During sleep the cerebrospinal fluid clears out the waste products of brains cells. Sleep fragmentation or sleep deprivation can prevent this process, or reduce its efficiency. So I think the accumulation of waste products cause that you have to sleep more after sleep deprivation and extreme sleep deprivation (e.g. by fatal insomnia) can cause death. Low quality sleep and sleep deprivation can cause or worsen both neural (e.g. Alzheimer's disease), and metabolic diseases (e.g. diabetes mellitus, etc...), so you should avoid it, if you can (I cannot :D).
Daily sleep is regulated by the circadian clock. Many hormones can affect that clock, e.g. melatonin (dependent on blue light), insulin, etc...
The conservation of sleep across all animal species suggests that
sleep serves a vital function. We here report that sleep has a
critical function in ensuring metabolic homeostasis. Using real-time
assessments of tetramethylammonium diffusion and two-photon imaging in
live mice, we show that natural sleep or anesthesia are associated
with a 60% increase in the interstitial space, resulting in a striking
increase in convective exchange of cerebrospinal fluid with
interstitial fluid. In turn, convective fluxes of interstitial fluid
increased the rate of β-amyloid clearance during sleep. Thus, the
restorative function of sleep may be a consequence of the enhanced
removal of potentially neurotoxic waste products that accumulate in
the awake central nervous system.
According to the traditional understanding of cerebrospinal fluid
(CSF) physiology, the majority of CSF is produced by the choroid
plexus, circulates through the ventricles, the cisterns, and the
subarachnoid space to be absorbed into the blood by the arachnoid
villi. This review surveys key developments leading to the traditional
concept. Challenging this concept are novel insights utilizing
molecular and cellular biology as well as neuroimaging, which indicate
that CSF physiology may be much more complex than previously believed.
The CSF circulation comprises not only a directed flow of CSF, but in
addition a pulsatile to and fro movement throughout the entire brain
with local fluid exchange between blood, interstitial fluid, and CSF.
Astrocytes, aquaporins, and other membrane transporters are key
elements in brain water and CSF homeostasis. A continuous
bidirectional fluid exchange at the blood brain barrier produces flow
rates, which exceed the choroidal CSF production rate by far. The CSF
circulation around blood vessels penetrating from the subarachnoid
space into the Virchow Robin spaces provides both a drainage pathway
for the clearance of waste molecules from the brain and a site for the
interaction of the systemic immune system with that of the brain.
Important physiological functions, for example the regeneration of the
brain during sleep, may depend on CSF circulation.
Sleep fragmentation is present in numerous sleep pathologies and
constitutes a major feature of patients with obstructive sleep apnea.
A prevalence of metabolic syndrome, diabetes and obesity has been
shown to be associated to obstructive sleep apnea. While sleep
fragmentation has been shown to impact sleep homeostasis, its specific
effects on metabolic variables are only beginning to emerge. In this
context, it is important to develop realistic animal models that would
account for chronic metabolic effects of sleep fragmentation. We
developed a 14-day model of instrumental sleep fragmentation in mice,
and show an impact on both brain-specific and general metabolism. We
first report that sleep fragmentation increases food intake without
affecting body weight. This imbalance was accompanied by the inability
to adequately decrease brain temperature during fragmented sleep. In
addition, we report that sleep-fragmented mice develop glucose
intolerance. We also observe that sleep fragmentation slightly
increases the circadian peak level of glucocorticoids, a factor that
may be involved in the observed metabolic effects. Our results confirm
that poor-quality sleep with sustained sleep fragmentation has similar
effects on general metabolism as actual sleep loss. Altogether, these
results strongly suggest that sleep fragmentation is an aggravating
factor for the development of metabolic dysfunctions that may be
relevant for sleep disorders such as obstructive sleep apnea.
Inadequate sleep simultaneously modulates the levels of multiple
hormones that govern metabolism, In general, with sleep deprivation,
the following hormones are decreased: insulin, growth hormone (GH),
growth hormone releasing hormone (GHRH), and leptin levels. In
contrast, ghrelin and somatostatin are increased. Essentially,
hormones that signal that the body has plenty of energy are decreased,
while those that signal energy need are increased. Experiments
utilizing knockout animals as well as pharmacological agonists,
antagonists, and immunodepletion of the proteins, illustrate that
these hormones affect sleep regulation. Diabetic rats have decreased
sleep time and consolidation while replacement of insulin increases
increases slow-wave sleep.
In humans, melatonin is produced by the pineal gland, a small
endocrine gland located in the center of the brain but outside the
blood–brain barrier. The melatonin signal forms part of the system
that regulates the sleep–wake cycle by chemically causing drowsiness
and lowering the body temperature, but it is the central nervous
system (specifically the suprachiasmatic nuclei, or SCN) that
controls the daily cycle in most components of the paracrine and
endocrine systems rather than the melatonin signal (as was