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J Appl Physiol 89: 38-46, 2000;
8750-7587/00 $5.00
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Vol. 89, Issue 1, 38-46, July 2000

Sprint training normalizes Ca2+ transients and SR function in postinfarction rat myocytes

Lian-Qin Zhang1, Xue-Qian Zhang1, Yuk-Chow Ng2, Lawrence I. Rothblum3, Timothy I. Musch4, Russell L. Moore5, and Joseph Y. Cheung1,3

Departments of 1 Medicine, 2 Pharmacology, and 3 Cellular and Molecular Physiology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033; 4 Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506; and 5 Department of Kinesiology, University of Colorado, Boulder, Colorado 80309

Previous studies have shown that myocytes isolated from sedentary (Sed) rat hearts 3 wk after myocardial infarction (MI) undergo hypertrophy, exhibit altered intracellular Ca2+ concentration ([Ca2+]i) dynamics and abnormal contraction, and impaired sarcoplasmic reticulum (SR) function manifested as prolonged half-time of [Ca2+]i decline. 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 restore [Ca2+]i dynamics and SR function in MI myocytes toward normal. In MI rats, HIST ameliorated myocyte hypertrophy as indicated by significant (P <=  0.05) decreases in whole cell capacitances [Sham-Sed 179 ±12 (n = 20); MI-Sed 226 ± 7 (n = 20); MI-HIST 183 ± 11 pF (n = 19)]. HIST significantly (P < 0.0001) restored both systolic [Ca2+]i [Sham-Sed 421 ± 9 (n = 79); MI-Sed 350 ± 6 (n = 70); MI-HIST 399 ± 9 nM (n = 70)] and half-time of [Ca2+]i decline (Sham-Sed 0.197 ± 0.005; MI-Sed 0.247 ± 0.006; MI-HIST 0.195 ± 0.006 s) toward normal. Compared with Sham-Sed myocytes, SR Ca2+-ATPase expression significantly (P < 0.001) decreased by 44% in MI-Sed myocytes. Surprisingly, expression of SR Ca2+-ATPase was further reduced in MI-HIST myocytes to 26% of that measured in Sham-Sed myocytes. There were no differences in calsequestrin expression among the three groups. Expression of phospholamban was not different between Sham-Sed and MI-Sed myocytes but was significantly (P < 0.01) reduced in MI-HIST myocytes by 25%. Our results indicate that HIST instituted shortly after MI improves [Ca2+]i dynamics in surviving myocytes. Improvement in SR function by HIST is mediated not by increased SR Ca2+-ATPase expression, but by modulating phospholamban regulation of SR Ca2+-ATPase activity.

exercise training; excitation-contraction coupling; sarcoplasmic reticulum calcium uptake; sarco(endo)plasmic reticulum calcium-adenosinetriphosphatase 2; fura 2 quantitative fluorescence microscopy; cardiac hypertrophy


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