Journal Article

Early exercise training after myocardial infarction prevents contractile but not electrical remodelling or hypertrophy

Virginie Bito, Monique C. de Waard, Liesbeth Biesmans, Ilse Lenaerts, Semir Ozdemir, Elza van Deel, Yousra Abdel-Mottaleb, Ronald Driesen, Patricia Holemans, Dirk J. Duncker and Karin R. Sipido

in Cardiovascular Research

Published on behalf of European Society of Cardiology

Volume 86, issue 1, pages 72-81
Published in print April 2010 | ISSN: 0008-6363
Published online December 2009 | e-ISSN: 1755-3245 | DOI: https://dx.doi.org/10.1093/cvr/cvp381
Early exercise training after myocardial infarction prevents contractile but not electrical remodelling or hypertrophy

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Aims

Exercise started early after myocardial infarction (MI) improves in vivo cardiac function and myofilament responsiveness to Ca2+. We investigated whether this represents partial or complete reversal of cellular remodelling.

Methods and results

Mice with MI following left coronary ligation were given free access to a running wheel (MIEXE, N = 22) or housed sedentary (MISED, N = 18) for 8 weeks and compared with sedentary sham-operated animals (SHAM, N = 11). Myocytes were enzymatically isolated from the non-infarcted left ventricle. Myocytes in MI were significantly longer and even more so with exercise (165 ± 3 µm in MIEXE vs. 148 ± 3 µm in MISED and 136 ± 2 µm in SHAM; P < 0.05, mean ± SEM); cell width was not different. Contraction was measured during electrical field stimulation at 1, 2, and 4 Hz. Unloaded cell shortening was significantly reduced in MISED (at 1 Hz, L/L0=4.4 ± 0.3% vs. 6.7 ± 0.4% in SHAM; P < 0.05, also at 2 and 4 Hz). Exercise restored cell shortening to SHAM values (MIEXE, L/L0=6.4 ± 0.5%). Membrane currents and [Ca2+]i were measured via whole-cell patch clamping, with Fluo-3 as Ca2+ indicator, all at 30°C. Ca2+ transient amplitude, ICaL and sarcoplasmic reticulum Ca2+ content were not different between the three groups. Diastolic Ca2+ levels at 4 Hz were significantly elevated in MISED only, with a trend to increased spontaneous Ca2+ release events (sparks). Action potential duration was increased and transient outward K+ currents significantly reduced after MI; this was unaffected by exercise.

Conclusions

Early voluntary exercise training after MI restores cell contraction to normal values predominantly because of changes in the myofilament Ca2+ response and has a beneficial effect on diastolic Ca2+ handling. However, the beneficial effect is not a complete reversal of remodelling as hypertrophy and loss of repolarizing K+ currents are not affected.

Keywords: Calcium; Exercise; Arrhythmias; Myocardial infarction; Potassium currents

Journal Article.  5407 words.  Illustrated.

Subjects: Cardiovascular Medicine

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