Gloger Elana M, Hong Joanna H, Mogle Jacqueline, Almeida David M, Greaney Jody L
Department of Human Development and Family Studies, The Pennsylvania State University, University Park, Pennsylvania, United States.
Center for Healthy Aging, The Pennsylvania State University, University Park, Pennsylvania, United States.
J Appl Physiol (1985). 2025 May 1;138(5):1251-1260. doi: 10.1152/japplphysiol.00886.2024. Epub 2025 Apr 29.
Despite mounting evidence that greater affective responsivity to naturally occurring daily stressors is associated with increased risk of cardiovascular diseases (CVDs), few studies have examined dysregulation of the sympathetic nervous system as a potential mechanism. We hypothesized that greater affective responsivity to daily stressful events would be related to increased urinary catecholamine excretion. Daily stress processes (8-day daily diary) were assessed in 715 middle-aged adults (56 ± 11 yr; 57% female) from the Midlife in the United States Study. Urinary norepinephrine and epinephrine concentrations were also measured (24 h; normalized to creatinine). Multilevel modeling was used to calculate negative and positive affective responsivity (i.e., the slope of the within-person differences in negative and positive affect on stressor days compared with stressor-free days). Analyses controlled for relevant covariates (e.g., sex, age, affect on stressor-free days, etc.). On stressor days, negative affect increased (0.1 ± 0.2 stressor-free days vs. 0.3 ± 0.4 au stressor days; < 0.0001) and positive affect decreased (2.8 ± 0.7 stressor-free days vs. 2.6 ± 0.8 au stressor days; < 0.0001). Greater negative affectivity responsivity to daily stressors was related to increased urinary norepinephrine ( = 0.42, SE = 0.14, = 0.003), but not epinephrine ( = 0.142), excretion. Positive affective responsivity to daily stressors was not related to either urinary norepinephrine ( = -0.33, SE = 0.29, = 0.24) or epinephrine ( = 0.626) excretion. Heightened negative affective responsivity to daily stressors was associated with greater urinary norepinephrine excretion, suggesting that sympathetic overactivation may contribute to the link between emotional vulnerability to daily stressors and increased CVD risk. Few studies have examined sympathetic dysregulation as a potential mechanism linking affective responsivity to daily stressors to future cardiovascular diseases. Using a large national sample, our findings show that amplified negative affective responsivity to daily stressors is related to increased urinary norepinephrine excretion independent of the frequency of stressor occurrence. These data suggest that chronic sympathetic overactivation may contribute to the link between emotional vulnerability to daily stressors and increased risk of future cardiovascular comorbidities.
尽管越来越多的证据表明,对自然发生的日常压力源有更强的情感反应性与心血管疾病(CVD)风险增加有关,但很少有研究将交感神经系统失调作为一种潜在机制进行研究。我们假设,对日常压力事件有更强的情感反应性与尿儿茶酚胺排泄增加有关。对来自美国中年研究的715名中年成年人(56±11岁;57%为女性)进行了日常压力过程(为期8天的每日日记)评估。还测量了24小时尿去甲肾上腺素和肾上腺素浓度(以肌酐标准化)。使用多层次模型计算消极和积极情感反应性(即与无压力源日相比,压力源日消极和积极情绪的个体内差异斜率)。分析控制了相关协变量(如性别、年龄、无压力源日的情绪等)。在压力源日,消极情绪增加(无压力源日为0.1±0.2,压力源日为0.3±0.4;<0.0001),积极情绪减少(无压力源日为2.8±0.7,压力源日为2.6±0.8;<0.0001)。对日常压力源更强的消极情感反应性与尿去甲肾上腺素排泄增加有关(β = 0.42,标准误 = 0.14,P = 0.003),但与肾上腺素排泄无关(β = 0.142)。对日常压力源的积极情感反应性与尿去甲肾上腺素(β = -0.33,标准误 = 0.29,P = 0.24)或肾上腺素(β = 0.626)排泄均无关。对日常压力源增强的消极情感反应性与更高的尿去甲肾上腺素排泄有关,这表明交感神经的过度激活可能有助于解释对日常压力源的情绪易感性与CVD风险增加之间的联系。很少有研究将交感神经失调作为一种潜在机制,来研究对日常压力源的情感反应性与未来心血管疾病之间的联系。通过一个大型全国样本,我们的研究结果表明,对日常压力源增强的消极情感反应性与尿去甲肾上腺素排泄增加有关,且与压力源发生频率无关。这些数据表明,慢性交感神经过度激活可能有助于解释对日常压力源的情绪易感性与未来心血管合并症风险增加之间的联系。