The DOI matches its Crossref record; 85 of the 86 references it cites were found in a registry or an index.
Signals mediating skeletal muscle remodeling by resistance exercise: PI3-kinase independent activation of mTORC1
Abstract
For over 10 years, we have known that the activation of the mammalian target of rapamycin complex 1 (mTORC1) has correlated with the increase in skeletal muscle size and strength that occurs following resistance exercise. Initial cell culture and rodent models of muscle growth demonstrated that the activation of mTORC1 is common to hypertrophy induced by growth factors and increased loading. The further observation that high loads increased the local production of growth factors led to the paradigm that resistance exercise stimulates the autocrine production of factors that act on membrane receptors to activate mTORC1, and this results in skeletal muscle hypertrophy. Over the last few years, there has been a paradigm shift. From both human and rodent studies, it has become clear that the phenotypic and molecular responses to resistance exercise occur in a growth factor-independent manner. Although the mechanism of load-induced mTORC1 activation remains to be determined, it is clear that it does not require classical growth factor signaling.
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In the citing paper
“However, resistance exercise activates mTOR in a growth factor-independent manner [12].”
From Using Molecular Biology to Maximize Concurrent Training (2014) · cites this paper as [12]
In the citing paper
“linked kinases have each been proposed as mechanosensors that initiate the signal that generates greater subsequent activity of the mechanistic target of rapamycin complex 1 (mTORC1).”
From Concurrent exercise training: do opposites distract? (2017) · cites this paper as Philp et al., 2011
In the citing paper
“The downstream effectors of mTORC1 are the 70KDa ribosomal S6 protein kinase (S6K) and eukaryotic initiation factor 4E binding protein (4E-BP) that have been shown to have key roles in promoting translation initiation and ribosome biogenesis (Philp et al., 2011).”
From Concurrent exercise training: do opposites distract? (2017) · cites this paper as Philp et al., 2011
Citations
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1 of the 86 references couldn’t be matched to a known paper.
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Metadata
- Authors
- Philp, A., Hamilton, D. L., & Baar, K.
- Affiliations
- University of California, Davis (US)
- University of Dundee (GB)
- Corresponding author
- Baar, Keith
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2011-02
- Volume
- 110
- Issue
- 2
- Pages
- 561-568
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W1993994764
- Cited by
- 131
- References
- 86
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 1 · 2023: 9 · 2022: 8 · 2021: 3 · 2020: 5 · 2019: 4 · 2018: 6 · 2017: 11 · 2016: 11 · 2015: 10 · 2014: 14 · 2013: 21 · 2012: 13
- FWCI
- 5.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Stirling Online Research Repository (University of Stirling) (submittedVersion)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- 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
- Keywords
- resistance training, skeletal muscle remodeling, mTORC1, muscle hypertrophy, mechanical loading, autocrine growth factor, muscle growth
- MeSH terms
- Mechanistic Target of Rapamycin Complex 1, Animals, Humans, Models, Biological, Proteins, Signal Transduction, Muscle, Skeletal, Phosphatidylinositol 3-Kinases, Multiprotein Complexes, TOR Serine-Threonine Kinases
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