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Cutaneous warming promotes sleep onset.

机译:皮肤变暖促进睡眠发作。

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Sleep occurs in close relation to changes in body temperature. Both the monophasic sleep period in humans and the polyphasic sleep periods in rodents tend to be initiated when core body temperature is declining. This decline is mainly due to an increase in skin blood flow and consequently skin warming and heat loss. We have proposed that these intrinsically occurring changes in core and skin temperatures could modulate neuronal activity in sleep-regulating brain areas (Van Someren EJW, Chronobiol Int 17: 313-54, 2000). We here provide results compatible with this hypothesis. We obtained 144 sleep-onset latencies while directly manipulating core and skin temperatures within the comfortable range in eight healthy subjects under controlled conditions. The induction of a proximal skin temperature difference of only 0.78 +/- 0.03 degrees C (mean +/- SE) around a mean of 35.13 +/- 0.11 degrees C changed sleep-onset latency by 26%, i.e., by 3.09 minutes [95% confidence interval (CI), 1.91 to 4.28] around a mean of 11.85 min (CI, 9.74 to 14.41), with faster sleep onsets when the proximal skin was warmed. The reduction in sleep-onset latency occurred despite a small but significant decrease in subjective comfort during proximal skin warming. The induction of changes in core temperature (delta = 0.20 +/- 0.02 degrees C) and distal skin temperature (delta = 0.74 +/- 0.05 degrees C) were ineffective. Previous studies have demonstrated correlations between skin temperature and sleep-onset latency. Also, sleep disruption by ambient temperatures that activate thermoregulatory defense mechanisms has been shown. The present study is the first to experimentally demonstrate a causal contribution to sleep-onset latency of skin temperature manipulations within the normal nocturnal fluctuation range. Circadian and sleep-appetitive behavior-induced variations in skin temperature might act as an input signal to sleep-regulating systems.
机译:睡眠与体温变化密切相关。当核心体温下降时,人类的单相睡眠期和啮齿动物的多相睡眠期都趋于开始。这种下降主要是由于皮肤血液流量增加,因此皮肤变暖和热量损失。我们已经提出,核心和皮肤温度的这些固有发生的变化可以调节睡眠调节脑区域的神经元活动(Van Someren EJW,Chronobiol Int 17:313-54,2000)。我们在这里提供与该假设兼容的结果。我们获得了144次睡眠发作延迟,同时在受控条件下直接在8位健康受试者的舒适范围内调节了核心和皮肤温度。大约35.13 +/- 0.11℃的平均值引起的近端皮肤温度差仅为0.78 +/- 0.03摄氏度(平均+/- SE),使睡眠发作潜伏期缩短了26%,即3.09分钟[ 95%置信区间(CI)为1.91到4.28],平均约为11.85分钟(CI为9.74到14.41),近端皮肤变暖时睡眠开始更快。尽管近端皮肤变暖期间主观舒适度有小幅但显着的下降,但睡眠开始潜伏期却有所减少。诱导核心温度(δ= 0.20 +/- 0.02摄氏度)和远端皮肤温度(δ= 0.74 +/- 0.05摄氏度)的变化是无效的。先前的研究表明皮肤温度与睡眠开始潜伏期之间存在相关性。而且,已经显示出环境温度激活了温度调节防御机制而导致睡眠中断。本研究是第一个通过实验证明在正常夜间波动范围内对皮肤温度操纵的睡眠发作潜伏期的因果关系的研究。昼夜节律和睡眠竞争行为引起的皮肤温度变化可能充当睡眠调节系统的输入信号。

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