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首页> 外文期刊>Medicine and science in sports and exercise >Cyclosporin A does not block exercise-induced cardiac hypertrophy.
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Cyclosporin A does not block exercise-induced cardiac hypertrophy.

机译：环孢菌素A不会阻止运动引起的心脏肥大。

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Cyclosporin A (CsA) has been shown to inhibit pathophysiological models of overload-induced cardiac hypertrophy, indicating a role for the calcium dependent signal pathways. It is unclear what impact CsA may have on the myocardial response to exercise, a physiological model of overload.PURPOSE: The purpose of the study was to determine whether CsA would alter exercise-induced cardiac hypertrophy. METHODS: Thirty male rats were assigned to vehicle or CsA injection (15 mg.kg.d(-1)) and then assigned to sedentary or exercise training. Animals were swum for 60 min.d(-1) for 1 wk. RESULTS: One week of swim training significantly increased plantaris cytochrome oxidase activity, as well as significantly increasing left ventricular (LV) weight and the left ventricular:body weight (LV/BW) ratio. Exercise did not alter right ventricular (RV) weight or the RV/BW ratio. RNA analysis found that exercise significantly increased atrial natriuretic factor (ANF)-mRNA levels but did not influence alpha-myosin heavy chain (MHC) expression. CsA treatment, but not exercise, was associated with a significant increase in betaMHC expression. Western blot analysis determined that betaMHC protein was also significantly increased in the CsA-treated animals. CONCLUSION: CsA did not block exercise-induced cardiac hypertrophy but did significantly influence the myocardial phenotype. The CsA-sensitive calcium dependent pathways, important for pathological forms of overload-induced hypertrophy, were not essential to the early adaptations to exercise and that a different mechanism or signal transduction pathway was engaged. The data also indicate that CsA alone may induce a shift in the MHC isoform expression toward that associated with a pathological phenotype. Whether this phenotype shift contributes to the lowered exercise capacity found in transplant patients remains to be determined.
机译：已显示环孢菌素A（CsA）抑制超负荷引起的心脏肥大的病理生理模型，表明其对钙依赖性信号通路的作用。尚不清楚CsA对运动对心肌的反应有什么影响，这是一种超负荷的生理模型。目的：本研究的目的是确定CsA是否会改变运动引起的心脏肥大。方法：将30只雄性大鼠分为媒介物或CsA注射液（15 mg.kg.d（-1）），然后进行久坐或运动训练。使动物游泳60分钟.d（-1），持续1周。结果：游泳训练的一周显着增加了植物细胞色素氧化酶的活性，并显着增加了左心室（LV）重量和左心室：体重（LV / BW）的比率。运动并没有改变右心室（RV）的重量或RV / BW比。 RNA分析发现，运动可显着增加心房利钠因子（ANF）-mRNA的水平，但不影响α-肌球蛋白重链（MHC）的表达。 CsA治疗（而非运动）与betaMHC表达的显着增加有关。蛋白质印迹分析确定在经CsA处理的动物中betaMHC蛋白也显着增加。结论：CsA不能阻止运动引起的心脏肥大，但确实可以显着影响心肌表型。 CsA敏感的钙依赖性途径对于超负荷引起的肥大的病理形式很重要，对于早期适应运动并不重要，并且采用了不同的机制或信号转导途径。数据还表明单独的CsA可能诱导MHC亚型表达向与病理表型有关的表达转变。这种表型的改变是否有助于降低移植患者的运动能力尚待确定。

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