Impaired Insulin Profiles Following a Single Night of Sleep Restriction: The Impact of Acute Sprint Interval Exercise

Experimental sleep restriction (SR) has demonstrated reduced insulin sensitivity in healthy individuals. Exercise is well-known to be beneficial for metabolic health. A single bout of exercise has the capacity to increase insulin sensitivity for up to 2 days. Therefore, the current study aimed to determine if sprint interval exercise could attenuate the impairment in insulin sensitivity after one night of SR in healthy males. Nineteen males were recruited for this randomized crossover study which consisted of four conditions—control, SR, control plus exercise, and sleep restriction plus exercise. Time in bed was 8 hr (2300–0700) in the control conditions and 4 hr (0300–0700) in the SR conditions. Conditions were separated by a 1-week entraining period. Participants slept at home, and compliance was assessed using wrist actigraphy. Following the night of experimental sleep, participants either conducted sprint interval exercise or rested for the equivalent duration. An oral glucose tolerance test was then conducted. Blood samples were obtained at regular intervals for measurement of glucose and insulin. Insulin concentrations were higher in SR than control (p = .022). Late-phase insulin area under the curve was significantly lower in sleep restriction plus exercise than SR (862 ± 589 and 1,267 ± 558; p = .004). Glucose area under the curve was not different between conditions (p = .207). These findings suggest that exercise improves the late postprandial response following a single night of SR

Effects of work-related sleep restriction on acute physiological and psychological stress responses and their interactions: A review among emergency service personnel

Emergency work can expose personnel to sleep restriction. Inadequate amounts of sleep can negatively affect physiological and psychological stress responses. This review critiqued the emergency service literature (e.g., firefighting, police/law enforcement, defense forces, ambulance/paramedic personnel) that has investigated the effect of sleep restriction on hormonal, inflammatory and psychological responses. Furthermore, it investigated if a psycho-physiological approach can help contextualize the significance of such responses to assist emergency service agencies monitor the health of their personnel. The available literature suggests that sleep restriction across multiple work days can disrupt cytokine and cortisol levels, deteriorate mood and elicit simultaneous physiological and psychological responses. However, research concerning the interaction between such responses is limited and inconclusive. Therefore, it is unknown if a psycho-physiological relationship exists and as a result, it is currently not feasible for agencies to monitor sleep restriction related stress based on psycho- physiological interactions. Sleep restriction does however, appear to be a major stressor contributing to physiological and psychological responses and thus, warrants further investigation

Metabolic consequences of chronic sleep restriction in rats:Changes in body weight regulation and energy expenditure

Epidemiological studies have shown an association between short or disrupted sleep and an increased risk to develop obesity. In animal studies, however, sleep restriction leads to an attenuation of weight gain that cannot be explained by changes in energy intake. In the present study, we assessed whether the attenuated weight gain under conditions of restricted sleep is a consequence of an overall increase in energy expenditure. Adult male rats were subjected to a schedule of chronic sleep restriction (SR) for 8 days with a 4 h window of unrestricted rest per day. Electroencephalogram and electromyogram recordings were performed to quantify the effect of the sleep restriction schedule on sleep-wake patterns. In a separate experiment, we measured sleep restriction-induced changes in body weight, food intake, and regulatory hormones such as glucose, insulin, leptin and corticosterone. To investigate whether a change in energy expenditure underlies the attenuation of weight gain, energy expenditure was measured by the doubly labeled water method from day 5 until day 8 of the SR protocol. Results show a clear attenuation of weight gain during sleep restriction but no change in food intake. Baseline plasma glucose, insulin and leptin levels are decreased after sleep restriction which presumably reflects the nutritional status of the rats. The daily energy expenditure during SR was significantly increased compared to control rats. Together, we conclude that the attenuation of body weight gain in sleep restricted rats is explained by an overall increase in energy expenditure together with an unaltered energy intake. Published by Elsevier Inc

Hemodynamic effects of sleep restriction and laboratory stress

Neðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenThe reactivity hypothesis of hypertension states that persistent and exaggerated blood pressure (BP) responses to common stressful events may lead to the development of hypertension and cardiovascular disease. This experiment aimed to examine hemodynamic profile induced by behavioural challenges in the form of sleep restriction and psychosocial stress induced by time-pressured cognitive performance. Participants were 96 healthy male and female adults who received 40% of their usual overnight sleep on 2 of 4 nights preceding 4 morning visits to the research laboratory. Consistent with previous studies, sleep restriction had no appreciable effect on BP level. However, Finapres measurements of CO and TPR showed that the null effect of sleep restriction on BP concealed a pronounced vascular response in the form of marked increases in TPR, suggesting that a lifestyle characterised by persistent sleep loss could contribute significantly to the development of cardiovascular disease

Impact Of Sleep Restriction And Recovery On Motivation During Repeated Cognitive Performance Testing

Introduction: Both motivation and sleep deprivation affect cognitive performance. Especially during long-lasting studies with repeated cognitive performance tasks there is concern that subjects will lose motivation over time. Results may be confounded due to changes in motivation. Methods: In an ongoing study, 29 healthy volunteers performed 55 cognitive performance tasks at three-hourly intervals in a 12-day inpatient study. After two baseline nights with 8 h time in bed (TIB) the intervention group (N=20; mean age 26 ± 4 years, 9 females) underwent chronic sleep restriction for 5 nights (5 h TIB) with a following recovery night of 8 h TIB. The control group (N=9; mean age 25 ± 5 years, 3 females) had the opportunity to sleep 8 hours every night. Participants completed the Karolinska Sleepiness Scale (KSS) and a questionnaire about their motivation (from 1=very little/not motivated to 5=very motivated) at 6 p.m. on all days. Results: Wilcoxon signed-rank tests showed a significant decrease in motivation (p=.0439) and a significant increase in subjective sleepiness (p=.0184) from baseline (motivation: 2.8 ± 0.6 (SD), sleepiness: 3.2 ± 1.2) to the last day of chronic sleep restriction (motivation: 2.2 ± 0.5, sleepiness: 5.1 ± 1.8) for the experimental group. Motivation remained low after recovery sleep (2.2 ± 0.8; p=.0198). Sleepiness and motivation scores showed a significant Spearman correlation (r=-0.43, p<0.001). Discussion: Chronic sleep restriction for five days leads to an increase in sleepiness and a decrease in motivation. One night of recovery is insufficient to reverse the motivation loss, contrasting with the beneficial effect on sleepiness. During chronic sleep restriction conditions subjective motivation seems to decrease as a function of subjective sleepiness

Physiological and autonomic stress responses after prolonged sleep restriction and subsequent recovery sleep in healthy young men

Purpose Sleep restriction is increasingly common and associated with the development of health problems. We investigated how the neuroendocrine stress systems respond to prolonged sleep restriction and subsequent recovery sleep in healthy young men. Methods After two baseline (BL) nights of 8 h time in bed (TIB), TIB was restricted to 4 h per night for five nights (sleep restriction, SR, n = 15), followed by three recovery nights (REC) of 8 h TIB, representing a busy workweek and a recovery weekend. The control group (n = 8) had 8 h TIB throughout the experiment. A variety of autonomic cardiovascular parameters, together with salivary neuropeptide Y (NPY) and cortisol levels, were assessed. Results In the control group, none of the parameters changed. In the experimental group, heart rate increased from 60 +/- 1.8 beats per minute (bpm) at BL, to 63 +/- 1.1 bpm after SR and further to 65 +/- 1.8 bpm after REC. In addition, whole day low-frequency to-high frequency (LF/HF) power ratio of heart rate variability increased from 4.6 +/- 0.4 at BL to 6.0 +/- 0.6 after SR. Other parameters, including salivary NPY and cortisol levels, remained unaffected. Conclusions Increased heart rate and LF/HF power ratio are early signs of an increased sympathetic activity after prolonged sleep restriction. To reliably interpret the clinical significance of these early signs of physiological stress, a follow-up study would be needed to evaluate if the stress responses escalate and lead to more unfavourable reactions, such as elevated blood pressure and a subsequent elevated risk for cardiovascular health problems.Peer reviewe

Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses.

Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency. In both approaches, blood transcriptome and serum metabolome were analysed. Sleep loss decreased the expression of genes encoding cholesterol transporters and increased expression in pathways involved in inflammatory responses in both paradigms. Metabolomic analyses revealed lower circulating large HDL in the population cohorts among subjects reporting insufficient sleep, while circulating LDL decreased in the experimental sleep restriction study. These findings suggest that prolonged sleep deprivation modifies inflammatory and cholesterol pathways at the level of gene expression and serum lipoproteins, inducing changes toward potentially higher risk for cardiometabolic diseases

Influence of food restriction on lipid profile and spontaneous glucose levels in male rats subjected to paradoxical sleep deprivation

OBJECTIVES: The purpose of this study was to determine the paired consequences of food restriction and paradoxical sleep deprivation on lipid profile and spontaneous glucose levels in male rats. METHOD: Food restriction began at weaning, with 6 g of food being provided per day, which was subsequently increased by 1 g per week until reaching 15 g per day by the eighth week. At adulthood, both rats subjected to food restriction and those fed ad libitum were exposed to paradoxical sleep deprivation for 96 h or were maintained in their home-cage groups. RESULTS: Animals subjected to food restriction exhibited a significant increase in high-density lipoprotein levels compared to animals that were given free access to food. After the paradoxical sleep deprivation period, the foodrestricted animals demonstrated reduced concentrations of high-density lipoprotein relative to their respective controls, although the values for the food-restricted animals after sleep deprivation were still higher than those for the ad libitum group. The concentration of low-density lipoproteins was significantly increased in sleep-deprived animals fed the ad libitum diet. The levels of triglycerides, very low-density lipoproteins, and glucose in foodrestricted animals were each decreased compared to both ad libitum groups. CONCLUSION: These results may help to illustrate the mechanisms underlying the relationship between sleep curtailment and metabolism and may suggest that, regardless of sleep deprivation, dietary restriction can minimize alterations in parameters related to cardiovascular risk.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Associacao Fundo de Incentivo a Pesquisa (AFIP)Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP-CEPID)Universidade Federal de São Paulo (UNIFESP) Departamento de PsicobiologiaUNIFESP, Depto. de Psicobiologia98/14303-311/12325-6 e 10/14768-0SciEL

Blood Pressure Non-Dipping and Obstructive Sleep Apnea Syndrome: A Meta-Analysis

AIM: We examined the reduced blood pressure (BP) nocturnal fall in patients with obstructive sleep apnea (OSA) by a meta-analysis including studies that provided data on prevalence rates of non-dipping (ND) pattern during 24-h ambulatory blood pressure monitoring (ABPM). DESIGN: The PubMed, OVID-MEDLINE, and Cochrane CENTRAL literature databases were searched for appropriate articles without temporal restriction up to April 2019 through focused and sensitive search methods. Studies were identified by crossing the search terms as follows: "obstructive sleep apnea", "sleep quality", "non dipping", "reduced nocturnal BP fall", "circadian BP variation", "night-time BP", and "ambulatory blood pressure monitoring". RESULTS: Meta-analysis included 1562 patients with OSA from different clinical settings and 957 non-OSA controls from 14 studies. ND pattern prevalence in patients with OSA widely varied among studies (36.0-90.0%). This was also the case for non-OSA controls (33.0% to 69.0%). Overall, the ND pattern, assessed as an event rate in the pooled OSA population, was 59.1% (confidence interval (CI): 52.0-65.0%). Meta-analysis of the seven studies comparing the prevalence of ND pattern in participants with OSA and controls showed that OSA entails a significantly increased risk of ND (Odds ratio (OR) = 1.47, CI: 1.07-1.89, p < 0.01). After the exclusion of patients with mild OSA, OR increased to 1.67 (CI: 1.21-2.28, p < 0.001). CONCLUSIONS: The present meta-analysis, extending previous information on the relationship between OSA and impaired BP dipping, based on single studies, suggests that this condition increases by approximately 1.5 times the likelihood of ND, which is a pattern associated with a greater cardiovascular risk than normal BP dipping