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睡眠剥夺对警觉性和生化变量的多重影响。

Multiplex influences on vigilance and biochemical variables induced by sleep deprivation.

作者信息

Liu Shiqi, Ma Xiaohong, Chen Ying, Zhao Yuanyuan, Luo Rujia, Wu Zhouying, Li Yicheng, Qian Yongyu, Wang Wenwen, Dong Shuohan, Zhou Zengxuan, Li Silin, Xiao Yi, Zhu Xinhai, Tian Yu, Guo Jinhu

机构信息

School of Life Sciences, Ministry of Education (MOE) Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, Sun Yat-sen University, Guangzhou, China.

Engineering Research Center of Human Circadian Rhythm and Sleep, Space Science and Technology Institute, Shenzhen, China.

出版信息

Front Sports Act Living. 2024 Jun 28;6:1412044. doi: 10.3389/fspor.2024.1412044. eCollection 2024.

DOI:10.3389/fspor.2024.1412044
PMID:39005627
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11239445/
Abstract

INTRODUCTION

Sleep loss and sleep deprivation (SD) cause deleterious influences on health, cognition, mood and behaviour. Nevertheless, insufficient sleep and SD are prevalent across many industries and occur in various emergencies. The deleterious consequences of SD have yet to be fully elucidated. This study aimed to assess the extensive influences of SD on physiology, vigilance, and plasma biochemical variables.

METHODS

Seventeen volunteers were recruited to participate in a 32.5-h SD experiment. Multiple physiological and cognitive variables, including tympanic temperature, blood oxygen saturation (SaO), and vigilance were recorded. Urinal/salivary samples were collected and subjected to cortisol or cortisone analysis, and plasma samples were subjected to transcriptomic analysis of circular RNA (circRNA) expression using microarray. Plasma neurotransmitters were measured by targeted metabolic analysis, and the levels of inflammatory factors were assessed by antibody microarray.

RESULTS

The volunteers showed significantly increased sleepiness and decreased vigilance during SD, and the changes in circadian rhythm and plasma biochemistry were observed. The plasma calcium (= 0.0007) was induced by SD, while ischaemia-modified albumin (IMA, = 0.0030) and total bile acid (TBA, = 0.0157) decreased. Differentially expressed circRNAs in plasma were identified, which are involved in multiple signaling pathways including neuronal regulation and immunity. Accordingly, SD induced a decrease in 3-hydroxybutyric acid (3OBH, = 0.0002) and an increase in thyroxine (T4, < 0.0001) in plasma. The plasma anti-inflammatory cytokine IL-10 was downregulated while other ten inflammatory factors were upregulated.

CONCLUSION

This study demonstrates that SD influences biochemical, physiological, cognitive variables, and the significantly changed variables may serve as candidates of SD markers. These findings may further our understanding of the detrimental consequence of sleep disturbance at multiple levels.

摘要

引言

睡眠不足和睡眠剥夺(SD)会对健康、认知、情绪和行为产生有害影响。然而,睡眠不足和SD在许多行业中普遍存在,并发生在各种紧急情况下。SD的有害后果尚未完全阐明。本研究旨在评估SD对生理、警觉性和血浆生化变量的广泛影响。

方法

招募了17名志愿者参加32.5小时的SD实验。记录了多个生理和认知变量,包括鼓膜温度、血氧饱和度(SaO)和警觉性。收集尿液/唾液样本并进行皮质醇或可的松分析,血浆样本使用微阵列进行环状RNA(circRNA)表达的转录组分析。通过靶向代谢分析测量血浆神经递质,并通过抗体微阵列评估炎症因子水平。

结果

志愿者在SD期间表现出明显的嗜睡增加和警觉性下降,并观察到昼夜节律和血浆生化的变化。SD诱导血浆钙(=0.0007)升高,而缺血修饰白蛋白(IMA,=0.0030)和总胆汁酸(TBA,=0.0157)降低。鉴定出了血浆中差异表达的circRNAs,它们参与了包括神经元调节和免疫在内的多个信号通路。相应地,SD诱导血浆中3-羟基丁酸(3OBH,=0.0002)降低和甲状腺素(T4,<0.0001)升高。血浆抗炎细胞因子IL-10下调,而其他十种炎症因子上调。

结论

本研究表明SD会影响生化、生理、认知变量,且显著变化的变量可能作为SD标志物的候选者。这些发现可能会在多个层面上加深我们对睡眠障碍有害后果的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/994be0bd83e9/fspor-06-1412044-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/698d7b3869d8/fspor-06-1412044-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/c001491f6751/fspor-06-1412044-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/8239198e1cb2/fspor-06-1412044-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/4f7d1ba6d590/fspor-06-1412044-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/994be0bd83e9/fspor-06-1412044-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/698d7b3869d8/fspor-06-1412044-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/c001491f6751/fspor-06-1412044-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/8239198e1cb2/fspor-06-1412044-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/4f7d1ba6d590/fspor-06-1412044-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/11239445/994be0bd83e9/fspor-06-1412044-g005.jpg

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