Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes.
Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes.
复制标题
短跑训练可减轻心肌细胞肥大并改善梗死后肌细胞的 Ca2 稳态。
DOI：
10.1152/jappl.1998.84.2.544
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Cheung,JY
中科院分区：
文献类型：
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作者：
Zhang,XQ;Ng,YC;Musch,TI;Moore,RL;Zelis,R;Cheung,JY
张雪倩，吴玉周，Timothy I.Musch，Russell L.Moore，R.Zelis，and Joseph Y.Cheung.短跑训练减轻心肌细胞肥大，改善心肌细胞钙稳态.应用期刊.从心肌梗死(MI)后3wk的大鼠心脏分离的心肌细胞减少了Na+/Ca~(2+)交换电流(Ina/Ca；3 Na~+Out：1 Ca~(2+)In)和肌浆网(SR)可释放的Ca~(2+)含量。这些钙离子调节缺陷可能是心肌细胞收缩异常的原因之一。由于运动训练引起心肌收缩功能和心肌钙调节的正向适应，本研究探讨了6-8wk的高强度短跑训练(HIST)是否能改善运动受限(SED)的MI后大鼠的部分细胞适应不良。在MI大鼠，HIST不影响足底肌柠檬酸合成酶活性，但显著增加心肌α-肌球蛋白重链亚型的百分比(MI-HIST组为57.2±1.9vs.49.3±3.5vs.MI-SED组49.3±3.5.P≤0.05)。在单个心肌细胞水平，心肌梗死后细胞肥大程度减轻，表现为心肌梗死后心肌细胞长度(112±4vs.130±5μm，P≤0.005)和细胞容量(心肌梗死后212±8pF比心肌梗死后242±9pF，P≤0.015)的减少。MI-SED组大鼠心肌细胞INa/Ca值显著低于假手术组和久坐组(P≤0.0001)。HIST使心肌细胞INa/Ca逆转(P≤0.0 5)，但不影响心肌细胞Na+/Ca~(2+)交换量(免疫印迹法检测)。HIST对咖啡因诱导的心肌细胞肌浆网钙离子释放也有明显的促进作用(P≤0.02)。我们得出结论，心肌梗死后大鼠的心输出量和每搏量的增加至少部分是由心肌梗死后细胞适应不良的逆转所介导的。
Zhang, Xue-Qian, Yuk-Chow Ng, Timothy I. Musch, Russell L. Moore, R. Zelis, and Joseph Y. Cheung.Sprint training attenuates myocyte hypertrophy and improves Ca2+homeostasis in postinfarction myocytes.J. Appl. Physiol.84(2): 544–552, 1998.—Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na+/Ca2+exchange currents (INa/Ca; 3 Na+out:1 Ca2+in) and sarcoplasmic reticulum (SR)-releasable Ca2+contents. These defects in Ca2+regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac α-myosin heavy chain (MHC) isoforms (57.2 ± 1.9 vs. 49.3 ± 3.5 in MI-HIST vs. MI-Sed, respectively;P≤ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 ± 4 vs. 130 ± 5 μm in MI-HIST vs. MI-Sed, respectively;P≤ 0.005) and cell capacitances (212 ± 8 vs. 242 ± 9 pF in MI-HIST vs. MI-Sed, respectively;P≤ 0.015). ReverseINa/Cawas significantly lower (P≤ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverseINa/Ca(P≤ 0.05) without affecting the amount of Na+/Ca2+exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca2+content, as estimated by integrating forwardINa/Caduring caffeine-induced SR Ca2+release, was also significantly increased (P≤ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.