Background: Duchenne muscular dystrophy (DMD) is caused by mutation of dystrophin, the main component of the Dystrophin-glycoprotein complex. Absence of dystrophin entails damage to
skeletal muscle during contractions and lesions requires repetitive cycles of muscle fiber degeneration and regeneration to repair the damage. In DMD, after muscle injury, quiescent satellite cells is
activated by inflammatory cells that up-regulates members of myogenic regulatory factors expression (MyoD and myogenin), in order to regulate myogenesis process. MyoD stimulates differentiation of
satellite cells into myogenic cells, and activate myogenin, which is characterized by promote the differentiation and development of myofibrils and myotubes. Therefore, myogenin is an important
modulator of cell cycle exit during differentiation, while MyoD is involved in the determination of myogenic cells. In mdx mice, eccentric exercise promotes sarcolema rupture, causes muscular
weakness, muscle degeneration, and increased the inflammatory profile of skeletal muscle. The aim of this study was to analyze the effects of eccentric training in myogenic regulatory factors (MyoD
and myogenin) of skeletal muscle in mdx mice.
Methods: C57BL/10 and C57BL/10-Dmdmdx male mice with eight weeks old were distributed into four groups (n=5): Sedentary Control (SC), Trained Control (TC), Sedentary Mdx (S-Mdx) and
Trained Mdx (T-Mdx). Procedures were approved by the Experimental Animal Use Committee of UNIFESP (CEUA 8165240614). Trained groups were submitted to seven weeks of aerobic exercise, five times a week
at a high intensity speed for 60 minutes with treadmill downward of -15°. After euthanasia, gastrocnemius muscles were taken and the specimens were evaluated by MyoD and myogenin immunohistochemistry.
Immunoreactive nuclei percentage were determined using photomicrographs obtained with the aid of computerized imaging system (Axio Visio-Zeiss) attached to a binocular light microscope (Axio Observer
D1, Zeiss). Statistical analysis of data was performed using two-way ANOVA.
Results: MyoD and Myogenin were detected in muscle fiber nuclei. S-Mdx and T-Mdx immunoexpression of MyoD showed lower percentage of immunoreactive nuclei when compared with SC and
TC. MyoD evaluation was not influenced by physical training. Concerning myogenin immunoexpression, Mdx animals (S-Mdx and T-Mdx) had lower percentage of immunoreactive nuclei to myogenin when compared
with C group, as viewed in MyoD analysis. However, the protocol training was able to increase the percentage of myogenin immunoreactive nuclei in trained groups when compared with respective controls:
ST>SC and T-Mdx >S-Mdx.
Conclusions: The exercise training protocol did not influenced MyoD but increased myogenin immunoexpression in gastrocnemius muscle of mdx mice.