Lee Young I, Cho Joon Y, Kim Mun H, Kim Kee B, Lee Dong J, Lee Kyu S
Exercise Biochemistry Laboratory, Korea National Sport University, 88-15 Oryun-dong, 138-763, Songpa-gu, Seoul, Korea.
Eur J Appl Physiol. 2006 May;97(2):216-24. doi: 10.1007/s00421-006-0161-5. Epub 2006 Apr 1.
This study determined whether exercise training prevents pathological hypertrophy in the left ventricle by modulation of myocardial and apoptosis-associated genes. We used spontaneously hypertensive rats (n=15, non-exercise SHR), exercise-trained SHR (n=15, treadmill exercise for 12 weeks), and sedentary Wistar-Kyoto (WKY) rats (n=15). Exercise-trained SHR expressed adaptive changes such as reduced body weight, heart rate, blood pressures, left ventricle wall thickness, lipid profiles, and homocysteine level. The mRNA expression of angiotensin converting enzyme, endothelin-1, and brain natriuretic peptides in the heart was lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR, whereas mRNA expression of caveolin-3 and eNOS in the heart was higher. Bcl-2 protein was higher in the exercise-trained SHR than in the WKY and the non-exercise SHR. In contrast, Bax protein levels were lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR. Furthermore, the levels of the active forms of caspase-3 (20 kDa) were lower in the exercise-trained SHR and in the WKY than in the non-exercise SHR. These findings suggest that exercise training prevents pathological hypertrophy in the left ventricle by modulation of myocardial genes and that it interferes with a signal transduction pathway of apoptosis secondary to the pathological cardiac hypertrophy.
本研究确定运动训练是否通过调节心肌和凋亡相关基因来预防左心室病理性肥大。我们使用了自发性高血压大鼠（n = 15，非运动SHR）、运动训练的SHR（n = 15，进行12周跑步机运动）和久坐不动的Wistar - Kyoto（WKY）大鼠（n = 15）。运动训练的SHR表现出适应性变化，如体重、心率、血压、左心室壁厚度、血脂谱和同型半胱氨酸水平降低。运动训练的SHR和WKY心脏中血管紧张素转换酶、内皮素 - 1和脑钠肽的mRNA表达低于非运动SHR，而心脏中小窝蛋白 - 3和eNOS的mRNA表达较高。运动训练的SHR中Bcl - 2蛋白高于WKY和非运动SHR。相反，运动训练的SHR和WKY中Bax蛋白水平低于非运动SHR。此外，运动训练的SHR和WKY中活性形式的caspase - 3（20 kDa）水平低于非运动SHR。这些发现表明运动训练通过调节心肌基因来预防左心室病理性肥大，并且它干扰了病理性心脏肥大继发的凋亡信号转导途径。
