Nocturnal Cortisol Release in Relation to Sleep Structure

Abstract

The relationship between the temporal organization of cortisol secretion and sleep structure is controversial. To determine whether the cortisol profile is modified by 4 hours of sleep deprivation, which shifts slow-wave sleep (SWS) episodes, 12 normal men were studied during a reference night, a sleep deprivation night and a recovery night. Plasma cortisol was measured in 10-minute blood samples. Analysis of the nocturnal cortisol profiles and the concomitant patterns of sleep stage distribution indicates that the cortisol profile is not influenced by sleep deprivation. Neither the starting time of the cortisol increase nor the mean number and amplitude of pulses was significantly different between the three nights. SWS episodes were significantly associated with declining plasma cortisol levels (p less than 0.01). This was especially revealed after sleep deprivation, as SWS episodes were particularly present during the second half of the night, a period of enhanced cortisol secretion. In 73% of cases, rapid eye movement sleep phases started when cortisol was reflecting diminished adrenocortical activity. Cortisol increases were not concomitant with a specific sleep stage but generally accompanied prolonged waking periods. These findings tend to imply that cortisol-releasing mechanisms may be involved in the regulation of sleep.

Association of salivary-assessed oxytocin and cortisol levels with time of night and sleep stage

“…It is unclear whether this circadian CT secretion is modulated by sleep stage. There are indications that onset of REM episodes may be accompanied by decreased secretion of CT (Born et al 1986;Follenius et al 1992;Gronfier et al 1999), although this was not found by Bierwolf et al (1997), and Follenius et al (1992) conclude that CT increases do not seem to be related to any specific sleep stage. Furthermore, a lack of relationship between sleep stage at awakening and cortisol awakening response was found by Elder et al (2012).…”

“…N2 was used as a comparison condition, because, unlike NREM stage 3 [N3, or slow wave sleep (SWS)], it is abundant throughout the night. In contrast, N3 episodes predominate during the first half of the night and have been related to an additional decrease in cortisol beyond the circadian nadir occurring at this time of night (Follenius et al 1992;Gronfier et al 1997;Pannain and Van Cauter 2007;Van Cauter and Tasali 2011).…”

Nocturnal Intermittent Hypoxia and Metabolic Syndrome; the Effect of being Overweight: the CIRCS Study

“…Inhibition of slow wave sleep decreased growth hormone levels, leading to a reduction in metabolism, and serum leptin levels and increased serum grhelin levels, leading to the stimulation of appetite. Activation of the hypothalamic-pituitaryadrenal axis increased serum cortisol levels 28) , leading to hyperglycemia and insulin resistance 29) . Lastly, an experimental study has shown that intermittent hypoxia caused an increase in hepatic levels of triglyceride and phospholipid, and upregulated the expression of genes involved in lipid biosynthesis in mice 30) .…”

Delta Sleep Response to Metyrapone in Post-Traumatic Stress Disorder

“…Aging is also associated with increased cortisol response and more decreases in delta sleep in response to mild laboratory stressors (Prinz et al, 2000). Several studies in which subjects were forced to sleep in the second half of the night when HPA activity is enhanced have shown that delta sleep emerges only during troughs of cortisol activity (Follenius et al, 1992;Orth et al, 1967;Spath-Schwalbe et al, 1992Van Cauter et al, 1991;Weibel et al, 1995;Weitzman et al, 1974Weitzman et al, , 1983. In the most sophisticated set of studies of peripheral cortisol and delta sleep to date, Gronfier and colleagues calculated secretory rates of cortisol measured every 10 min using a deconvolutional procedure.…”