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. 2010:2010:759234.
doi: 10.1155/2010/759234. Epub 2010 Jun 9.

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

Marcella Balbo  1 , Rachel Leproult, Eve Van Cauter
Affiliations

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

Marcella Balbo et al. Int J Endocrinol. 2010.

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.

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Figures

Figure 1
Figure 1
24-hour individual cortisol profile (solid line).The smoothing curve (dotted line) is calculated to determine the minimum (nadir), the maximum (acrophase), the onset of the circadian rise, and the amplitude (50% of the difference between the acrophase and the nadir) of the cortisol profile. The black bar represents the sleep period.
Figure 2
Figure 2
Effects of age and sex on cortisol profile: Mean 24-hour (+ or − SEM) cortisol profiles in men (left profiles) and women (right profiles) for 2 age groups that is, 50 years of age and older (solid lines) and 20 to 29 years old (hatched lines). (adapted from Van Cauter [30])
Figure 3
Figure 3
Effect of an 8-hour sleep delay on cortisol profiles. Mean 24-hour (+ SEM) cortisol profiles under baseline conditions (bedtimes from 23:00 to 7:00), and one, three, five days after an 8-hour delay of the sleep-wake and dark-light cycles (bedtimes from 7:00 to 15:00). Black bars represent the sleep periods. (Adapted from Buxton et al. [67].)
Figure 4
Figure 4
Effect of an 8-hour sleep advance on cortisol profiles. Mean (+ SEM) cortisol profiles obtained during 68 consecutive hours including baseline conditions and 2 postshift periods, that is, after an 8-hour advance of the sleep-wake and dark-light cycles. Black bars represent the sleep periods whereas wake time was spent in dim light conditions. (Adapted from Caufriez et al. [68].)
Figure 5
Figure 5
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].)
Figure 6
Figure 6
Cortisol rhythm under different sleep conditions. (a) and (b): 24-hour (+ SEM) cortisol profiles under 4 hours (a) and 12 hours (b) bedtimes (Adapted from Spiegel et al. [84]). (c) and (d): 24-hour (+ SEM) cortisol profiles in young insomniacs (c) and age, and BMI-matched controls (d) (Adapted from Vgontzas et al. [105]). Black bars represent the sleep periods.
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