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

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 Universi...

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Published in:Journal of applied physiology (1985) 2001-05, Vol.90 (5), p.1720-1728
Main Authors: Zhang, Xue-Qian, Zhang, Lian-Qin, Palmer, Bradley M, Ng, Yuk-Chow, Musch, Timothy I, Moore, Russell L, Cheung, Joseph Y
Format: Article
Language:English
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Summary: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 ( I to ) density. Because high-intensity sprint training (HIST) ameliorated myocyte hypertrophy and improved myocyte Ca 2+ homeostasis and contractility after MI, the present study evaluated whether 6-8 wk of HIST would shorten the prolonged APD and improve the depressed I to 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  
ISSN:8750-7587
1522-1601
DOI:10.1152/jappl.2001.90.5.1720