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Impact of exercise training on myostatin expression in the myocardium and skeletal muscle in a chronic heart failure model
Author(s) -
Lenk Karsten,
Schur Robert,
Linke Axel,
Erbs Sandra,
Matsumoto Yasuharu,
Adams Volker,
Schuler Gerhard
Publication year - 2009
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1093/eurjhf/hfp020
Subject(s) - myostatin , skeletal muscle , medicine , endocrinology , heart failure , cachexia , myokine , myocyte , regulator , follistatin , biology , biochemistry , cancer , gene
Aims In late‐stage chronic heart failure (CHF), elevated cytokines and cachexia are often observed. Several studies have shown that exercise training exerts beneficial effects on skeletal muscle in this setting. Furthermore, it has been shown that the expression of myostatin, a key regulator of skeletal muscle mass, is increased in a variety of cachectic states. This study aimed to investigate the expression of myostatin in CHF, the influence of exercise training on myostatin levels, and regulation of myostatin by tumour necrosis factor‐α (TNF‐α). Methods and results In an animal model of CHF (LAD‐ligation model), protein expression of myostatin was elevated 2.4‐fold in the skeletal muscle and more than four‐times in the myocardium, compared with control (Co). Exercise training on a treadmill over 4 weeks led to a significant reduction in myostatin protein expression in the skeletal muscle and the myocardium of CHF animals, with values returning to baseline levels. In differentiated C2C12 cells, TNF‐α induced the expression of myostatin through a p38MAPK‐dependent pathway involving nuclear factor kappa‐B (NF‐κB). The increased TNF‐α mRNA levels in the skeletal muscle of CHF animals correlated significantly with myostatin expression. Conclusion These alterations in myostatin expression in the skeletal and heart muscle following exercise training could help to explain the beneficial anti‐catabolic effects of exercise training in CHF.