ACUTE SLEEP REDUCTION NORMALLY CAUSES A HO- MEOSTATIC RESPONSE DURING THE NEXT SLEEP OP- PORTUNITY, CHARACTERIZED BY INCREASED amounts

217 ACUTE SLEEP REDUCTION NORMALLY CAUSES A HOMEOSTATIC RESPONSE DURING THE NEXT SLEEP OPPORTUNITY, CHARACTERIZED BY INCREASED amounts of stage 3 and 4 (slow wave sleep [SWS])1,2 This increase occurs at the expense of REM sleep, stage 2 sleep, stage 1 sleep, and stage wake. The latter study also showed that spectral power density in the 0.5–8 Hz range increased but was most pronounced in the 0.5–4 Hz band, called “delta power.” However, repeated partial sleep restriction does not seem to cause the same homeostatic response of SWS or of delta activity. Thus, Webb and Agnew3 found that stage 4 sleep was maintained at baseline levels for 8 days with 3 h of sleep, while all other stages were reduced. Values returned to baseline on the first recovery night. Carskadon and Dement4 found similar results for 5 h/night across 7 days, except for an increase in REM sleep during recovery sleep. The same lack of SWS response was reported by Brunner et al.5 for 4 days of 4 h sleep, but total sleep time (TST), REM, SWS, and delta power (during the first 4 h of sleep) were increased for 2 days of recovery sleep. Interestingly, though, the span of 1/4 Hz bands with increased spectral power increased beyond the 0.5–4 Hz band during partial sleep deprivation (PSD) nights, suggesting a compensation for the partial sleep deprivation. In a study across 14 days, Van Dongen et al.6 showed that a reduction to 6 or 4 h of sleep per day caused a reduction on the first restricted night of summed NREM power in the 0.5–4 Hz band, TST, and all sleep stages except SWS. The changes across the days with sleep restriction were marginal and mostly nonsignificant, but REM latency decreased by 2.2 min/day in the 4-h condition, and SWS increased marginally. Similar observations (mainly lack of significant change in SWS across the experiment) were made across 7 days with 5 h sleep.7 Recovery was apparently complete on the first recovery night, since no difference from baseline was seen. In rodents Kim et al.8 showed an increase of NREM sleep during the first PSD sleep (of 4 h of sleep/day), but this was followed by a decrease of NREM and delta power during the subsequent 3 days. During recovery sleep, NREM did not respond during the first day, whereas delta power increased. During the next day, delta power actually decreased. The discrepancy between the homeostatic response of SWS delta power after acute sleep loss and that during repeated partial sleep loss is puzzling in view of the homeostatic response after acute sleep reduction, but it may reflect a basic property of sleep. However, it could also be due to a lack of depth of analysis—the previous studies did not focus on the dynamics of sleep architecture. It might, for example, be fruitful to examine a wider part of the EEG spectrum. It might also help to focus attention on the smallest common TST denominator (≈4 h), since modest responses may be lost when the entire sleep period is used for analysis. The purpose of the present study was, therefore, to emphasize the previous 2 points in a study of the effects of partial sleep deprivation (4 h/night) across 5 days, followed by 3 days of recovery sleep (8 h in bed), on sleep polysomnography and EEG spectral content. The design of the study was an attempt to reflect the working week, with cumulative sleep restriction and subsequent recovery during the weekend. The main finding to come out of this study was a clear homeostatic response in EEG power from 1.25 to 7.25 Hz (summed across each sleep) during the nights of partial sleep deprivation, as well a clear homeostatic recovery during the first night of recovery sleep. Sleep HomeoStaSiS during Sleep reStriction and recovery