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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 561-568 |
| Number of pages | 8 |
| Journal | Journal of Applied Physiology |
| Volume | 110 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 2011 |
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Keywords
- Mammalian target of rapamycin complex 1
ASJC Scopus subject areas
- Physiology
- Physiology (medical)
- Medicine(all)
Cite this
Highlighted topic signals mediating skeletal muscle remodeling by activity signals mediating skeletal muscle remodeling by resistance exercise : PI3-kinase independent activation of mTORC1. / Philp, Andrew; Hamilton, D. Lee; Baar, Keith.
In: Journal of Applied Physiology, Vol. 110, No. 2, 02.2011, p. 561-568.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Highlighted topic signals mediating skeletal muscle remodeling by activity signals mediating skeletal muscle remodeling by resistance exercise
T2 - PI3-kinase independent activation of mTORC1
AU - Philp, Andrew
AU - Hamilton, D. Lee
AU - Baar, Keith
PY - 2011/2
Y1 - 2011/2
N2 - 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.
AB - 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.
KW - Mammalian target of rapamycin complex 1
UR - http://www.scopus.com/inward/record.url?scp=79851497642&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79851497642&partnerID=8YFLogxK
U2 - 10.1152/japplphysiol.00941.2010
DO - 10.1152/japplphysiol.00941.2010
M3 - Article
C2 - 21071597
AN - SCOPUS:79851497642
VL - 110
SP - 561
EP - 568
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 2
ER -