Abstract：
OBJECTIVE: To synthesise the literature examining the autonomic nervous system (ANS) and cortisol responses to an acute stressor following total sleep deprivation (TSD) in healthy adult subjects.
METHODS: We conducted a systematic review (CRD42022293857) following the latest PRISMA statement. We searched Medline (via Ovid), Embase (via Ovid), PsycINFO (via Ovid), CINAHL complete and Scopus databases, without year restriction, using search terms related to \"sleep deprivation\", \"stress\", \"autonomic nervous system\" and \"cortisol\". Two independent team members used pre-defined inclusion/exclusion criteria to assess eligibility and extract data. We used RoB 2 to assess the risk of bias in randomised controlled trials, and ROBINS-I for non-randomised studies.
RESULTS: Sixteen studies, with 581 participants (mean age = 29 ± 12 years), were eligible for inclusion in the descriptive syntheses. Half of the studies (n = 8) were conducted in the United States of America. The most commonly used study designs were randomised crossover studies (n = 7) and randomised controlled trials (n = 5). Most studies used a single night of TSD (n = 13) which was followed by a psychological (n = 6), physical (n = 5) or psychological and physical (n = 5) acute stressor event. Heart rate (n = 8), cortisol (n = 7) and blood pressure (n =6) were the most reported outcomes, while only a single study used forearm vascular conductance and forearm blood flow. Ten studies found that TSD changed, at least, one marker of ANS or cortisol response. TSD compared with a sleep control condition increased cortisol level (n=1), systolic blood pressure (n=3), diastolic blood pressure (n=2), mean arterial pressure (n=1), and electrodermal activity (n=1) after acute stress. Also, compared with a sleep control, TSD blunted cortisol (n=2), heart rate (n=1) and systolic blood pressure (n=2) responses after acute stress. However, TSD did not change ANS or cortisol responses to acute stressors in 73 % of the total reported outcomes. Furthermore, 10 RCT studies (62.5 %) were assigned as \"some concerns\" and two RCT studies (12.5 %) were attributed \"high\" risk of bias. Additionally, one non-randomised trial was classified as \"moderate\" and three non-randomised trials as \"serious\" risk of bias.
CONCLUSIONS: The markers of ANS and cortisol responses to acute stress after TSD in healthy individuals reveal a scarcity of consistent evidence. The included studies present enough evidence that TSD induces either blunted or exaggerated ANS or cortisol responses to laboratory stresses supporting the \"bidirectional multi-system reactivity hypothesis.\". It appears that a comprehensive understanding of this phenomenon still lacks robust evidence, and further research is needed to clarify these relationships.
METHODS: We conducted a systematic review (CRD42022293857) following the latest PRISMA statement. We searched Medline (via Ovid), Embase (via Ovid), PsycINFO (via Ovid), CINAHL complete and Scopus databases, without year restriction, using search terms related to \"sleep deprivation\", \"stress\", \"autonomic nervous system\" and \"cortisol\". Two independent team members used pre-defined inclusion/exclusion criteria to assess eligibility and extract data. We used RoB 2 to assess the risk of bias in randomised controlled trials, and ROBINS-I for non-randomised studies.
RESULTS: Sixteen studies, with 581 participants (mean age = 29 ± 12 years), were eligible for inclusion in the descriptive syntheses. Half of the studies (n = 8) were conducted in the United States of America. The most commonly used study designs were randomised crossover studies (n = 7) and randomised controlled trials (n = 5). Most studies used a single night of TSD (n = 13) which was followed by a psychological (n = 6), physical (n = 5) or psychological and physical (n = 5) acute stressor event. Heart rate (n = 8), cortisol (n = 7) and blood pressure (n =6) were the most reported outcomes, while only a single study used forearm vascular conductance and forearm blood flow. Ten studies found that TSD changed, at least, one marker of ANS or cortisol response. TSD compared with a sleep control condition increased cortisol level (n=1), systolic blood pressure (n=3), diastolic blood pressure (n=2), mean arterial pressure (n=1), and electrodermal activity (n=1) after acute stress. Also, compared with a sleep control, TSD blunted cortisol (n=2), heart rate (n=1) and systolic blood pressure (n=2) responses after acute stress. However, TSD did not change ANS or cortisol responses to acute stressors in 73 % of the total reported outcomes. Furthermore, 10 RCT studies (62.5 %) were assigned as \"some concerns\" and two RCT studies (12.5 %) were attributed \"high\" risk of bias. Additionally, one non-randomised trial was classified as \"moderate\" and three non-randomised trials as \"serious\" risk of bias.
CONCLUSIONS: The markers of ANS and cortisol responses to acute stress after TSD in healthy individuals reveal a scarcity of consistent evidence. The included studies present enough evidence that TSD induces either blunted or exaggerated ANS or cortisol responses to laboratory stresses supporting the \"bidirectional multi-system reactivity hypothesis.\". It appears that a comprehensive understanding of this phenomenon still lacks robust evidence, and further research is needed to clarify these relationships.
摘要：
目的：综合研究健康成年受试者完全睡眠剥夺（TSD）后自主神经系统（ANS）和皮质醇对急性应激源的反应的文献。
方法：我们根据最新的PRISMA声明进行了系统评价（CRD42022293857）。我们搜索了Medline（通过Ovid），Embase（通过Ovid），PsycINFO（通过Ovid），CINAHL完整数据库和Scopus数据库，没有年份限制,使用与“睡眠剥夺”相关的搜索词，“压力”，“自主神经系统”和“皮质醇”。两名独立团队成员使用预定义的纳入/排除标准来评估资格并提取数据。我们使用RoB2评估随机对照试验中的偏倚风险，和ROBINS-I用于非随机研究。
结果：16项研究，581名参与者（平均年龄=29±12岁），有资格纳入描述性综合。一半的研究（n=8）在美国进行。最常用的研究设计是随机交叉研究（n=7）和随机对照试验（n=5）。大多数研究使用了一个晚上的TSD（n=13），然后是心理（n=6），身体（n=5）或心理和身体（n=5）急性应激源事件。心率（n=8），皮质醇（n=7）和血压（n=6）是报告最多的结果，而只有一项研究使用了前臂血管电导和前臂血流量。十项研究发现TSD改变了，至少,ANS或皮质醇反应的一个标记。与睡眠控制条件相比，TSD增加了皮质醇水平（n=1），收缩压（n=3），舒张压（n=2），平均动脉压（n=1），和急性应激后的皮肤电活动（n=1）。此外，与睡眠控制相比，TSD减弱皮质醇（n=2），急性应激后的心率（n=1）和收缩压（n=2）反应。然而,在73%的总报告结局中，TSD没有改变ANS或皮质醇对急性应激源的反应。此外，10项RCT研究（62.5%）被列为“一些担忧”，2项RCT研究（12.5%）被列为“高”偏倚风险。此外,一项非随机试验被归类为"中度",三项非随机试验被归类为"严重"偏倚风险.
结论：健康个体对TSD后急性应激的ANS和皮质醇反应的标志物显示缺乏一致的证据。所包括的研究提供了足够的证据，表明TSD诱导对实验室压力的钝化或夸大的ANS或皮质醇反应，支持“双向多系统反应性假说”。\."看来，对这一现象的全面了解仍然缺乏有力的证据，需要进一步的研究来澄清这些关系。
方法：我们根据最新的PRISMA声明进行了系统评价（CRD42022293857）。我们搜索了Medline（通过Ovid），Embase（通过Ovid），PsycINFO（通过Ovid），CINAHL完整数据库和Scopus数据库，没有年份限制,使用与“睡眠剥夺”相关的搜索词，“压力”，“自主神经系统”和“皮质醇”。两名独立团队成员使用预定义的纳入/排除标准来评估资格并提取数据。我们使用RoB2评估随机对照试验中的偏倚风险，和ROBINS-I用于非随机研究。
结果：16项研究，581名参与者（平均年龄=29±12岁），有资格纳入描述性综合。一半的研究（n=8）在美国进行。最常用的研究设计是随机交叉研究（n=7）和随机对照试验（n=5）。大多数研究使用了一个晚上的TSD（n=13），然后是心理（n=6），身体（n=5）或心理和身体（n=5）急性应激源事件。心率（n=8），皮质醇（n=7）和血压（n=6）是报告最多的结果，而只有一项研究使用了前臂血管电导和前臂血流量。十项研究发现TSD改变了，至少,ANS或皮质醇反应的一个标记。与睡眠控制条件相比，TSD增加了皮质醇水平（n=1），收缩压（n=3），舒张压（n=2），平均动脉压（n=1），和急性应激后的皮肤电活动（n=1）。此外，与睡眠控制相比，TSD减弱皮质醇（n=2），急性应激后的心率（n=1）和收缩压（n=2）反应。然而,在73%的总报告结局中，TSD没有改变ANS或皮质醇对急性应激源的反应。此外，10项RCT研究（62.5%）被列为“一些担忧”，2项RCT研究（12.5%）被列为“高”偏倚风险。此外,一项非随机试验被归类为"中度",三项非随机试验被归类为"严重"偏倚风险.
结论：健康个体对TSD后急性应激的ANS和皮质醇反应的标志物显示缺乏一致的证据。所包括的研究提供了足够的证据，表明TSD诱导对实验室压力的钝化或夸大的ANS或皮质醇反应，支持“双向多系统反应性假说”。\."看来，对这一现象的全面了解仍然缺乏有力的证据，需要进一步的研究来澄清这些关系。
