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Impact of sleep and its disturbances on hypothalamo-pituitary-adrenal axis activity.

Balbo M, Leproult R, Van Cauter E - Int J Endocrinol (2010)

Bottom Line: Sleep has modest but clearly detectable modulatory effects on HPA axis activity.During waking, an association between cortisol secretory bursts and indices of central arousal has also been detected.Abrupt shifts of the sleep period induce a profound disruption in the daily cortisol rhythm, while sleep deprivation and/or reduced sleep quality seem to result in a modest but functionally important activation of the axis.

View Article: PubMed Central - PubMed

Affiliation: Sleep, Chronobiology and Neuroendocrinology Research Laboratory, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA.

ABSTRACT
The daily rhythm of cortisol secretion is relatively stable and primarily under the influence of the circadian clock. Nevertheless, several other factors affect hypothalamo-pituitary-adrenal (HPA) axis activity. Sleep has modest but clearly detectable modulatory effects on HPA axis activity. Sleep onset exerts an inhibitory effect on cortisol secretion while awakenings and sleep offset are accompanied by cortisol stimulation. During waking, an association between cortisol secretory bursts and indices of central arousal has also been detected. Abrupt shifts of the sleep period induce a profound disruption in the daily cortisol rhythm, while sleep deprivation and/or reduced sleep quality seem to result in a modest but functionally important activation of the axis. HPA hyperactivity is clearly associated with metabolic, cognitive and psychiatric disorders and could be involved in the well-documented associations between sleep disturbances and the risk of obesity, diabetes and cognitive dysfunction. Several clinical syndromes, such as insomnia, depression, Cushing's syndrome, sleep disordered breathing (SDB) display HPA hyperactivity, disturbed sleep, psychiatric and metabolic impairments. Further research to delineate the functional links between sleep and HPA axis activity is needed to fully understand the pathophysiology of these syndromes and to develop adequate strategies of prevention and treatment.

No MeSH data available.


Related in: MedlinePlus

Inverse “dose-response” relationship between evening cortisol levels and sleep duration. Mean 24-hour (+ SEM) cortisol profiles and AUC (black areas) under 4 hours, 8 hours, and 12 hours bedtimes. Black bars represent the sleep periods. (Adapted from Spiegel et al. [84].)
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fig5: Inverse “dose-response” relationship between evening cortisol levels and sleep duration. Mean 24-hour (+ SEM) cortisol profiles and AUC (black areas) under 4 hours, 8 hours, and 12 hours bedtimes. Black bars represent the sleep periods. (Adapted from Spiegel et al. [84].)

Mentions: The first systematic study of HPA axis activity in a state of sleep debt assessed the effect of 6 consecutive nights of 4 hours in bed in eleven young men [83]. The sleep debt condition was compared with a fully rested condition, obtained after 6 nights of 12 hours in bed. Plasma and salivary cortisol were measured under both conditions. The state of sleep debt, as compared to the fully rested state, was associated with elevated cortisol concentrations in the afternoon and in the early evening and with a shorter quiescent period, due to a delay in its onset by nearly 1.5 hour. In addition, the rate of decrease of free cortisol concentrations in saliva between 16.00 hours and 21.00 hours was about six times slower in the sleep-debt than in the fully rested condition. Nine of the eleven subjects of the previous study participated, one year later, in a separate protocol with 8-hour bedtime, using the same experimental procedures. Interestingly, cortisol evening levels observed under 8-hour bedtime condition were intermediate between those measured under 4-hour and 12-hour bedtime conditions [84] (Figure 5).


Impact of sleep and its disturbances on hypothalamo-pituitary-adrenal axis activity.

Balbo M, Leproult R, Van Cauter E - Int J Endocrinol (2010)

Inverse “dose-response” relationship between evening cortisol levels and sleep duration. Mean 24-hour (+ SEM) cortisol profiles and AUC (black areas) under 4 hours, 8 hours, and 12 hours bedtimes. Black bars represent the sleep periods. (Adapted from Spiegel et al. [84].)
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2902103&req=5

fig5: Inverse “dose-response” relationship between evening cortisol levels and sleep duration. Mean 24-hour (+ SEM) cortisol profiles and AUC (black areas) under 4 hours, 8 hours, and 12 hours bedtimes. Black bars represent the sleep periods. (Adapted from Spiegel et al. [84].)
Mentions: The first systematic study of HPA axis activity in a state of sleep debt assessed the effect of 6 consecutive nights of 4 hours in bed in eleven young men [83]. The sleep debt condition was compared with a fully rested condition, obtained after 6 nights of 12 hours in bed. Plasma and salivary cortisol were measured under both conditions. The state of sleep debt, as compared to the fully rested state, was associated with elevated cortisol concentrations in the afternoon and in the early evening and with a shorter quiescent period, due to a delay in its onset by nearly 1.5 hour. In addition, the rate of decrease of free cortisol concentrations in saliva between 16.00 hours and 21.00 hours was about six times slower in the sleep-debt than in the fully rested condition. Nine of the eleven subjects of the previous study participated, one year later, in a separate protocol with 8-hour bedtime, using the same experimental procedures. Interestingly, cortisol evening levels observed under 8-hour bedtime condition were intermediate between those measured under 4-hour and 12-hour bedtime conditions [84] (Figure 5).

Bottom Line: Sleep has modest but clearly detectable modulatory effects on HPA axis activity.During waking, an association between cortisol secretory bursts and indices of central arousal has also been detected.Abrupt shifts of the sleep period induce a profound disruption in the daily cortisol rhythm, while sleep deprivation and/or reduced sleep quality seem to result in a modest but functionally important activation of the axis.

View Article: PubMed Central - PubMed

Affiliation: Sleep, Chronobiology and Neuroendocrinology Research Laboratory, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA.

ABSTRACT
The daily rhythm of cortisol secretion is relatively stable and primarily under the influence of the circadian clock. Nevertheless, several other factors affect hypothalamo-pituitary-adrenal (HPA) axis activity. Sleep has modest but clearly detectable modulatory effects on HPA axis activity. Sleep onset exerts an inhibitory effect on cortisol secretion while awakenings and sleep offset are accompanied by cortisol stimulation. During waking, an association between cortisol secretory bursts and indices of central arousal has also been detected. Abrupt shifts of the sleep period induce a profound disruption in the daily cortisol rhythm, while sleep deprivation and/or reduced sleep quality seem to result in a modest but functionally important activation of the axis. HPA hyperactivity is clearly associated with metabolic, cognitive and psychiatric disorders and could be involved in the well-documented associations between sleep disturbances and the risk of obesity, diabetes and cognitive dysfunction. Several clinical syndromes, such as insomnia, depression, Cushing's syndrome, sleep disordered breathing (SDB) display HPA hyperactivity, disturbed sleep, psychiatric and metabolic impairments. Further research to delineate the functional links between sleep and HPA axis activity is needed to fully understand the pathophysiology of these syndromes and to develop adequate strategies of prevention and treatment.

No MeSH data available.


Related in: MedlinePlus