Molecular biological studies of skeletal muscle adaptations to physical exercise

乳酸阈值（LT）运动是可以促进健康益处的最低强度。这种轻度运动训练可以推荐给运动能力非常有限的人，包括老年人和患有代谢综合征和冠状动脉疾病（CAD）的人。事实上，监督下的低氧训练可以改善健康成人的生理适应性、血脂、胰岛素敏感性和心肺压力反射。本研究通过分子生物学的方法进一步探讨了诱导上述适应性的机制。我们为此目的开发了非侵入性注射器活检来获取肌肉样本。我们发现，PGC-1α基因的表达可能在线粒体生物发生、脂质代谢和胰岛素敏感性中发挥重要作用，但在LT以下的运动中，单次运动可以激活PGC-1α基因的表达。此外，LT训练还可以协调诱导线粒体能量代谢、脂肪氧化以及葡萄糖和肌酸代谢的转录物编码酶。其中一些变化，特别是线粒体功能的变化，已知在代谢综合征和肌肉萎缩的个体中是反向调节的。与LT训练相关的另一个分子特征是编码强效抗氧化酶和分子伴侣的转录本增加，这些转录本是参与兴奋-收缩耦合和电解质运输的关键基因，以及负责蛋白质周转的基因。我们还发现，I型纤维中的CD36随着LT训练而增加，但没有改变线粒体含量。

Exercise at lactate threshold (LT) is the minimum intensity that can promote health benefits. This mild-exercise training can be recommended to people with very limited range of exercise capacity, including the elderly and individuals with metabolic syndrome and coronary artery diseases (CAD). Indeed, supervised LT training improves physiological fitness, lipid profile, insulin sensitivity and cardio-pulmonary baroreflex in healthy adults. In this study we further investigated the mechanism to induce the above mentioned adaptation by the molecular biological approach. We developed rather noninvasive syringe biopsy to obtain the muscle sample for this purpose. We found that PGC-1α gene expression, which may play an important role for the mitochondrial biogenesis, lipid metabolism and insulin sensitivity, was activated by a single session of exercise at the LT but not by the exercise below the LT. Further the LT training has coordinately induced transcripts encoding enzymes in mitochondrial energy metabolism and fat oxidation as well as glucose and creatine metabolisms in young adult. Some of these changes, especially in mitochondrial function, are known to be inversely modulated in individuals with metabolic syndrome as well as atrophied muscle. Another molecular feature associated with LT training is the increases in transcripts encoding potent antioxidant enzymes and molecular chaperons, key genes involved in excitation-contraction coupling and electrolyte transport, and genes responsible for protein turnover. We also showed that CD36 in type I fiber increased with the LT training but did not change mitochondrial content.