背景:最近的一项荟萃分析显示,在月经周期的黄体期,迷走神经介导的心率变异性(vmHRV;情绪调节能力的生物标志物)显著降低。正如两项后续研究表明的那样,这些vmHRV下降主要是由黄体孕酮(P4)增加所致.然而,分析还显示,vmHRV对循环的反应性存在显著的个体差异,这与长期证据一致,表明个体间对周期的情绪敏感性存在差异。本研究开始调查vmHRV周期性的这些个体间差异是否可以解释谁出现经前情绪变化的风险较高。我们预计黄体中期vmHRV降低的程度会更大,从而预示着负面影响的经前增加。
方法:我们对自然循环社区样本(N=31,M=26.03年)进行了观察性研究。在六个星期的时间里,参与者完成(a)负面情绪的每日评级和(b)在排卵中平衡实验室访问,黄体中期,和外围阶段。根据阳性排卵试验安排实验室访视,并包括基线vmHRV和唾液卵巢类固醇水平的评估。
结果:与先前的研究一致,多水平模型表明,大多数样本显示排卵至黄体中期vmHRV降低,然而,与经前情绪变化无关。有趣的是,只有vmHRV黄体增加的亚组,其负面影响在月经前明显恶化,而在月经后改善。
结论:本研究开始研究vmHRV的周期性变化,作为情绪对月经周期敏感性的潜在生物标志物。结果表明,这些关联的复杂性比最初预期的要高。鉴于vmHRV中只有非典型的黄体增加与更大的经前负面影响相关。讨论了潜在的潜在机制,其中黄体vmHRV可能会增加经前负面影响较大的患者调节情绪的指数补偿努力。然而,未来的研究应在这些发现的基础上,进一步探讨vmHRV周期性与经期相关情绪变化之间的关联.
BACKGROUND: A recent meta-analysis revealed that vagally mediated heart rate variability (vmHRV; a biomarker of emotion regulation capacity) significantly decreases in the luteal phase of the menstrual cycle. As two follow-up studies suggest, these vmHRV decreases are driven primarily by increased luteal progesterone (P4). However, analyses also revealed significant interindividual differences in vmHRV reactivity to the cycle, which is in line with longstanding evidence for interindividual differences in mood sensitivity to the cycle. The present study begins to investigate whether these interindividual differences in vmHRV cyclicity can explain who is at higher risk of showing premenstrual emotional changes. We expected a greater degree of midluteal vmHRV decrease to be predictive of a greater premenstrual increase in negative affect.
METHODS: We conducted an observational study with a naturally cycling community sample (N = 31, M = 26.03 years). Over a span of six weeks, participants completed (a) daily ratings of negative affect and (b) counterbalanced lab visits in their ovulatory, midluteal, and perimenstrual phases. Lab visits were scheduled based on positive ovulation tests and included assessments of baseline vmHRV and salivary ovarian steroid levels.
RESULTS: In line with previous research, multilevel models suggest that most of the sample shows ovulatory-to-midluteal vmHRV decreases which, however, were not associated with premenstrual emotional changes. Interestingly, it was only the subgroup with luteal increases in vmHRV whose negative affect markedly worsened premenstrually and improved postmenstrually.
CONCLUSIONS: The present study begins to investigate cyclical changes in vmHRV as a potential biomarker of mood sensitivity to the menstrual cycle. The results demonstrate a higher level of complexity in these associations than initially expected, given that only atypical midluteal increases in vmHRV are associated with greater premenstrual negative affect. Potential underlying mechanisms are discussed, among those the possibility that luteal vmHRV increases index compensatory efforts to regulate emotion in those with greater premenstrual negative affect. However, future studies with larger and clinical samples and more granular vmHRV assessments should build on these findings and further explore associations between vmHRV cyclicity and menstrually related mood changes.