Compared with that in the wake state, there is a reduction in sympathetic activity and an increase in parasympathetic activity during NREM sleep. There is a further decrease in sympathetic activity, as well as an increase in parasympathetic activity, during REM sleep compared with NREM sleep. Transient increases in sympathetic activity may develop during phasic REM sleep.
Respiration is under both metabolic (ie, pH, Pao2, and Paco2) and behavioral control during wakefulness. Behavioral influences are lost during sleep in which only metabolic control is present. Both hypoxic and hypercapnic ventilatory responses decrease during NREM sleep compared with that during wake and decrease further during REM sleep. There appear to be gender differences in hypoxic ventilatory responses, with a reduction in drive from wake to sleep in men but a similar drive during wake and NREM sleep in women.
During sleep compared with wakefulness, Pao2 falls by approximately 2 to 12 mm Hg, arterial oxygen saturation (Sao2) drops by 2%, and Paco2 rises by 2 to 8 mm Hg. Upper airway dilator muscle tone and activity of accessory muscles of respiration progressively fall during NREM and REM sleep compared with that in wakefulness. Tidal volume, minute ventilation, and ventilatory response to added inspiratory resistance also decrease during sleep compared with that in wakefulness.
Respiratory patterns often change during sleep, with periodic breathing and episodes of hypopneas and hyperpneas developing during stage N1 sleep. Respiration stabilizes with a regular frequency and amplitude of respiration during N3 sleep. An irregular pattern of respiration with variable respiratory rates and tidal volumes typically characterizes REM sleep. Central apneas or periodic breathing may occur during phasic REM sleep.
The upper airway acts much like a collapsible cylinder, with flow through it determined by the difference in upstream (ie, nasal) vs downstream pressure, as well as by airway resistance. Thus, airflow is greater with higher upstream pressure, lower downstream pressure, and decreased airway resistance. The patency of the upper airway is dependent on the balance of factors that either maintain airway opening (activation of dilator muscles) or promote airway closure (reduction in intraluminal extrathoracic airway pressure).
During NREM sleep, there is a decrease in heart rate, reduction in cardiac output, lowered BP, and either a reduction or no change in systemic vascular resistance compared with levels during wakefulness. Tonic REM sleep is associated with further reductions in heart rate, cardiac output, BP, and systemic vascular resistance compared with that in NREM sleep. In contrast, heart rate, cardiac output, BP, and systemic vascular resistance all increase during phasic REM sleep compared with that in NREM and tonic REM sleep, as well as during awakenings, the latter due to enhanced sympathetic tone. Nighttime systolic BP is commonly about 10% less than daytime systolic BP, referred to as the dipping phenomenon.
Sleep is associated with a decrease in swallowing rate, diminished salivary production, and reduced esophageal motility. There is a circadian rhythmicity in basal gastric acid secretion, which peaks between 10:00 pm and 2:00 am and has a nadir between 5:00 am and 11:00 am. A decrease in intestinal motility (ie, migrating motor complex) and motor tone occurs during sleep.
Sleep is associated with an increase in water reabsorption, reduced glomerular filtration, and increase in renin release, which, collectively, reduces urine volume.
Penile tumescence in men and clitoral tumescence and vaginal engorgement in women can occur during REM sleep.
Although release of growth hormone occurs primarily during N3 sleep, growth hormone secretion can also occur without N3 sleep, such as during a relaxed supine position. There is typically one peak in growth hormone secretion at sleep onset in men, whereas several peaks in growth hormone secretion occurring throughout the day and night may be seen in women. Sleep deprivation may suppress growth hormone secretion. Secretion of prolactin increases during N3 sleep and decreases during REM sleep; its secretion is suppressed by sleep fragmentation. Prolactin secretion is also influenced by circadian rhythms during wakefulness, with lower levels at noon and higher levels in the evening.
Thyroid stimulating hormone secretion is linked to both sleep and circadian rhythms; levels are low during the daytime, with a nadir between 10:00 am and 7:00 pm and increase during the night from 9:00 pm to 6:00 am, peaking prior to sleep onset. Thyroid stimulating hormone secretion is inhibited by sleep, particularly N3 sleep, and increases with awakenings and sleep deprivation. Thyroid hormone levels decrease at night.
Levels of parathyroid hormone increase during sleep.
Cortisol secretion is linked primarily to the circadian rhythm rather than to sleep. Levels of cortisol begin to rise about 2 h prior to awakening, with peak levels at 8:00 am to 9:00 am; thereafter, cortisol levels decline, with a nadir at 12:00 am. Sleep, especially N3 sleep, suppresses cortisol secretion. Secretion of cortisol increases during prolonged awakenings of > 20 min.
Levels of melatonin rise in the evening. Peak levels occur in the early morning between 2:00 am and 5:00 am; levels decline thereafter, even if no sleep occurs during the night. Synthesis and secretion of melatonin are suppressed by light exposure.
Secretion of testosterone is primarily linked to sleep. Levels increase during sleep, particularly in young adult men. Peak levels occur about 90 min prior to the first REM period.
Luteinizing hormone levels increase during sleep, mainly during NREM sleep, in adolescents and adult men. Luteinizing hormone secretion may remain unchanged or even decline during sleep in adult women, especially during the follicular phase of the menstrual cycle.
Antidiuretic hormone levels increase at night. The secretion of renin is linked to the NREM-REM sleep cycle, with greater secretion during NREM sleep; levels peak during stage N3 sleep. There is lower secretion during REM sleep. Levels are increased during recovery sleep following sleep deprivation.
Insulin levels are decreased during sleep. Insulin levels are higher in NREM sleep compared with that in REM sleep.
Insulin resistance may develop during sleep deprivation. Leptin is released from peripheral adipocytes and is involved with the regulation of energy balance, primarily by reducing appetite. Secretion of leptin is influenced by both sleep and circadian rhythms, with greater secretion at night. Highest levels are from 12:00 am to 4:00 am; lowest levels, from 1:00 pm to 2:00 pm. Secretion of leptin declines during sleep restriction.
Ghrelin stimulates appetite and increases food intake; levels increase at night. In summary, levels of growth hormone are increased and levels of cortisol and adrenocorticotropic hormone decrease during the first half of the sleep period. Conversely, during the second half of the sleep period, there are lower levels of growth hormone and higher levels of cortisol and adrenocorticotropic hormone.
Skeletal muscle relaxation, either hypotonia or atonia, and inhibition of deep tendon reflexes occur during sleep.
Pupillary constriction is seen during NREM and tonic REM sleep, whereas pupillary dilatation occurs during phasic REM sleep.
Proinflammatory cytokines, such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α, enhance sleep. Specifically, they increase NREM sleep and delta EEG waves. Conversely, levels of IL-1β and TNF-α increase during sleep. IL-1β and TNF-α act via nuclear factor-κβ; IL-1β and TNF-α increase, and are increased by, nuclear factor-κβ in a positive-feedback-loop fashion. Nuclear factor-κβ, in turn, promotes sleep by enhancing nitric oxide synthase. Antiinflammatory cytokines, such as IL-4, IL-10, and transforming growth factor-β, suppress sleep. Acute infectious and inflammatory processes can give rise to sleepiness.
Neurons in the preoptic and anterior hypothalamus are involved with thermoregulation. Activity of warmth-sensing neurons increases during sleep and decreases during the wake state; activity of cold-sensing neurons, on the other hand, decreases during sleep and increases during wakefulness. Core body temperature peaks in the late afternoon and early evening (6:00 pm to 8:00 pm) and falls at the onset of sleep. Temperature nadir occurs about 2 h prior to the usual wake time (4:00 am to 5:00 am).
Changes in thermoregulation occurring during sleep include (1) fall in core body temperature; (2) decline in thermal set point; (3) reduced thermoregulatory responses to thermal challenges (lower during REM sleep compared with NREM sleep); (4) decrease in metabolic heat production; (5) loss of heat production from shivering during REM sleep; and (6) increased heat loss due to sweating and peripheral vasodilatation.10
Sleep latency and architecture are influenced by changes in body temperature at bedtime. Exposure to extreme hot or cold environmental temperatures suppresses sleep onset and causes sleep disruption. Nocturnal sleep typically occurs during the falling phase of the temperature rhythm after maximum core body temperature. Awakening, on the other hand, occurs during the rising phase of the temperature rhythm after minimum core body temperature.
Initiating sleep during the falling phase of the temperature rhythm results in a shortened sleep-onset latency and increases both total sleep time and stage N3 sleep. In contrast, initiating sleep during the rising phase of the temperature rhythm will produce a more prolonged sleep onset latency, decrease in total sleep time, reduced stage N3 sleep, and increase in REM sleep.
Metabolic rate decreases during NREM sleep compared with that in the wake state. Metabolic rate during REM sleep is either similar to, or greater than, that during NREM sleep.
Dreaming can occur during both REM sleep (accounts for 80% of dreams) and NREM sleep (20% of dreams). In contrast to REM-related dreams, which are generally more complex and irrational, NREM dreams tend to be simpler and more realistic.