| Grant number: | 11/15962-7 |
| Support Opportunities: | Scholarships in Brazil - Master |
| Start date: | March 01, 2012 |
| End date: | August 31, 2013 |
| Field of knowledge: | Health Sciences - Physical Education |
| Principal Investigator: | Marco Túlio de Mello |
| Grantee: | Marcos Mônico Neto |
| Host Institution: | Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil |
Abstract Sleep is an important factor in the process of muscle recovery. Changes caused by sleep deprivation and sleep restriction, cause damage in specific hormonal axes, such as hypothalamic-pituitary-adrenal and hypothalamic-pituitary-gonadal axis. The increase on the secretion of corticosterone and decreases testosterone, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels, creates a catabolic environment and promotes the process of muscle atrophy. On the other hand, resistance exercise promotes important physiological adaptations, with emphasis on the metabolic, hormonal and intracellular respond by increasing strength, cross-sectional area and maintenance / synthesis of contractile proteins. The aim of this project is evaluate the effects of resistance exercise in the way trophic and atrophic skeletal muscle of rats subjected to deprivation of paradoxical sleep for 96 hours. Will be used male rats, subjected to a protocol of high intensity resistance training for 8 weeks followed by a protocol of paradoxical sleep deprivation for 96 hours. After the animals are euthanized and gastrocnemius muscle blood will be taken for biochemical, histological and blood. To evaluate the anabolic and catabolic hormonal responses will be measured levels of testosterone, IGF-1 and corticosterone. Histology of the gastrocnemius muscle is made with hematoxylin and eosin (HE) and ATPase histomorphometry to evaluate the different types of muscle fibers. Biochemical analysis will be performed by Western blotting of proteins key pathways of synthesis and protein degradation, and the AKT, mTOR, p70S6K1, FOXO, MuRF1, and myostatin and their active forms. | |
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