Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes

被引:31
作者
Zhang, XQ
Ng, YC
Musch, TI
Moore, RL
Zelis, R
Cheung, JY [1 ]
机构
[1] Penn State Univ, Milton S Hershey Med Ctr, Div Nephrol, Dept Med, Hershey, PA 17033 USA
[2] Penn State Univ, Milton S Hershey Med Ctr, Dept Pharmacol, Hershey, PA 17033 USA
[3] Penn State Univ, Milton S Hershey Med Ctr, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA
[4] Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA
[5] Univ Colorado, Dept Kinesiol, Boulder, CO 80309 USA
关键词
exercise training; excitation-contraction coupling; patch clamp; ventricular remodeling; cardiac hypertrophy;
D O I
10.1152/jappl.1998.84.2.544
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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 (KIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with Limited exercise activity (Sed). In MI rats, KIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac cr-myosin heavy chain (MHC) isoforms (57.2 +/- 1.9 vs. 49.3 +/- 3.5 in MI-KIST vs. MI-Sed, respectively; P less than or equal to 0.05). At the single myocyte level, KIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 +/- 4 vs. 130 +/- 5 mu m in MI-KIST vs. MI-Sed, respectively; P less than or equal to 0.005) and cell capacitances (212 +/- 8 vs. 242 +/- 9 pF in MI-KIST vs. MI-Sed, respectively; P less than or equal to 0.015). Reverse I-Na/Ca was significantly lower (P less than or equal to 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. KIST significantly increased reverse I-Na/Ca (P less than or equal to 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 less than or equal to 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to KIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.
引用
收藏
页码:544 / 552
页数:9
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