Effect of high intensity interval training and detraining on gene expression of AKT/FoxO3a in cardiac and soleus muscle of male rats

The Akt / FoxO3a pathways is an important player in skeletal and cardiac muscle atrophy. In this study, the expression of Akt / FoxO3a / MAFbx / MuRF1 genes in soleus and heart muscle following exercise and detraining was investigated.

Male mice were randomly assigned to the control and exercise group after familiarization. HIIT training group was randomly divided into three groups of eight after six weeks of intermittent training. After a six-week training period, tissue removal was performed for the 1st, 2nd, and 3rd groups respectively after 48 hours, seven days, and 14 days of inactivity. The RT-PCR method was used to investigate gene expresion changes.

Exercise significantly increased the weight of the heart and soleus muscle relative to body weight. However, it decreased after seven and 14 days of inactivity [15% and 22% in the heart muscle (p=0.002) and 9% and 16% in the soleus muscle (p=0.001), respectively]. AKT expression increased in both the heart and the soleus muscles after exercise, while FoxO3a decreased. During exercise, increased FoxO3a activity lead to activation of MAFbx and MuRF1 in the heart muscle and only MAFbx in the soleus muscle.

In cardiomyocytes, like skeletal muscle, FoxO3a activates MAFbx transcroption, which slows or prevents hypertrophy. But changes in MuRF1 showed that the FoxO3a / MuRF1 pathway in the heart and skeletal muscles may have different regulatory mechanisms and react differently.