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

V Bito, Monique Waard, L Biesmans, I Lenaerts, S Ozdemir, Elza Deel, Y Abdel-Mottaleb, R Driesen, P Holemans, Dirk-jan Duncker, KR Sipido

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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. 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 mu m in MIEXE vs. 148 +/- 3 mu m in MISED and 136 +/- 2 mu m 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/L-0=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/L-0=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 degrees C. Ca2+ transient amplitude, I-CaL 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. 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.
Original languageUndefined/Unknown
Pages (from-to)72-81
Number of pages10
JournalCardiovascular Research
Issue number1
Publication statusPublished - 2010

Research programs

  • EMC COEUR-09
  • EMC MGC-01-12-03

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