Activating the Protein Synthesis Signaling by HIIT Concomitant with the Suppression of Protein Degradation in Wistar Rats’ Skeletal Muscle

Muscle loss occurs in some conditions such as aging, sarcopenia, and cancer. The interaction between protein synthesis and degradation signaling components induced by high-intensity interval training (HIIT) is not well studied.

The purpose of the present study was to simultaneously examine the effect of eight-week HIIT on the gene expression of both signaling components.

Sixteen male Wistar rats were randomly assigned to HIIT and non-exercise control groups. The HIIT group ran on a treadmill, five days/week for eight weeks, with 0º slope, including five interval sets of high and low intensity. Forty-eight hours after the last exercise session, dissected soleus muscles were stored at -80°C for later analyses.

The gene expression of Akt1, mTORC1, and S6K1 were increased in the HIIT group compared with the control group (All P ≤ 0.031) concomitant with the suppression of eIF4EBP1. The results of the S6K1 and eIF4EBP1 mRNA were also confirmed by the Western blotting. According to the inhibitory effect of Akt1, the gene expressions of FoxO3a and, consequently, MuRF1 and LC3A were significantly inhibited (All P ≤ 0.003). Western blot analysis did not confirm the LC3A protein expression, which may underline the role of LC3A in autophagy to promote cell survival.

The intensities and durations of the exercise training protocol are sufficient to increase protein synthesis signaling components and especially inhibit the atrophy-related gene expression, which may lead to attenuating muscle loss and increasing muscle mass. Accordingly, it may be considered for rehabilitation and/or prevention of some conditions such as sarcopenia and cachexia.