Age-related changes in the circadian and homeostatic regulation of human sleep
Age-related changes in the circadian and homeostatic regulation of human sleep
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DOI：
10.1080/07420520500545813
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发表时间：
2006-01-01
影响因子：
2.8
通讯作者：
Wirz-Justice, A
中科院分区：
文献类型：
--
作者：
Cajochen, C;Münch, M;Wirz-Justice, A
脑电图（EEG）慢波活动（SWA）（EEG功率密度在0.75-4.5 Hz之间）和纺锤波频率活动的减少，以及睡眠期间不自主觉醒的增加，代表了人类睡眠随年龄变化的标志。据推测，这种非快速眼动（NREM）睡眠巩固的减少反映了睡眠稳态驱动的年龄相关衰减。为了验证这一假设，我们测量了睡眠EEG特征（即，SWA，睡眠纺锤波）在健康老年志愿者响应高（睡眠剥夺协议）和低睡眠压力（午睡协议）条件。尽管老年志愿者的睡眠巩固受损，SWA水平降低，但他们对高和低睡眠压力条件的相对SWA反应与年轻人相似。只有在额叶脑区，我们发现了与年龄相关的SWA对高睡眠压力的反应减弱。另一方面，我们有明确的证据表明，在40小时午睡协议期间，睡眠的昼夜节律调节发生了变化，使得老年研究参与者晚上的昼夜节律觉醒信号较弱。更多的睡眠发生在清醒维持区，下午晚些时候和晚上的主观嗜睡评分高于年轻的参与者。此外，我们发现褪黑激素分泌减少，REM睡眠和纺锤波频率的昼夜节律调制减少，后者相对于昼夜节律褪黑激素分布是相位提前的。因此，我们倾向于这样的假设，即与年龄相关的睡眠变化是由于睡眠和觉醒的昼夜节律调节减弱。我们的数据表明，昼夜节律计时系统的操作，而不是睡眠稳态，可能提供一个潜在的策略，以减轻与年龄相关的睡眠和白天警觉水平的下降。
The reduction of electroencephalographic (EEG) slow-wave activity (SWA) (EEG power density between 0.75-4.5 Hz) and spindle frequency activity, together with an increase in involuntary awakenings during sleep, represent the hallmarks of human sleep alterations with age. It has been assumed that this decrease in non-rapid eye movement (NREM) sleep consolidation reflects an age-related attenuation of the sleep homeostatic drive. To test this hypothesis, we measured sleep EEG characteristics (i.e., SWA, sleep spindles) in healthy older volunteers in response to high (sleep deprivation protocol) and low sleep pressure (nap protocol) conditions. Despite the fact that the older volunteers had impaired sleep consolidation and reduced SWA levels, their relative SWA response to both high and low sleep pressure conditions was similar to that of younger persons. Only in frontal brain regions did we find an age-related diminished SWA response to high sleep pressure. On the other hand, we have clear evidence that the circadian regulation of sleep during the 40 h nap protocol was changed such that the circadian arousal signal in the evening was weaker in the older study participants. More sleep occurred during the wake maintenance zone, and subjective sleepiness ratings in the late afternoon and evening were higher than in younger participants. In addition, we found a diminished melatonin secretion and a reduced circadian modulation of REM sleep and spindle frequency-the latter was phase-advanced relative to the circadian melatonin profile. Therefore, we favor the hypothesis that age-related changes in sleep are due to weaker circadian regulation of sleep and wakefulness. Our data suggest that manipulations of the circadian timing system, rather than the sleep homeostat, may offer a potential strategy to alleviate age-related decrements in sleep and daytime alertness levels.