In two separate experiments, sleep patterns of 17 young male adults were examined following single and repeated doses (0.9 g/kg body weight) of alcohol. A third study of 10 additional Ss measured the rate of elimination of alcohol from blood during sleep and waking. With a single dose of alcohol, onset of sleep was brisk, the latency of SW sleep (stages 3-1-4) was reduced and the first episode of stage REM was shortened. These transient alterations were accompanied by loss of high-frequency beta rhythms in the EEG and a gain in abundance and synchrony of activity in the alpha-rhythm range.
Experiment 3 found no significant difference between sleep and waking for rate of elimination of alcohol from blood. Starting with peak blood alcohol concentrations (BACs) of about 75 mg percent, average BACs after 4 h of bedtime had decreased to about 30 mg percent. The effects noted above, associated with higher BACs, were confined to the first half of the night. Thus, these results are consistent with conclusions of previous investigators that the depressant effects on EEG sleep patterns of a moderate dose of alcohol are due to its direct action on the brain.
There are, however, longer range compensation and adaptation effects associated with single and repeated doses of alcohol which cannot be directly related to its presence in the brain. For example, in the single-dose study reported here, and in most previous studies, rebound of stage REM occurred during the second half of the alcohol night. Further, in the repeated-dose study, most of the effects of alcohol on sleep stages and EEG frequencies observed during the first dose session, disappeared on the second and third alcohol sessions. Finally, heart and respiration rates increased whereas eye movements during stage REM, sigma spindles in stage 2 and non-specific GSR responses in SW sleep tended to be suppressed throughout the night in each alcohol session. Several mechanisms are discussed which might account for these more persistent alterations.