Homeostasis and Sleep Propensity

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Homeostasis in physiology refers to the mechanisms and patterns in the body to maintain a constant state. Homeostasis refers to body temperature, pH levels of bodily fluids, weight, and sleep propensity as well as a host of other characteristics of the body. Life presents external factors that tend to knock the body out of balance and homeostatic processes bring internal stability needed to sustain the organism over longer periods of time.

How do we know there is homeostasis? Easy. When people are deprived of sleep they add extra sleep time when allowed to sleep again. They make up the lost sleep. When the brain is allowed to sleep after deprivation, the NREM sleep is more intense REM sleep does not increase in intensity by any measure we have but the brain does make up for lost REM sleep.

Subjectively we feel sleep propensity – the pressure to sleep – especially when we have been up for a while. When sleep intensity is high, sleep is less fragmented – there are fewer nighttime awakenings.

The intensity appears to be for NREM sleep. While there is some homeostasis for just REM, the person does not appear to experience an extra drive for sleep when deprived of only REM.

The two-process model is the dominant model for sleep behavior and even if scientists understand it lacks nuance and may regard it as oversimplified, to a first approximation the model does a good job at describing and predicting sleep cycles. Homeostasis is called Process S in this model

Even before little was known about brain biochemistry, observers could see there was a homeostatic process and that the propensity for sleep increased over the course of the waking period. They used the term “sonogen” to indicate the unknown constituents that promoted sleep. Today we know that the neurotransmitter dopamine appears to play a part in the homeostatic process, although the mechanism is not understood. We do know that if mice are altered to have higher levels of dopamine in their brains, the homeostatic drive is higher. When deprived of sleep, their recovery sleep is stronger – less fragmented and deeper.

The old-timey chemical theory of sleep – made obsolete by discoveries in recent decades – posited somnogens. Today we know there are such things as somnogens of a sort. Adenosine (made by ATP breakdown over the course of the day) is a somnogen (caffeine counteracts is) as are cytokines.

Separate from NREM, there is something of a homeostat for REM sleep, too.

Sleep propensity accumulates over the course of the day, but here is an interesting question: does it accumulate at a steady rate (as we show in the graph) or does the rate depend on what the person is doing? Does an hour of intense study increase sleep propensity (but not necessarily immediate sleepiness) more than an hour of watching television. Does time spent jogging in the Sun cause more of a build-up than time spent walking in the mall?

The answer is not totally clear, but animal experiments suggest that the activity while awake does affect the rate of sleep propensity build-up. Rats that spent time exploring mazes subsequently experienced more slow-wave sleep than those who were less challenged.

“Delta power” is a characteristic of EEG activity graphs during stage 3 and has emerged in science as more-or-less and indicator of the depth and intensity of sleep. If someone stays awake too long (sleep deprivation), their subsequent stage 3 readings show greater delta power. A surplus of sleep results in a lower delta power. This is true for individuals, but the difference from person to person in delta power can vary considerably, suggesting a strong genetic component in the regulation of the homeostatic process.

The neurotransmitter dopamine is implicated in much of human behavior, and there is indication the dopamine transporter neurosubstrate mechanism in the brain plays a part in sleep homeostasis, but the actual mechanism or magnitude of the effect is unknown.

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