Nocturnal arousals are associated with endothelial dysfunction in individuals with high exposure to adverse childhood experiences

Gavin Power; Laura E Schwager; Kylee S. West; Manoela Lima Oliveira; Thomas W Hart; Junjie liu; Emily B. K. Thomas; Nathaniel D. M. Jenkins

doi:10.1152/physiol.2026.41.S1.2301581

Abstract only Background: Adverse childhood experiences (ACEs) are psychosocial stressors that occur during vulnerable developmental periods and are associated with sleep disturbances and increased cardiovascular disease risk in later life. Stress-related disruption of sleep may be characterized by changes in nocturnal arousals and autonomic function (e.g., cortical and autonomic arousals), despite intact sleep macroarchitecture (i.e., sleep stages). Thus, we hypothesized that prior ACE exposure would be associated with an increased frequency of nocturnal arousals and indices of nocturnal autonomic function, and that these would be negatively related to in vivo vascular endothelial function. Methods: We assessed endothelial function using the brachial artery flow-mediated dilation (FMD) technique followed by collection of 2 nights of at-home polysomnography recordings including a familiarization night in a cohort of otherwise healthy young adults (n=48; 39F/9M) with high (ACEsHIGH; ³4 ACEs, n=24) or low (ACEsLOW; 0-3 ACEs n=24) exposure to ACEs. Sleep macro- and microarchitecture (i.e., arousals) were automatically scored according to AASM guidelines using a validated algorithm. Results: FMD was lower in ACEsHIGH vs. ACEsLOW (6.0 ± 0.3% vs. 7.6 ± 0.6%, p=0.037). There were no observed differences in total sleep duration (6.1 ± 0.3 h vs 6.1 ± 0.3 h, p=0.863), efficiency (88.1 ± 5.6% vs. 87.2 ± 5.9%, p=0.496), nor any indices of macroarchitecture (e.g., Non-REM sleep1-3, REM sleep). Similarly, there were no differences in the frequency of cortical (12.7 ± 1.1 vs. 13.4 ± 1.3 arousals/h, p=0.698) or autonomic arousals (30.8 ± 2.4 vs. 31.5 ± 3.0 arousals/h, p=0.858) between ACEsHIGH and ACEsLOW. However, microarousal frequency (1.4 ± 0.2 vs. 0.9 ± 0.1 arousals/h, p=0.044), head movement arousal frequency (4.3 ± 0.5 vs. 3.1 ± 0.4, p=0.055), autonomic arousal frequency during non-REM sleep (30.1 ± 2.7 vs. 21.0 ± 2.0, p=0.024), and mean sleep heart rate (66 ± 2 vs. 60 ± 1 bpm, p=0.031) were elevated in ACEsHIGH vs. ACEsLOW. Autonomic arousals (r=-0.29, p=0.051) and sleep efficiency (r=-0.35, p=0.018) were negatively associated with FMD across the full sample, while mean nocturnal heart rate (r=-0.42, p=0.047) and head movement arousal frequency (r=-0.48, p=0.025) were negatively associated with FMD in ACEsLOW. Conclusions: These findings support the notion that individuals with prior ACE exposure demonstrate disrupted sleep microarchitecture and potential impairments in nocturnal autonomic function, which are associated with reduced endothelial function. These findings also have important implications for measurement and interpretation of stress-related sleep disruption, where traditionally reported sleep duration and quality (i.e., efficiency) metrics may lack sensitivity to detect meaningful, cardiovascular health-related differences in sleep architecture. This abstract was presented at the American Physiology Summit 2026 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.

Nocturnal arousals are associated with endothelial dysfunction in individuals with high exposure to adverse childhood experiences

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