2017 Volume 93 Issue 1 Pages 11-23
In this article, we examined the development of a model for “karoshi” (death by cerebrovascular and cardiovascular diseases due to overwork) in terms of sleep architecture. The normal sleep architecture mainly consists of slow wave sleep (SWS) and rapid eye movement (REM) sleep which result in different time courses and functions. Slow wave sleep is associated with homeostatic regulation, and on the other hand, distribution of REM sleep is entrained by the circadian rhythm. In the normal sleep, the absolute amount of REM sleep is much higher than that of SWS. When working hours are prolonged and prior wakefulness duration increases, SWS pressure is estimated to simultaneously rise and then the amount of REM sleep will decrease and REM sleep pressure will be much higher. After that, REM latency could result in premature sleep-onset REM periods (SOREMPs). In this condition, homeostatic regulation in SWS and circadian regulation in REM sleep will be changed under further allostatic regulation (McEwen;1998). Therefore, we may hypothesize that if allostatic load continually repeats over time, then sympathetic nerves system activity during REM sleep will be elevated. This may result in increased brain and cardiovascular loads that will lead to a prodromal stage of karoshi.