0194 Impact of Sleep Deprivation Combined with Alcohol or Oxycodone on Sleep Architecture in Healthy Young Adults

Abstract Introduction Alcohol and opioids disturb sleep, but the impact of substance use on recovery sleep after sleep deprivation is largely unknown. Here we piloted a study protocol to assess the combined impact of total sleep deprivation (TSD) and substance administration on recovery sleep. Methods N=6 healthy normal sleepers (ages 28.2±5.6y; 4 males) completed two 24h laboratory study sessions. During each session, which began at 15:00, participants were kept awake for 15h until 06:00 the next day. They were then given an 8h recovery sleep opportunity (06:00–14:00) and went home. During the second study session, participants were randomly assigned to receive alcohol (n=3; peak BAC of 0.043±0.008% at 00:55, decayed to zero by 06:00) or an opioid (n=3; 10mg oxycodone administered at 22:30). Recovery sleep was recorded polysomnographically and scored using AASM criteria; analyses focused on total sleep time (TST), sleep efficiency, sleep latency, sleep stages N1–N3 and REM, and latency to each of the sleep stages. Results Session 1 (pre-substance) TST was considerably shorter in the opioid group (282±28min) than the alcohol group (403±24min). Therefore, we analyzed sleep variables for the two groups separately, using mixed-effects ANOVA with a fixed effect for study session (TSD vs. TSD+drug) and a random effect over subjects on the intercept. For the opioid group, latency to N3 sleep was significantly longer by 10±2min after opioid administration compared to TSD alone (F=33.8, p=0.028). There were no significant effects of TSD+alcohol compared to TSD alone. Conclusion Opioid administration during TSD delayed N3 onset, but no other effects of opioid or alcohol administration were seen during recovery sleep. Our sample was small, but the within-subjects study design provided considerable statistical power – substance effects on neurobehavioral performance during TSD (reported elsewhere) were readily detectable. However, BAC at the onset of recovery sleep had decayed to zero, and elevated homeostatic sleep pressure from TSD may have negated any residual substance effects other than the opioid-induced delay in N3. Investigating the impact of substances on recovery sleep after TSD, as well as post-recovery neurobehavioral functioning, is important for safety and health in today’s sleep-deprived society. Support (if any) National Safety Council