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J Appl Physiol 90: 1720-1728, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 5, 1720-1728, May 2001

Sprint training shortens prolonged action potential duration in postinfarction rat myocyte: mechanisms

Xue-Qian Zhang1, Lian-Qin Zhang2, Bradley M. Palmer6, Yuk-Chow Ng3, Timothy I. Musch4, Russell L. Moore5, and Joseph Y. Cheung1

1 Weis Center for Research, Geisinger Medical Center, Danville 17822; Departments of 2 Cellular and Molecular Physiology and 3 Pharmacology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey, Pennsylvania 17033; 4 Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506; 5 Department of Kinesiology, University of Colorado, Boulder, Colorado 80309; and 6 Department of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont 05405

Two electrophysiological manifestations of myocardial infarction (MI)-induced myocyte hypertrophy are prolongation of action potential duration (APD) and reduction of transient outward current (Ito) density. Because high-intensity sprint training (HIST) ameliorated myocyte hypertrophy and improved myocyte Ca2+ homeostasis and contractility after MI, the present study evaluated whether 6-8 wk of HIST would shorten the prolonged APD and improve the depressed Ito in post-MI myocytes. There were no differences in resting membrane potential and action potential amplitude (APA) measured in myocytes isolated from sham-sedentary (Sed), MI-Sed, and MI-HIST groups. Times required for repolarization to 50 and 90% APA were significantly (P < 0.001) prolonged in MI-Sed myocytes. HIST reduced times required for repolarization to 50 and 90% APA to values observed in Sham-Sed myocytes. The fast and slow components of Ito were significantly (P < 0.0001) reduced in MI-Sed myocytes. HIST significantly (P < 0.001) enhanced the fast and slow components of Ito in MI myocytes, although not to levels observed in Sham-Sed myocytes. There were no significant differences in steady-state Ito inactivation and activation parameters among Sham-Sed, MI-Sed, and MI-HIST myocytes. Likewise, recovery from time-dependent inactivation was also similar among the three groups. We suggest that normalization of APD after MI by HIST may be mediated by restoration of Ito toward normal levels.

transient outward current; excitation-contraction coupling; heart hypertrophy; exercise training; electrophysiology


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