期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 593, 期 18, 页码 4275-4284出版社
WILEY
DOI: 10.1113/JP271219
关键词
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资金
- BBSRC New Investigator Award [BB/L023547/1]
- National Institutes of Health (NIH) [R01 AG043120, R24 HD050837, P30 AR061303, P30 AR058878]
- Sir Henry Wellcome Post-doctoral Fellowship
- ACSM Research Endowment
- Society for Endocrinology Young Investigator Award
- National Science and Engineering Research Council of Canada [RGPIN227870-05]
- NIH [R01 AG045375]
- BBSRC [BB/L023547/1] Funding Source: UKRI
- MRC [MR/K00414X/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/L023547/1] Funding Source: researchfish
- Medical Research Council [MR/K00414X/1] Funding Source: researchfish
The present study aimed to investigate the role of the mechanistic target of rapamycin complex 1 (mTORC1) in the regulation of myofibrillar (MyoPS) and mitochondrial (MitoPS) protein synthesis following endurance exercise. Forty-two female C57BL/6 mice performed 1 h of treadmill running (18 m min(-1); 5 degrees grade), 1 h after I.P. administration of rapamycin (1.5 mg.kg(-1)) or vehicle. To quantify skeletal muscle protein fractional synthesis rates, a flooding dose (50 mg.kg(-1)) of L-[ring-C-13(6)] phenylalanine was administered via I.P. injection. Blood and gastrocnemius muscle were collected in non-exercised control mice, as well as at 0.5, 3 and 6 h after completing exercise (n = 4 per time point). Skeletal muscle MyoPS and MitoPS were determined by measuring isotope incorporation in their respective protein pools. Activation of the mTORC1-signalling cascade was measured via direct kinase activity assay and immunoblotting, whereas genes related to mitochondrial biogenesis were measured via a quantitative RT-PCR. MyoPS increased rapidly in the vehicle group post-exercise and remained elevated for 6 h, whereas this response was transiently blunted (30 min post-exercise) by rapamycin. By contrast, MitoPS was unaffected by rapamycin, and was increased over the entire post-exercise recovery period in both groups (P < 0.05). Despite rapid increases in both MyoPS and MitoPS, mTORC1 activation was suppressed in both groups post-exercise for the entire 6 h recovery period. Peroxisome proliferator activated receptor-gamma coactivator-1 alpha, pyruvate dehydrogenase kinase 4 and mitochondrial transcription factor A mRNA increased post-exercise (P < 0.05) and this response was augmented by rapamycin (P < 0.05). Collectively, these data suggest that endurance exercise stimulates MyoPS and MitoPS in skeletal muscle independently of mTORC1 activation.
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