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Sleep loss disrupts the neural signature of successful learning.
Guttesen, AÁV, Gaskell, MG, Madden, EV, Appleby, G, Cross, ZR, Cairney, SA
Cerebral cortex (New York, N.Y. : 1991). 2023;33(5):1610-1625
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Understanding how sleep disturbances impair learning and memory is increasingly important in modern society, where many people fail to regularly obtain an adequate amount of sleep. The aim of this study was to investigate the relationship between sleep-associated consolidation and next-day learning and how suppressing slow-wave activity (SWA) [during slow-wave sleep, electrical activity in the brain changes while the body relaxes into deep and restorative rest] contributes to this relationship. This study was a within-subjects (n = 30), crossover design which showed that sleep improved both memory retention and next-day learning however, there was no evidence of a relationship between these measures or with SWA. Furthermore, an absence of sleep disrupts the neural operations underpinning memory encoding, leading to suboptimal performance. Authors conclude that an extended lack of sleep might disrupt the ability to draw upon semantic knowledge when encoding novel associations, necessitating the use of more surface-based and ultimately suboptimal routes to learning.
Abstract
Sleep supports memory consolidation as well as next-day learning. The influential "Active Systems" account of offline consolidation suggests that sleep-associated memory processing paves the way for new learning, but empirical evidence in support of this idea is scarce. Using a within-subjects (n = 30), crossover design, we assessed behavioral and electrophysiological indices of episodic encoding after a night of sleep or total sleep deprivation in healthy adults (aged 18-25 years) and investigated whether behavioral performance was predicted by the overnight consolidation of episodic associations from the previous day. Sleep supported memory consolidation and next-day learning as compared to sleep deprivation. However, the magnitude of this sleep-associated consolidation benefit did not significantly predict the ability to form novel memories after sleep. Interestingly, sleep deprivation prompted a qualitative change in the neural signature of encoding: Whereas 12-20 Hz beta desynchronization-an established marker of successful encoding-was observed after sleep, sleep deprivation disrupted beta desynchrony during successful learning. Taken together, these findings suggest that effective learning depends on sleep but not necessarily on sleep-associated consolidation.
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Effects of Two Physical Activity Interventions on Sleep and Sedentary Time in Pregnant Women.
Alomairah, SA, Knudsen, SP, Roland, CB, Molsted, S, Clausen, TD, Bendix, JM, Løkkegaard, E, Jensen, AK, Larsen, JE, Jennum, P, et al
International journal of environmental research and public health. 2023;20(7)
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Pregnant women benefit from physical activity (PA) during pregnancy. The aim of this study was to assess the effect of the FitMum PA interventions on sleep quantity and quality and sedentary time (SED). This study was a secondary analysis of the FitMum study which included 220 healthy pregnant women. Participants were randomised to one of three groups. Results showed that pregnant women are prone to low sleep quality and high SED, which worsens as pregnancy progresses. Pregnant women who received structured supervised exercise training had better sleep quality and less SED than pregnant women receiving standard prenatal care when self-reported. Furthermore, when measured by a consumer activity tracker, no differences were observed between groups. Authors conclude that interventions that increase PA levels might improve sleep quality and decrease SED in pregnant women. Future behavioural interventions targeting pregnant women should include evidence-based content to improve sleep quality and reduce SED.
Abstract
Pregnancy is often associated with poor sleep and high sedentary time (SED). We investigated the effect of physical activity (PA) interventions on sleep and SED in pregnant women. A secondary analysis of a randomized controlled trial (n = 219) explored the effect of structured supervised exercise training (EXE) or motivational counseling on PA (MOT) compared to standard prenatal care (CON) on sleep and SED during pregnancy. Three times during pregnancy, sleep was determined by the Pittsburgh Sleep Quality Index (PSQI) and SED by the Pregnancy Physical Activity Questionnaire (PPAQ). Also, a wrist-worn consumer activity tracker measured sleep and SED continuously. Data from the activity tracker confirmed that sleep time decreases, and SED increases by approx. 30 and 24 min/day, respectively, from baseline (maximum gestational age (GA) week 15) to delivery. Compared to CON, the global PSQI score was better for EXE in GA week 28 (-0.8 [-1.5; -0.1], p = 0.031) and for both EXE and MOT in GA week 34 (-1 [-2; -0.5], p = 0.002; -1 [-2; -0.1], p = 0.026). In GA week 28, SED (h/day) from PPAQ was lower in EXE compared to both CON and MOT (-0.69 [-1; -0.0], p = 0.049; -0.6 [-1.0; -0.02], p = 0.042). In conclusion, PA interventions during pregnancy improved sleep quality and reduced SED.
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Increased Hunger, Food Cravings, Food Reward, and Portion Size Selection after Sleep Curtailment in Women Without Obesity.
Yang, CL, Schnepp, J, Tucker, RM
Nutrients. 2019;11(3)
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Insufficient sleep is a risk factor for overweight and obesity. A number of maladaptive changes take place that promote increased intake and weight gain. The aim of this randomised crossover study was to examine the impact of sleep deprivation on hunger, food cravings, food reward and portion size among 24 healthy women. Participants were randomised to either one normal night sleep or curtailed night sleep, where time in bed was reduced by 33%. Crossover visits occurred two weeks apart. Sleep duration was measured through imaging and sleep quality, hunger, tiredness, and food cravings were observed through questionnaires. This study found an increase in hunger, food cravings, food reward and portion sizes after a night of sleep deprivation. Based on this study the authors conclude reduced sleep duration can lead to increased energy intake and therefore an increased risk of obesity.
Abstract
This study examined the effects of one night of sleep curtailment on hunger, food cravings, food reward, and portion size selection. Women who reported habitually sleeping 7⁻9 h per night, were aged 18⁻55, were not obese, and had no sleep disorders were recruited. Sleep conditions in this randomized crossover study consisted of a normal night (NN) and a curtailed night (CN) where time in bed was reduced by 33%. Hunger, tiredness, sleep quality, sleepiness, and food cravings were measured. A progressive ratio task using chocolates assessed the food reward. Participants selected portions of various foods that reflected how much they wanted to eat at that time. The sleep duration was measured using a single-channel electroencephalograph. Twenty-four participants completed the study. The total sleep time was shorter during the CN (p < 0.001). Participants reported increased hunger (p = 0.013), tiredness (p < 0.001), sleepiness (p < 0.001), and food cravings (p = 0.002) after the CN. More chocolate was consumed after the CN (p = 0.004). Larger portion sizes selected after the CN resulted in increased energy plated for lunch (p = 0.034). In conclusion, the present study observed increased hunger, food cravings, food reward, and portion sizes of food after a night of modest sleep curtailment. These maladaptive responses could lead to higher energy intake and, ultimately, weight gain.
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Sleep restriction increases the neuronal response to unhealthy food in normal-weight individuals.
St-Onge, MP, Wolfe, S, Sy, M, Shechter, A, Hirsch, J
International journal of obesity (2005). 2014;38(3):411-6
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Sleep patterns influence eating behaviour and the body’s response to food. Previous studies suggest that short sleep duration leads to increased caloric intake and a desire for high-fat foods, however the specific neural mechanisms explaining how sleep restriction modulates this response is unknown. The aim of this study was to determine whether a specific area of the brain is activated in response to unhealthy compared with healthy foods. 25 participants were included, all of which were normal weight and had normal sleeping patterns. Each participant was tested after five nights of either 4 or 9 hours in bed by functional magnetic resonance imaging (fMRI). The test was performed while the participant was shown healthy and unhealthy food photos in the fasted state. This study found that after a period of restricted sleep compared with habitual sleep, unhealthy foods led to greater activation in brain regions associated with reward compared with healthy foods. This finding provides a model of neuronal mechanisms relating short sleep duration to obesity and cardio-metabolic risk factors and warrants further investigation.
Abstract
CONTEXT Sleep restriction alters responses to food. However, the underlying neural mechanisms for this effect are not well understood. OBJECTIVE The purpose of this study was to determine whether there is a neural system that is preferentially activated in response to unhealthy compared with healthy foods. PARTICIPANTS Twenty-five normal-weight individuals, who normally slept 7-9 h per night, completed both phases of this randomized controlled study. INTERVENTION Each participant was tested after a period of five nights of either 4 or 9 h in bed. Functional magnetic resonance imaging (fMRI) was performed in the fasted state, presenting healthy and unhealthy food stimuli and objects in a block design. Neuronal responses to unhealthy, relative to healthy food stimuli after each sleep period were assessed and compared. RESULTS After a period of restricted sleep, viewing unhealthy foods led to greater activation in the superior and middle temporal gyri, middle and superior frontal gyri, left inferior parietal lobule, orbitofrontal cortex, and right insula compared with healthy foods. These same stimuli presented after a period of habitual sleep did not produce marked activity patterns specific to unhealthy foods. Further, food intake during restricted sleep increased in association with a relative decrease in brain oxygenation level-dependent (BOLD) activity observed in the right insula. CONCLUSION This inverse relationship between insula activity and food intake and enhanced activation in brain reward and food-sensitive centers in response to unhealthy foods provides a model of neuronal mechanisms relating short sleep duration to obesity.