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为了进一步探讨运动心脏重塑的发生机制，以大鼠１８Ｓ－ＲＮＡ为内参照，采用先进的定量反转录聚合酶链反应（ＱＲＴ－ＰＣＲ）技术，对２０只经１２周耐力训练的 ＳＤ大鼠心脏中原癌基因ｃ－ｍｙｃ的表达进行了研究。结果表明，与安静对照组相比，耐力训练组大鼠心室中ｃ－ｍｙｃ的表达非但没有提高，反而出现非常显著的下降（Ｐ＜０．００１）；尽管训练组大鼠心房中ｃ－ｍｙｃ的表达较对照组有明显升高，但无显著性统计学意义（ｐ＜ ０．０５）。训练组大鼠。心室中 ｃ－ｍｙｃ的表达显著低于心房中 ｃ－ｍｙｃ的表达（Ｐ＜ ０．０１），而安静对照组心室中 ｃ－ｍｙｃ的表达则与相应心房中 ｃ－ｍｙｃ的表达无显著性差异（ｐ＞ ０．０５）。研究结果提示，训练后心室中ｃ－ｍｙｃ表达的显著下降，一方面，可能是由于在耐力训练应激下，ｃ－ｍｙｃ主要为早期瞬间表达，在训练后早期，甚至几小时即快速表达，然后启动心肌结构基因，如ＭＨＣ、ａ－ａｃｔｉｎ、ＭＬＣ－２、ＡＮＦ等的表达，而自身则由于受反馈抑制的影响，后期表达下降；另一方面，可能由于训练大鼠心房中ｃ－ｍｙｃ表达的触发机制不同于心室中相应机制的缘故。
In order to further explore the mechanism of exercise heart remodeling, 18S-RNA was used as an internal reference and advanced quantitative reverse transcription-polymerase chain reaction (QRT-PCR) The expression of proto-oncogene c-myc in rat heart was studied. The results showed that, compared with the quiet control group, endurance training group of rats ventricular c-myc expression not only did not improve, but a very significant decline (P <0.001); although training group atrial c-myc (P <0.05), but there was no significant difference between the two groups (p <0.05). Training group rats. The expression of c-myc in the ventricles was significantly lower than that in the atria (P <0.01), while the expression of c-myc in the ventricular of the quiet control group was not significantly different from the expression of c-myc in the corresponding atria (P> 0.05). The results suggest that after training, the expression of c-myc in the ventricle significantly decreased, on the one hand, may be due to endurance training stress, c-myc mainly for the early moment of expression, early in the training, or even hours after the rapid expression, And then start the myocardial structural genes, such as MHC, a-actin, MLC-2, ANF expression, but itself due to the impact of feedback inhibition, decreased expression at the late; the other hand, may be due to training in the rat atrial c-myc The trigger mechanism of expression is different from the corresponding mechanism in the ventricle.