Background and Objective:
Exercise-induced muscle hypertrophy occurs through increased rate of muscle protein synthesis that is regulated via molecular signaling pathways. The mammalian target of rapamycin (mTOR) pathway is believed to play a major role, via phosphorylation of the ribosomal protein S6 kinase of 70 kDa (p70S6K). Results concerning the effect of concurrent training on these factors have been contradictory. This study was done to determine the effect of 8 weeks of resistance training and concurrent resistance and aerobic training on phospho-mTOR (p-mTOR) and phospho-p70S6K (p-p70S6K) responses in skeletal muscle in rats.
In this experimental study, 24 wistar rats (age: 8 weeks) were randomly allocated into resistance training (n=8), concurrent training (n=8), and control (n=8) groups in equal laboratorial condition. Resistance group performed 5 sessions per week consisted of 10 repetitions ladder climbing with load suspended from the tail between 30-80% individual maximum overload test that was weekly performed to adjust the individual load throughout the week. The concurrent group performed resistance training followed by 5 minutes rest and endurance training consisted of treadmills run, that speed and duration of running gradually increased during training period, from 9 m/min and 10 minutes in the first week to 30 m/min and 60 minutes in the last week. The flexor hallucis longus (FHL) muscle of rats were removed under sterile condition at 24 hours after the last session of training and the proteins levels of p-mTOR and p-p70S6K were measured by ELISA method.
The level of p-mTOR was significantly greater in resistance training and concurrent training groups in compared to control group. No significant difference was observed between training groups. However, the significant increase of p-p70S6K was observed only in resistance group in compared to control group.
Because of the increased of p-mTOR in concurrent group was not accompanied by increase of p-p70S6K compared with resistance group, thus concurrent training probably attenuate signaling responses of downstream targets of mTOR.