Morning sympathetic activity after evening binge alcohol consumption

Abstract

Binge alcohol consumption elicits acute and robust increases of muscle sympathetic nerve activity (MSNA), yet the impact of evening binge drinking on morning-after MSNA is unknown. The present study examined the effects of evening binge alcohol consumption on polysomnographic sleep and morning-after MSNA. We hypothesized that evening binge drinking (i.e. 4-5 drink equivalent in <2 h) would reduce sleep quality and increase morning-after blood pressure (BP) and MSNA. Following a familiarization night within the sleep laboratory, 22 participants (12 men, 10 women; 25 ± 1 yr) were examined after simulated binge drinking or fluid control (randomized, crossover design). Morning MSNA was successfully recorded across both conditions in 16 participants (8 men, 8 women) during a 10-min baseline and three Valsalva's maneuvers (VM). Binge drinking reduced rapid eye movement (REM) sleep (15 ± 1 vs. 20 ± 1%, P = 0.003), increased stage II sleep (54 ± 1 vs. 51 ± 1%, P = 0.002), and increased total urine output (2.9 ± 0.2 vs. 2.1 ± 0.1 liters, P < 0.001) but did not alter morning-after urine specific gravity. Binge drinking increased morning-after heart rate [65 (54-72) vs. 58 (51-67) beats/min, P = 0.013] but not resting BP or MSNA. Binge drinking elicited greater sympathoexcitation during VM (38 ± 3 vs. 43 ± 3 bursts/min, P = 0.036). Binge drinking augmented heart rate (P = 0.002), systolic BP (P = 0.022), and diastolic BP (P = 0.037) reactivity to VM phase IV and blunted cardiovagal baroreflex sensitivity during VM phases II (P = 0.028) and IV (P = 0.043). In conclusion, evening binge alcohol consumption disrupted REM sleep and morning-after autonomic function. These findings provide new mechanistic insight into the potential role of binge drinking on cardiovascular risk.NEW & NOTEWORTHY Chronic binge alcohol consumption is associated with future cardiovascular disease (CVD) risk in both men and women. In addition, binge alcohol consumption is known to disrupt normal sleep quality during the early morning hours, coinciding with the morning sympathetic surge. In the present study, an evening of binge alcohol consumption increased baseline morning heart rate and cardiovascular reactivity during the Valsalva maneuver (VM) strain. Specifically, muscle sympathetic nerve activity and phase IV hemodynamic responses increased during VM the morning after binge alcohol consumption. The autonomic dysfunction and increased cardiovascular reactivity during VM suggests a contributing mechanism to CVD risk present in individuals who binge drink.

Keywords: autonomic activity; baroreflex sensitivity; ethanol; hypertension; sleep.

Figure 1.

Tracings of heart rate, blood pressure, and muscle sympathetic nerve activity during the 15-s Valsalva’s maneuver (VM) for 1 representative participant following fluid control (A) and binge alcohol dose (B). Phase II of VM is outlined with a dashed line, which constitutes the first blood pressure decrease from strain onset to strain termination. Phase IV of VM is represented with a solid line and begins with the first blood pressure increase after strain termination to first blood pressure decrease during blood pressure overshoot.

Figure 2.

Experimental design of the present study consisting of familiarization (FAM) night and two testing protocols where binge alcohol or fluid control were provided. A 1-mo interval was allotted between each laboratory visit.

Figure 3.

Morning muscle sympathetic nerve activity (MSNA) during a 15-s Valsalva maneuver (VM) after fluid control and evening binge alcohol consumption. MSNA burst frequency (P = 0.036), but not burst incidence (P = 0.447), was elevated following binge alcohol consumption during VM. *P < 0.05 between conditions via paired-samples t tests between alcohol and fluid control.

Figure 4.

Changes in heart rate (HR), systolic arterial pressure (SAP), and diastolic arterial pressure (DAP) during phase II and IV of Valsalva’s maneuver (VM). Increases in HR during VM were augmented during both phase II (P = 0.018) and IV (P = 0.002) after evening binge alcohol consumption. Phase II SAP and DAP drop (expressed as absolute changes for visual purposes) were not different between conditions (P = 0.059 and 0.301, respectively). Morning SAP (P = 0.022) and DAP (P = 0.037) “overshoot” during phase IV VM were augmented following binge alcohol consumption. *P < 0.05 between conditions via paired-samples t tests between alcohol and fluid control.

Figure 5.

Cardiovagal baroreflex sensitivity (cvBRS) during phase II and IV of Valsalva’s maneuver (VM). cvBRS during phase II (P = 0.028) and IV (P = 0.043) of VM were significantly blunted the morning after binge alcohol consumption. *P < 0.05 between conditions via paired-samples t tests between alcohol and fluid control.