Sleep duration and chronic sleep debt: Are 6 hours enough?
University of Pennsylvania School of Medicine, Department of Psychiatry, Unit for Experimental Psychiatry, Division of Sleep and Chronobiology, Philadelphia, PA, USA.Biological psychology (Impact Factor: 3.4). 02/2011; 87(1):15-6. DOI: 10.1016/j.biopsycho.2011.02.015
- Biological psychology 03/2011; 87(2). DOI:10.1016/j.biopsycho.2011.03.007 · 3.40 Impact Factor
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ABSTRACT: Much of the current science on, and mathematical modeling of, dynamic changes in human performance within and between days is dominated by the two-process model of sleep-wake regulation, which posits a neurobiological drive for sleep that varies homeostatically (increasing as a saturating exponential during wakefulness and decreasing in a like manner during sleep), and a circadian process that neurobiologically modulates both the homeostatic drive for sleep and waking alertness and performance. Endogenous circadian rhythms in neurobehavioral functions, including physiological alertness and cognitive performance, have been demonstrated using special laboratory protocols that reveal the interaction of the biological clock with the sleep homeostatic drive. Individual differences in circadian rhythms and genetic and other components underlying such differences also influence waking neurobehavioral functions. Both acute total sleep deprivation and chronic sleep restriction increase homeostatic sleep drive and degrade waking neurobehavioral functions as reflected in sleepiness, attention, cognitive speed, and memory. Recent evidence indicating a high degree of stability in neurobehavioral responses to sleep loss suggests that these trait-like individual differences are phenotypic and likely involve genetic components, including circadian genes. Recent experiments have revealed both sleep homeostatic and circadian effects on brain metabolism and neural activation. Investigation of the neural and genetic mechanisms underlying the dynamically complex interaction between sleep homeostasis and circadian systems is beginning. A key goal of this work is to identify biomarkers that accurately predict human performance in situations in which the circadian and sleep homeostatic systems are perturbed.Progress in molecular biology and translational science 07/2013; 119:155-90. DOI:10.1016/B978-0-12-396971-2.00007-5 · 3.49 Impact Factor
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ABSTRACT: Circadian rhythms control a wide range of physiological events in all organisms. Typical of our modern lifestyles is the flexibility to rest, exercise, eat, or socialize at any time of the circadian day or night; yet, these allowances correlate with rising disorders of a metabolic nature, which are thought to be mediated by changes in the molecular events underlying metabolic gene expression. Because the clock confers on gene expression changes in activity that are not necessarily related to changes in DNA sequence, the study of circadian rhythms is inseparable from epigenetics. Increasingly evident is that energy balance at the systems level relies on precise and collaborative circadian timing of epigenetic events within individual cells and tissues of the body. At the center of these rhythms resides the circadian clock machinery, a remarkably well-orchestrated transcription-translation feedback system that incorporates a fluctuating landscape of mRNA expression, protein stability, chromatin state, and metabolite abundance to keep correct time. Understanding more fully the ties that exist between cellular metabolism and the circadian clock at the epigenetic level will produce not only needed insights about circadian physiology but also novel strategies for the pharmacological and nonpharmacological treatment of metabolic disorders.Progress in molecular biology and translational science 07/2013; 119:29-50. DOI:10.1016/B978-0-12-396971-2.00002-6 · 3.49 Impact Factor
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