Psychological, Psychophysiological, and Biochemical Correlates of Prolonged Sleep Deprivation

Kollar, Edward J.; Pasnau, Robert; Rubín, Robert T.; Naitoh, Paul; Slater, Grant G.; Kales, Anthony

doi:10.1176/ajp.126.4.488

Cited by 54 publications

(25 citation statements)

References 22 publications

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“…By comparison, in the present study, sleep-deprived rats showed only a mild tendency for increased corticosteroid concentrations by 50%, and not more than was recorded at various times for the other two groups. This result replicates previous findings (8,20) and corroborates the mild or unchanged values found in the results of human studies of selective sleep deprivation (37,38,70). Although changes in corticosteroid receptors, sensitivity, and catabolism cannot yet be ruled out, corticosterone concentration in sleep-deprived rats appears consistent with what may be expected to mobilize fuel to support metabolic and cellular requirements.…”

Section: Discussionsupporting

confidence: 91%

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Everson¹,

Crowley²

2004

American Journal of Physiology-Endocrinology and Metabolism

181

136

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Everson, Carol A., and William R. Crowley. Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats. Am J Physiol Endocrinol Metab 286: E1060 -E1070, 2004. First published February 10, 2004 10.1152/ajpendo.00553.2003The main systemic disorders resulting from prolonged sleep deprivation in laboratory animals are a negative energy balance, low circulating thyroid hormones, and host defense impairments. Low thyroid hormones previously have been found caused by altered regulation at the level of the hypothalamus with possible pituitary involvement. The present studies investigated the effects of sleep deprivation on other major anabolic hormonal systems. Plasma growth hormone (GH) concentrations and major secretory bursts were characterized. Insulin-like growth factor I (IGF-I) was evaluated as an integrative marker of peripheral GH effector activity. Prolactin (PRL) was assessed by basal concentrations and by stimulating the pituitary with exogenous thyrotropin-releasing hormone. Leptin was studied for its linkage to metabolic signs of sleep loss and its correspondence to altered neuroendocrine regulation in other disease states. Last, plasma corticosterone was measured to investigate the degree of hypothalamic-pituitary-adrenal activation. Sleep deprivation was produced by the disk-over-water method, a well-established means of selective deprivation of sleep and noninterference with normal waking behaviors. Hormone concentrations were determined in sham comparisons and at intervals during baseline and experimental periods lasting at least 15 days in partially and totally sleep-deprived rats. The results indicate that high-amplitude pulses of GH were nearly abolished and that concentrations of GH, IGF-I, PRL, and leptin all were suppressed by sleep deprivation. Corticosterone concentration was relatively unaffected. Features of these results, such as low GH and low IGF-I, indicate failed negative feedback and point to hypothalamic mechanisms as containing the foci responsible for peripheral signs. growth hormone; thyroxine; prolactin; insulin-like growth factor I; leptin; corticosterone SLEEP IS CONSIDERED CRITICAL for the maintenance of health (2, 14, 49b, 77a) and support of life (18,35,54). Some of the clinical states associated with abnormal sleep include pulmonary and cardiovascular disorders, cerebrovascular disease, thrombotic disease, epilepsy, arthritis, mood disorders, chronic pain, and shortened life span (reviewed in Refs. 39 and 49a). The physical consequences of sleep deprivation have not been localized. Evidence from studies in laboratory animals suggest that multitropic factors in immune and hormonal systems contribute to the absence of localization.The three principal consequences of prolonged sleep deprivation in the rat are a progressively deepening negative energy balance (8,18,23), reduced thyroid hormone concentrations (8,19,20), and abnormal control of microorganisms (22). Sleep-deprived rats become strikingly and progressively hyperphagic but do not gain we...

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Section: Discussionsupporting

confidence: 91%

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Everson¹,

Crowley²

2004

American Journal of Physiology-Endocrinology and Metabolism

181

136

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“…The abnormally low level appears compensatory and points to increased negative feedback to the brain and pituitary, perhaps serving a permissive action for effector functions that tend to be reciprocally related to glucocorticoid action (49). Corticosterone otherwise remained unchanged by sleep loss, consistent with earlier findings in laboratory rats studied under this paradigm (17,18,21), and with a lack of a cortisol stress response in human sleep deprivation or extended sleep restriction studies (2,9,31,41,42,51,52,55,62,64,71,72). Findings opposite to these, that is, decreased circulating leukocytes and marked increases in corticosterone, have been reported in laboratory rodents sleep deprived by the pedestal technique (73), also known as the platform or inverted flower-pot technique, which is considered nonspecific for sleep deprivation (48,66).…”

Section: Discussionsupporting

confidence: 87%

Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

Everson¹,

Thalacker²,

Hogg³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The relative lack of response on REe2 night is in contrast with several studies in which stage 1 (16,(20)(21)(22)24) and wakefulness (20) remained lower than baseline; latencies to stage 1, 2, and 3 remained lower (20); and REM sleep (which in general shows no change on the REel night) was significantly increased on REe2 night (16,19,23). It should be noted, however, that the sleep loss period was> 1 night in three of these studies (19,21,23). Although the sleep records in this study were scored using the standard (11) amplitude criterion for stages 3 and 4 sleep, a striking change in slow wave sleep was seen on recovery nights.…”

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confidence: 72%

Sleep Loss in Elderly Volunteers

Carskadon

Dement

1985

Sleep

103

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Summary: Sleep, perfonnance, and sleepiness were assessed in 10 elderly volunteers (8 women, 2 men; aged 61-77 years) before, during, and after 38 h of sleep loss. Recovery night 1 sleep showed increased total sleep and stages 3 and 4 sleep and decreased stage I sleep, wakefulness, brief arousals, and latency to stages 3 and 4 sleep. An increase in stage 4 sleep persisted to the second recovery night. Increased arousal threshold was suggested by a lengthening of respiratory events and a reduction in arousals associated with leg movements. Performance was impaired during sleep loss, associated with an increased tendency to fall asleep. Reported sleepiness increased, except in three subjects who denied sleepiness. Latency to sleep onset declined. All measures returned to basal values after a night of sleep. Sleep in one volunteer failed to respond to sleep loss. With this exception, the response was similar to that reported in younger volunteers, although shorter-lived.

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Psychological, Psychophysiological, and Biochemical Correlates of Prolonged Sleep Deprivation

Cited by 54 publications

References 22 publications

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

Sleep Loss in Elderly Volunteers

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