Responses of skeletal muscle hypertrophy in Wistar rats to different resistance exercise models
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
27982685
DOI
10.33549/physiolres.933256
PII: 933256
Knihovny.cz E-zdroje
- MeSH
- kondiční příprava zvířat metody MeSH
- kosterní svaly anatomie a histologie fyziologie MeSH
- krysa rodu Rattus MeSH
- odporový trénink metody MeSH
- potkani Wistar MeSH
- protoonkogenní proteiny c-akt metabolismus MeSH
- svalová síla fyziologie MeSH
- TOR serin-threoninkinasy metabolismus MeSH
- velikost orgánu fyziologie MeSH
- výsledek terapie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- mTOR protein, rat MeSH Prohlížeč
- protoonkogenní proteiny c-akt MeSH
- TOR serin-threoninkinasy MeSH
This study aimed to compare the effects of three different resistance exercise models on the quadriceps muscle cross-sectional area, as well as on mTOR phosphorylation and other pivotal molecules involved in the upstream regulation of mTOR. Twenty-four male Wistar rats were divided into untrained (control), endurance resistance training, strength resistance training, and hypertrophy resistance training (HRT) groups (n=6). After 12 weeks of training, the red portion of the quadriceps was removed for histological and Western blot analyses. The results showed that the quadriceps weight and cross-sectional areas in the exercised groups were higher than those of the untrained rats. However, the HRT group presented better results than the other two experimental groups. This same pattern was observed for mTOR phosphorylation and for the most pivotal molecules involved in the upstream control of mTOR (increase of PKB, 14-3-3, ERK, p38 MAPK, and 4E-BP1 phosphorylation, and reduction of tuberin, sestrin 2, REDD1, and phospho AMPK). In summary, our study showed that HRT leads to high levels of mTOR phosphorylation as well as of other proteins involved in the upstream regulation of mTOR.
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