ABSTRACT

　The aim of this study is to investigate whether adropin, a novel regulator of metabolic homeostasis, is involved in lowered exercise capacity and skeletal muscle atrophy due to aging (sarcopenia). We focused on heart failure, which is a representative disease of sarcopenia, and tested this hypothesis in clinical studies for patients with heart failure and in experimental settings using heart failure model after myocardial infarction. The serum adropin levels of heart failure patients was 1.44±0.09 (ng/mL), which was significantly lower than that of the healthy control group (1.64±0.07). Moreover, serum adropin levels showed a significant positive correlation with the maximum oxygen uptake and anaerobic metabolic threshold, which are indicators of exercise tolerance (r=0.65, 0.59, respectively). In addition, serum adropin levels showed a significant negative correlation with the ventilatory response which is an index of shortness of breath (r=-0.61). We created post-infarct heart failure model by ligating left coronary artery of 10-12 week old C57BL/6J mice. In this model, the exercise time, exercise distance, and maximum oxygen uptake were all significantly reduced compared to the Sham group. These lowered exercise capacities were associated with a reduction in mitochondrial oxidative capacity in the skeletal muscle of those mice. As a future plan, we will quantify adropin concentration in those skeletal muscle tissues and will examine whether adropoin levels are associated with muscle mitochondrial oxidative capacities under each energy substrate. Our findings suggest that serum adropin levels may a new surrogate marker for sarcopenia and exercise intolerance associated with heart failure as well as aging.

DESCENTE SPORTS SCIENCE Vol.39/THE DESCENTE AND ISHIMOTO MEMORIAL FOUNDATION FOR THE PROMOTION SPORTS SCIENCE