Energy metabolism differs between sleep stages and begins to increase prior to awakening.

PURPOSE: Human sleep is generally consolidated into a single prolonged period, and its metabolic consequence is to impose an extended period of fasting. Changes in sleep stage and homeostatic sleep drive following sleep onset may affect sleeping metabolic rate through cross talk between the mechanisms controlling energy metabolism and sleep. The purpose of this study was to isolate the effects of sleep stage and time after sleep onset on sleeping metabolic rate. METHODS: The sleeping metabolic rate of 29 healthy adults was measured using whole room indirect calorimetry, during which polysomnographic recording of sleep was performed. The effects of sleep stage and time after sleep onset on sleeping metabolic rate were evaluated using a semi-parametric regression analysis. A parametric analysis was used for the effect of sleep stage and a non-parametric analysis was used for the effect of time. RESULTS: Energy expenditure differed significantly between sleep stages: wake after sleep onset (WASO)>stage 2, slow wave sleep (SWS), and REM; stage 1>stage 2 and SWS; and REM>SWS. Similarly, carbohydrate oxidation differed significantly between sleep stages: WASO > stage 2 and SWS; and stage 1>SWS. Energy expenditure and carbohydrate oxidation decreased during the first half of sleep followed by an increase during the second half of sleep. CONCLUSIONS: This study identified characteristic phenotypes in energy expenditure and carbohydrate oxidation indicating that sleeping metabolic rate differs between sleep stages.

The effect of nocturnal blue light exposure from light-emitting diodes on wakefulness and energy metabolism the following morning.

OBJECTIVES: The control of sleep/wakefulness is associated with the regulation of energy metabolism. The present experiment was designed to assess the effect of nocturnal blue light exposure on the control of sleep/wakefulness and energy metabolism until next noon. METHODS: In a balanced cross-over design, nine young male subjects sitting in a room-size metabolic chamber were exposed either to blue LEDs or to no light for 2 h in the evening. Wavelength of monochromatic LEDs was 465 nm and its intensity was 12.1 µW/cm(2). RESULTS: During sleep, sleep architecture and alpha and delta power of EEG were similar in the two experimental conditions. However, the following morning, when subjects were instructed to stay awake in a sitting position, duration judged as sleep at stages 1 and 2 was longer for subjects who received than for those who received no light exposure. Energy metabolism during sleep was not affected by evening blue light exposure, but the next morning energy expenditure, oxygen consumption, carbon dioxide production and the thermic effect of breakfast were significantly lower in subjects who received blue light exposure than in those who received no light exposure. CONCLUSIONS: Exposure to low intensity blue light in the evening, which does not affect sleep architecture and energy metabolism during sleep, elicits drowsiness and suppression of energy metabolism the following morning.

Effect of norepinephrine on RhoA, MAP kinase, proliferation and VEGF expression in human umbilical vein endothelial cells.

Norepinephrine is a well known major vasoconstricting factor. Recent reports suggest that norepinephrine, in addition to acting as a vasoconstricting factor, may also play several additional roles in endothelial cells. These include: 1] induction of NO release. It has been demonstrated that a small GTP-binding protein, Rho, and its downstream effecter, Rho kinase (ROCK), negatively regulate endothelial nitric oxide synthase (eNOS) production. However, it is not known whether ROCK is directly involved in norepinephrine-induced NO release. 2] Norepinephrine is reported to induce a mitogenic effect, but whether MAPKs are involved in this process is unknown. 3] Recently, we demonstrated an increase in vascular endothelial growth factor (VEGF) mRNA/protein expression in human pheochromocytoma tissue in comparison to normal adrenomedullary tissue. Thus, it is reasonable to speculate that norepinephrine may stimulate the level of VEGF mRNA. The aim of the present study was to clarify the role of norepinephrine and related endothelial adrenoceptor systems in various pathophysiological conditions, such as hypertension and in particular pheochromocytoma, using human umbilical vein endothelial cells (HUVEC). Norepinephrine-induced RhoA attenuation, through cAMP/protein kinase A (PKA) activation coupled with beta-adrenoceptors, may lead to eNOS activation in acute conditions. Norepinephrine stimulates the production of VEGF mRNA through cAMP/PKA activation coupled with beta-adrenoceptors. Norepinephrine stimulates a mitogenic effect through ERK activation coupled with the alpha(1)-adrenoceptor. In conclusion, norepinephrine stimulates eNOS activity via RhoA attenuation, VEGF mRNA synthesis and mitogenic activity in endothelial cells. We propose that an excess of norepinephrine can lead to endothelial dysfunction due to these aforementioned processes.