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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,
Souza Rodrigo Wagner Alves,
Almeida Fernanda Losi Alves,
Carani Fernanda,
Carvalho Robson Francisco,
Cicogna Antonio Carlos,
Silva Maeli Dal Pai
Publication year - 2016
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep085552
Subject(s) - myod , myogenin , heart failure , muscle hypertrophy , medicine , skeletal muscle , cardiology , endocrinology , myod protein , ventricular hypertrophy , population , left ventricular hypertrophy , environmental health , myogenesis , blood pressure
New FindingsWhat is the central question of this study ? We investigated the effects of physical training on phenotypic (fibre‐type content) and myogenic features (MyoD and myogenin expression) in skeletal muscle during the transition from cardiac hypertrophy to heart failure.What is the main finding and its importance ? We provide new insight into skeletal muscle adaptations by showing that physical training increases the type I fibre content during the transition from cardiac hypertrophy to heart failure, without altering MyoD and myogenin expression. These results have important clinical implications for patients with heart failure, because this population has reduced muscle oxidative capacity.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 18 weeks 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 10 week 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 .