Sleep Pressure

Introduction

Sleep pressure, or homeostatic pressure, reflects on the need to sleep; this depends on prior wakefulness duration and prior sleep duration1. Furthermore, sleep pressure often rises during waking hours, subsides during sleep and intensifies with sleep deprivation1. We know that different sleep stages possess different sleep pressure mechanics. 

This post will explore various characteristics of sleep pressure and some personal differences and responses to sleep pressure. However, some of these materials may or may not reliably apply to polyphasic sleeping. 

Content

  1. Mechanics
  2. SOREM
  3. SWS Pressure
    1. Homeostatic Regulation
    2. Circadian Regulation
  4. REM Pressure
    1. Homeostatic Regulation
    2. Circadian Regulation

Overall Mechanics of Sleep Pressure

Obviously, REM sleep and SWS are both necessary for the body to function properly. Thus, reduction of their amount causes sleep pressures to build until the body tries to get necessary rest. However, REM and SWS have different speeds of building pressure, and feel different.

Severe sleep deprivation results in change in sleep architecture and proportion of time spent in the individual sleep stages. The body also prioritizes SWS and REM over light sleep. Therefore, this leads to Sleep Onset REM (SOREM) or Sleep Onset SWS (SOSWS) depending on which homeostatic pressure is highest at the moment.

If a person is sleeping a reduced amount of REM or SWS from their daily needs, sleep pressure will build over time. REM deprivation typically happens on any reducing sleep schedule, while SWS deprivation is typically only problematic with schedules that have fewer than 3 core cycles (nominally 4.5h of core time).

It should be noted that if you schedule more sleep than necessary, you will wake up naturally once you are done sleeping. This needs to be highlighted because there are underaged people who claim to need less sleep on monophasic sleep than they would get on biphasic schedules, which shows that they were actually restricting their sleep when monophasic. Following the standard scheduling protocols on this website is still recommended. 

Achieving SOREM

Achieving SOREM plays an important factor in naps. When initiating sleep, the body starts with NREM1 and then transitions to NREM2, where it spends roughly 20 minutes. Theoretically, this is because NREM2 is very easy to wake from, which means that you’ll wake up easily if a predator attacks. The 20 minutes of light sleep at the beginning of a sleep is consequently called the “watchdog mode” by the polyphasic sleep community.

However, if the REM pressure is high enough, the body can learn to put REM in this time frame instead. This is at the expense of the vestigial watchdog mode. Thus, this leads to a restructuring of the sleep cycle. Once sleep pressures normalize, this ability often remains, leading to REM in naps.

  • NREM2 never gets prioritized. During a study, a person was able to recover 53% of missed REM, 68% of missed SWS, yet only 7% of missed NREM22. These observations serve to support the belief that NREM1 and 2 are¬†less essential parts¬†of sleep.¬†
  • After a sufficient amount of recovery sleep, the brain switches back to the usual sleep cycle architecture.
  • With SOREM, this still happens roughly 25 minutes in, where after the SOREM period, SWS will begin. In other words, only the watchdog mode will be replaced by REM sleep. Consequently, this is the reason why the vast majority of naps should last for 20 minutes.

Slow-wave Sleep Pressure

Homeostatic Regulation of Slow-wave Sleep

Researchers conclude that the duration of wake periods dictate SWS in the next sleep blocks; as a result, daytime or evening napping results in a decrease in SWS onset latency in the main core sleep at night3. Unlike REM sleep, this suggests that there is only a finite amount of daily SWS to fulfill4,5. Extending sleep duration excessively will result in virtually non-existent SWS.

Most importantly, the homeostatic drive for SWS is directly linked to the concentration of adenosine. Adenosine is an endogenous somnogen, which dictates your tiredness levels. There are also other somnogens, like prostaglandin, but adenosine is the main one. However, it is currently unknown which somnogens build up to represent SWS deprivation symptoms. 

Thus, there are multiple implications for polyphasic sleeping:

  • Short daytime naps (e.g, 20m) can still contain a trace amount of SWS especially around afternoon or even late morning hours, but most likely if there is even a small amount of SWS pressure built up.
  • SWS can get into any daytime sleep block, with varying amounts. This contradicts previous hypotheses that daytime naps contain only REM sleep or light sleep. Nevertheless, this largely depends on the current level of homeostatic pressure by the time of the daytime sleep.
  • A core sleep of at least 4.5h is more than likely to cover all daily SWS requirements. Similarly, having more than one core sleep (e.g, Dual Core) also facilitates SWS.¬†
  • During sleep deprivation stages of the adaptation, SWS pressure can lead to oversleeping. Furthermore, SWS rebounds are intensified on extreme schedules. So far, SWS is the prime culprit behind oversleeping during adaptation, from any sleep blocks.
  • There is no guaranteed easy adaptations to extreme schedules for short sleepers. This is because their usually normal SWS baseline likely will suffer on radically restrictive sleep.

Circadian Regulation of Slow-wave Sleep

Interestingly, it is also a consensus that SWS occurrences seem independent of circadian phases3; this notion suggests that deep sleep can still creep into morning hours, where REM sleep often dominates. What this means is that SWS pressure is more likely to unpredictably override REM and light sleep. This is because its pressure heavily depends on homeostatic pressure rather than circadian pressure.

However, this usually only happens in cases with supposedly poor sleep hygiene, SWS rebounds, disrupted sleep, etc. In addition, even though SWS is primarily regulated through the homeostatic drive, there is still some involvement of minor circadian timing. Because of this, there is a SWS peak, similar to how there is a REM peak. However, this peak needs to be taken into considerations only on schedules where a large amount of sleep is reduced (less than 3 cycles during the SWS-heavy core).

REM Sleep Pressure

Regulation of REM stage

Up to date, it is common knowledge that REM stage predominantly occurs in the second half of the night, in the last sleep cycles. These last 2 sleep cycles often end around sunrise hours. However, REM also occurs in the previous sleep cycles; the amount is often minimal compared to slow-wave sleep. 

Under a polyphasic sleep regime where nocturnal sleep drastically reduces, the behavior of REM sleep changes over time with the addition of naps and repartitioning. Otherwise, it is also necessary to understand the regulation of REM stage under partial sleep deprivations (e.g, adapting to a polyphasic schedule). On any schedules with a core sleep (at least ~3h), REM stage receives the penalty until repartitioning kicks in and stabilize REM duration.

Homeostatic Regulation of REM sleep

Shortened Monophasic Sleep

Researchers have reached the common ground on how REM stage operates under partial sleep deprivation conditions; these conditions mostly showcase the almost intact amount of deep sleep while REM accrues radical deficits. In the following nights, REM rebounds occur in the core sleep with much shorter latency than usual. Additionally, REM duration also increases to abnormal levels especially where SWS pressure is low6.

Therefore, this idea cements the fact that REM sleep is a vital sleep stage, which takes over lighter sleep stages and even has an effect on the delta EEG of SWS. Especially, the study also hints at the possibility of the repartitioning of REM stage with its appearance in earlier sleep cycles of a core.

Polyphasic Sleep and Naps

Most REM sleep in the second core sleep

The aforementioned study mentioned that suppressing REM sleep with nocturnal awakening (similar to Segmented sleep) increases REM duration in the next sleep session and reduces REM latency5. This may explain how the second core sleep of Dual Core or any other Multi-core schedules with a core sleep around dawn have plenty of REM. 

Under napping condition, the amount of obtained REM stage is not finite. This means that the previous nap session with some amount of REM stage does not delay REM latency or reduce REM duration in the following night7. The importance of this detail is to suggest that extending sleep perpetually can break normal REM baselines. Getting as much sleep as possible will inflate the amount of REM sleep in an unhealthy way. 

Thus, unlike SWS, there is an absence of homeostatic regulation of REM stage. The previous waking duration before a sleep session does not determine the amount of time one would spend in REM. 

Circadian Regulation of REM sleep

The circadian clock primarily drives the occurrences of REM during a particular sleep session1. What this means is that REM stage is dominant during daytime hours, especially during the REM peak (6-9 AM). The polyphasic community over years has gathered a lot of evidence that any sleep blocks around these morning hours are filled with REM. 

Daytime naps, especially later naps in the day, also suppress REM in favor of NREM stages (including SWS). Thus, this is something to note when scheduling late daytime naps on polyphasic sleep schedules. 

Main author: Crimson & GeneralNguyen

Page last updated: 19 January 2021

Reference

  1. Taillard, J., Philip, P., Coste, O., Sagaspe, P., & Bioulac, B. (2003). The circadian and homeostatic modulation of sleep pressure during wakefulness differs between morning and evening chronotypes. Journal of Sleep Research, 12(4), 275‚Äď282. doi:10.1046/j.0962-1105.2003.00369.x. [PubMed]
  2. GULEVICH G. Psychiatric and EEG Observations on a Case of Prolonged (264 Hours) Wakefulness. A. 1966;15(1):29. doi:10.1001/archpsyc.1966.01730130031005. [PubMed]
  3. Dijk, Derk-Jan. “Regulation and functional correlates of slow wave sleep.” Journal of Clinical Sleep Medicine 5.2 suppl (2009): S6-S15. [PubMed]
  4. Campbell, Ian G., and Irwin Feinberg. “Homeostatic sleep response to naps is similar in normal elderly and young adults.” Neurobiology of aging 26.1 (2005): 135-144. [PubMed]
  5. Dinges DF. Differential effects of prior wakefulness and circadian phase on nap sleep. E. 1986;64(3):224-227. doi:10.1016/0013-4694(86)90170-7. [PubMed]
  6. Brunner, D. P., Dijk, D.-J., Tobler, I., & Borb√©ly, A. A. (1990). Effect of partial sleep deprivation on sleep stages and EEG power spectra: evidence for non-REM and REM sleep homeostasis. Electroencephalography and Clinical Neurophysiology, 75(6), 492‚Äď499. doi:10.1016/0013-4694(90)90136-8. [PubMed]
  7. Barbato, Giuseppe, and Thomas A. Wehr. “Homeostatic regulation of REM sleep in humans during extended sleep.” Sleep 21.3 (1998): 267-276.¬†