<p><b>Session:</b> Symposium—Maternal stress during pregnancy may shape the rest of your life.</p><p><b>Presentation:</b> Long-term effects of perinatal stress exposure on adult health in animal models.</p><p><b>Speaker:</b> Viviana Lo Martire, Italy.</p><p><b>Summary</b></p><p>The Developmental Origins of Health and Disease (DOHaD) theory hypothesizes that environmental exposures during early life (particularly the in-utero period) can permanently influence health and vulnerability to diseases later in life. Adult-onset diseases may be linked to early life environmental conditions. The brain regions involved have not yet been identified but, among other areas, the hippocampus is likely to be permanently modulated by early life stress. This structure is involved in the regulation of the activity of the hypothalamic–pituitary–adrenal (HPA) axis, the primary component of stress response. A growing body of evidence suggests that perinatal stress exposure leads to diseases in adult life associated to a hyperactivation of the HPA axis, possibly through an epigenetic programming of the hippocampus, a key structure in the coordination of the hormonal stress response. The persistent hyperactivation of the HPA axis has several consequences also on wake–sleep bahavior, since its mediators acts as wake-promoting molecules. There is a bidirectional relationship between stress and sleep: stress inducing factors may alter sleep–wake architecture and sleep impairment may deeply impact several biological pathways, including stress responses and, eventually, quality of life. However, a new aspect is emerging: the moment of life in which stress is acting should be considered as a relevant factor in mediating the effects of this bidirectional relationship. Here, data from animal studies are collected and presented in order to demonstrate that perinatal stress exposure has long-term effects on sleep phenotype during adulthood. Moreover, the hypothesis that maternal sleep loss during pregnancy can be considered as a prenatal stress factors with the potential to program wake–sleep behaviour, leading to sleep disturbances in adulthood, will be considered. Animal studies produce compelling evidence that: (1) perinatal stress may lead, possibly through epigenetic mechanisms, to health problems in adults, including sleep derangements; (2) sleep loss during pregnancy may be responsible for long-term negative outcomes, including wake–sleep disorders. In conclusion, stress exposure during pregnancy should be considered a big issue not only for mothers but also for children's health in the long-term. Thus, preserving mothers' mental health during pregnancy should be a worldwide priority.</p><p><b>Conflict of Interest</b>: No.</p><p><b>Session:</b> Symposium—What can we learn about sleep from aperiodic neural activity?</p><p><b>Presentation:</b> Fractal cycles of sleep: A new aperiodic activity-based definition of sleep cycles.</p><p><b>Speaker:</b> Yevgenia Rosenblum, Netherl
牙医也可以在预防和早期诊断睡眠磨牙症方面发挥作用，识别口腔内的征兆，例如：牙齿折断、釉质断裂、畸形或裂隙、颞下颌关节疼痛或不适、咬合不正或牙齿排列不齐、舌痕和颊粘膜上的 "白线"。此外，咬指甲、咬东西和吸吮拇指等副功能性习惯也可能是相关的征兆。SB 的治疗应着眼于保护口腔结构免受 SB 的影响，采取的保守策略包括：口腔夹板（主要推荐用于成人）、生物反馈行为疗法、放松或冥想、针灸、理疗和改善睡眠卫生。药物治疗（抗抑郁药、肌肉松弛剂、苯二氮卓类药物等）也有使用。然而，还需要进一步的研究来确认药物的疗效：无：特邀专题讨论会--欧洲牙科睡眠医学学会（EADSM）--睡眠医学中的牙科医学：一个综合的合作模式：演讲题目：牙科医学与睡眠医学：整合模式合作：演讲人：Susana Falardo Ramos演讲人：葡萄牙的苏珊娜-法拉多-拉莫斯（Susana Falardo Ramos）。牙科医生、颌面外科医生和其他口腔卫生专业人员对睡眠相关障碍的了解和认识也在不断提高。由于需要筛查与睡眠相关的呼吸障碍、运动障碍以及睡眠与口腔疼痛之间的关系，因此睡眠专家之间有必要开展多学科合作。作为以同一屋檐下的睡眠医学为目标的综合模式的一部分，本次研讨会旨在探讨多学科合作：无：专题讨论会--小儿 OSA 的呼吸相关唤醒：对诊断和管理的影响：演讲人：苏珊娜-法拉尔多-拉莫斯（Susana Falardo Ramos）：Susana Falardo Ramos，葡萄牙.摘要：牙科医学对睡眠医学的兴趣一直在上升。牙科医生、颌面外科医生和其他口腔卫生专业人员对睡眠相关障碍的了解和认识也在增加。由于需要筛查与睡眠相关的呼吸障碍、运动障碍以及睡眠与口腔疼痛之间的关系，因此睡眠专家之间有必要开展多学科合作。作为以同一屋檐下的睡眠医学为目标的综合模式的一部分，本次研讨会旨在探讨多学科合作：无：专题讨论会-涣散的洞察力：了解眼睛在睡眠-觉醒控制中的作用：睡眠剥夺不会改变小鼠的视网膜电图：汤姆-德布尔（Tom De Boer），荷兰.摘要睡眠平衡压力和昼夜节律是否以及如何相互作用并影响彼此的功能是睡眠研究中的一个重要问题，尤其是在睡眠调节的双过程模型中。过去的研究表明，二者之间存在相互作用，尤其是睡眠压力可能会影响昼夜节律钟的功能。对昼夜节律钟功能影响最大的是昼夜节律钟对光线的移相能力，当动物睡眠不足时，这种能力会大大降低。将这项工作与咖啡因的应用相结合，表明这种影响是通过在剥夺睡眠期间释放腺苷来介导的，腺苷会降低相移诱导通路（可能在嗜铬细胞上核（SCN））中的神经元活动。使用咖啡因进行的其他研究表明，昼夜节律周期也可能受到腺苷的影响。这些研究结果将结合光信息从视网膜到SCN，再到下游时钟输出的路径进行讨论。此外，还将讨论咖啡因治疗的效果，咖啡因可抵消睡眠压力增加的影响。在此背景下，将讨论行为的昼夜节律周期和这种行为的相移，还将讨论SCN神经元活动的变化，以及视网膜电图的推测变化，因为眼睛是该路径的第一站：无：专题讨论会-稀释的洞察力：了解眼睛在睡眠-觉醒控制中的作用：咖啡因影响人类睡眠-觉醒调节的视网膜机制：摘要睡眠压力会调节昼夜节律，而昼夜节律是通过所谓的内在光敏神经节细胞（ipRGCs）在眼睛中提取的光-暗信息与外部世界同步的。体外实验表明，腺苷会降低ipRGCs对光的反应，腺苷是一种神经调节剂，在剥夺睡眠时会增加，并被咖啡因拮抗。
{"title":"Invited Speaker Abstracts","authors":"","doi":"10.1111/jsr.14347","DOIUrl":"https://doi.org/10.1111/jsr.14347","url":null,"abstract":"<p><b>Session:</b> Symposium—Maternal stress during pregnancy may shape the rest of your life.</p><p><b>Presentation:</b> Long-term effects of perinatal stress exposure on adult health in animal models.</p><p><b>Speaker:</b> Viviana Lo Martire, Italy.</p><p><b>Summary</b></p><p>The Developmental Origins of Health and Disease (DOHaD) theory hypothesizes that environmental exposures during early life (particularly the in-utero period) can permanently influence health and vulnerability to diseases later in life. Adult-onset diseases may be linked to early life environmental conditions. The brain regions involved have not yet been identified but, among other areas, the hippocampus is likely to be permanently modulated by early life stress. This structure is involved in the regulation of the activity of the hypothalamic–pituitary–adrenal (HPA) axis, the primary component of stress response. A growing body of evidence suggests that perinatal stress exposure leads to diseases in adult life associated to a hyperactivation of the HPA axis, possibly through an epigenetic programming of the hippocampus, a key structure in the coordination of the hormonal stress response. The persistent hyperactivation of the HPA axis has several consequences also on wake–sleep bahavior, since its mediators acts as wake-promoting molecules. There is a bidirectional relationship between stress and sleep: stress inducing factors may alter sleep–wake architecture and sleep impairment may deeply impact several biological pathways, including stress responses and, eventually, quality of life. However, a new aspect is emerging: the moment of life in which stress is acting should be considered as a relevant factor in mediating the effects of this bidirectional relationship. Here, data from animal studies are collected and presented in order to demonstrate that perinatal stress exposure has long-term effects on sleep phenotype during adulthood. Moreover, the hypothesis that maternal sleep loss during pregnancy can be considered as a prenatal stress factors with the potential to program wake–sleep behaviour, leading to sleep disturbances in adulthood, will be considered. Animal studies produce compelling evidence that: (1) perinatal stress may lead, possibly through epigenetic mechanisms, to health problems in adults, including sleep derangements; (2) sleep loss during pregnancy may be responsible for long-term negative outcomes, including wake–sleep disorders. In conclusion, stress exposure during pregnancy should be considered a big issue not only for mothers but also for children's health in the long-term. Thus, preserving mothers' mental health during pregnancy should be a worldwide priority.</p><p><b>Conflict of Interest</b>: No.</p><p><b>Session:</b> Symposium—What can we learn about sleep from aperiodic neural activity?</p><p><b>Presentation:</b> Fractal cycles of sleep: A new aperiodic activity-based definition of sleep cycles.</p><p><b>Speaker:</b> Yevgenia Rosenblum, Netherl","PeriodicalId":17057,"journal":{"name":"Journal of Sleep Research","volume":"33 S1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jsr.14347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142313416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hugo Saner, Kevin Möri, Narayan Schütz, Philipp Buluschek, Tobias Nef
Little is known about the correlation between subjective perception and objective measures of sleep quality in particular in the oldest-old. The aim of this study was to perform longitudinal home sleep monitoring in this age group, and to correlate results with self-reported sleep quality. This is a prospective longitudinal home sleep-monitoring study in 12 oldest-old persons (age 83-100 years, mean 93 years, 10 females) without serious sleep disorders over 1 month using a contactless piezoelectric bed sensor (EMFIT QS). Participants provided daily information about perceived sleep. Duration in bed: 264-639 min (M = 476 min, SD = 94 min); sleep duration: 239-561 min (M = 418 min, SD = 91 min); sleep efficiency: 83.9%-90.7% (M = 87.4%, SD = 5.0%); rapid eye movement sleep: 21.1%-29.0% (M = 24.9%, SD = 5.5%); deep sleep: 13.3%-19.6% (M = 16.8%, SD = 4.5%). All but one participant showed a weak (r = 0.2-0.39) or very weak (r = 0-0.19) positive or negative correlation between self-rated sleep quality and the sleep score. In conclusion, longitudinal sleep monitoring in the home of elderly people by a contactless piezoelectric sensor system is feasible and well accepted. Subjective perception of sleep quality does not correlate well with objective measures in our study. Our findings may help to develop new approaches to sleep problems in the oldest-old including home monitoring. Further studies are needed to explore the full potential of this approach.
{"title":"Sleep characteristics and self-reported sleep quality in the oldest-old: Results from a prospective longitudinal cohort study.","authors":"Hugo Saner, Kevin Möri, Narayan Schütz, Philipp Buluschek, Tobias Nef","doi":"10.1111/jsr.14348","DOIUrl":"https://doi.org/10.1111/jsr.14348","url":null,"abstract":"<p><p>Little is known about the correlation between subjective perception and objective measures of sleep quality in particular in the oldest-old. The aim of this study was to perform longitudinal home sleep monitoring in this age group, and to correlate results with self-reported sleep quality. This is a prospective longitudinal home sleep-monitoring study in 12 oldest-old persons (age 83-100 years, mean 93 years, 10 females) without serious sleep disorders over 1 month using a contactless piezoelectric bed sensor (EMFIT QS). Participants provided daily information about perceived sleep. Duration in bed: 264-639 min (M = 476 min, SD = 94 min); sleep duration: 239-561 min (M = 418 min, SD = 91 min); sleep efficiency: 83.9%-90.7% (M = 87.4%, SD = 5.0%); rapid eye movement sleep: 21.1%-29.0% (M = 24.9%, SD = 5.5%); deep sleep: 13.3%-19.6% (M = 16.8%, SD = 4.5%). All but one participant showed a weak (r = 0.2-0.39) or very weak (r = 0-0.19) positive or negative correlation between self-rated sleep quality and the sleep score. In conclusion, longitudinal sleep monitoring in the home of elderly people by a contactless piezoelectric sensor system is feasible and well accepted. Subjective perception of sleep quality does not correlate well with objective measures in our study. Our findings may help to develop new approaches to sleep problems in the oldest-old including home monitoring. Further studies are needed to explore the full potential of this approach.</p>","PeriodicalId":17057,"journal":{"name":"Journal of Sleep Research","volume":" ","pages":"e14348"},"PeriodicalIF":3.4,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142289831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jonathon Jacobs, Caitlin E. Martin, Bernard Fuemmeler, Shanshan Chen
SummarySleep is a complex biological process regulated by networks of neurons and environmental factors. As one falls asleep, neurotransmitters from sleep–wake regulating neurones work in synergy to control the switching of different sleep states throughout the night. As sleep disorders or underlying neuropathology can manifest as irregular switching, analysing these patterns is crucial in sleep medicine and neuroscience. While hypnograms represent the switching of sleep states well, current analyses of hypnograms often rely on oversimplified temporal descriptive statistics (TDS, e.g., total time spent in a sleep state), which miss the opportunity to study the sleep state switching by overlooking the complex structures of hypnograms. In this paper, we propose analysing sleep hypnograms using a seven‐state continuous‐time Markov model (CTMM). This proposed model leverages the CTMM to depict the time‐varying sleep‐state transitions, and probes three types of insomnia by distinguishing three types of wake states. Fitting the proposed model to data from 2056 ageing adults in the Multi‐Ethnic Study of Atherosclerosis (MESA) Sleep study, we profiled sleep architectures in this population and identified the various associations between the sleep state transitions and demographic factors and subjective sleep questions. Ageing, sex, and race all show distinctive patterns of sleep state transitions. Furthermore, we also found that the perception of insomnia and restless sleep are significantly associated with critical transitions in the sleep architecture. By incorporating three wake states in a continuous‐time Markov model, our proposed method reveals interesting insights into the relationships between objective hypnogram data and subjective sleep quality assessments.
{"title":"Profiling the sleep architecture of ageing adults using a seven‐state continuous‐time Markov model","authors":"Jonathon Jacobs, Caitlin E. Martin, Bernard Fuemmeler, Shanshan Chen","doi":"10.1111/jsr.14331","DOIUrl":"https://doi.org/10.1111/jsr.14331","url":null,"abstract":"SummarySleep is a complex biological process regulated by networks of neurons and environmental factors. As one falls asleep, neurotransmitters from sleep–wake regulating neurones work in synergy to control the switching of different sleep states throughout the night. As sleep disorders or underlying neuropathology can manifest as irregular switching, analysing these patterns is crucial in sleep medicine and neuroscience. While hypnograms represent the switching of sleep states well, current analyses of hypnograms often rely on oversimplified temporal descriptive statistics (TDS, e.g., total time spent in a sleep state), which miss the opportunity to study the sleep state switching by overlooking the complex structures of hypnograms. In this paper, we propose analysing sleep hypnograms using a seven‐state continuous‐time Markov model (CTMM). This proposed model leverages the CTMM to depict the time‐varying sleep‐state transitions, and probes three types of insomnia by distinguishing three types of wake states. Fitting the proposed model to data from 2056 ageing adults in the Multi‐Ethnic Study of Atherosclerosis (MESA) Sleep study, we profiled sleep architectures in this population and identified the various associations between the sleep state transitions and demographic factors and subjective sleep questions. Ageing, sex, and race all show distinctive patterns of sleep state transitions. Furthermore, we also found that the perception of insomnia and restless sleep are significantly associated with critical transitions in the sleep architecture. By incorporating three wake states in a continuous‐time Markov model, our proposed method reveals interesting insights into the relationships between objective hypnogram data and subjective sleep quality assessments.","PeriodicalId":17057,"journal":{"name":"Journal of Sleep Research","volume":"18 1","pages":"e14331"},"PeriodicalIF":4.4,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emma Hertel, Elaxmi Sathiyalingam, Linea Pilgaard, Simone Juline Brommann, Rocco Giordano, Kristian Kjær‐Staal Petersen
SummarySleep disturbances exacerbate chronic pain, increase psychological load, and increase inflammation. Delayed onset muscle soreness (DOMS) mimics aspects of chronic pain, predominantly affecting peripheral pain mechanisms, while experimental sleep provocations have been shown to impact central pain mechanisms. This study aimed to combine a DOMS model with total sleep deprivation (TSD) to create a novel model affecting both peripheral and central pain mechanisms. A total of 30 healthy participants attended two sessions (baseline and follow‐up) separated by 24 h of TSD and a home rating after 48 h. Assessments of interleukin 6 (IL‐6) levels, sleep quality, pain catastrophising, affect, and symptoms of depression and anxiety were included in the baseline and follow‐up sessions. Additionally, pressure pain and tolerance thresholds, temporal summation, and conditioned pain modulation (CPM) were assessed using cuff‐pressure algometry in the baseline and follow‐up sessions. DOMS was induced with eccentric calf raises during the baseline session followed by 24 h of TSD. At follow‐up pain tolerance (p = 0.012) was significantly reduced, and CPM (p = 0.036) was significantly impaired compared to baseline. Psychological changes included decreases in pain catastrophising (p = 0.027), positive affect (p < 0.001), negative affect (p = 0.003), and anxiety (p = 0.012). Explorative regression models predicted 58% and 68% of DOMS pain intensity after 24 and 48 h, respectively, based on baseline body mass index, pain thresholds, psychological measures, and IL‐6 (p < 0.01). Combining DOMS with 1 night of TSD induced pain hypersensitivity, impaired CPM, and altered psychological states. A combination of baseline inflammation, psychological measures, and pain sensitivity significantly predicted DOMS pain intensity after 24 and 48 h.
{"title":"Psychophysical changes after total sleep deprivation and experimental muscle pain","authors":"Emma Hertel, Elaxmi Sathiyalingam, Linea Pilgaard, Simone Juline Brommann, Rocco Giordano, Kristian Kjær‐Staal Petersen","doi":"10.1111/jsr.14329","DOIUrl":"https://doi.org/10.1111/jsr.14329","url":null,"abstract":"SummarySleep disturbances exacerbate chronic pain, increase psychological load, and increase inflammation. Delayed onset muscle soreness (DOMS) mimics aspects of chronic pain, predominantly affecting peripheral pain mechanisms, while experimental sleep provocations have been shown to impact central pain mechanisms. This study aimed to combine a DOMS model with total sleep deprivation (TSD) to create a novel model affecting both peripheral and central pain mechanisms. A total of 30 healthy participants attended two sessions (baseline and follow‐up) separated by 24 h of TSD and a home rating after 48 h. Assessments of interleukin 6 (IL‐6) levels, sleep quality, pain catastrophising, affect, and symptoms of depression and anxiety were included in the baseline and follow‐up sessions. Additionally, pressure pain and tolerance thresholds, temporal summation, and conditioned pain modulation (CPM) were assessed using cuff‐pressure algometry in the baseline and follow‐up sessions. DOMS was induced with eccentric calf raises during the baseline session followed by 24 h of TSD. At follow‐up pain tolerance (<jats:italic>p</jats:italic> = 0.012) was significantly reduced, and CPM (<jats:italic>p</jats:italic> = 0.036) was significantly impaired compared to baseline. Psychological changes included decreases in pain catastrophising (<jats:italic>p</jats:italic> = 0.027), positive affect (<jats:italic>p</jats:italic> < 0.001), negative affect (<jats:italic>p</jats:italic> = 0.003), and anxiety (<jats:italic>p</jats:italic> = 0.012). Explorative regression models predicted 58% and 68% of DOMS pain intensity after 24 and 48 h, respectively, based on baseline body mass index, pain thresholds, psychological measures, and IL‐6 (<jats:italic>p</jats:italic> < 0.01). Combining DOMS with 1 night of TSD induced pain hypersensitivity, impaired CPM, and altered psychological states. A combination of baseline inflammation, psychological measures, and pain sensitivity significantly predicted DOMS pain intensity after 24 and 48 h.","PeriodicalId":17057,"journal":{"name":"Journal of Sleep Research","volume":"11 1","pages":"e14329"},"PeriodicalIF":4.4,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Landon S. Deru, Cameron G. Jacobsen, Elizabeth Z. Gipson, Parker G. Graves, Andrew J. Stevens, Garrett B. Duncan, William F. Christensen, Bruce W. Bailey
SummaryUtilizing a randomized control design, 42 healthy adults (22.5 ± 2.8 years) participated in alternate‐day modified fasting over a 12‐day treatment period. Assessments of sleep included sleep time, efficiency, latency and wake after sleep onset, and assessments of physical activity included steps, energy expenditure, sedentary time, time spent in light physical activity and time spent in moderate‐to‐vigorous activity. Additional measurements included body composition and mood. The alternate‐day modified fasting group consumed 25.8% ± 0.3% fewer calories compared with the control group (p = 0.03). There were no differences between groups for change in body mass index (p = 0.87), total fat mass (p = 0.91) or total lean mass (p = 0.88). Daily energy expenditure did not differ between groups (p = 0.11). On fast days, participants spent 34.5 ± 12.7 more minutes sedentary (p = 0.01), took 1100 ± 362 fewer steps (p < 0.01), and engaged in 27.2 ± 8.4 fewer minutes of moderate‐to‐vigorous physical activity (p = 0.00) compared with non‐fasting days. Sleep duration, efficiency, latency or wake after sleep onset were not different between conditions (p = 0.92, p = 0.10, p = 0.09 and p = 0.66, respectively). We conclude that alternate‐day modified fasting does not alter sleep time, efficiency, latency or wake after sleep onset in people reporting poor sleep quality, and does not alter overall physical activity. Although average daily physical activity is not altered, fasting in this manner does tend to result in more sedentary time and less physical activity with compensation on non‐fasting days.
{"title":"The effects of alternate‐day fasting on sleep and physical activity in poor sleeping adults: A randomized control trial","authors":"Landon S. Deru, Cameron G. Jacobsen, Elizabeth Z. Gipson, Parker G. Graves, Andrew J. Stevens, Garrett B. Duncan, William F. Christensen, Bruce W. Bailey","doi":"10.1111/jsr.14341","DOIUrl":"https://doi.org/10.1111/jsr.14341","url":null,"abstract":"SummaryUtilizing a randomized control design, 42 healthy adults (22.5 ± 2.8 years) participated in alternate‐day modified fasting over a 12‐day treatment period. Assessments of sleep included sleep time, efficiency, latency and wake after sleep onset, and assessments of physical activity included steps, energy expenditure, sedentary time, time spent in light physical activity and time spent in moderate‐to‐vigorous activity. Additional measurements included body composition and mood. The alternate‐day modified fasting group consumed 25.8% ± 0.3% fewer calories compared with the control group (<jats:italic>p</jats:italic> = 0.03). There were no differences between groups for change in body mass index (<jats:italic>p</jats:italic> = 0.87), total fat mass (<jats:italic>p</jats:italic> = 0.91) or total lean mass (<jats:italic>p</jats:italic> = 0.88). Daily energy expenditure did not differ between groups (<jats:italic>p</jats:italic> = 0.11). On fast days, participants spent 34.5 ± 12.7 more minutes sedentary (<jats:italic>p</jats:italic> = 0.01), took 1100 ± 362 fewer steps (<jats:italic>p</jats:italic> < 0.01), and engaged in 27.2 ± 8.4 fewer minutes of moderate‐to‐vigorous physical activity (<jats:italic>p</jats:italic> = 0.00) compared with non‐fasting days. Sleep duration, efficiency, latency or wake after sleep onset were not different between conditions (<jats:italic>p</jats:italic> = 0.92, <jats:italic>p</jats:italic> = 0.10, <jats:italic>p</jats:italic> = 0.09 and <jats:italic>p</jats:italic> = 0.66, respectively). We conclude that alternate‐day modified fasting does not alter sleep time, efficiency, latency or wake after sleep onset in people reporting poor sleep quality, and does not alter overall physical activity. Although average daily physical activity is not altered, fasting in this manner does tend to result in more sedentary time and less physical activity with compensation on non‐fasting days.","PeriodicalId":17057,"journal":{"name":"Journal of Sleep Research","volume":"116 1","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Liborio Parrino, Francesco Rausa, Giulia Balella, Dario Bottignole, Ivana Rosenzweig, Carlotta Mutti
SummaryThis article aims at providing a comprehensive review of the historical discovery and following research on rapid eye movement (REM) sleep, highlighting its manifold nature as a behavioural, electrophysiological and dreaming state. Pioneering works conducted by Aserinsky, Kleitman, Dement and Jouvet established the foundational understanding of REM sleep recurrence, brainstem mechanisms, and the paradoxical coexistence of electroencephalographic activation and muscle atonia. We focus on REM sleep homeostasis, emphasising its role in emotional recovery and the consequences of REM deprivation, such as the REM rebound effect. We also analyse the periodicity of REM sleep, its ultradian rhythm, and the physiological mechanisms underlying its regulation. Additionally, the article discusses the entangled relationship between arousals, sleep, and consciousness, pointing out the distinction between non‐REM and REM sleep‐related arousals, and the similarities between REM sleep and wakefulness.
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