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Cardiovascular Research 2002 54(1):162-174; doi:10.1016/S0008-6363(01)00565-X
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Aerobic exercise reduces cardiomyocyte hypertrophy and increases contractility, Ca2+ sensitivity and SERCA-2 in rat after myocardial infarction

Ulrik Wisløffa, Jan P. Loennechena, Susan Currieb, Godfrey L. Smithb and Øyvind Ellingsena,*

aDepartment of Physiology and Biomedical Engineering, Norwegian University of Science and Technology, OLav Kyrres gt. 3., N-7489 Trondheim, Norway
bInstitute of Biomedical and Life Sciences, University of Glasgow, Glasgow, UK

Oyvind.Ellingsen{at}medisin.ntnu.no

* Corresponding author. Tel.: +47-735-98-822; fax: +47-735-98-613

Objective: Although it is generally accepted that endurance training improves cardiac function after myocardial infarction the sub-cellular mechanisms are uncertain. The present study reports the effects of aerobic endurance training on myocardial mass, myocyte dimensions, contractile function, Ca2+ handling, and myofilament responsiveness to Ca2+ in cardiomyocytes from healthy and failing rat hearts. Methods: Adult female Sprague–Dawley rats ran on a treadmill 1.5 h/day, 5 days a week for 8 weeks. Exercise intervals alternated between 8 min at 85–90% of VO2max and 2 min at 50–60%. Training started 4 weeks after ligation of the left coronary artery (TR-INF, n=11) or sham operation (TR-SHAM, n=6). Sedentary animals (SED-SHAM, n=6; SED-INF, n=13) were controls. Results: After 6 weeks VO2max in TR-INF and TR-SHAM leveled off 65% above sedentary controls. In TR-SHAM, left and right ventricle weights were ~25% higher than in SED-SHAM, myocytes were ~13% longer; width remained unchanged. At physiological stimulation frequencies, relative myocyte shortening was markedly higher whereas peak systolic [Ca2+] and t1/2 of Ca2+ transient decay were 10–20% lower, indicating higher Ca2+ sensitivity in cardiomyocytes from trained rats, compared to respective controls. In TR-INF the left and right ventricular weights, and myocyte length and width were 15, 23, 12, and 20% less than in SED-INF. Endurance training significantly increased the myocardial SR Ca2+ pump (SERCA-2) and sarcolemmal Na+–Ca2+-exchanger (NCX) protein levels to the extent that TR-INF did not differ from SED-SHAM. Conclusion: This is the first study to show that aerobic endurance training attenuates the ventricular and cellular hypertrophy in failing hearts. Furthermore, training consistently restores contractile function, intracellular Ca2+ handling, and Ca2+-sensitivity in cardiomyocytes from rats with myocardial infarction.

KEYWORDS Heart failure; Hypertrophy; Myocytes


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