Passive body heating improves sleep patterns in female patients with fibromyalgia

OBJECTIVE: To assess the effect of passive body heating on the sleep patterns of patients with fibromyalgia. METHODS: Six menopausal women diagnosed with fibromyalgia according to the criteria determined by the American College of Rheumatology were included. All women underwent passive immersion in a warm bath at a temperature of 36 ±1 °C for 15 sessions of 30 minutes each over a period of three weeks. Their sleep patterns were assessed by polysomnography at the following time-points: pre-intervention (baseline), the first day of the intervention (acute), the last day of the intervention (chronic), and three weeks after the end of the intervention (follow-up). Core body temperature was evaluated by a thermistor pill during the baseline, acute, chronic, and follow-up periods. The impact of this treatment on fibromyalgia was assessed via a specific questionnaire termed the Fibromyalgia Impact Questionnaire. RESULTS: Sleep latency, rapid eye movement sleep latency and slow wave sleep were significantly reduced in the chronic and acute conditions compared with baseline. Sleep efficiency was significantly increased during the chronic condition, and the awakening index was reduced at the chronic and follow-up time points relative to the baseline values. No significant differences were observed in total sleep time, time in sleep stages 1 or 2 or rapid eye movement sleep percentage. The core body temperature and Fibromyalgia Impact Questionnaire responses did not significantly change over the course of the study. CONCLUSION: Passive body heating had a positive effect on the sleep patterns of women with fibromyalgia.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo (UNIFESP) Departamento de PsicobiologiaCentro de Estudos em Psicobiologia e ExercícioUNIFESP, Depto. de Psicobiologia98/14303-3 e 07/56620-6 e 09/13881-0SciEL

Circadian Rhythm and Sleep Disruption: Causes, Metabolic Consequences and Countermeasures.

Circadian (∼ 24 hour) timing systems pervade all kingdoms of life, and temporally optimize behaviour and physiology in humans. Relatively recent changes to our environments, such as the introduction of artificial lighting, can disorganize the circadian system, from the level of the molecular clocks that regulate the timing of cellular activities to the level of synchronization between our daily cycles of behaviour and the solar day. Sleep/wake cycles are intertwined with the circadian system, and global trends indicate that these too are increasingly subject to disruption. A large proportion of the world's population is at increased risk of environmentally-driven circadian rhythm and sleep disruption, and a minority of individuals are also genetically predisposed to circadian misalignment and sleep disorders. The consequences of disruption to the circadian system and sleep are profound and include myriad metabolic ramifications, some of which may be compounded by adverse effects on dietary choices. If not addressed, the deleterious effects of such disruption will continue to cause widespread health problems; therefore, implementation of the numerous behavioural and pharmaceutical interventions that can help restore circadian system alignment and enhance sleep will be important

Muscle adaptations induced by sleep deprivation

Aims: To evaluate the effects of sleep deprivation and recovery on the muscle regeneration process and muscle IGF-1 concentrations in rats submitted to cryolesion. The present study also evaluated the histopathological changes, oxidative damage and the modulatory effects of corticosterone on different types muscle fibers in sleep deprived rats. Methods: Male Wistar rats, 3-month-old, were submitted to cryolesion of the anterior tibial muscle and after 4 groups were established: control group (CTL, n=8), sleep deprivation group for 96h (SD96, n=8), group CTL + sleep recovery period (CTL+R, n=8) and SD96 + sleep recovery period for 96h (PS96+R, n=8). The SD96 and SD96+R groups were submitted to sleep deprivation for 96h and in the end; the PS96+R group remained for another 96h with sleep ad libitum. Control groups remained in the housing box for the same period of sleep deprivation and sleep recovery. The muscle IGF-1, hormone profile (testosterone and corticosterone), PCNA protein expression and histopathological changes of the tibialis anterior muscle were analyzed. A second experiment distributed animals of the same lineage and age into three groups, the CTL group treated with vehicle (CTL, n = 10), SD treated with metyrapone (SD+MET, n=10) and SD treated with vehicle (SD+VEI, n=10). The metyrapone drug is corticosterone synthesis inhibitor and propyleneglycol was used as vehicle. The soleus muscle (oxidative fibers) and plantaris muscle (glycolytic fibers) were analyzed for histopathological pattern, oxidative damage, mitochondrial and lysosomal activity. Results: Sleep deprivation reduced muscle IGF-1, minimized its increase in the injured muscle, and sleep recovery was effective in restoring growth factor concentrations. A delay in the muscle regeneration process was observed in the animals of the SD96+R group when compared to the CTL+R group. When comparing the different types muscle fibers, pathological processes were observed in sleep deprived animals, in both analyzed muscles (soleus and plantaris), being more intense in the soleus, with interstitial edema and tissue degeneration. Oxidative damage was observed in both muscles, being more intense in the soleus muscle. Oxidative damage and lysosomal activity increased in the SD+VEI group only in the soleus muscle and, lysosomal activity increased in the SD+MET group only in the plantaris muscle. Conclusions: Sleep deprivation impairs the muscle regeneration process in rats and reduces muscle IGF-1 concentrations. Sleep recovery restored the hormonal pattern, but it was not enough to normalize the process of muscle regeneration. Histopathological changes induced by sleep deprivation in the skeletal muscle occur according to the type of muscle fiber, and type I fibers undergo greater oxidative damage. In addition, the data suggest that corticosterone potentiates oxidative damage in the soleus muscle and muscle fiber type seems to be determinant for the outcome of corticosterone effects during sleep deprivation.Objetivos: Avaliar os efeitos da privação e da recuperação de sono no processo de regeneração muscular e nas concentrações musculares de IGF-1 em ratos submetidos à criolesão. O presente estudo também avaliou as alterações histopatológicas, o dano oxidativo e os efeitos modulatórios da corticosterona em diferentes tipos de fibras musculares de ratos privados de sono. Métodos: Ratos machos, Wistar, com 3 meses de idade, foram submetidos à criolesão do músculo tibial anterior e após, 4 grupos foram estabelecidos: grupo controle (CTL, n=8), grupo privação de sono por 96h (PS96, n=8), grupo CTL+ período de recuperação de sono (CTL+R, n=8) e grupo PS96+período de recuperação de sono por 96h (PS96+R, n=8). Os grupos PS96 e PS96+R foram submetidos à privação de sono por 96 h e ao final, o grupo PS96+R permaneceu por mais 96 h com sono ad libitum. Os grupos controles permaneceram nas caixas moradias pelo mesmo período de privação de sono e recuperação de sono. Foram analisadas as concentrações de IGF-1 muscular, o perfil hormonal (testosterona e corticosterona), a expressão da proteína PCNA e o padrão histopatológico do músculo tibial anterior. Um segundo experimento distribuiu animais da mesma linhagem e idade em três grupos, sendo o grupo CTL tratado com veículo (CTL, n=10), grupo PS tratado com metirapona (PS+MET, n=10) e o grupo PS tratado com veículo (PS+VEI, n=10). A droga metirapona é inibidora da síntese de corticosterona e o propilenoglicol foi utilizado como veículo. Foram analisados o músculo sóleo (fibras oxidativas) e o músculo plantar (fibras glicolíticas) quanto ao padrão histopatológico, o dano oxidativo, a atividade mitocondrial e lisossomal. Resultados: A privação de sono reduziu o IGF-1 muscular, minimizou seu aumento no músculo lesionado e a recuperação do sono foi eficaz para restabelecer as concentrações dos fatores de crescimento. Foi observado um atraso no processo de regeneração muscular nos animais do grupo PS96+R quando comparado ao grupo CTL+R. Ao comparar os diferentes tipos de fibras musculares, foi observado processos patológicos nos animais privados de sono, em ambos os músculos analisados (sóleo e plantar), sendo mais intensos no músculo sóleo, com edema intersticial e degeneração celular. O dano oxidativo foi observado em ambos os músculos, sendo mais intenso no músculo sóleo. O dano oxidativo e a atividade lisossomal aumentaram no grupo PS+VEI, apenas no músculo sóleo e a atividade lisossomal aumentou no grupo PS+MET, apenas no músculo plantar. Conclusões: A privação de sono prejudica o processo de regeneração muscular em ratos e reduz as concentrações de IGF-1 muscular. A recuperação do sono restaurou o padrão hormonal, mas não foi o suficiente para normalizar o processo de regeneração muscular. As alterações histopatológicas induzidas pela privação de sono no musculoesquelético ocorreram de acordo com o tipo de fibra muscular, sendo que as fibras do tipo I sofreram maior dano oxidativo. Além disso, os dados sugerem que a corticosterona potencializa o dano oxidativo no músculo sóleo e o tipo de fibra muscular parece ser determinante para o desfecho dos efeitos da corticosterona durante a privação de sono.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Associação Fundo de Incentivo à Pesquisa (AFIP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)FAPESP: 2013/00152-5Dados abertos - Sucupira - Teses e dissertações (2018