Abstract

This study investigated whether different exercise intensities during detraining could maintain muscle hypertrophy and mitochondrial biogenesis signaling pathways activated high-intensity interval training (HIIT) in the flexor pollicis longus and soleus muscles of Sprague-Dawley rats. Fiver groups were studied: non-exercise ([NEG], n=6), HIIT only ([CTG], n=6), resting control ([CD], n=6), low-intensity exercise (LID, n=6), moderate-intensity exercise ([MID], n=6). The HIIT program consisted of 30-minute sessions of 24 m/min for eight weeks. During detraining (two weeks), LID and MID groups exercise three times per week at 8 m/min and 16 m/min, respectively. Muscle hypertrophy and mitochondrial biogenesis-related protein expression in the flexor pollicis longus and soleus muscles were analyzed using Western blotting. Compared to NEG, PI3K was higher in the CTG and LID in the flexor pollicis longus, while Akt and p-mTOR signaling pathways were significantly activated in MID and CTG. In the soleus muscle, p-AMPK expression was higher in CD and MID than in NEG, and FNDC5 was upregulated in LID compared to CTG and CD. These findings suggest that moderate-intensity exercise during detraining may help maintain HIIT-induced muscle hypertrophy signaling, while low-intensity exercise may contribute to sustaining HIIT-activated aerobic metabolism in skeletal muscle.

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