Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/22562
Appears in Collections:Faculty of Health Sciences and Sport Journal Articles
Peer Review Status: Refereed
Title: Rapamycin does not prevent increases in myofibrillar or mitochondrial protein synthesis following endurance exercise
Authors: Philp, Andrew
Schenk, Simon
Perez-Schindler, Joaquin
Hamilton, David Lee
Breen, Leigh
Laverone, Erin
Jeromson, Stewart
Phillips, Stuart M
Baar, Keith
Contact Email: d.l.hamilton@stir.ac.uk
Issue Date: 15-Sep-2015
Publisher: Wiley-Blackwell
Citation: Philp A, Schenk S, Perez-Schindler J, Hamilton DL, Breen L, Laverone E, Jeromson S, Phillips SM & Baar K (2015) Rapamycin does not prevent increases in myofibrillar or mitochondrial protein synthesis following endurance exercise, Journal of Physiology, 593 (18), pp. 4275-4284.
Abstract: 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 1h of treadmill running (18mmin−1; 5° grade), 1h afteri.p.administration of rapamycin (1.5mg · kg−1) or vehicle. To quantify skeletal muscle protein fractional synthesis rates, a flooding dose (50mg · kg−1) ofl-[ring-13C6]phenylalanine was administered viai.p.injection. Blood and gastrocnemius muscle were collected in non-exercised control mice, as well as at 0.5, 3 and 6h 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 6h, whereas this response was transiently blunted (30min 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 6h recovery period. Peroxisome proliferator activated receptor-γ coactivator-1α, 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.
Type: Journal Article
URI: http://hdl.handle.net/1893/22562
DOI Link: http://dx.doi.org/10.1113/JP271219
Rights: The publisher does not allow this work to be made publicly available in this Repository. Please use the Request a Copy feature at the foot of the Repository record to request a copy directly from the author. You can only request a copy if you wish to use this work for your own research or private study.
Affiliation: University of Birmingham
University of California, San Diego
University of Birmingham
Sport
University of Birmingham
University of California, Davis
Sport
McMaster University
University of California, Davis

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