PMID- 32256674
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220413
IS  - 1743-7075 (Print)
IS  - 1743-7075 (Electronic)
IS  - 1743-7075 (Linking)
VI  - 17
DP  - 2020
TI  - Crucial role of androgen receptor in resistance and endurance trainings-induced 
      muscle hypertrophy through IGF-1/IGF-1R- PI3K/Akt- mTOR pathway.
PG  - 26
LID - 10.1186/s12986-020-00446-y [doi]
LID - 26
AB  - BACKGROUND: Androgen receptor (AR) has been reported to play vital roles in 
      exercise-induced increase of muscle mass in rats, but needs to be further 
      verified and the mechanism behind remains unclear. As AR target genes, insulin 
      growth factor-1 (IGF-1) and IGF-1 receptor (IGF-1R) promote muscle hypertrophy 
      through activating PI3K/Akt- mammalian target of rapamycin (mTOR) pathway, a 
      classic pathway of muscle hypertrophy. So the main purpose of this study was 
      using AR antagonist flutamide to demonstrate AR's effect on training-induced 
      muscle hypertrophy and its possible mechanism: IGF-1/IGF-1R- PI3K/Akt- mTOR 
      pathway? METHODS: Forty-eight Sprague Dawley male rats aged 7 weeks were randomly 
      divided into six groups: control (C), flutamide (F), resistance training (R), 
      resistance training plus flutamide (R + F), endurance training (E), and endurance 
      training plus flutamide (E + F) groups. Flutamide was used to block AR in rats. 
      Rats in R and R + F groups fulfilled 3 weeks of ladder climbing with 
      progressively increased load, while E and E + F rats completed 3-week moderate 
      intensity aerobic exercise on a treadmill. The relative muscle mass (muscle 
      mass/body weight) of rats was detected. Serum levels of testosterone and IGF-1 of 
      rats were determined by ELISA, and mRNA levels of IGF-1R and mTOR in muscles by 
      real-time PCR. Protein levels of AR, IGF-1, IGF-1R, mTOR, PI3K, Akt, p-PI3K and 
      p-Akt in muscles were detected by Western blot. RESULTS: (1) The training-induced 
      rise in the relative muscle mass and the expression levels of AR were only found 
      in the gastrocnemius of R rats and in the soleus of E rats (selective muscle 
      hypertrophy), which were blocked by flutamide. (2) Serum testosterone in the R 
      and E rat were increased, and flutamide exerted no effect. (3) The levels of 
      IGF-1, IGF-1R and mTOR as well as the activities of PI3K and Akt were enhanced 
      selectively (in the gastrocnemius of R rats and in the soleus of E rats), which 
      were reduced by flutamide. Conclusions: AR exerted an essential role in both 
      resistance training and endurance training-induced muscle hypertrophy, which was 
      mediated at least partly through IGF-1/IGF-1R- PI3K/Akt- mTOR pathway.
CI  - (c) The Author(s) 2020.
FAU - Yin, Lijun
AU  - Yin L
AD  - Department of Kinesiology, Shanghai University of Sport, 188 Hengren Road, Yangpu 
      District, Shanghai, 200438 People's Republic of China. GRID: grid.412543.5. ISNI: 
      0000 0001 0033 4148
FAU - Lu, Lin
AU  - Lu L
AD  - Department of Kinesiology, Shanghai University of Sport, 188 Hengren Road, Yangpu 
      District, Shanghai, 200438 People's Republic of China. GRID: grid.412543.5. ISNI: 
      0000 0001 0033 4148
FAU - Lin, Xiaojing
AU  - Lin X
AD  - Department of Kinesiology, Shanghai University of Sport, 188 Hengren Road, Yangpu 
      District, Shanghai, 200438 People's Republic of China. GRID: grid.412543.5. ISNI: 
      0000 0001 0033 4148
FAU - Wang, Xiaohui
AU  - Wang X
AD  - Department of Kinesiology, Shanghai University of Sport, 188 Hengren Road, Yangpu 
      District, Shanghai, 200438 People's Republic of China. GRID: grid.412543.5. ISNI: 
      0000 0001 0033 4148
LA  - eng
PT  - Journal Article
DEP - 20200330
PL  - England
TA  - Nutr Metab (Lond)
JT  - Nutrition & metabolism
JID - 101231644
PMC - PMC7106900
OTO - NOTNLM
OT  - Androgen receptor
OT  - IGF-1
OT  - IGF-1R
OT  - Muscle hypertrophy
OT  - PI3K/Akt/mTOR
OT  - Training
COIS- Competing interestsWe declare that we have no competing interests.
EDAT- 2020/04/08 06:00
MHDA- 2020/04/08 06:01
PMCR- 2020/03/30
CRDT- 2020/04/08 06:00
PHST- 2019/12/25 00:00 [received]
PHST- 2020/03/21 00:00 [accepted]
PHST- 2020/04/08 06:00 [entrez]
PHST- 2020/04/08 06:00 [pubmed]
PHST- 2020/04/08 06:01 [medline]
PHST- 2020/03/30 00:00 [pmc-release]
AID - 446 [pii]
AID - 10.1186/s12986-020-00446-y [doi]
PST - epublish
SO  - Nutr Metab (Lond). 2020 Mar 30;17:26. doi: 10.1186/s12986-020-00446-y. 
      eCollection 2020.