The increase in longitudinally measured sleepiness across adolescence is related to the maturational decline in low-frequency EEG power.

DECLINING SLEEP DURATION IS COMMONLY CITED AS THE REASON THAT DAYTIME SLEEPINESS EMERGES IN ADOLESCENTS (C.F. 1), I.E., ADOLESCENTS ARE BECOMING sleepy because they are becoming sleep deprived. It is certainly the case that sleep schedules change dramatically with age across adolescence. Compared to younger children, adolescents delay their bedtimes but wake up as early or earlier due to school schedules. This pattern is widespread in developed nations.2–11 It results in reduced time in bed and sleep duration. Actigraphy and polysomnography studies have documented reductions of about 1 hour in total sleep duration on school days across adolescence (reviewed in 12). However, there is evidence that declining sleep duration is not the sole factor responsible for the development of daytime sleepiness in adolescence. In a study that fixed time in bed at 10 hours for both adolescents and preadolescents, adolescents had total sleep times as long as those of preadolescents but still had shorter sleep latencies in Multiple Sleep Latency Tests (MSLT), indicating increased sleepiness.13 Thus, adolescents had greater daytime sleepiness without decreased nocturnal sleep duration. This study indicates that some maturational factor must also play a role in the development of adolescent daytime sleepiness. This maturational factor could be a change in circadian or homeostatic regulation or a separate brain maturational change that reduces daytime arousal levels. In addition to changes in sleep schedule, sleep duration, and daytime sleepiness, the sleep electroencephalogram (EEG) undergoes dramatic developmental changes during adolescence. The most well-described adolescent EEG change is a steep decline in non-rapid eye movement (NREM) slow-wave EEG (delta) activity.14, 15 We have proposed that this decline is one component of a widespread brain maturational process driven by synaptic pruning.15,16 According to our model, declining synaptic connectivity decreases the intensity of waking brain activity and, therefore, cerebral metabolic rate. It is now becoming recognized that the need for the sleep-dependent recuperation depends not only on waking duration, but also on the intensity of waking brain activity.17,18 A decrease in the intensity of waking neuronal activity should reduce the need for the recuperative processes of sleep and thus reduce the NREM delta intensity. We recently reported that delta EEG activity is constant between ages 9 and 11 years but declines steeply between ages 12 and 14 years.19 Another prominent change of adolescence is pubertal development and the associated hormonal changes driven by reactivation of gonadotropin-releasing hormone secretion.20 We found that the delta EEG decline between ages 12 and 14 is strongly related to age but is independent of pubertal development.19 Here we hypothesize that increasing daytime sleepiness is related to this decline in slow-wave EEG. Prior to adolescence, nocturnal sleep is very deep, waking brain activity (metabolic rate21) is very intense, and daytime sleepiness is normally absent. As the intensity of waking brain activity diminishes across adolescence, daytime sleepiness emerges. If our hypothesis is correct, daytime sleepiness in adolescents should be related to the decline in NREM delta power. Thus, we propose that sleep-schedule changes and brain maturational processes independently contribute to the development of daytime sleepiness. Most previous studies on adolescent sleep have been cross-sectional. Longitudinal studies can more effectively determine how the development of sleepiness relates to changes in other variables. Thus the main goal of this study is to use longitudinal data to test the hypothesis that increasing sleepiness in adolescence is related to declining delta EEG independently of sleep-schedule changes. We also describe longitudinally measured changes, from ages 9 to 12 and 12 to 15 years, in the following variables: subjective daytime sleepiness, sleep schedule, sleep duration, and slow-wave EEG power.