Influence of acute alcohol ingestion on sympathetic neural responses to orthostatic stress in humans

Abstract

Acute alcohol consumption is reported to decrease mean arterial pressure (MAP) during orthostatic challenge, a response that may contribute to alcohol-mediated syncope. Muscle sympathetic nerve activity (MSNA) increases during orthostatic stress to help maintain MAP, yet the effects of alcohol on MSNA responses during orthostatic stress have not been determined. We hypothesized that alcohol ingestion would blunt arterial blood pressure and MSNA responses to lower body negative pressure (LBNP). MAP, MSNA, and heart rate (HR) were recorded during progressive LBNP (-5, -10, -15, -20, -30, and -40 mmHg; 3 min/stage) in 30 subjects (age 24 ± 1 yr). After an initial progressive LBNP (pretreatment), subjects consumed either alcohol (0.8 g ethanol/kg body mass; n = 15) or placebo (n = 15), and progressive LBNP was repeated (posttreatment). Alcohol increased resting HR (59 ± 2 to 65 ± 2 beats/min, P < 0.05), MSNA (13 ± 3 to 19 ± 4 bursts/min, P < 0.05), and MSNA burst latency (1,313 ± 16 to 1,350 ± 17 ms, P < 0.05) compared with placebo (group × treatment interactions, P < 0.05). During progressive LBNP, a pronounced decrease in MAP was observed after alcohol but not placebo (group × time × treatment, P < 0.05). In contrast, MSNA and HR increased during all LBNP protocols, but there were no differences between trials or groups. However, alcohol altered MSNA burst latency response to progressive LBNP. In conclusion, the lack of MSNA adjustment to a larger drop in arterial blood pressure during progressive LBNP, coupled with altered sympathetic burst latency responses, suggests that alcohol blunts MSNA responses to orthostatic stress.

Fig. 1.

Changes in systolic (SAP), diastolic (DAP), and mean (MAP) arterial pressures and heart rate (HR) during progressive lower body negative pressure (LBNP). Alcohol attenuated SAP, DAP, and MAP responses to progressive LBNP (all group × time × treatment interactions, P < 0.05) but did not alter HR responses (group × time × treatment interaction, P > 0.05). A significant time effect (P < 0.05) demonstrated increases in HR and decreases in SAP for each treatment in both groups. *P < 0.05 vs. corresponding post-alcohol value.

Fig. 2.

Changes in muscle sympathetic nerve activity (MSNA) quantified as bursts/min, bursts/100 heart beats (100HB), and total MSNA during progressive LBNP. Progressive LBNP elicited similar increases of MSNA during both treatments (pre- vs. posttreatment) and groups (alcohol vs. placebo). Group × time × treatment interactions were P > 0.05 for all MSNA variables, whereas the time effect was P < 0.001 for each treatment in both groups. AU, arbitrary units.

Fig. 3.

Changes in MSNA burst latency during progressive LBNP before and after alcohol (n = 9) or placebo (n = 8). Burst latency responses to progressive LBNP were altered by alcohol but not placebo (group × time × treatment interaction, P < 0.01). *P < 0.05 vs. corresponding post-alcohol value.

Fig. 4.

Changes in forearm blood flow (FBF), forearm vascular resistance (FVR), and forearm vascular conductance (FVC) during progressive LBNP. Increases in FVR were significantly blunted by alcohol (group × time × treatment, P < 0.05). Group × time × treatment interactions were P > 0.05 for both FBF and FVC, whereas the time effect was P < 0.01 for each treatment in both groups. *P < 0.05 vs. corresponding post-alcohol value.