Effects of exercise training on brain-derived neurotrophic factor in skeletal muscle and heart of rats post myocardial infarction

Exercise training post myocardial infarction (MI) attenuates progressive left ventricle (LV) remodeling and dysfunction, but the peripheral stimuli induced by exercise which trigger these beneficial effects are still unclear. We investigated as possible mediators fibronectin type III domain-containing protein 5 (FNDC5) and brain-derived neurotrophic factor (BDNF) in the skeletal muscle and heart. Male Wistar rats underwent either sham surgery or ligation of left descending coronary artery, and surviving MI rats were allocated to either sedentary (Sed-MI) or exercise group (ExT-MI). Exercise training was done for 4 weeks on a motor- driven treadmill. At the end, LV function was evaluated, and FNDC5 and BDNF mRNA and protein were assessed in soleus muscle, quadriceps, and non-, peri- and infarct areas of the LV. At 5 weeks post MI, FNDC5 mRNA was decreased in soleus muscle and all areas of the LV, but FNDC5 protein was increased in the soleus muscle and the infarct area. Mature BDNF (mBDNF) protein was decreased in the infarct area without change in mRNA. Exercise training attenuated the decrease in EF and the increase in LVEDP post MI. Exercise training had no effect on FNDC5 mRNA and protein, but increased mBDNF protein in soleus muscle, quadriceps and non-infarct area of the LV. mBDNF protein in the non-infarct area correlated positively with EF and inversely with LVEDP. In conclusion, mBDNF is induced by exercise training in skeletal muscle and non-infarct area of the LV, which may contribute to improvement of muscle dysfunction and cardiac function post MI.