A influência da perda de peso no perfil inflamatório de mulheres com síndrome dos ovários policísticos

The polycystic ovary syndrome (PCOS) is considered the most common endocrine disorder in reproductive age women, with a prevalence ranging from 15 to 20%. In addition to hormonal and reproductive changes, it is common in PCOS the presence of risk factors for developing cardiovascular disease (CVD) and diabetes mellitus, insulin resistance (IR), visceral obesity, chronic low-grade inflammation and dyslipidemia. Due to the high frequency of obesity associated with PCOS, weight loss is considered as the first-line treatment for the syndrome by improving metabolic and normalizes serum androgens, restoring reproductive function of these patients. Objectives: To evaluate the inflammatory markers and IR in women with PCOS and healthy ovulatory with different nutritional status and how these parameters are displayed after weight loss through caloric restriction in with Down syndrome. Methods: Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and C-reactive protein (CRP) were assessed in serum samples from 40 women of childbearing age. The volunteers were divided into four groups: Group I (not eutrophic with PCOS, n = 12); Group II (not eutrophic without PCOS, n = 10), Group III (eutrophic with PCOS, n = 08) and Group IV (eutrophic without PCOS, n = 10). The categorization of groups was performed by body mass index (BMI), according to the World Health Organization (WHO) does not eutrophic, overweight and obesity (BMI> 25 kg / m²) and normal weight (BMI <24.9 kg / m²). IR was determined by HOMA-IR index. In the second phase of the study a controlled dietary intervention was performed and inflammatory parameters were evaluated in 21 overweight and obese women with PCOS, before and after weight loss. All patients received a low-calorie diet with reduction of 500 kcal / day of regular consumption with standard concentrations of macronutrients. Results: Phase 1: PCOS patients showed increased levels of CRP (p <0.01) and HOMAIR (p <0.01). When divided by BMI, both not eutrophic group with PCOS (I) as eutrophic with PCOS (III) showed increased levels of CRP (I = 2.35 ± 0,55mg / L and 2.63 ± III = 0,65mg / L; p <0.01) and HOMA-IR (I = 2.16 ± 2.54 and III = 1.07 ± 0.55; p <0.01). There were no differences in TNF-α and IL-6 between groups. Step 2: After the weight loss of 5% of the initial weight was reduced in all of the components of serum assessed inflammatory profile, PCR (154.75 ± 19:33) vs (78.06 ± 8.9) TNF α (10.89 ± 5.09) vs (6:39 ± 1:41) and IL6 (154.75 ± 19:33) vs (78.06 ± 08.09) (p <0:00) in association with improvement some hormonal parameters evaluated. Conclusion: PCOS contributed to the development of chronic inflammation and changes in glucose metabolism by increasing CRP, insulin and HOMA-IR, independent of nutritional status. The weight loss, caloric restriction has improved the inflammatory condition and hormonal status of the evaluated patients.

The functional and clinical outcomes of exercise training following a very low energy diet for severely obese women: study protocol for a randomised controlled trial

BACKGROUND: Clinical practice guidelines globally recommend lifestyle modification including diet and exercise training as first-line treatment for obesity. The clinical benefits of exercise training in adults with obesity is well-documented; however, there is no strong evidence for the effectiveness of exercise training for weight loss in class II and class III obesity. The purpose of the randomised controlled trial described in this protocol article is to examine the effect of exercise training, in addition to a very low energy diet (VLED), in clinically severe obese women for changes in body composition, physical function, quality of life, and markers of cardiometabolic risk.

METHODS/DESIGN: Sixty women, aged 18-50 years with a body mass index (BMI) greater than 34.9 kg.m(2) and at least one obesity-related co-morbidity, will be recruited for this 12-month study. Participants will be randomised to either exercise plus energy restriction (n = 30), or energy restriction alone (n = 30). All participants will follow an energy-restricted individualised diet incorporating a VLED component. The exercise intervention group will also receive exercise by supervised aerobic and resistance training and a home-based exercise programme totalling 300 minutes per week. Primary outcome measures include body composition and aerobic fitness. Secondary outcome measures include: physical function, cardiometabolic risk factors, quality of life, physical activity, and mental health. All outcome measures will be conducted at baseline, 3, 6 and 12 months.

DISCUSSION: Previous research demonstrates various health benefits of including exercise training as part of a healthy lifestyle at all BMI ranges. Although clinical practice guidelines recommend exercise training as part of first-line treatment for overweight and obesity, there are few studies that demonstrate the effectiveness of exercise in class II and class III obesity. The study aims to determine whether the addition of exercise training to a VLED provides more favourable improvements in body composition, physical function, quality of life, and markers of cardiometabolic risk for women with clinically severe obesity, compared to VLED alone.

Reversing diet-induced metabolic dysregulation by diet switching leads to altered hepatic de novo lipogenesis and glycerolipid synthesis

In humans, low-energy diets rapidly reduce hepatic fat and improve/normalise glycemic control. Due to difficulties in obtaining human liver, little is known about changes to the lipid species and pathway fluxes that occur under these conditions. Using a combination of stable isotope, and targeted metabolomic approaches we investigated the acute (7–9 days) hepatic effects of switching high-fat high-sucrose diet (HFD) fed obese mice back to a chow diet. Upon the switch, energy intake was reduced, resulting in reductions of fat mass and hepatic triacyl- and diacylglycerol. However, these parameters were still elevated compared to chow fed mice, thus representing an intermediate phenotype. Nonetheless, glucose intolerance and hyperinsulinemia were completely normalized. The diet reversal resulted in marked reductions in hepatic de novo lipogenesis when compared to the chow and HFD groups. Compared with HFD, glycerolipid synthesis was reduced in the reversal animals, however it remained elevated above that of chow controls, indicating that despite experiencing a net loss in lipid stores, the liver was still actively esterifying available fatty acids at rates higher than that in chow control mice. This effect likely promotes the re-esterification of excess free fatty acids released from the breakdown of adipose depots during the weight loss period.

Feed restriction and a diet's caloric value: The influence on the aerobic and anaerobic capacity of rats

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Dietary restriction, caloric value and the accumulation of hepatic fat

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Depot-specific modulation of adipokine levels in rat adipose tissue by diet-induced obesity: The effect of aerobic training and energy restriction

The present study examined the effects of aerobic training and energy restriction on adipokines levels in mesenteric (MEAT) and retroperitoneal (RPAT) white adipose tissue from obese rats. Male Wistar rats were fed with standard laboratory diet (Control group) or high fat diet (HFD). After 15 weeks, HFD rats were randomly assigned to the following groups: rats submitted to HFD, which were sedentary (sedentary HFD, n = 8) or trained (trained HFD, n = 8); or submitted to energy-restriction (ER), which were sedentary (sedentary ER, n = 8) or trained (trained ER, n = 8). Trained rats ran on a treadmill at 55% VO(2max) for 60 min/day, 5 days/week, for 10 weeks. ER rats were submitted to a reduction of 20% daily caloric ingestion compared to the Control group. ER and aerobic training decreased body weight, MEAT and RPAT absolute weight, and fat mass. IL-6, IL-10 and TNF-alpha levels were decreased and adiponectin did not change in RPAT in response to ER protocol. On the other hand, ER and the aerobic training protocol decreased IL-6, TNF-alpha and adiponectin levels in MEAT. Absolute MEAT weight showed a positive correlation with IL-6 (r = 0.464), INF-alpha (r = 0.508); and adiponectin (r = 0.342). These results suggest a tissue-specific heterogeneous response in adipokines level. The combination of the protocols (aerobic training and energy restriction) did not induce an enhanced effect. Published by Elsevier Ltd.

Determinants of participation restriction among community dwelling stroke survivors : a path analysis

Background: Apart from promoting physical recovery and assisting in activities of daily living, a major challenge in stroke rehabilitation is to minimize psychosocial morbidity and to promote the reintegration of stroke survivors into their family and community. The identification of key factors influencing long-term outcome are essential in developing more effective rehabilitation measures for reducing stroke-related morbidity. The aim of this study was to test a theoretical model of predictors of participation restriction which included the direct and indirect effects between psychosocial outcomes, physical outcome, and socio-demographic variables at 12 months after stroke.--------- Methods: Data were collected from 188 stroke survivors at 12 months following their discharge from one of the two rehabilitation hospitals in Hong Kong. The settings included patients' homes and residential care facilities. Path analysis was used to test a hypothesized model of participation restriction at 12 months.---------- Results: The path coefficients show functional ability having the largest direct effect on participation restriction (β = 0.51). The results also show that more depressive symptoms (β = -0.27), low state self-esteem (β = 0.20), female gender (β = 0.13), older age (β = -0.11) and living in a residential care facility (β = -0.12) have a direct effect on participation restriction. The explanatory variables accounted for 71% of the variance in explaining participation restriction at 12 months.---------- Conclusion: Identification of stroke survivors at risk of high levels of participation restriction, depressive symptoms and low self-esteem will assist health professionals to devise appropriate rehabilitation interventions that target improving both physical and psychosocial functioning.

Differentiation of Rice Tungro Bacilliform Virus Strains by Restriction Analysis and DNA Hybridization

Rice tungro bacilliform virus (RTBV) is one of the two viruses that cause tungro disease. Four RTBV strains maintained in the greenhouse for 4 years, G1, G2, Ic, and L, were differentiated by restriction fragment length polymorphism (RFLP) analysis of the native viral DNA. Although strains G1 and Ic had identical restriction patterns when cleaved with Pst1, BamHI, EcoRI, and EcoRV, they can be differentiated from strains G2 and L by EcoRI and EcoRV digestion. These same endonucleases also differentiate strain G2 from strain L. When total DNA extracts from infected plants were used instead of viral DNA, and digested with EcoRV, identical restriction patterns for each strain (G2 and L) were obtained from roots, leaves, and leaf sheaths of infected plants. The restriction patterns were consistent from plant to plant, in different varieties, and at different times after inoculation. This technique can be used to differentiate RTBV strains and determine the variability of a large number of field samples.

Comparing the medium-term effects of exercise or dietary restriction on appetite regulation and compensatory responses

Previous studies have shown that exercise (Ex) interventions create a stronger coupling between energy intake (EI) and energy expenditure (EE) leading to increased homeostasis of the energy-balance (EB) regulatory system compared to a diet intervention where an un-coupling between EI and EE occurs. The benefits of weight loss from Ex and diet interventions greatly depend on compensatory responses. The present study investigated an 8-week medium-term Ex and diet intervention program (Ex intervention comprised of 500kcal EE five days per week over four weeks at 65-75% maximal heart rate, whereas the diet intervention comprised of a 500kcal decrease in EI five days per week over four weeks) and its effects on compensatory responses and appetite regulation among healthy individuals using a between- and within-subjects design. Effects of an acute dietary manipulation on appetite and compensatory behaviours and whether a diet and/or Ex intervention pre-disposes individuals to disturbances in EB homeostasis were tested. Energy intake at an ad libitum lunch test meal after a breakfast high- and low-energy pre-load (the high energy pre-load contained 556kcal and the low energy pre-load contained 239kcal) were measured at the Baseline (Weeks -4 to 0) and Intervention (Weeks 0 to 4) phases in 13 healthy volunteers (three males and ten females; mean age 35 years [sd + 9] and mean BMI 25 kg/m2 [sd + 3.8]) [participants in each group included Ex=7, diet=5 (one female in the diet group dropped out midway), thus, 12 participants completed the study]. At Weeks -4, 0 and 4, visual analogue scales (VAS) were used to assess hunger and satiety and liking and wanting (L&W) for nutrient and taste preferences using a computer-based system (E-Prime v1.1.4). Ad libitum test meal EI was consistently lower after the HE pre-load compared to the LE pre-load. However, this was not consistent during the diet intervention however. A pre-load x group interaction on ad libitum test meal EI revealed that during the intervention phase the Ex group showed an improved sensitivity to detect the energy content between the two pre-loads and improved compensation for the ad libitum test meal whereas the diet group’s ability to differentiate between the two pre-loads decreased and showed poorer compensation (F[1,10]=2.88, p-value not significant). This study supports previous findings of the effect Ex and diet interventions have on appetite and compensatory responses; Ex increases and diet decreases energy balance sensitivity.

Meal induced thermogenesis and appetite : methodological issues and responses to energy restriction

Diet Induced Thermogenesis (DIT) is the energy expended consequent to meal consumption, and reflects the energy required for the processing and digestion of food consumed throughout each day. Although DIT is the total energy expended across a day in digestive processes to a number of meals, most studies measure thermogenesis in response to a single meal (Meal Induced Thermogenesis: MIT) as a representation of an individual’s thermogenic response to acute food ingestion. As a component of energy expenditure, DIT may have a contributing role in weight gain and weight loss. While the evidence is inconsistent, research has tended to reveal a suppressed MIT response in obese compared to lean individuals, which identifies individuals with an efficient storage of food energy, hence a greater tendency for weight gain. Appetite is another factor regulating body weight through its influence on energy intake. Preliminary research has shown a potential link between MIT and postprandial appetite as both are responses to food ingestion and have a similar response dependent upon the macronutrient content of food. There is a growing interest in understanding how both MIT and appetite are modified with changes in diet, activity levels and body size. However, the findings from MIT research have been highly inconsistent, potentially due to the vastly divergent protocols used for its measurement. Therefore, the main theme of this thesis was firstly, to address some of the methodological issues associated with measuring MIT. Additionally this thesis aimed to measure postprandial appetite simultaneously to MIT to test for any relationships between these meal-induced variables and to assess changes that occur in MIT and postprandial appetite during periods of energy restriction (ER) and following weight loss. Two separate studies were conducted to achieve these aims. Based on the increasing prevalence of obesity, it is important to develop accurate methodologies for measuring the components potentially contributing to its development and to understand the variability within these variables. Therefore, the aim of Study One was to establish a protocol for measuring the thermogenic response to a single test meal (MIT), as a representation of DIT across a day. This was done by determining the reproducibility of MIT with a continuous measurement protocol and determining the effect of measurement duration. The benefit of a fixed resting metabolic rate (RMR), which is a single measure of RMR used to calculate each subsequent measure of MIT, compared to separate baseline RMRs, which are separate measures of RMR measured immediately prior to each MIT test meal to calculate each measure of MIT, was also assessed to determine the method with greater reproducibility. Subsidiary aims were to measure postprandial appetite simultaneously to MIT, to determine its reproducibility between days and to assess potential relationships between these two variables. Ten healthy individuals (5 males, 5 females, age = 30.2 ± 7.6 years, BMI = 22.3 ± 1.9 kg/m2, %Fat Mass = 27.6 ± 5.9%) undertook three testing sessions within a 1-4 week time period. During the first visit, participants had their body composition measured using DXA for descriptive purposes, then had an initial 30-minute measure of RMR to familiarise them with the testing and to be used as a fixed baseline for calculating MIT. During the second and third testing sessions, MIT was measured. Measures of RMR and MIT were undertaken using a metabolic cart with a ventilated hood to measure energy expenditure via indirect calorimetry with participants in a semi-reclined position. The procedure on each MIT test day was: 1) a baseline RMR measured for 30 minutes, 2) a 15-minute break in the measure to consume a standard 576 kcal breakfast (54.3% CHO, 14.3% PRO, 31.4% FAT), comprising muesli, milk toast, butter, jam and juice, and 3) six hours of measuring MIT with two, ten-minute breaks at 3 and 4.5 hours for participants to visit the bathroom. On the MIT test days, pre and post breakfast then at 45-minute intervals, participants rated their subjective appetite, alertness and comfort on visual analogue scales (VAS). Prior to each test, participants were required to be fasted for 12 hours, and have undertaken no high intensity physical activity for the previous 48 hours. Despite no significant group changes in the MIT response between days, individual variability was high with an average between-day CV of 33%, which was not significantly improved by the use of a fixed RMR to 31%. The 95% limits of agreements which ranged from 9.9% of energy intake (%EI) to -10.7%EI with the baseline RMRs and between 9.6%EI to -12.4%EI with the fixed RMR, indicated very large changes relative to the size of the average MIT response (MIT 1: 8.4%EI, 13.3%EI; MIT 2: 8.8%EI, 14.7%EI; baseline and fixed RMRs respectively). After just three hours, the between-day CV with the baseline RMR was 26%, which may indicate an enhanced MIT reproducibility with shorter measurement durations. On average, 76, 89, and 96% of the six-hour MIT response was completed within three, four and five hours, respectively. Strong correlations were found between MIT at each of these time points and the total six-hour MIT (range for correlations r = 0.990 to 0.998; P < 0.01). The reproducibility of the proportion of the six-hour MIT completed at 3, 4 and 5 hours was reproducible (between-day CVs ≤ 8.5%). This indicated the suitability to use shorter durations on repeated occasions and a similar percent of the total response to be completed. There was a lack of strong evidence of any relationship between the magnitude of the MIT response and subjective postprandial appetite. Given a six-hour protocol places a considerable burden on participants, these results suggests that a post-meal measurement period of only three hours is sufficient to produce valid information on the metabolic response to a meal. However while there was no mean change in MIT between test days, individual variability was large. Further research is required to better understand which factors best explain the between-day variability in this physiological measure. With such a high prevalence of obesity, dieting has become a necessity to reduce body weight. However, during periods of ER, metabolic and appetite adaptations can occur which may impede weight loss. Understanding how metabolic and appetite factors change during ER and weight loss is important for designing optimal weight loss protocols. The purpose of Study Two was to measure the changes in the MIT response and subjective postprandial appetite during either continuous (CONT) or intermittent (INT) ER and following post diet energy balance (post-diet EB). Thirty-six obese male participants were randomly assigned to either the CONT (Age = 38.6 ± 7.0 years, weight = 109.8 ± 9.2 kg, % fat mass = 38.2 ± 5.2%) or INT diet groups (Age = 39.1 ± 9.1 years, weight = 107.1 ± 12.5 kg, % fat mass = 39.6 ± 6.8%). The study was divided into three phases: a four-week baseline (BL) phase where participants were provided with a diet to maintain body weight, an ER phase lasting either 16 (CONT) or 30 (INT) weeks, where participants were provided with a diet which supplied 67% of their energy balance requirements to induce weight loss and an eight-week post-diet EB phase, providing a diet to maintain body weight post weight loss. The INT ER phase was delivered as eight, two-week blocks of ER interspersed with two-week blocks designed to achieve weight maintenance. Energy requirements for each phase were predicted based on measured RMR, and adjusted throughout the study to account for changes in RMR. All participants completed MIT and appetite tests during BL and the ER phase. Nine CONT and 15 INT participants completed the post-diet EB MIT and 14 INT and 15 CONT participants completed the post-diet EB appetite tests. The MIT test day protocol was as follows: 1) a baseline RMR measured for 30 minutes, 2) a 15-minute break in the measure to consume a standard breakfast meal (874 kcal, 53.3% CHO, 14.5% PRO, 32.2% FAT), and 3) three hours of measuring MIT. MIT was calculated as the energy expenditure above the pre-meal RMR. Appetite test days were undertaken on a separate day using the same 576 kcal breakfast used in Study One. VAS were used to assess appetite pre and post breakfast, at one hour post breakfast then a further three times at 45-minute intervals. Appetite ratings were calculated for hunger and fullness as both the intra-meal change in appetite and the AUC. The three-hour MIT response at BL, ER and post-diet EB respectively were 5.4 ± 1.4%EI, 5.1 ± 1.3%EI and 5.0 ± 0.8%EI for the CONT group and 4.4 ± 1.0%EI, 4.7 ± 1.0%EI and 4.8 ± 0.8%EI for the INT group. Compared to BL, neither group had significant changes in their MIT response during ER or post-diet EB. There were no significant time by group interactions (p = 0.17) indicating a similar response to ER and post-diet EB in both groups. Contrary to what was hypothesised, there was a significant increase in postprandial AUC fullness in response to ER in both groups (p < 0.05). However, there were no significant changes in any of the other postprandial hunger or fullness variables. Despite no changes in MIT in both the CONT or INT group in response to ER or post-diet EB and only a minor increase in postprandial AUC fullness, the individual changes in MIT and postprandial appetite in response to ER were large. However those with the greatest MIT changes did not have the greatest changes in postprandial appetite. This study shows that postprandial appetite and MIT are unlikely to be altered during ER and are unlikely to hinder weight loss. Additionally, there were no changes in MIT in response to weight loss, indicating that body weight did not influence the magnitude of the MIT response. There were large individual changes in both variables, however further research is required to determine whether these changes were real compensatory changes to ER or simply between-day variation. Overall, the results of this thesis add to the current literature by showing the large variability of continuous MIT measurements, which make it difficult to compare MIT between groups and in response to diet interventions. This thesis was able to provide evidence to suggest that shorter measures may provide equally valid information about the total MIT response and can therefore be utilised in future research in order to reduce the burden of long measurements durations. This thesis indicates that MIT and postprandial subjective appetite are most likely independent of each other. This thesis also shows that, on average, energy restriction was not associated with compensatory changes in MIT and postprandial appetite that would have impeded weight loss. However, the large inter-individual variability supports the need to examine individual responses in more detail.

Association and linkage analyses of restriction fragment length polymorphisms for the human renin and antithrombin III genes in essential hypertension

Essential hypertension is a highly hereditable disorder in which genetic influences predominate over environmental factors. The molecular genetic profiles which predispose to essential hypertension are not known. In rats with genetic hypertension, there is some recent evidence pointing to linkage of renin gene alleles with blood pressure. The genes for renin and antithrombin III belong to a conserved synteny group which, in humans, spans the q21.3-32.3 region of chromosome I and, in rats, is linkage group X on chromosome 13. The present study examined the association of particular human renin gene (REN) and antithrombin III gene (AT3) polymorphisms with essential hypertension by comparing the frequency of specific alleles for each of these genes in 50 hypertensive offspring of hypertensive parents and 91 normotensive offspring of normotensive parents. In addition, linkage relationships were examined in hypertensive pedigrees with multiple affected individuals. Alleles of a REN HindIII restriction fragment length polymorphism (RFLP) were detected using a genomic clone, λHR5, to probe Southern blots of HindIII-cut leucocyte DNA, and those for an AT3 Pstl RFLP were detected by phATIII 113 complementary DNA probe. The frequencies of each REN allele in the hypertensive group were 0.76 and 0.24 compared with 0.74 and 0.26 in the normotensive group. For AT3, hypertensive allele frequencies were 0.49 and 0.51 compared with normotensive values of 0.54 and 0.46. These differences were not significant by χ2 analysis (P > 0.2). Linkage analysis of a family (data from 16 family members, 10 of whom were hypertensive), informative for both markers, without an age-of-onset correction, and assuming dominant inheritance of hypertension, complete penetrance and a disease frequency of 20%, did not indicate linkage of REN with hypertension, but gave a positive, although not significant, logarithm of the odds for linkage score of 0.784 at a recombination fraction of 0 for AT3 linkage to hypertension. In conclusion, the present study could find no evidence for an association of a REN HindIII RFLP with essential hypertension or for a linkage of the locus defined by this RFLP in a family segregating for hypertension. In the case of an AT3 Pstl RFLP, although association analysis was negative, linkage analysis suggested possible involvement (odds of 6:1 in favour) of a gene located near the 1q23 locus with hypertension in one informative family.

Moderate sleep restriction in treated older male OSA participants: Greater impairment during monotonous driving compared with controls

Objectives To examine the effects on monotonous driving of normal sleep versus one night of sleep restriction in continuous positive airway pressure (CPAP) treated obstructive sleep apnoea (OSA) patients compared with age matched healthy controls. Methods Nineteen CPAP treated compliant male OSA patients (OSA-treated patients (OPs)), aged 50–75 years, and 20 healthy age-matched controls underwent both a normal night’s sleep and sleep restriction to 5 h (OPs remained on CPAP) in a counterbalanced design. All participants completed a 2 h afternoon monotonous drive in a realistic car simulator. Driving was monitored for sleepiness-related minor and major lane deviations, with ‘safe’ driving time being total time driven prior to first major lane deviation. EEGs were recorded continuously, and subjective sleepiness ratings were taken at regular intervals throughout the drive. Results After a normal night’s sleep, OPs and controls did not differ in terms of driving performance or in their ability to assess the levels of their own sleepiness, with both groups driving ‘safely’ for approximately 90 min. However, after sleep restriction, OPs had a significantly shorter (65 min) safe driving time and had to apply more compensatory effort to maintain their alertness compared with controls. They also underestimated the enhanced sleepiness. Nevertheless, apart from this caveat, there were generally close associations between subjective sleepiness, likelihood of a major lane deviation and EEG changes indicative of sleepiness. Conclusions With a normal night’s sleep, effectively treated older men with OSA drive as safely as healthy men of the same age. However, after restricted sleep, driving impairment is worse than that of controls. This suggests that, although successful CPAP treatment can alleviate potential detrimental effects of OSA on monotonous driving following normal sleep, these patients remain more vulnerable to sleep restriction.

One night CPAP withdrawal impairs performance at a driving simulator task faster than sleep restriction to 5 hours with treatment in OSA patients

Introduction Sleep restriction and missing 1 night’s continuous positive air pressure (CPAP) treatment are scenarios faced by obstructive sleep apnoea (OSA) patients, who must then assess their own fitness to drive. This study aims to assess the impact of this on driving performance. Method 11 CPAP treated participants (50–75 yrs), drove an interactive car simulator under monotonous motorway conditions for 2 hours on 3 afternoons, following;(i)normal night’s sleep (average 8.2 h) with CPAP (ii) sleep restriction (5 h), with CPAP (iii)normal length of sleep, without CPAP. Driving incidents were noted if the car came out of the designated driving lane. EEG was recorded continually and KSS reported every 200 seconds. Results Driving incidents: Incidents were more prevalent following CPAP withdrawal during hour 1, demonstrating a significant condition time interaction [F(6,60) = 3.40, p = 0.006]. KSS: At the start of driving participants felt sleepiest following CPAP withdrawal, by the end of the task KSS levels were similar following CPAP withdrawal and sleep restriction, demonstrating a significant condition, time interaction [F(3.94,39.41) = 3.39, p = 0.018]. EEG: There was a non significant trend for combined alpha and theta activity to be highest throughout the drive following CPAP withdrawal. Discussion CPAP withdrawal impairs driving simulator performance sooner than restricting sleep to 5 h with CPAP. Participants had insight into this increased sleepiness reflected by the higher KSS reported following CPAP withdrawal. In the practical terms of driving any one incident could be fatal. The earlier impairment reported here demonstrates the potential danger of missing CPAP treatment and highlights the benefit of CPAP treatment even when sleep time is short.

The effects of sleep restriction on executive inhibitory control and affect in young adults

Purpose: Young adults regularly experience restricted sleep due to a range of social, educational and vocational commitments. Evidence suggests that extended periods of sleep deprivation negatively impact affective and inhibitory control mechanisms leading to behavioural consequences such as increased emotional reactivity and impulsive behaviour. It is less clear whether acute periods of restricted sleep produce the same behavioural consequences. Methods: Nineteen young adults (m = 8, f = 12) with habitual late bed-time (after 22:30 h) and wake-time (after 06:30 h) completed a range of objective and subjective measures assessing sleepiness (Psychomotor Vigilance Task, Karolinska Sleepiness Scale), inhibitory control (Emotional Go/No-go Task and a Balloon Analog Risk Task) and affect (Positive and Negative Affective Schedule). Testing was counterbalanced across participants, and occurred on two occasions once following restricted sleep and once following habitual sleep one week apart. Results: Compared to habitual sleep, sleep restriction produced significantly slower performance on the Psychomotor Vigilance Task, and higher subjective ratings of sleepiness on the Karolinska Sleepiness Scale. Sleep restriction also caused a significant decrease in positive affect, but no change in negative affect on the Affective Schedule. Inhibitory control efficiency was significantly differentiated, with participants showing an increase in risk taking on the Balloon Analog Risk Task, but there was no evidence of increased reactivity to negative stimuli on the Emotional Go/No-go task. Conclusions: Results suggest that even acute periods of sleep loss may cause deficits in affective experiences and increase impulsive and potentially high risk behaviour in young adults.