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Vol. 84, Issue 2, 544-552, February 1998
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
Zhang, Xue-Qian, Yuk-Chow Ng, Timothy I. Musch, Russell L. Moore, R. Zelis, and Joseph Y. Cheung. Sprint training attenuates myocyte hypertrophy and improves
Ca2+ homeostasis in postinfarction
myocytes. J. Appl. Physiol. 84(2): 544-552, 1998.
Myocytes isolated from rat hearts 3 wk after
myocardial infarction (MI) had decreased
Na+/Ca2+
exchange currents
(INa/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 
-myosin heavy chain (MHC) isoforms (57.2 ± 1.9 vs. 49.3 ± 3.5 in MI-HIST vs. MI-Sed, respectively;
P 
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 µm in MI-HIST vs. MI-Sed, respectively;
P 0.005) and cell capacitances (212 ± 8 vs. 242 ± 9 pF in MI-HIST vs. MI-Sed, respectively; P 0.015). Reverse
INa/Ca was
significantly lower (P 0.0001) in
myocytes from MI-Sed rats compared with those from rats that were sham
operated and sedentary. HIST significantly increased reverse
INa/Ca
(P 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
INa/Ca during
caffeine-induced SR Ca2+ release,
was also significantly increased (P 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.
exercise training; excitation-contraction coupling; patch clamp; ventricular remodeling; cardiac hypertrophy
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