Sleep Deprivation Interferes with JAK/STAT Signaling Pathway and Myogenesis in the Masseter Muscle of Rats.

OBJECTIVES: The aim of the study was to study the Janus kinase/tyrosine kinase-activated transduction factor (JAK/STAT) signaling pathway and myogenesis on the masseter muscle after sleep deprivation and to investigate the role of stress in this scenario. SUBJECTS AND METHODS: A total of 18 male Wistar rats were divided into the following groups: control (n = 6): animals were not submitted to any procedures, and paradoxical sleep deprivation and vehicle (PSD + V; n = 6): animals were subjected to PSD for 96 h and (PSD + MET; n = 6): animals were subjected to PSD for 96 h with administration of metyrapone. Paradoxical sleep deprivation was performed by the modified multiple platforms method. Histopathological analysis, histomorphometry, and immunohistochemistry were performed. RESULTS: The results showed the presence of inflammatory infiltrate in the PSD + V and PSD + MET groups and atrophy. Histomorphometry showed that the cellular profile area decreased, while cellular density increased in both experimental groups. Expression of p-STAT 3, MyoD, and MyoG increased in the PSD + V group, while the PSD + MET group showed increased expression of IL-6 and p-STAT 3. CONCLUSION: Our results suggest that sleep deprivation induces an inflammatory response and atrophy in the masseter muscle of rats.

Paradoxical sleep deprivation induces differential biological response in rat masticatory muscles: Inflammation, autophagy and myogenesis.

BACKGROUND: The aim of this study was to evaluate whether sleep deprivation (SD) induces inflammation, autophagy and myogenesis in the following masticatory muscles: masseter and temporal. METHODS: In this study, 18 animals were randomly distributed into three groups: control group (CTL, n = 6), SD for 96 hours (SD96, n = 6), and SD for 96 hours and more 96 hours of sleep recovery (SD96 + R, n = 6). RESULTS: In the histopathological analysis, SD 96 was able to induce inflammation in masseter and temporal. Nevertheless, the lack of inflammatory process was evidenced to the masseter in the group SD96 + R. Upregulation of TNF-alpha production was detected in the SD96 group, while SD96 + R decreased TNF immunoexpression for both skeletal muscles evaluated. MyoD and myogenin increased in rats submitted to SD96. By contrast, the levels of MyoD decreased in the group SD96 + R. Myogenin pointed out high immunoexpression in SD96 + R groups. In temporal, pAkt decreased in animals submitted to SD96, but it increased in the group SD96 + R. The levels of LC3 protein increased in both skeletal muscles studied, and masseter decreased LC3 protein expression in the SD96 + R. CONCLUSION: In summary, our results demonstrate that SD is able to induce inflammation, atrophy and myogenesis in rat masticatory muscles, being more intense in temporal when compared to masseter.

Physical activity as a moderator for obstructive sleep apnoea and cardiometabolic risk in the EPISONO study.

Obstructive sleep apnoea (OSA) is positively associated with cardiometabolic diseases; however, high levels of physical activity could decrease the incidence of OSA and associated comorbidities.In this study we aimed to examine the incidence of OSA in relation to physical activity, and its role as a protective factor in individuals with OSA on the incidence of cardiometabolic diseases, in an 8-9-year follow-up study. We analysed data of 658 volunteers from the São Paulo Epidemiologic Sleep Study (EPISONO), a cohort study of individuals aged 20-80 years, collected through polysomnography, the International Physical Activity Questionnaire and an assessment of cardiometabolic profile.Active subjects had a lower risk of developing OSA compared with nonactive subjects (relative risk 0.877, 95% CI 0.296-0.855) and there was a reduced risk of developing type 2 diabetes mellitus in active/apnoeic subjects (relative risk 0.493, 95% CI 0.252-0.961) compared with nonactive subjects. Metabolic equivalent was negatively associated to cardiometabolic markers, such as C-reactive protein (exp(B)=0.720; p=0.001), interleukin-6 (exp(B)=0.991; p=0.03), insulin (exp(B)=0.982; p=0.03), triglycerides (exp(B)=0.997; p<0.001), homeostasis model assessment for insulin resistance (exp(B)≤0.946; p<0.024), quantitative insulin sensitivity check index (exp(B)=992.4; p<0.001) and mean arterial pressure (exp(B)=0.987; p=0.001).Physical activity was a protective factor against type 2 diabetes mellitus in apnoeic individuals; moreover, being active reduced the risk of developing OSA and was associated with a better cardiometabolic profile.

One-month of a low-energy diet, with no additional effect of high-protein, reduces Obstructive Sleep Apnea severity and improve metabolic parameters in obese males.

PURPOSE: Obstructive Sleep Apnea (OSA) is closely associated with obesity. Weight loss ameliorates OSA and its associated metabolic disorders. A high protein intake may improve weight loss through increased energy expenditure, and fat-free mass maintenance during weight loss. OBJECTIVES: To evaluate the effects of a low-energy, high-protein diet on OSA severity and metabolic parameters in obese men. METHODS: Forty-five OSA obese (BMI ≥ 30 kg/m2) males were included in this randomized study and submitted to nocturnal polysomnography, body composition measured by plethysmography, biochemical analyses of blood glucose, insulin and lipids, and food intake evaluations before and after one month of a low-energy diet. Diets were designed to create a 30% deficit in total energy expenditure with 1.6 g of protein/kg/day (High Protein group - HP) or 0.8 g of protein/kg/day (Low Protein group - LP). RESULTS: Only a time effect of the intervention was observed in body mass (-3.7 ± 2.0% for the LP group and -4.0 ± 1.5% for the HP group; p < 0.001), Body Mass Index (p < 0.001), fat mass in kg (p < 0.01) and fat-free mass in kg (p < 0.01). Significant improvements in Apnea Hypopnea Index were observed in both groups (54.0 ± 25.0 to 33.7 ± 31.7 in LP group; 39.7 ± 24.3 to 21.4 ± 25.9 in HP group; p = 0.06). Improvements of 38% and 46% in the Apnea-Hypopnea Index were observed in the LP and HP groups, respectively. Both interventions provided equivalent metabolic benefits as reductions in glucose (p < 0.001), insulin (p < 0.001), HOMA-IR (p = 0.005), triglycerides (p = 0.002), and in total cholesterol (p = 0.004). CONCLUSION: One month of a low-energy diet resulted in significant improvements in OSA severity in obese men. Increased protein intake during a short period of low-energy diet had no further beneficial effects on OSA severity or biochemical parameters than a standard protein diet. Registered under ClinicalTrials.gov Identifier no. NCT01985035.

Relationship of evening meal with sleep quality in obese individuals with obstructive sleep apnea.

PURPOSE: To determine the relationship between habitual food intake, resting energy expenditure and sleep pattern in obstructive sleep apnea (OSA) patients. METHODS: Forty-five OSA obese males were included in the study. All participants were submitted to nocturnal polysomnography, body composition measurements by plethysmography, resting energy expenditure (REE) analysis by indirect calorimetry and they filled in a 3-day food record. RESULTS: No differences in body composition, REE and food intake were found between the moderate and severe OSA groups. A trend towards higher energy intake in the severe OSA group was observed, compared to the moderate group (p = 0.08). Significant associations between apnea-hypopnea index (AHI) with body weight, body mass index (BMI) and resting energy expenditure (REE) were found. Higher food intake in the evening period was positively correlated with sleep stage NREM1, arousal index, and AHI and negatively correlated with sleep stage NREM3 and sleep efficiency. A multivariate linear regression showed energy intake at breakfast to be a significant negative predictor of AHI; protein intake (g/kg) showed a positive association, while energy intake at breakfast and at dinner were negative predictors of sleep efficiency; and energy intake at dinner was a negative predictor of stage NREM1 sleep. CONCLUSIONS: We conclude that higher amounts of food intake during the evening period may diminish sleep quality in moderate and severe sleep apnea patients. In addition, despite observing no differences between OSA severity groups, a moderate correlation between REE and sleep quality and OSA exists.