Alcohol alters sensory processing to respiratory stimuli in healthy men and women during wakefulness

Abstract

Study objectives: Alcohol can cause sleep-disordered breathing in healthy men, increase O2 desaturation in men who snore, and worsen obstructive sleep apnea (OSA) severity in men with OSA. These findings are less consistent among women, and the underlying mechanisms are incompletely understood. Respiratory-load sensory processing, which underpins upper-airway and respiratory responses to increased breathing load, is potentially impaired by alcohol. Using respiratory-related evoked potentials (RREPs) during wakefulness, this study aimed to test the hypothesis that alcohol impairs respiratory-load sensory processing and to explore potential sex differences.

Design: Within-subjects cross-over design in men versus women.

Setting: Sleep physiology laboratory.

Participants: Twenty healthy individuals (9 women) aged 18 to 38 years.

Interventions: Within each subject, RREP waveform components were generated by approximately 60 brief early-inspiratory negative-pressure pulses (-13 cm H2O mask pressure, 200 ms) before and after acute alcohol administration (1.5 mL/kg body weight). Choanal and epiglottic pressures were recorded to monitor stimulus magnitude and upper-airway resistance.

Measurements and results: The latency of several RREP waveform components increased after the administration of alcohol (deltaN1 = 11 +/- 5 ms, deltaN2 = 6 +/- 3 ms, deltaP3 = 26 +/- 10 ms), and P2 amplitude decreased (3.4 +/- 1.5 microV vs 1.2 +/- 0.8 microV). There were no changes in P1 latency or amplitude. During relaxed breathing, nasal resistance increased after alcohol ingestion (1.38 +/- 0.16 vs 1.86 +/- 0.18 cm H2O x l(-1) x s(-1)), but pharyngeal and supraglottic resistances remained unchanged. RREP waveform components and upper-airway resistance measures were not different in men versus women before or after alcohol ingestion.

Conclusions: These data demonstrate that alcohol alters sensory processing of respiratory neural information, but not early neural transmission (P1), to a similar extent in healthy men and women. Altered sensory processing to respiratory stimuli, as well as nasal congestion, may be important mechanisms contributing to alcohol-related sleep disordered breathing.

Figure 1

Schematic of the experimental protocol. B refers to baseline; NPP, negative-pressure pulses; Alcohol, 1.5 mL/kg (body weight) 100-proof vodka in orange juice; BAC, estimated blood alcohol concentration via Breathalyzer test.

Figure 2

Respiratory-related evoked potential (RREP) group-average waveforms and stimulus characteristics. P_mask refers to mask pressure, P_cho: choanal pressure, P_epi: epiglottic pressure before and after alcohol consumption. *Denotes a significant difference in the latency of a peak between conditions. ^†Indicates a significant difference in the amplitude of a peak between conditions.