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Association Between Short Sleep Duration and Increased Cardiovascular Reactivity to Nocturnal Arousal
Abstract   Open access   Peer reviewed

Association Between Short Sleep Duration and Increased Cardiovascular Reactivity to Nocturnal Arousal

Jeremy Bigalke, Ian Greenlund, Jennifer Nicevski, Neha John-Henderson and Jason Carter
The FASEB journal, Vol.35(S1), p.n/a
05/2021
DOI: 10.1096/fasebj.2021.35.S1.02387
url
https://doi.org/10.1096/fasebj.2021.35.S1.02387View
Published (Version of record) Open Access

Abstract

Abstract only Reduced habitual total sleep time (TST) is associated with an increased prevalence of hypertension, coronary heart disease, and other cardiovascular complications. Nocturnal arousal intensity, assessed by overnight polysomnography (PSG), and its subsequent impact on nocturnal heart rate (HR) reactivity have been implicated as a potential link between arousal strength and heightened cardiovascular strain. Despite evidence of a positive relationship between nocturnal arousal intensity and heart rate reactivity, little research has established if habitual sleep parameters are associated with these associations. The purpose of the present study was to examine the relationship between objectively measured TST and HR responsiveness to nocturnal arousal in stage 2 (N2) and stage 3 (N3) sleep. We hypothesized that short objective TST would be associated with an augmented HR reactivity to arousals in both N2 and N3 sleep. Habitual TST was measured in 17 adults (10 men, 7 women; 33±4 years; 26±1 kg/m 2 ) using actigraphy monitoring over a duration of 7‐14 days (mean, 13±1 days). On a separate occasion, participants underwent a full night of PSG testing, in addition to continuous HR recording (electrocardiogram) throughout the sleep period. Arousals were scored by a certified PSG technician, and verified by a board‐certified sleep physician following American Academy of Sleep Medicine guidelines. Peak HR response to arousal was determined as the highest HR measured within 20 seconds following an arousal onset, while the peak change was identified as the post‐arousal peak HR minus the average HR taken from 10 cardiac cycles prior to the arousal. Bivariate correlations were utilized to compare associations between the two parameters. The number of arousals varied from 4 ‐ 47 (mean, 19±3 arousals) during N2 sleep, and 0 – 9 (mean, 4±1 arousals) during N3 sleep. There were no associations between habitual, actigraphy‐based TST and number of arousals in either sleep stage (P > 0.05). Similarly, there were no significant correlations between pre‐arousal HR and TST in either N2 or N3 sleep (P > 0.05). However, our results demonstrated a significant negative correlation between TST and both peak HR reactivity (R = ‐0.490, P < 0.05) and absolute change in peak HR (R = ‐0.487, P < 0.05) following arousals during N2 sleep. Similarly, peak HR (R = ‐0.542, P < 0.05) and change in peak HR (R = ‐0.577, P < 0.05) after arousals were significantly associated with habitual TST during N3 sleep. Our results indicate a relationship between poor sleep duration and heightened cardiovascular reactivity to nocturnal arousal during both N2 and N3 sleep. These findings suggest that short sleep duration and dysregulated HR reactivity may be underlying mechanisms propagating impaired cardiovascular functioning in chronically sleep restricted individuals. Further research is necessary to fully elucidate the direction of this relationship.

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