Morning Sympathetic Nerve Activity After a Night of Binge Alcohol Consumption
Authors: Greenlund Ian M. , Cunningham Hannah A. , Tikkanen Anne L. , Durocher John J. , Smoot Carl A. , Carter Jason R. 
Published: April 2020

Epidemiological studies report a significant relationship between binge alcohol consumption and the incidence of hypertension and stroke. While sympathoexcitation is a suspected mechanism, this has not been definitively demonstrated. Acute consumption of alcohol has been shown to consistently activate the sympathetic nervous system, yet the impact of evening alcohol consumption on sympathetic activity the morning after consumption remains unknown. The purpose of the present study was to determine the impact of evening binge alcohol consumption on morning blood pressure and sympathetic neural activity. We hypothesized that blood pressure and neural activity would be augmented the morning after binge alcohol consumption. Using a randomized, crossover design, fifteen young adults (10 men, 5 women; 23±1 years, 27±1 kg/m2) were tested during both a binge alcohol condition and fluid control condition (one month apart). Participants arrived to the laboratory in the early evening for a standardized dinner and were instructed to relax in a semi‐recumbent position. Two beverages were administered to each participant over the course of two hours, designed to mimic an episode of binge drinking. Each alcohol dose was 1 g/kg or 0.85 g/kg in men and women, respectively (diluted in a 1:3 ratio with fruit juice), while fluid control was simply the fruit juice in similar volume. Participants were allotted 8 hours of polysomnography‐monitored sleep (data not included) prior to morning autonomic testing. Heart rate (HR), beat‐to‐beat blood pressure (NOVA, Finapres), and muscle sympathetic nerve activity (MSNA, microneurography) were recorded during a 10‐minute supine baseline and three 15‐second Valsalva maneuvers (VM). During VM, participants forcefully exhaled into a modified pressure manometer to 40 mmHg for 15 seconds and breathed normally during 1‐minute recovery period between each of the three VM strains. Statistical analysis included paired t‐tests across conditions (p<0.05). Baseline morning mean arterial pressure (81±2 vs. 80±2 mmHg) and MSNA (18±3 vs. 20±2 burst/min) were not different between alcohol and fluid control (p>0.05 for both). In contrast, HR was higher the morning after alcohol consumption compared to fluid control (64±3 vs. 59±2 beats/min, p=0.031). Increased sympathoexcitation (i.e. MSNA bursts/min) was exhibited during Phase II of VM strain after evening alcohol consumption when compared to fluid control (53±4 vs. 45±4 bursts/min, p=0.013). Cardiovagal baroreflex sensitivity (BRS) was assessed during Phase II and IV of VM strain, where phase II BRS was significantly blunted the morning after binge alcohol consumption (11±2 vs. 8±1 ms/mmHg, p=0.05). Phase IV BRS trended lower the morning after alcohol consumption (17±3 vs. 13±1 ms/mmHg, p=0.085). During Phase IV of the VM strain, systolic arterial pressure “overshoot” was augmented the morning after binge alcohol consumption compared to fluid control (Δ36±3 vs. Δ28±4 mmHg, p=0.021). These findings provide new mechanistic insight into the relation between binge drinking and cardiovascular disease.

Support or Funding Information

Support provided by the National Institutes of Health (R01 AA‐024892) and the Portage Health Foundation.