交感神经活动（MSNA）增强的研究。尽管两组之间感知疼痛水平的增加相似，但睡眠障碍组在冷加压试验期间MSNA反应性增加更快。睡眠障碍组和非睡眠障碍组之间的基线MSNA爆发发生率和爆发频率以及血压和心率相似。
