title: Early exercise training after myocardial infarction prevents contractile but not electrical remodelling or hypertrophy.
abstract: OBJECTIVE
  Exercise started early after myocardial infarction (MI) improves in vivo cardiac function and myofilament responsiveness to Ca(2+). We investigated whether this represents partial or complete reversal of cellular remodelling.
  
  
  RESULTS
  Mice with MI following left coronary ligation were given free access to a running wheel (MI(EXE), N = 22) or housed sedentary (MI(SED), 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 microm in MI(EXE) vs. 148 +/- 3 microm in MI(SED) and 136 +/- 2 microm 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 MI(SED) (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 (MI(EXE), L/L(0)=6.4 +/- 0.5%). Membrane currents and [Ca(2+)](i) were measured via whole-cell patch clamping, with Fluo-3 as Ca(2+) indicator, all at 30 degrees C. Ca(2+) transient amplitude, I(CaL) and sarcoplasmic reticulum Ca(2+) content were not different between the three groups. Diastolic Ca(2+) levels at 4 Hz were significantly elevated in MI(SED) only, with a trend to increased spontaneous Ca(2+) 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 Ca(2+) response and has a beneficial effect on diastolic Ca(2+) handling. However, the beneficial effect is not a complete reversal of remodelling as hypertrophy and loss of repolarizing K(+) currents are not affected.
authors.affiliation: Laboratory of Experimental Cardiology, University of Leuven, KUL, Campus Gasthuisberg O/N 7th floor, Herestraat 49, B-3000 Leuven, Belgium.
authors.forename: Virginie
authors.initials: V
authors.lastname: Bito
authors.forename: Monique C
authors.initials: MC
authors.lastname: de Waard
authors.forename: Liesbeth
authors.initials: L
authors.lastname: Biesmans
authors.forename: Ilse
authors.initials: I
authors.lastname: Lenaerts
authors.forename: Semir
authors.initials: S
authors.lastname: Ozdemir
authors.forename: Elza
authors.initials: E
authors.lastname: van Deel
authors.forename: Yousra
authors.initials: Y
authors.lastname: Abdel-Mottaleb
authors.forename: Ronald
authors.initials: R
authors.lastname: Driesen
authors.forename: Patricia
authors.initials: P
authors.lastname: Holemans
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: Duncker
authors.forename: Karin R
authors.initials: KR
authors.lastname: Sipido
mesh_terms: D008841:Actin Cytoskeleton / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D020746:Calcium Channels, L-Type / Q000502:physiology; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D003971:Diastole / Q000502:physiology; D004195:Disease Models, Animal; D005081:Exercise Therapy; D051379:Mice; D009200:Myocardial Contraction / Q000502:physiology*; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D020746:Calcium Channels, L-Type; D011188:Potassium; D002118:Calcium