Heart Rate Responsiveness to Anticipatory Stress is Elevated in Individuals with Stress-Induced Insomnia Susceptibility

Insomnia is a prevalent sleep disorder characterized by difficulty initiating or maintaining sleep, and negatively impacts cardiometabolic and cardiovascular health. Some individuals experience greater sleep disturbance following stress exposure, and this enhanced stress susceptibility is associated with the development of insomnia. However, the physiological mechanisms underlying this association remain unclear. The purpose of the present study was to evaluate cardiovascular responsiveness to anticipatory stress in individuals with elevated likelihood of developing stress-induced insomnia. We hypothesized that individuals with heightened stress-induced insomnia susceptibility would exhibit an exaggerated cardiovascular reactivity to acute laboratory stress. Fourty-three healthy individuals (22 male, 21 female; 21±4 yrs; 23±3 kg/m 2 ) participated in this study. Participants completed the Ford Insomnia Response to Stress Test (FIRST) which categorizes an individual’s likelihood to experience sleep disturbance following stress exposure. Higher FIRST scores indicate greater vulnerability to stress-induced sleep disturbance. During the laboratory session, participants’ heart rate (HR; electrocardiogram), beat-by-beat mean arterial pressure (MAP; finger plethysmography), and respiration (pneumobelt) were monitored. Cardiac output (CO) was estimated from the beat-by-beat arterial pressure waveform. Following a 10-minute, non-recorded baseline, all participants underwent 10 minutes of recorded autonomic and cardiovascular assessment. Participants then underwent the Trier Social Stress Test (TSST), which included a speech preparation (5min), speech (5min), and mental arithmetic (5min) task in front of two laboratory judges and a video recording. Elevated FIRST scores were positively correlated with HR reactivity to the speech preparation phase of the TSST (r=0.480, p=0.001). A significant association was also observed between estimated CO reactivity and FIRST scores during the speech prep phase (r=0.422, p=0.005). There was no association between FIRST scores and HR (Speech: r=0.258, p=0.095 Math: r=0.121, p=0.441) or CO (Speech: r=0.287, p=0.062, Math: r=0.168, p=0.282) reactivity during the other phases of the TSST. FIRST scores were not associated with MAP reactivity during the prep (r=0.029, p=0.855), speech (r=0.030, p=0.846) or math (r=-0.022, p=0.891) phases of the TSST. These findings indicate that a greater vulnerability to stress-induced sleep disruption was associated with augmented HR and CO reactivity during the anticipatory stress phase of the TSST. Exaggerated cardiac reactivity to anticipatory stress may partially explain the association between high FIRST scores and greater risk of insomnia development. Sleep Research Society Foundation This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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Journal
Physiology
Published
2025-05-01
DOI
https://doi.org/10.1152/physiol.2025.40.s1.1669
Primary Topic
Heart Rate Variability and Autonomic Control
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article
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article

Heart Rate Responsiveness to Anticipatory Stress is Elevated in Individuals with Stress-Induced Insomnia Susceptibility

Ankita Talukdar, Jason Carter, Jeremy A. Bigalke, Jennifer Bigalke et al.
Physiology
Heart Rate Variability and Autonomic Control
article

Heart Rate Responsiveness to Anticipatory Stress is Elevated in Individuals with Stress-Induced Insomnia Susceptibility

Ankita Talukdar, Jason Carter, Jeremy A. Bigalke, Jennifer Bigalke, Anna Murvich
article en

Abstract

Insomnia is a prevalent sleep disorder characterized by difficulty initiating or maintaining sleep, and negatively impacts cardiometabolic and cardiovascular health. Some individuals experience greater sleep disturbance following stress exposure, and this enhanced stress susceptibility is associated with the development of insomnia. However, the physiological mechanisms underlying this association remain unclear. The purpose of the present study was to evaluate cardiovascular responsiveness to anticipatory stress in individuals with elevated likelihood of developing stress-induced insomnia. We hypothesized that individuals with heightened stress-induced insomnia susceptibility would exhibit an exaggerated cardiovascular reactivity to acute laboratory stress. Fourty-three healthy individuals (22 male, 21 female; 21±4 yrs; 23±3 kg/m 2 ) participated in this study. Participants completed the Ford Insomnia Response to Stress Test (FIRST) which categorizes an individual’s likelihood to experience sleep disturbance following stress exposure. Higher FIRST scores indicate greater vulnerability to stress-induced sleep disturbance. During the laboratory session, participants’ heart rate (HR; electrocardiogram), beat-by-beat mean arterial pressure (MAP; finger plethysmography), and respiration (pneumobelt) were monitored. Cardiac output (CO) was estimated from the beat-by-beat arterial pressure waveform. Following a 10-minute, non-recorded baseline, all participants underwent 10 minutes of recorded autonomic and cardiovascular assessment. Participants then underwent the Trier Social Stress Test (TSST), which included a speech preparation (5min), speech (5min), and mental arithmetic (5min) task in front of two laboratory judges and a video recording. Elevated FIRST scores were positively correlated with HR reactivity to the speech preparation phase of the TSST (r=0.480, p=0.001). A significant association was also observed between estimated CO reactivity and FIRST scores during the speech prep phase (r=0.422, p=0.005). There was no association between FIRST scores and HR (Speech: r=0.258, p=0.095 Math: r=0.121, p=0.441) or CO (Speech: r=0.287, p=0.062, Math: r=0.168, p=0.282) reactivity during the other phases of the TSST. FIRST scores were not associated with MAP reactivity during the prep (r=0.029, p=0.855), speech (r=0.030, p=0.846) or math (r=-0.022, p=0.891) phases of the TSST. These findings indicate that a greater vulnerability to stress-induced sleep disruption was associated with augmented HR and CO reactivity during the anticipatory stress phase of the TSST. Exaggerated cardiac reactivity to anticipatory stress may partially explain the association between high FIRST scores and greater risk of insomnia development. Sleep Research Society Foundation This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

PhysiologyVol. 40(S1)
Baylor University (US)
Openalex Percentile: Top 73%
Heart Rate Variability and Autonomic Control
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