过度训练的大鼠心肌中氧化磷酸化受损。
Impaired oxidative phosphorylation in overtrained rat myocardium.
作者信息
Kadaja Lumme, Eimre Margus, Paju Kalju, Roosimaa Mart, Põdramägi Taavi, Kaasik Priit, Pehme Ando, Orlova Ehte, Mudist Margareeta, Peet Nadezhda, Piirsoo Andres, Seene Teet, Gellerich Frank N, Seppet Enn K
机构信息
Institute of General and Molecular Pathology, Faculty of Medicine;
出版信息
Exp Clin Cardiol. 2010 Winter;15(4):e116-27.
The present study was undertaken to characterize and review the changes in energy metabolism in rat myocardium in response to chronic exhaustive exercise. It was shown that a treadmill exercise program applied for six weeks led the rats into a state characterized by decreased performance, loss of body weight and enhanced muscle catabolism, indicating development of overtraining syndrome. Electron microscopy revealed disintegration of the cardiomyocyte structure, cellular swelling and appearance of peroxisomes. Respirometric assessment of mitochondria in saponin-permeabilized cells in situ revealed a decreased rate of oxidative phosphorylation (OXPHOS) due to diminished control over it by ADP and impaired functional coupling of adenylate kinase to OXPHOS. In parallel, reduced tissue content of cytochrome c was observed, which could limit the maximal rate of OXPHOS. The results are discussed with respect to relationships between the volume of work and corresponding energy metabolism. It is concluded that overtraining syndrome is not restricted to skeletal muscle but can affect cardiac muscle as well.
本研究旨在描述和综述大鼠心肌能量代谢对慢性力竭运动的反应变化。结果显示，为期六周的跑步机运动方案使大鼠进入一种表现为运动能力下降、体重减轻和肌肉分解代谢增强的状态，表明出现了过度训练综合征。电子显微镜检查显示心肌细胞结构解体、细胞肿胀以及过氧化物酶体出现。对皂素通透处理的原位细胞中线粒体进行呼吸测定评估发现，由于ADP对氧化磷酸化（OXPHOS）的控制减弱以及腺苷酸激酶与OXPHOS的功能偶联受损，氧化磷酸化速率降低。同时，观察到细胞色素c的组织含量减少，这可能会限制OXPHOS的最大速率。结合工作量与相应能量代谢之间的关系对结果进行了讨论。得出的结论是，过度训练综合征不仅限于骨骼肌，也会影响心肌。
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