M9 Sleep architecture and circadian rhythms

Topic

Sleep propensity arises from the combination of two distinct processes, according to Borbely’s two-process model: a homeostatic pressure that builds up progressively during wakefulness and dissipates during sleep, and a central circadian oscillator generated by the suprachiasmatic nucleus—formalized here using the Kuramoto phase oscillator model described elsewhere in this catalog—which synchronizes its phase with environmental light signals. The greater the accumulated homeostatic pressure and the more favorable the phase of the central circadian oscillator at a given moment, the higher the resulting sleep propensity.

Throughout the night, this same sleep propensity determines the sleeper's progression through various sleep stages—wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep—in a sequence of transitions following the pattern of a Markov chain: the probability of moving from one sleep stage to the next depends solely on the current sleep stage, and higher sleep propensity increases the likelihood of transitioning to deeper sleep stages.

During deep sleep within this progression of stages, slow-wave electrical activity emerges; its intensity directly reflects the amount of homeostatic pressure accumulated during the preceding period of wakefulness. The greater the accumulated homeostatic pressure, the higher the slow-wave activity during deep sleep; it is precisely this slow-wave activity that progressively dissipates the accumulated homeostatic pressure, thereby closing the cycle of pressure buildup and decay with which this description began. That same suprachiasmatic nucleus—which generates the central circadian oscillator—also modulates the secretion of the hormone melatonin, the release of which is directly suppressed by exposure to light: the more ambient light a person receives, the less melatonin the suprachiasmatic nucleus allows to be released.

When the central circadian oscillator generated by the suprachiasmatic nucleus falls out of alignment with the environmental schedule a person must follow—for instance, after a long-haul flight across time zones or an abrupt shift-work change—this misalignment is quantified as a phase difference between the central circadian oscillator and the required environmental schedule; the greater this phase difference, the more the person's sleep propensity becomes desynchronized from the times they actually need to sleep or remain awake. Ultimately, it is this very sleep propensity—combining the homeostatic pressure that accumulates and dissipates through slow-wave activity with the central circadian oscillator (which the suprachiasmatic nucleus generates, synchronizes with ambient light, and translates into melatonin secretion)—that determines when and how much a person sleeps, and that becomes desynchronized from the required schedule when the phase difference between the two oscillators becomes too great.

ID:4281