Different physical exercise models lead to innumerable benefits in the organism, being able to help in the treatment of diseases and increase performance in sports. Each model of exercise use majorly different types of muscle fiber, energetic system, and signaling pathways activating, for example, the mammalian target of rapamycin (mTOR) pathway, and the AMP-activated protein kinase (AMPK) pathway. The activation of these pathways also regulates the physiology process like autophagy, one way of "cellular recycling" reusing damaged organelles for energy generation. Recently it was discovered that NR1D1 shows relation with these phenomena, introducing itself as a potential modulator of aerobic capacity in skeletal muscle and regulator of genes related with muscular atrophy and autophagy. The NR1D1 also suffer influence of circadian cycle, being able to be characterized like a clock gene. Therefore, the main objective of the present research study is investigating the responses of NR1D1 to the acute physical exercise in both more classic models, strength and endurance, taking into account their behavior during the circadian cycle. For this objective, will be used mice C57B16 which will be divided in those groups: control group (CT: sedentary mice), endurance group (END: mice submitted to the protocol of acute aerobic exercise), and resistance group (RES: mice submitted to the protocol of acute strength exercise). Will be extracted the gastrocnemius muscle immediately after the acute exercise and after 6, 12, 18 hours of recovery. Will be performed the techniques of immunoblotting, RT-PCR, and autophagy flux. In accord to the statistic distribution of data, will use parametric test or not parametric. The significance level of p <0.05 will be adopted.
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