Abstract
Sedentary life has been associated with several chronic diseases, including cardiovascular and metabolic diseases such as obesity dyslipidemia and type 2 diabetes, demonstrating the importance of exercising regularly. Only recently the mechanisms involved in the muscle adaptation to physical exercise have been elucidated. Different exercise, such as endurance and strength training, activate distinct signaling pathways which generate muscle adaptations to increase energy production (through AMPK) or protein synthesis (through Akt/mTOR), respectively. One important proteolytic system, the ubiquitin-proteasome system (UPS), activated under muscular disuse, has its activity modulated by exercise. On the other hand, branched chain amino acids, especially leucin, are efficient anabolic agents, activating Akt/mTOR pathway, but modulates insulin secretion as well. The three pathways, AMPK, mTOR and UPS suffer interference from each other. AMPK inhibits mTOR pathway, reducing protein synthesis, and strength training (via Akt) and even leucin supplementation are capable of inhibiting or reducing UPS activity in muscle. Endurance exercise may also play this role. In this way, this project aims to investigate in mice the effects of swimming exercise and leucin supplementation on muscle glucose and protein metabolism and gene and protein expression of the main proteins involved in the regulation of these processes (AMPK, Akt/mTOR e UPS) and insulin secretion by isolated islets. (AU)
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