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Roles of Sleep‐Wake and Dark‐Light Cycles in the Control of Endocrine, Metabolic, Cardiovascular, and Cognitive Function

Eve Van Cauter, Fred W. Turek

10.1002/cphy.cp070415

Source: Supplement 23: Handbook of Physiology, The Endocrine System, Coping with the Environment: Neural and Endocrine Mechanisms

Originally published: 2001

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Mechanisms Underlying Diurnal Rhythmicity
2 Diurnal Rhythms in Physiology and Behavior in Normal Conditions
2.1 Endocrine, Metabolic, and Cardiovascular Function
2.2 Diurnal Rhythms in Subjective Fatigue, Mood, and Cognitive Performance
3 Effects of Sleep Curtailment
4 Effects of Environmental Light
5 Conditions of Misalignment Between Circadian Rhythmicity and the Rest‐Activity Cycle
5.1 Jet Lag
5.2 Shift Work
6 Conclusions
Figure 1. Figure 1.

Schematic representation of the organization of the mammalian circadian system. SCN, suprachiasmatic nucleus; NPY, neuropeptide Y; 5‐HT, 5‐hydroxytryptamine (serotonin).
Figure 2. Figure 2.

Mean 24 h profiles of (from top to bottom) systolic blood pressure (SBP), heart rate (HR), plasma glucose, insulin secretion rate (ISR), plasma growth hormone (GH), and plasma cortisol in eight normal young men who ate three identical carbohydrate‐rich meals (M) at the times indicated by the arrows. Bedtimes are represented by black bars. At each time point, the vertical line represents the standard error of the mean.

From Biston et al. 10 with permission
Figure 3. Figure 3.

Mean (+ standard error) profiles of plasma cortisol, growth hormone (GH) and thyroid‐stimulating hormone (TSH) in a group of eight normal young men studied over a 53 h period including 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h of daytime recovery sleep.
Figure 4. Figure 4.

Mean profiles of body temperature, subjective sleepiness (using the Stanford Sleepiness Score), positive affect (using the Positive and Negative Affect Scale), and performance on a vigilance task in normal young men studied during 40 h of continuous wakefulness at bed rest. Data are represented as mean (black bar) and standard error (open bar) for each 2 h interval.
Figure 5. Figure 5.

Representative profiles of plasma cortisol levels (left panels) in a subject who had a normal night of sleep (top) and in a subject who underwent total sleep deprivation (bottom). Shaded areas show the area under the curve between 18:00 and 23:00 in both conditions on day 1 (before sleep or sleep deprivation) and on day 2 (after sleep or sleep deprivation). Histograms (right) represent the mean and standard error of plasma cortisol levels between 18:00 and 23:00 in both groups of subjects on days 1 and 2.

From Leproult et al. 66 with permission
Figure 6. Figure 6.

Mean (+ SEM) profiles of blood glucose (top panels) and serum insulin (lower panels) in 11 young men who received an intravenous injection of glucose at 09:00 when their bedtimes had been restricted to 4 hours per night for 5 nights (left; sleep debt) and after their bedtimes had been extended to 12 hours per night for 5 nights (right; sleep recovery). The shaded areas highlight the postinjection glucose response and the acute insulin response to glucose.

From Spiegel, Leproult and Van Cauter 94, with permission
Figure 7. Figure 7.

Mean 24 h profiles of plasma cortisol and prolactin levels observed in six normal young men studied under baseline conditions at 1, 3, and 5 days after an abrupt 8 h delay shift of the light‐dark and sleep‐wake cycles in the laboratory. The vertical bar at each sampling time represents the standard error of the mean. Scheduled sleep periods are shown as black bars.

From Van Cauter and Turek 105 with permission
Figure 8. Figure 8.

Mean profiles of plasma cortisol, plasma prolactin (PRL) and plasma growth hormone (GH) in two groups of normal young night workers (right) and day workers (left). The black bar represents the scheduled sleep periods.

From refs. 93,116,117.


Figure 1.

Schematic representation of the organization of the mammalian circadian system. SCN, suprachiasmatic nucleus; NPY, neuropeptide Y; 5‐HT, 5‐hydroxytryptamine (serotonin).



Figure 2.

Mean 24 h profiles of (from top to bottom) systolic blood pressure (SBP), heart rate (HR), plasma glucose, insulin secretion rate (ISR), plasma growth hormone (GH), and plasma cortisol in eight normal young men who ate three identical carbohydrate‐rich meals (M) at the times indicated by the arrows. Bedtimes are represented by black bars. At each time point, the vertical line represents the standard error of the mean.

From Biston et al. 10 with permission


Figure 3.

Mean (+ standard error) profiles of plasma cortisol, growth hormone (GH) and thyroid‐stimulating hormone (TSH) in a group of eight normal young men studied over a 53 h period including 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h of daytime recovery sleep.



Figure 4.

Mean profiles of body temperature, subjective sleepiness (using the Stanford Sleepiness Score), positive affect (using the Positive and Negative Affect Scale), and performance on a vigilance task in normal young men studied during 40 h of continuous wakefulness at bed rest. Data are represented as mean (black bar) and standard error (open bar) for each 2 h interval.



Figure 5.

Representative profiles of plasma cortisol levels (left panels) in a subject who had a normal night of sleep (top) and in a subject who underwent total sleep deprivation (bottom). Shaded areas show the area under the curve between 18:00 and 23:00 in both conditions on day 1 (before sleep or sleep deprivation) and on day 2 (after sleep or sleep deprivation). Histograms (right) represent the mean and standard error of plasma cortisol levels between 18:00 and 23:00 in both groups of subjects on days 1 and 2.

From Leproult et al. 66 with permission


Figure 6.

Mean (+ SEM) profiles of blood glucose (top panels) and serum insulin (lower panels) in 11 young men who received an intravenous injection of glucose at 09:00 when their bedtimes had been restricted to 4 hours per night for 5 nights (left; sleep debt) and after their bedtimes had been extended to 12 hours per night for 5 nights (right; sleep recovery). The shaded areas highlight the postinjection glucose response and the acute insulin response to glucose.

From Spiegel, Leproult and Van Cauter 94, with permission


Figure 7.

Mean 24 h profiles of plasma cortisol and prolactin levels observed in six normal young men studied under baseline conditions at 1, 3, and 5 days after an abrupt 8 h delay shift of the light‐dark and sleep‐wake cycles in the laboratory. The vertical bar at each sampling time represents the standard error of the mean. Scheduled sleep periods are shown as black bars.

From Van Cauter and Turek 105 with permission


Figure 8.

Mean profiles of plasma cortisol, plasma prolactin (PRL) and plasma growth hormone (GH) in two groups of normal young night workers (right) and day workers (left). The black bar represents the scheduled sleep periods.

From refs. 93,116,117.
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Article Title: Roles of Sleep‐Wake and Dark‐Light Cycles in the Control of Endocrine, Metabolic, Cardiovascular, and Cognitive Function
 

How to Cite

Eve Van Cauter, Fred W. Turek. Roles of Sleep‐Wake and Dark‐Light Cycles in the Control of Endocrine, Metabolic, Cardiovascular, and Cognitive Function. Compr Physiol 2011, Supplement 23: Handbook of Physiology, The Endocrine System, Coping with the Environment: Neural and Endocrine Mechanisms: 313-330. First published in print 2001. doi: 10.1002/cphy.cp070415