SLEEP DEPRIVATION INDUCES DIFFERENTIAL BIOLOGICAL RESPONSE IN RAT MASTICATORY MUSCLES: INFLAMMATION AND MYOGENESIS

Abstract

Sleep plays an important role in promoting human health since it is closely involved in the maintenance of homeostasis of the human body. The aim of this study was to evaluate if sleep deprivation induces inflammation, autophagy, and myogenesis in rat masticatory muscles: the masseter and temporal muscle. A total of 18 animals were distributed into 3 groups: the control group (CTL, n = 6), subjected to sleep deprivation for 96 hours (SD96, n = 6) and subjected to sleep deprivation for 96 hours and 96 hours of sleep recovery (SD96R, n = 6). In the group SD96R, no inflammatory process was noted in the mas- seter only. Up-regulation of tumor necrosis factor-alpha (TNFa) production was detected in the SD96 group, while SD96R decreased TNF immunoexpression for both skeletal muscles evaluated. MyoD and myogenin increased in rats subjected to SD96. Nevertheless, the levels of MyoD decreased immunoexpression. Myogenin had high immunoexpression in SDR groups. Akt decreased in animals submitted to SD whereas, LC3 protein increased in the temporal muscle only. In summary, our results show that SD is able to induce inflammation, atrophy, and myogenesis in rat masticatory muscles and is dependent on skeletal muscle type and the recovery process. Sleep plays an important role in promoting human health since it is closely involved in the maintenance of homeostasis of the human body. The aim of this study was to evaluate if sleep deprivation induces inflammation, autophagy, and myogenesis in rat masticatory muscles: the masseter and temporal muscle. A total of 18 animals were distributed into 3 groups: the control group (CTL, n = 6), subjected to sleep deprivation for 96 hours (SD96, n = 6) and subjected to sleep deprivation for 96 hours and 96 hours of sleep recovery (SD96R, n = 6). In the group SD96R, no inflammatory process was noted in the mas- seter only. Up-regulation of tumor necrosis factor-alpha (TNFa) production was detected in the SD96 group, while SD96R decreased TNF immunoexpression for both skeletal muscles evaluated. MyoD and myogenin increased in rats subjected to SD96. Nevertheless, the levels of MyoD decreased immunoexpression. Myogenin had high immunoexpression in SDR groups. Akt decreased in animals submitted to SD whereas, LC3 protein increased in the temporal muscle only. In summary, our results show that SD is able to induce inflammation, atrophy, and myogenesis in rat masticatory muscles and is dependent on skeletal muscle type and the recovery process.