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Resistance training‐induced muscle hypertrophy is mediated by TGF‐β1‐Smad signaling pathway in male Wistar rats
Author(s) -
Nikooie Rohollah,
JafariSardoie Sohil,
Sheibani Vahid,
Nejadvaziri Chatroudi Amir
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29497
Subject(s) - smad , muscle hypertrophy , signal transduction , pi3k/akt/mtor pathway , endocrinology , phosphorylation , protein kinase b , transforming growth factor , medicine , foxo1 , downregulation and upregulation , skeletal muscle , biology , chemistry , microbiology and biotechnology , biochemistry , gene
The TGF‐β1‐Smad pathway is a well‐known negative regulator of muscle growth; however, its potential role in resistance training‐induced muscle hypertrophy is not clear. The present study proposed to determine whether and how this pathway may be involved in resistance training‐induced muscle hypertrophy. Skeletal muscle samples were collected from the control, trained (RT), control + SB431542 (CI TGF ), and trained + SB431542 (RTI TGF ) animals following 3, 5, and 8 weeks of resistance training. Inhibition of the TGF‐β1‐Smad pathway by SB431542 augmented muscle satellite cells activation, upregulated Akt/mTOR/S6K1 pathway, and attenuated FOXO1 and FOXO3a expression in the CI TGF group (all p < .01), thereby causing significant muscle hypertrophy in animals from the CI TGF . Resistance training significantly decreased muscle TGF‐β1 expression and Smad3 (P‐Smad3 S423/425 ) phosphorylation at COOH‐terminal residues, augmented Smad2 (P‐Smad2‐L S245/250/255 ) and Smad3 (P‐Smad3‐L Ser208 ) phosphorylation levels at linker sites (all p < .01), and led to a muscle hypertrophy which was unaffected by SB431542, suggesting that the TGF‐β1‐Smad signaling pathway is involved in resistance training‐induced muscle hypertrophy. The effects of inhibiting the TGF‐β1‐Smad signaling pathway were not additive to the resistance training effects on FOXO1 and FOXO3a expression, muscle satellite cells activation, and the Akt/mTOR/S6K1 pathway. Resistance training effect of satellite cell differentiation was independent of the TGF‐β1‐Smad signaling pathway. These results suggested that the effect of the TGF‐β1‐Smad signaling pathway on resistance training‐induced muscle hypertrophy can be attributed mainly to its diminished inhibitory effects on satellite cell activation and protein synthesis. Suppressed P‐Smad3 S423/425 and enhanced P‐Smad2‐L S245/250/255 and P‐Smad3‐L Ser208 are the molecular mechanisms that link the TGF‐β1‐Smad signaling pathway to resistance training‐induced muscle hypertrophy.