Evidence map›Paper›PMID 27502839›Full record

ArticleScientific reports2016

The role of mTOR signalling in the regulation of skeletal muscle mass in a rodent model of resistance exercise.

Riki Ogasawara, Satoshi Fujita, Troy A Hornberger, Yu Kitaoka, Yuhei Makanae, Koichi Nakazato, Ishii Naokata

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

99 citing papers in PubMed, 2 syntheses or guidelines pooled it, 192 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Effects of electromyostimulation on sarcolipin and CaBiochemistry and biophysics reports · 2026
    Article
  8. TAK1 Regulates Skeletal Muscle Mass, Hypertrophic Signaling, and Metabolic Homeostasis in Male and Female Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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39 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Riki OgasawaraDepartment of Life Science and Applied Chemistry, Nagoya Institute of Technology, Nagoya, Japan.
Satoshi FujitaDepartment of Sport and Health Science, Ritsumeikan University, Kusatsu, Japan.
Troy A HornbergerDepartment of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Yu KitaokaDepartment of Life Sciences, The University of Tokyo, Tokyo, Japan.
Yuhei MakanaeDepartment of Sport and Health Science, Ritsumeikan University, Kusatsu, Japan.
Koichi NakazatoDepartment of exercise physiology, Nippon Sport Science University, Tokyo, Japan.
Ishii NaokataDepartment of Life Sciences, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPRitsumeikan University · JPNippon Sport Science University · JPUniversity of Wisconsin–Madison · US

Funding

Mechanotransduction and the Regulation of Skeletal Muscle MassR01AR057347 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI HORNBERGER, TROY A · 2010 to 2019
$3.6M
Mechanotransduction and the Regulation of Skeletal Muscle MassR56AR057347 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI HORNBERGER, TROY A · 2022 to 2022
$270k
NIAMS NIH HHS R01 AR057347NIAMS NIH HHS R56 AR057347
6 · The paper itself

Abstract

Resistance exercise (RE) activates signalling by the mammalian target of rapamycin (mTOR), and it has been suggested that rapamycin-sensitive mTOR signalling controls RE-induced changes in protein synthesis, ribosome biogenesis, autophagy, and the expression of peroxisome proliferator gamma coactivator 1 alpha (PGC-1α). However, direct evidence to support the aforementioned relationships is lacking. Therefore, in this study, we investigated the role of rapamycin-sensitive mTOR in the RE-induced activation of muscle protein synthesis, ribosome biogenesis, PGC-1α expression and hypertrophy. The results indicated that the inhibition of rapamycin-sensitive mTOR could prevent the induction of ribosome biogenesis by RE, but it only partially inhibited the activation of muscle protein synthesis. Likewise, the inhibition of rapamycin-sensitive mTOR only partially blocked the hypertrophic effects of chronic RE. Furthermore, both acute and chronic RE promoted an increase in PGC-1α expression and these alterations were not affected by the inhibition of rapamycin-sensitive mTOR. Combined, the results from this study not only establish that rapamycin-sensitive mTOR plays an important role in the RE-induced activation of protein synthesis and the induction of hypertrophy, but they also demonstrate that additional (rapamycin-sensitive mTOR-independent) mechanisms contribute to these fundamentally important events.

Indexed as

AnimalsExercise ToleranceMaleMuscle ProteinsMuscle, SkeletalPhysical Conditioning, AnimalProtein BiosynthesisRatsRats, Sprague-DawleySignal TransductionTOR Serine-Threonine KinasesmTOR protein, ratMuscle ProteinsTOR Serine-Threonine Kinases

Identifiers

PMID27502839
PMCPMC4977552
OpenAlexW2517574975

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.