mTOR Pathway is Up-regulated by Both Acute Endurance Exercise and Chronic Muscle Contraction in Rat Skeletal Muscle
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The purpose of this thesis was to examine changes in the expression of translation regulatory proteins following both an acute bout of endurance exercise and chronic muscle contractile activity. In experiment 1, female Sprague-Dawley rats ran for 2 h at 15 m/min followed by an increase in speed of 5 m/min every 5 min until volitional fatigue. Red gastrocnemius muscle was harvested from non-exercised animals (control), immediately following cessation of exercise (0 h) and after 3 hours of recovery (3 h). Compared to control, rpS6 mRNA was elevated (p < .05) at both 0 h (+32%) and 3 h (+47%). Both eIF2Bε (+127%) and mTOR mRNA (+44%) were higher than control at 3 h, while eIF4E decreased (-24%) immediately following exercise (p < .05). Phosphorylation of mTOR (+40%) and S6K1 (+266%) also increased immediately post-exercise (p < .05). In experiment 2, female Sprague-Dawley rats underwent chronic stimulation of the peroneal nerve continuously for 7 days. The red gastrocnemius muscle was removed 24 h following cessation of the stimulation. Chronic muscle stimulation up-regulated (P < .05) mTOR protein (+74%), rpS6 (+31%), and eIF2α (+44%, P < .07), and this was accompanied by an increase in cytochrome C (+31%). Phosphorylation of rpS6 (Ser235/Ser236) was increased (+51%, P < .05), while mTOR (Ser2448) and 4E-BP1 (Thr37/46) did not change. These experiments demonstrate that acute and chronic endurance contractile activity up-regulate the mTOR signalling pathway and mitochondrial content in murine skeletal muscle. This up-regulation of the mTOR pathway may increase translation efficiency and may also represent an important control point in exercise mediated mitochondrial biogenesis.