Department of Health, Human Performance, and Recreation, Baylor University, Waco, TX (J.A.B., T.X.S.-M., J.R.C.).
Department of Kinesiology and Integrative Physiology, Michigan Technological University, Houghton, MI (J.A.B., I.M.G., J.R.C.).
Hypertension. 2024 Oct;81(10):2140-2151. doi: 10.1161/HYPERTENSIONAHA.124.23416. Epub 2024 Aug 9.
Alcohol consumption is associated with cardiovascular disease, and the sympathetic nervous system is a suspected mediator. The present study investigated sympathetic transduction of muscle sympathetic nerve activity to blood pressure at rest and in response to cold pressor test following evening binge alcohol or fluid control, with the hypothesis that sympathetic transduction would be elevated the morning after binge alcohol consumption.
Using a randomized, fluid-controlled (FC) crossover design, 26 healthy adults (12 male, 14 female, 25±6 years, 27±4 kg/m) received an evening binge alcohol dose and a FC. All participants underwent next-morning autonomic-cardiovascular testing consisting of muscle sympathetic nerve activity, beat-to-beat blood pressure, and heart rate during a 10-minute rest period and a 2-minute cold pressor test. Sympathetic transduction was assessed at rest and during the cold pressor test in both experimental conditions.
Evening alcohol increased heart rate (FC: 60±9 versus alcohol: 64±9 bpm; =0.010) but did not alter resting mean arterial pressure (FC: 80±6 versus alcohol: 80±7 mm Hg; =0.857) or muscle sympathetic nerve activity (FC: 18±9 versus alcohol: 20±8 bursts/min; =0.283). Sympathetic transduction to mean arterial pressure (time×condition; =0.003), diastolic blood pressure (time×condition; =0.010), and total vascular conductance (time×condition; =0.004) was augmented after alcohol at rest. Sympathetic transduction during the cold pressor test was also elevated after evening binge alcohol consumption (=0.002).
These findings suggest that evening binge alcohol consumption leads to augmented morning-after sympathetic transduction of muscle sympathetic nerve activity to blood pressure, highlighting a new mechanism whereby chronic or excessive alcohol consumption contributes to cardiovascular disease progression via altered end-organ responsiveness to sympathetic neural outflow.
URL: https://clinicaltrials.gov/study/NCT03567434; Unique identifier: NCT03567434.
饮酒与心血管疾病有关,而交感神经系统是一个可疑的中介。本研究旨在调查在夜间 binge 饮酒或液体控制后,静息时和冷加压试验(CPP)期间,肌肉交感神经活动向血压的交感神经传递情况,假设 binge 饮酒后第二天早上交感神经传递会增加。
使用随机、液体控制(FC)交叉设计,26 名健康成年人(12 名男性,14 名女性,25±6 岁,27±4 kg/m)接受了夜间 binge 饮酒剂量和 FC。所有参与者在第二天早上进行自主心血管测试,包括肌肉交感神经活动、逐搏血压和心率,持续 10 分钟的休息期和 2 分钟的冷加压试验。在两种实验条件下,在休息时和冷加压试验期间评估交感神经传递。
夜间饮酒增加了心率(FC:60±9 比酒精:64±9 bpm;=0.010),但不改变静息平均动脉压(FC:80±6 比酒精:80±7 mmHg;=0.857)或肌肉交感神经活动(FC:18±9 比酒精:20±8 爆发/分钟;=0.283)。平均动脉压(时间×条件;=0.003)、舒张压(时间×条件;=0.010)和总血管传导率(时间×条件;=0.004)在静息时的交感神经传递在饮酒后增加。夜间 binge 饮酒后,冷加压试验期间的交感神经传递也升高(=0.002)。
这些发现表明,夜间 binge 饮酒会导致肌肉交感神经活动向血压的交感神经传递在第二天早上增加,这突显了一种新的机制,即慢性或过量饮酒通过改变终末器官对交感神经输出的反应,促进心血管疾病的进展。
网址:https://clinicaltrials.gov/study/NCT03567434;独特标识符:NCT03567434。