Training improves the oxidative phenotype of muscle during the transition from cardiac hypertrophy to heart failure without altering MyoD and myogenin

Author(s)

Pacagnelli, Francis Lopes ; Aguiar, Andreo Fernando ; Campos, Dijon Henrique S. ; Castan, Eduardo Paulino ; Alves de Souza, Rodrigo Wagner ; Alves de Almeida, Fernanda Losi ; Carani, Fernanda ; Carvalho, Robson Francisco ; Cicogna, Antonio Carlos ; Silva, Maeli Dal Pai

• Document type: Journal article
• Source: Experimental Physiology; v. 101, n. 8, p. 1075-1085, AUG 1 2016.
• Web of Science Citations: 0

Abstract

The purpose of this study was to investigate the effects of physical training (PT) on phenotypic features (fibre-type content) and myogenic regulatory factors (MyoD and myogenin) in rat skeletal muscle during the transition from cardiac hypertrophy to heart failure. We used the model of ascending aortic stenosis (AS) to induce heart failure in male Wistar rats. Sham-operated animals were used as age-matched controls. At 18weeks after surgery, rats with ventricular dysfunction were randomized into the following four groups: sham-operated, untrained (Sham-U; n=8); sham-operated, trained (Sham-T; n=6); aortic stenosis, untrained (AS-U; n=6); and aortic stenosis, trained (AS-T; n=8). The AS-T and Sham-T groups were submitted to a 10week aerobic PT programme, while the AS-U and Sham-U groups remained untrained for the same period of time. After the PT programme, the animals were killed and the soleus muscles collected for phenotypic and molecular analyses. Physical training promoted type IIa-to-I fibre conversion in the trained groups (Sham-T and AS-T) compared with the untrained groups (Sham-U and AS-U). No significant (P>0.05) differences were found in type I or IIa fibre content in the AS-U group compared with the Sham-U group. Additionally, there were no significant (P>0.05) differences in the myogenic regulatory factors MyoD and myogenin (gene and protein) expression between the groups. Therefore, our results indicate that PT may be a suitable strategy to improve the oxidative phenotype in skeletal muscle during the transition from cardiac hypertrophy to heart failure, without altering MyoD and myogenin. (AU)