Is the nap zone controlled by a light-sensitive circadian arousal process?

Abstract

This study attempts to identify the mechanism of the so-called afternoon nap zone. More specifically, it investigates a recent proposal that the afternoon nap zone represents the point in time after morning awakening when process-S has increased to a sufficiently high level to facilitate sleep onset, while at the same time an SCN-controlled circadian arousal process has not yet risen high enough to reverse this increased sleepiness. Eight normal male subjects aged 20--30 years, were monitored on two separate occasions under low ambient light (150 lux). Night sleep hours were maintained at 23:00--06:00h. PSG monitoring included EEG (C3-A2, O2-A1), right EOG-M1, left EOG-M2, submental EMG and core body temperature recorded continuously by a combination of the Oxford Medilog 9000 8-channel ambulatory recorder and the Minilogger temperature monitoring system. Following a baseline 24-hour day, bright light stimulation (10,000 lux) was given on two consecutive days either in the evening (20:00--22:00h) or morning (06:00--08:00h) in counter-balanced fashion with a 30 day washout periods between. Other than during a period of bright light stimulation, the level of daytime arousal was assessed every 60 min by quantified EEG spectral power followed by a 10 min duration simple reaction time test. In the baseline condition both the performance and Q-EEG variables confirmed the presence of a transitory afternoon nap zone as indexed by the timing of poorest performance and of greatest spectral power in a number of Q-EEG measures. Evening bright light treatment phase delayed these nap zone measures. Conversely, morning bright light phase advanced these measures. The finding that the timing of poorest performance and of the Q-EEG determined nap zone can be phase delayed by evening light and phase advanced by morning light supports the hypothesis tested, as well as supporting the existence of an SCN-dependent circadian arousal system in humans similar to that described by Edgar et al. (1993) in sub-human primates.