Circadian rhythms, sleep deprivation, and human performance.
Circadian rhythms, sleep deprivation, and human performance.
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DOI：
10.1016/b978-0-12-396971-2.00007-5
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发表时间：
2013
影响因子：
--
通讯作者：
Dinges, David F.
中科院分区：
文献类型：
--
作者：
Goel, Namni;Basner, Mathias;Rao, Hengyi;Dinges, David F.
目前，关于人在一天之内和一天之内的表现动态变化的科学和数学建模，大部分都是由睡眠-觉醒调节的双过程模型主导的，该模型假定睡眠的神经生物学驱动是动态变化的（在清醒期间以饱和指数增加，而在睡眠期间以类似方式减少），以及神经生物学调节睡眠和清醒时的警觉性和表现的体内平衡驱动的昼夜节律过程。神经行为功能中的内源性昼夜节律，包括生理警觉性和认知表现，已经使用特殊的实验室协议进行了证明，这些协议揭示了生物钟与睡眠稳态驱动的相互作用。昼夜节律的个体差异以及此类差异背后的遗传和其他成分也会影响清醒时的神经行为功能。急性完全睡眠剥夺和慢性睡眠限制都会增加稳态睡眠驱动力，并降低清醒时的神经行为功能，如嗜睡，注意力，认知速度和记忆。最近的证据表明，睡眠不足的神经行为反应具有高度稳定性，这表明这些性状样的个体差异是表型的，可能涉及遗传成分，包括昼夜节律基因。最近的实验已经揭示了睡眠稳态和昼夜节律对大脑代谢和神经激活的影响。对睡眠稳态和昼夜节律系统之间动态复杂相互作用的神经和遗传机制的研究正在开始。这项工作的一个关键目标是确定生物标志物，准确地预测人类在昼夜节律和睡眠稳态系统受到干扰的情况下的表现。
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.