Department of Cardiovascular Medicine, Japanese Red Cross Medical Center , Tokyo, Japan .
Department of Physiology, Yokohama City University, School of Medicine , Yokohama, Japan .
J Sports Sci Med. 2002 Dec 1;1(4):141-6. eCollection 2002 Dec.
Various substances have been introduced in relation with cardiac hypertrophy almost always with controversy in their roles in signal transduction. Those controversies may attribute to the diversity of cardiac hypertrophy. We previously showed that calcineurin was activated in physiological left ventricular hypertrophy (LVH) induced by voluntary exercise training, but not in decompensated pressure-overload LVH. In the current study, we advanced our search for the differences between the voluntary exercise-induced LVH and the pressure-overload LVH into several other hypertrophy-related substances including caveolin. Wistar rats were assigned to one of the following three groups: 10 weeks of voluntary exercise (EX), sedentary regimen (SED), and 4 weeks of ascending aortic constriction (AC). The EX rats voluntarily ran 1.6 ± 1.1 km/day in the specially manufactured cages resulting in LVH (24 % increase in left ventricular weight per body weight ratio). Myocardial tissue homogenate of the EX rats revealed different characteristics in signal transduction of hypertrophy from that of the AC. The EX rats had normal sarcoplasmic reticulum (SR) Ca(2+)ATPase mRNA level and normal myosin heavy chain isozyme pattern assessed by RNA protection assay, while AC rats had decreased SR Ca(2+)ATPase mRNA level and increased beta myosin heavy chain mRNA level. Myocardial caveolin-3 protein levels assessed by Western blotting increased in the EX rats but decreased in the AC rats. The voluntary exercise-induced LVH differed in signal transduction from the decompensated pressure-overload LVH. Caveolin-3 was induced in the voluntary exercise-induced LVH, while it was decreased in the decompensated pressure-overload LVH.
多种物质已被引入与心肌肥厚相关的研究，几乎总是在它们在信号转导中的作用方面存在争议。这些争议可能归因于心肌肥厚的多样性。我们之前的研究表明，在生理性左心室肥厚（LVH）中，钙调神经磷酸酶被激活，这是由自愿运动训练引起的，但在失代偿性压力超负荷 LVH 中没有被激活。在本研究中，我们进一步研究了自愿运动引起的 LVH 和压力超负荷引起的 LVH 之间的差异，涉及到几种其他与肥厚相关的物质，包括 caveolin。Wistar 大鼠被分为以下三组：10 周的自愿运动（EX）、久坐不动（SED）和 4 周的升主动脉缩窄（AC）。EX 大鼠在特制的笼子里自愿跑 1.6±1.1 公里/天，导致 LVH（左心室重量与体重比增加 24%）。EX 大鼠的心肌组织匀浆在信号转导方面表现出与 AC 大鼠不同的肥厚特征。EX 大鼠的肌浆网 Ca2+ATP 酶 mRNA 水平正常，肌球蛋白重链同工型模式通过 RNA 保护分析评估也正常，而 AC 大鼠的肌浆网 Ca2+ATP 酶 mRNA 水平降低，β肌球蛋白重链 mRNA 水平增加。Western blot 评估的心肌 caveolin-3 蛋白水平在 EX 大鼠中增加，但在 AC 大鼠中减少。自愿运动引起的 LVH 在信号转导方面与失代偿性压力超负荷引起的 LVH 不同。caveolin-3 在自愿运动引起的 LVH 中被诱导，而在失代偿性压力超负荷引起的 LVH 中被减少。
