Differential regulation of myofibrillar and mitochondrial protein synthesis following acute endurance exercise (702.3)

Endurance exercise leads to rapid transcriptional‐ and translational‐mediated remodeling in skeletal muscle. The purpose of this study was to investigate the role of the mechanistic target of rapamycin (mTORC1) in the molecular regulation of myofibrillar and mitochondrial protein synthesis in the first 6h after endurance exercise. Female C57BL/6 mice performed one‐hour of treadmill running after administration of rapamycin or vehicle. A flooding dose of L‐[ring‐13C6]phenylalanine was administered via IP injection and blood and gastrocnemius muscle collected 0.5, 3 and 6h post exercise and in a separate, non‐exercising control group (n=4/time). Skeletal muscle was analyzed for phenylalanine incorporation into the myofibrillar and mitochondrial pools via GC‐C‐IRMS. Myofibrillar fractional synthesis rate (FSR) increased rapidly in the vehicle group post‐exercise and remained elevated at all post‐exercise times. Rapamycin had no effect on basal FSR, but attenuated the rise in myofibrillar protein FSR at 0.5 and 3h post exercise. Interestingly, rapamycin did not affect mitochondrial protein FSR, which was increased at 3h and 6h post exercise in both groups. Taken together our data suggest that the initial increase (0‐3h) in myofibrillar FSR after endurance exercise is mTORC1 mediated, whereas at latter time points (3‐6h) myofibrillar and mitochondrial FSR are both stimulated, independent of mTORC1.