The effect of high-intensity training and detraining on FOXO3a/MuRF1 and MAFbx levels in soleus muscle of male rats

Inactivity may result in loss of muscle volume and subsequently reduce the power, by activating proteasome signaling pathways, which leads to a decrease in quality and expectations of life. The aim of this study was to evaluate the effect of high-intensity training and also detraining on the signaling pathways of FOXO3a, MAFbx, and MuRF1.
In this study, 32 2-month male Sprague-Dawley rats were used. At first, periodic exercise with intensity of 85-100% VO2max was performed for six weeks. Then, the groups (detrained for 48h, 7w, and 14w) were detrained and then soleus muscle was removed from hind limb. H&E staining and histochemical procedure were used to measure the amount and percentage of skeletal muscle fibers type. Also, RT-PCR method was used to examine gene changes.
The mean weight of the soleus muscle increased after exercise and decreased significantly after detraining (p=0.001).The fiber type conversion were happened from I to IIA (p=0.001). Hypertrophy was observed in fibers after training, whereas atrophy was seen after detraining in type II fibers (p=0.001). FOXO3a and MAFbx levels were significantly increased after training and decreased after detraining period (p=0.001).The MuRF1 expression shown an increase and a decrease after training and detraining, respectively (p=0.001).
The results of this study indicated that the exercise couldn’t prevent atrophy during the period of detraining. Also, the activation of pathway FOXO3a/MAFbx, not the FOXO3a/ MuRF1, is the atrophy inducer during detraining. In this regard, probably MuRF1 is an indirect target of FOXO3a and cannot always be an appropriate marker of atrophy. MuRF1 probably plays a more important role in pathological atrophy conditions.