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Muscle protein synthesis, degradation and the effect of mTORC1, after resistance exercise (1163.7)
Author(s) -
West Daniel,
Baehr Leslie,
Shamim Baubak,
Gomes Aldrin,
Bodine Sue,
Baar Keith
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1163.7
Subject(s) - mtorc1 , p70 s6 kinase 1 , stimulation , phosphorylation , endocrinology , chemistry , medicine , proteasome , protein degradation , biochemistry , protein kinase b
We aimed to measure mTORC1 signaling, rates of muscle protein synthesis (MPS), and proteasome activity after acute resistance exercise (REx). A second aim was to determine whether mTORC1 signaling impacted MPS in late recovery. Rats (8 m.o. FBN hybrids) underwent unilateral hindlimb stimulation that eccentrically contracted the tibialis anterior (TA). All measures in the stimulated TA were expressed relative to the contralateral control TA. TA muscles were collected at 1.5, 3, 6, 18, and 36 h after REx, and at 3 and 18 h after REx plus rapamycin treatment to block mTORC1 activity. There was a robust activation of mTORC1, whereby phosphorylation of S6K1 (T389) peaked at 3 h (134±22‐fold inc.) and returned to baseline by 18 h; phosphorylation of S6 (S240/244) peaked at 6 h (26±4‐fold inc.). MPS peaked at 6 h (67±31% inc.) before gradually declining toward baseline through 36 h. Principal proteasome activities, 26S and 20S beta5, tended to decrease (~15‐20% at 6‐12 h), and then increase at later time points (~15‐20% above rest at 18‐36 h). Interestingly, rapamycin treatment, while completely blocking increases in p‐S6K1, only partially blocked the elevation in MPS at 18 h. In summary, REx stimulated a large increase in mTORC1 signaling and a moderate sustained increase in MPS, and inhibiting mTORC1 did not fully abolish the MPS effect at 18 h. Further, for the first time, we have directly measured proteasome activity after REx. Grant Funding Source : Supported by NSERC and Veteran Affairs (RR&D Merit Grant E7766‐R)