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Paradoxical sleep deprivation induces muscle atrophy

Introduction: Because paradoxical sleep deprivation (PSD) induces a catabolic hormone profile, we sought to evaluate the morphology of the tibialis anterior (TA) muscle and testosterone and corticosterone levels of paradoxical sleep–deprived rats.Methods: Three study groups of rats were established: the first group was sleep deprived for 96 h; the second group was also sleep deprived for 96 h, but then returned to their home‐cage and allowed to sleep for the next 96 h; and the third group was the control group, with a normal sleep cycle. Results: PSD reduced the weight and fiber cross‐sectional area of the TA muscle. Moreover, PSD enhanced plasma corticosterone and reduced serum testosterone levels. The 96 h of sleep after PSD was sufficient to restore partially the morphology of TA, while hormones returned to basal levels. Conclusion: PSD induces hormonal alterations that may mediate muscle atrophy. Muscle Nerve, 2012

Resistance training minimizes catabolic effects induced by sleep deprivation in rats

Sleep deprivation (SD) can induce muscle atrophy. We aimed to investigate the changes underpinning SD-induced muscle atrophy and the impact of this condition on rats that were previously submitted to resistance training (RT). Adult male Wistar EPM-1 rats were randomly allocated into 1 of 5 groups: control, sham, SD (for 96 h), RT, and RT+SD. The major outcomes of this study were muscle fiber cross-sectional area (CSA), anabolic and catabolic hormone profiles, and the abundance of select proteins involved in muscle protein synthesis and degradation pathways. SD resulted in muscle atrophy; however, when SD was combined with RT, the reduction in muscle fiber CSA was attenuated. The levels of IGF-1 and testosterone were reduced in SD animals, and the RT+SD group had higher levels of these hormones than the SD group. Corticosterone was increased in the SD group compared with the control group, and this increase was minimized in the RT+SD group. The increases in corticosterone concentrations paralleled changes in the abundance of ubiquitinated proteins and the autophagic proteins LC3 and p62/SQSTM1, suggesting that corticosterone may trigger these changes. SD induced weight loss, but this loss was minimized in the RT+SD group. We conclude that SD induced muscle atrophy, probably because of the increased corticosterone and catabolic signal. High-intensity RT performed before SD was beneficial in containing muscle loss induced by SD. It also minimized the catabolic signal and increased synthetic activity, thereby minimizing the bodys weight loss.

Resistance exercise: A non-pharmacological strategy to minimize or reverse sleep deprivation-induced muscle atrophy

Sleep is important for maintenance of skeletal muscle health. Sleep debt can induce muscle atrophy by increasing glucocorticoids and decreasing testosterone, growth hormone and insulin-like growth factor-I. These hormonal alterations result in a highly proteolytic environment characterized by decreased protein synthesis and increased degradation. Given that sleep deprivation is increasingly prevalent in modern society, strategies to minimize or reverse its adverse effects need to be investigated. Resistance exercise has been suggested as an intervention that would benefit the muscle health. The practice of this type of exercise can increase the concentration of testosterone, growth hormone and insulin-like growth factor I and stimulate the protein synthesis through a key signaling molecule, mammalian target of rapamycin. Thus, we hypothesized that resistance exercise is an important non-pharmacological strategy to counteract deleterious effects of sleep debt on skeletal muscle.

Negative Energy Balance Induced by Paradoxical Sleep Deprivation Causes Multicompartmental Changes in Adipose Tissue and Skeletal Muscle

Objective. Describe multicompartmental changes in the fat and various muscle fiber types, as well as the hormonal profile and metabolic rate induced by SD in rats. Methods. Twenty adult male Wistar rats were equally distributed into two groups: experimental group (EG) and control group (CG). The EG was submitted to SD for 96 h. Blood levels of corticosterone (CORT), total testosterone (TESTO), insulin like growth factor-1 (IGF-1), and thyroid hormones (T3 and T4) were used to assess the catabolic environment. Muscle trophism was measured using a cross-sectional area of various muscles (glycolytic, mixed, and oxidative), and lipolysis was inferred by the weight of fat depots from various locations, such as subcutaneous, retroperitoneal, and epididymal. The metabolic rate was measured using oxygen consumption (V˙O2) measurement. Results. SD increased CORT levels and decreased TESTO, IGF-1, and T4. All fat depots were reduced in weight after SD. Glycolytic and mixed muscles showed atrophy, whereas atrophy was not observed in oxidative muscle. Conclusion. Our data suggest that glycolytic muscle fibers are more sensitive to atrophy than oxidative fibers during SD and that fat depots are reduced regardless of their location.

Sleep deprivation induces pathological changes in rat masticatory muscles: role of Toll like signaling pathway and atrophy†

The aim of this study was to evaluate the Toll like signaling pathway and atrophy after sleep deprivation (SD) in rat masticatory muscles: masseter and temporal. A total of 24 animals was distributed into three groups: Control group (CTL, n = 8), subjected to SD for 96 h (SD96, n = 8) and subjected to SD for 96 h more 96 h of sleep recovery (SD96 + R, n = 8). Histopathological analysis revealed the presence of acute inflammatory cells, congested vessels, fibrosis, and high cellularity in the skeletal muscle fibers from masseter and temporal submitted to SD. These morphological alterations were not observed in the control group since neither inflammatory cells nor congested vessels were observed to this group. In the group SD96 + R, the absence of inflammation was noticed to the masseter only. In this group, COX‐2 and TNF‐alpha downregulation were detected when comparing to control group. MyD88 and pIKK decreased in SD96 and SD96 + R groups being pNFKBp50 downregulatated in SD96 + R. MyD88 expression increased in rats submitted to SD96 and SD96 + R in temporal when compared to control group. On the other hand, pIKK decreased the protein expression in groups SD96 and SD96 + R while pNFKBp50 showed a decreased protein expression in group SD96 only. The activation of atrophy by means of MAFbx upregulation was detected in temporal muscle in SD96 and SD96 + R when compared to control. In summary, our results show that SD is able to induce morphological alterations in rat masticatory muscles. Toll like signaling pathway and atrophy play important roles in ethiopathogenesis induced by SD, being dependent of skeletal muscle type.

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. Physical activity reduces OSA incidence and protects against cardiometabolic diseases http://ow.ly/NxLh30leRPC

REM sleep deprivation impairs muscle regeneration in rats

Abstract Introduction: The aim was observe the influence of sleep deprivation (SD) and sleep recovery on muscle regeneration process in rats submitted to cryolesion. Methods: Thirty-two Wistar rats were randomly allocated in four groups: control (CTL), SD for 96 h (SD96), control plus sleep recovery period (CTL + R) and SD96h plus 96 h of sleep recovery (SD96 + R). The animals were submitted to muscle injury by cryolesioning, after to SD and sleep recovery. Results: The major outcomes of this study were the reduction of muscular IGF-1 in both legs (injured and uninjured) and a delay in muscle regeneration process of animals submitted to SD compared to animals that slept, with increase connective tissue, inflammatory infiltrate and minor muscle fibers. Conclusions: SD impairs muscle regeneration in rats, moreover reduces muscular IGF-1 and sleep recovery was able to restore it to basal levels, but it was not enough to normalize the muscle regeneration.

Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training

Background Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation. Methods Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated. Results Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway. Conclusions Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.

Effect Of Resistance Training On Myocardial Contractility In Vitro After Sleep Deprivation

Fundamento: O treinamento resistido promove beneficios a saude cardiovascular, a qual e influenciada pela privacao de sono. Objetivo: Investigar o efeito previo do treinamento resistido de alta intensidade sobre a contratilidade miocardica de ratos privados de sono paradoxal. Metodos: Quarenta ratos machos Wistar foram distribuidos nos grupos controle (CTRL), treinamento resistido (TRES), privacao de sono paradoxal por 96 horas (PSP96) e treinamento resistido seguido de privacao de sono paradoxal por 96 horas (TRES/PSP96). O treinamento resistido foi de alta intensidade, por 8 semanas, 5x/semana. Vinte e quatro horas apos a ultima sessao de treinamento, os grupos PSP96 e TRES/PSP96 foram submetidos ao protocolo de privacao de sono paradoxal e em seguida foi realizado o estudo in vitro da mecânica contratil do musculo papilar isolado. Resultados: Em comparacao ao CTRL, os grupos PSP96 e TRES/PSP96 apresentaram menor comprimento do musculo papilar e aumento da area de seccao transversa. Associado a essas alteracoes, verificou-se a diminuicao das derivadas temporais da forca na contracao e relaxamento em todas as condicoes avaliadas. Somente o grupo PSP96 apresentou reducao da tensao de repouso e lentidao no tempo de relaxamento, sendo este ultimo atenuado pelo treinamento resistido previo. Conclusao: O treinamento resistido previo a PSP foi parcialmente protetor contra as alteracoes contrateis do musculo papilar, minimizando a lentidao no tempo de relaxamento. Assim, o carater de alta intensidade do protocolo adotado parece nao proteger plenamente o tecido cardiaco frente a PSP.