Zhang X Q, Ng Y C, Musch T I, Moore R L, Zelis R, Cheung J Y
Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033, USA.
J Appl Physiol (1985). 1998 Feb;84(2):544-52. doi: 10.1152/jappl.1998.84.2.544.
Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na+/Ca2+ exchange currents (I Na/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 alpha-myosin heavy chain (MHC) isoforms (57.2 +/- 1.9 vs. 49.3 +/- 3.5 in MI-HIST vs. MI-Sed, respectively; P < or = 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 micrograms in MI-HIST vs. MI-Sed, respectively; P < or = 0.005) and cell capacitances (212 +/- 8 vs. 242 +/- 9 pF in MI-HIST vs. MI-Sed, respectively; P < or = 0.015). Reverse I Na/Ca was significantly lower (P < or = 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse I Na/Ca (P < or = 0.05) without affecting the amount of Na+/Ca2+ exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca2+ content, as estimated by integrating forward I Na/Ca during caffeine-induced SR Ca2+ release, was also significantly increased (P < or = 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.
从心肌梗死（MI）3周后的大鼠心脏分离出的心肌细胞，其钠钙交换电流（I Na/Ca；3个Na⁺外流：1个Ca²⁺内流）和肌浆网（SR）可释放的Ca²⁺含量降低。这些Ca²⁺调节缺陷可能导致MI心肌细胞收缩异常。由于运动训练能引起心脏收缩功能和心肌Ca²⁺调节的积极适应性变化，本研究探讨了6 - 8周的高强度短跑训练（HIST）是否能改善在运动活动受限的MI后大鼠（Sed）中观察到的一些细胞适应不良情况。在MI大鼠中，HIST不影响比目鱼肌的柠檬酸合酶活性，但显著增加了心脏α - 肌球蛋白重链（MHC）同工型的百分比（MI - HIST组为57.2±1.9，MI - Sed组为49.3±3.5；P≤0.05）。在单个心肌细胞水平，HIST减轻了MI后观察到的细胞肥大，这通过细胞长度的减少得以证明（MI - HIST组为112±4μm，MI - Sed组为130±5μm；P≤0.005）和细胞电容的减少（MI - HIST组为212±8 pF，MI - Sed组为242±9 pF；P≤0.015）。与假手术且久坐的大鼠相比，MI - Sed大鼠的心肌细胞中反向I Na/Ca显著更低（P≤0.0001）。HIST显著增加了反向I Na/Ca（P≤0.05），而不影响MI心肌细胞中钠钙交换体的量（通过免疫印迹检测）。通过在咖啡因诱导的SR Ca²⁺释放过程中对正向I Na/Ca进行积分估算的SR可释放Ca²⁺含量，也因HIST在MI心肌细胞中显著增加（P≤0.02）。我们得出结论，接受HIST的MI后大鼠心输出量和每搏输出量的增加至少部分是由MI后细胞适应不良的逆转介导的。
