Editing Sleep cycle (section)

== Characteristics ==
[[Electroencephalography]] shows the timing of sleep cycles by virtue of the marked distinction in [[brainwave]]s manifested during REM and non-REM sleep. [[Delta wave]] activity, correlating with slow-wave (deep) sleep, in particular shows regular oscillations throughout a good night's sleep. Secretions of various [[hormone]]s, including [[renin]], [[growth hormone]], and [[prolactin]], correlate positively with delta-wave activity, while secretion of [[thyroid-stimulating hormone]] correlates inversely.<ref name=GronfierEtAl1999>{{cite journal | last1 = Gronfier | first1 = Claude | last2 = Simon | first2 = Chantal | last3 = Piquard | first3 = François | last4 = Ehrhart | first4 = Jean | last5 = Brandenberger | first5 = Gabrielle | year = 1999|title=Neuroendocrine Processes Underlying Ultradian Sleep Regulation in Man | journal = Journal of Clinical Endocrinology & Metabolism | volume =  84| issue = 8| pages =  2686–2690| doi = 10.1210/jcem.84.8.5893 | pmid = 10443660 | doi-access = free }}</ref> [[Heart rate variability]], well known to increase during REM, predictably also correlates inversely with delta-wave oscillations over the ~90-minute cycle.<ref name=BrandenbergerEtAl2001>{{cite journal | last1 = Brandenberger | first1 = Gabrielle | last2 = Erhart | first2 = Jean | last3 = Piquard | first3 = François | last4 = Simon | first4 = Chantal | year = 2001| title = Inverse coupling between ultradian oscillations in delta wave activity and heart rate variability during sleep | url = https://pdfs.semanticscholar.org/db12/f3a46522450060675caad0a86d496434f01d.pdf | archive-url = https://web.archive.org/web/20170804113139/https://pdfs.semanticscholar.org/db12/f3a46522450060675caad0a86d496434f01d.pdf | url-status = dead | archive-date = 2017-08-04 | journal = Clinical Neurophysiology | volume =  112| issue = 6| pages =  992–996| doi = 10.1016/S1388-2457(01)00507-7 | pmid = 11377256 | s2cid = 206133162 }}</ref>

In order to determine in which stage of sleep the asleep subject is, electroencephalography is combined with other devices used for this differentiation. EMG ([[electromyography]]) is a crucial method to distinguish between sleep phases: for example, a decrease of [[muscle tone]] is in general a characteristic of the transition from wake to sleep,<ref name="Chase, M. H. 1990">{{cite journal|last1=Chase|first1=M. H.|last2=Morales|first2=F. R.|year=1990|title=The atonia and myoclonia of active (REM) sleep|journal=[[Annual Review of Psychology]]|volume=41|issue=1|pages=557–584|doi=10.1146/annurev.ps.41.020190.003013|pmid=1968326}}</ref><ref>Kleitman, N. (1963). Sleep and Wakefulness Chicago, Univ. ''Chicago Jfress''</ref> and during REM sleep, there is a state of muscle atonia (paralysis), resulting in an absence of signals in the EMG.<ref name="Chase, M. H. 1990"/>

[[Electrooculography|EOG (electrooculography)]], the measure of the eyes’ movement, is the third method used in the sleep architecture measurement;<ref>Berry, R. B., & Wagner, M. H. (2014). ''Sleep Medicine Pearls E-Book''. Elsevier Health Sciences.</ref> for example, REM sleep, as the name indicates, is characterized by a rapid eye movement pattern, visible thanks to the EOG.<ref>ber C., Ancoli-Israel S., Chesson A., and Quan SF. in The AASM Manual for the Scoring of Sleep and Associated Events:  Rules, Terminology and Technical Specifications, 1st. Ed.:  Westchester, Illinois:  American Academy of Sleep Medicine; 2007.</ref>

Moreover, methods based on cardiorespiratory parameters are also effective in the analysis of sleep architecture—if they are associated with the other aforementioned measurements (such as electroencephalography, electrooculography and the electromyography).<ref>Tataraidze, A., Korostovtseva, L., Anishchenko, L., Bochkarev, M., & Sviryaev, Y. (2016,). Sleep architecture measurement based on cardiorespiratory parameters.</ref>

[[Homeostasis|Homeostatic]] functions, especially [[thermoregulation]], occur normally during non-REM sleep, but not during REM sleep. Thus, during REM sleep, body temperature tends to drift away from its mean level, and during non-REM sleep, to return to normal. Alternation between the stages therefore maintains body temperature within an acceptable range.<ref>Pier Luigi Parmeggiani, "Modulation of body core temperature in NREM sleep and REM sleep"; in Mallick et al. (2011).</ref>

In humans, the transition between non-REM and REM is abrupt; in other animals, it is less so.<ref name=McCarley2007 />

Researchers have proposed different models to elucidate the undoubtedly complex rhythm of electrochemical processes that result in the regular alternation of REM and NREM sleep. [[Monoamine]]s are active during NREMS, but not REMS, whereas [[acetylcholine]] is more active during REMS. The [[activation-synthesis hypothesis|reciprocal interaction]] model proposed in the 1970s suggested a cyclic give-and-take between these two systems. More recent theories such as the "flip-flop" model, proposed in the 2000s, include the regulatory role of an inhibitory neurotransmitter [[gamma-aminobutyric acid]] (GABA).<ref>James T. McKenna, Lichao Chen, & Robert McCarley, "Neuronal models of REM-sleep control: evolving concepts"; in Mallick et al. (2011).</ref>