Cited by 297Muscle Physiology and DisordersPI3K/AKT/mTOR signaling in cancerMuscle metabolism and nutrition

The role of skeletal muscle mTOR in the regulation of mechanical load‐induced growth

Open access
Goodman, Craig A., Frey, John W., Mabrey, Danielle M., Jacobs, Brittany L., Lincoln, Hannah C., You, Jae‐Sung, Hornberger, Troy A.·2011·The Journal of Physiology

Abstract

Non‐Technical Summary Chronic mechanical loading (CML) of skeletal muscle induces growth and this effect can be blocked by the drug rapamycin. Rapamycin is considered to be a highly specific inhibitor of the mammalian target of rapamycin (mTOR), and thus, many have concluded that mTOR plays a key role in CML‐induced growth. However, direct evidence that mTOR confers the CML‐induced activation of growth promoting events such as hypertrophy, hyperplasia and ribosome biogenesis is lacking. This study addressed that gap in knowledge by using a specialized line of transgenic mice. Surprisingly, the results indicate that only a few of the growth promoting events induced by CML are fully dependent on mTOR signalling (e.g. hypertrophy). These results advance our understanding of the molecular mechanisms that regulate skeletal muscle mass and should help future studies aimed at identifying targets for therapies that can prevent the loss of muscle mass during conditions such as bedrest, immobilization, and ageing.

Integrity signals

Registry

Crossref · 10.1113/jphysiol.2011.218255

Cites

57 of 57 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Resistance exercise-induced muscle hypertrophy is completely dependent on mTOR.

    “These data showed conclusively that resistance exercise-induced muscle hypertrophy is completely dependent on mTOR.”

    From Using Molecular Biology to Maximize Concurrent Training (2014) · cites this paper as [29]

  • In wild-type animals rapamycin completely blocked muscle hypertrophy, whereas in mice expressing a rapamycin-resistant mutant of mTOR, muscle hypertrophy occurred normally both in the presence and absence of rapamycin.

    “As would be expected, in the wild-type animals rapamycin completely blocked muscle hypertrophy. However, in the mice expressing a rapamycin-resistant mutant of mTOR muscle, hypertrophy occurred normally both in the presence and absence of rapamycin [29].”

    From Using Molecular Biology to Maximize Concurrent Training (2014) · cites this paper as [29]

  • Readily digestible, leucine-rich protein consumed after resistance training maximizes mTOR recruitment to the lysosome.

    “Resistance exercise should be supported by readily digestible, leucine-rich protein as soon as possible after training to maximize leucine uptake [64], mTOR recruitment to the lysosome [29], and protein synthesis [25].”

    From Using Molecular Biology to Maximize Concurrent Training (2014) · cites this paper as [29]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Goodman, C. A., Frey, J. W., Mabrey, D. M., Jacobs, B. L., Lincoln, H. C., You, J., & Hornberger, T. A.
Affiliations
University of Wisconsin–Madison (US)
Venue
The Journal of Physiology
Publisher
Wiley
Published
2011-11
Volume
589
Issue
22
Pages
5485-5501
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W2117741579
Cited by
297
References
57
Citations by year
2026: 10 · 2025: 20 · 2024: 8 · 2023: 23 · 2022: 21 · 2021: 25 · 2020: 25 · 2019: 22 · 2018: 25 · 2017: 16 · 2016: 22 · 2015: 28 · 2014: 19 · 2013: 24 · 2012: 9
FWCI
6.75
Type
journal article
Language
en
Open access
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • University of Illinois at Urbana-Champaign
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-057347, R56AR057347, R03AR053280, AR053280, R01AR057347)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
Keywords
mTOR signaling, skeletal muscle, muscle hypertrophy, muscle hyperplasia, rapamycin, FOXO1, Akt phosphorylation, muscle growth regulation
MeSH terms
Animals, Hypertrophy, Male, Mice, Transgenic, Mutation, Ribosomes, Weight-Bearing, Muscle, Skeletal, Sirolimus, Mice, Ablation Techniques, TOR Serine-Threonine Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review