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Evening Binge Alcohol Disrupts Cardiovagal Tone and Baroreflex Function During Polysomnographic Sleep Stages
Abstract   Open access   Peer reviewed

Evening Binge Alcohol Disrupts Cardiovagal Tone and Baroreflex Function During Polysomnographic Sleep Stages

Ian Greenlund, Jeremy Bigalke, Anne Tikkanen, Carl Smoot, John Durocher and Jason Carter
The FASEB journal, Vol.35(S1)
05/2021
DOI: 10.1096/fasebj.2021.35.S1.02390
url
https://doi.org/10.1096/fasebj.2021.35.S1.02390View
Published (Version of record) Open Access

Abstract

Abstract only Evening alcohol consumption has been shown to attenuate nocturnal cardiovagal baroreflex sensitivity (cvBRS) and vagal tone, but the impact of alcohol on cvBRS during specific polysomnographic sleep stages remains unclear. We hypothesized that binge alcohol consumption would decrease nocturnal cardiovagal tone and cvBRS, particularly during slow wave (SWS) and rapid eye movement (REM) sleep due to their reported impact on cardiovascular health. Sixteen volunteers (9 women, 7 men; 25±1 years; 28±1 kg/m 2 ) participated in this study. Utilizing a randomized, crossover design, participants arrived to the laboratory for two testing nights (alcohol vs. fluid control) separated by one month. The alcohol condition simulated a binge drinking episode by consuming a 4‐5 drink equivalent within two hours. The alcohol dose was based on National Institute of Alcohol Abuse & Alcoholism (NIAAA) definitions of binge drinking, which includes differences based upon body weight and sex (1g/kg men, 0.85g/kg women). Overnight polysomnography (Natus, Middleton, WI), two‐lead electrocardiogram (ECG), and dual‐finger plethysmography (Finapres NOVA, Netherlands) were recorded during an 8‐hour in‐laboratory sleep acquisition period. The nocturnal ECG and continuous blood pressure signals were imported into custom software (WinCPRS, Absolute Aliens, Finland) for heart rate variability (HRV) and cvBRS analyses. A ten‐minute period of stable sleep was selected in each participant for each sleep stage, and was verified by a board‐certified sleep physician. Each segment of stable sleep was free of any scorable arousal, apneic event, and limb movement. Cardiovagal activity was assessed via fast‐Fourier transform and quantified as high frequency (HF; 0.15‐0.4 Hz), and cvBRS was assessed using up‐up (vagal activation) and down‐down (vagal withdrawal) sequence analyses. Evening binge alcohol consumption reduced HF during SWS (1429±279 vs. 698±146 ms 2 , p>0.001) and REM (1114±238 vs. 599±151 ms 2 , p=0.022), but not stage II (1619±453 vs. 901±258 ms 2 , p=0.137). Evening binge alcohol consumption decreased cvBRS during stage II (up‐up, 21±3 vs. 15±3 ms/mmHg, p=0.035; down‐down, 23±2 vs. 14±2 ms/mmHg, p=0.001) and REM sleep (up‐up, 21±4 vs. 15±3 ms/mmHg, p=0.008; down‐down, 19±3 vs. 12±2 ms/mmHg, p=0.008), but did not alter cvBRS during SWS (up‐up, 21±3 vs. 15±3 ms/mmHg, p=0.224; down‐down, 22±2 vs. 17±4 ms/mmHg, p=0.225). Taken together, our results indicate that the deleterious cardiovascular effects of binge alcohol consumption may be present across multiple sleep stages, but particularly during stable REM sleep.

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