Late exercise training improves non-uniformity of transmural myocardial function in rats with ischaemic heart failure

Cardiovasc Res. 2009 Feb 15;81(3):555-64. doi: 10.1093/cvr/cvn229. Epub 2008 Aug 14.


Aims: The exercise-induced beneficial mechanisms after long-term myocardial infarction (MI) are incompletely understood. The present study evaluated the effect of treadmill exercise training (5 weeks), started at a late stage of heart failure (HF) (13 weeks post-MI), on rat left ventricle remodelling and dysfunction of the regional global and cellular contractile functions.

Methods and results: In vivo echocardiography confirmed that sub-endocardial (ENDO) layers contract more (+86%) and faster (+50%) than the sub-epicardial (EPI) layers. This gradient was lost in MI rats due to a predominant reduction in the ENDO layer contractility. Exercise partially restored the amplitude and velocity of ENDO contraction, resulting in a partial recovery of the pump function indexed by the aortic blood-flow velocity time integral. At the cellular level, MI impaired ENDO contractile properties by reducing cell shortening (10-7%), calcium transient, and myofilament Ca(2+) sensitivity. These alterations were normalized by exercise. Sarcoplasmic reticulum Ca(2+)-ATPase (SERCA)2a expression and myosin light chain (MLC)-2 phosphorylation in ENDO cells were significantly reduced after MI and were restored by exercise. The EPI layer was only slightly reduced in vivo without cellular alterations.

Conclusion: This study shows that exercise performed at a late stage after MI restored a transmural non-uniformity of myocardium lost during HF. Recoveries of Ca(2+) homeostasis and myofilament function of cardiomyocytes contribute to this beneficial effect.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actin Cytoskeleton / metabolism
  • Animals
  • Calcium Signaling
  • Cardiac Myosins / metabolism
  • Disease Models, Animal
  • Exercise Therapy*
  • Heart Failure / etiology
  • Heart Failure / metabolism
  • Heart Failure / physiopathology
  • Heart Failure / therapy*
  • Male
  • Muscle Proteins / metabolism
  • Myocardial Contraction*
  • Myocardial Ischemia / complications*
  • Myocardial Ischemia / metabolism
  • Myocardial Ischemia / physiopathology
  • Myocardial Ischemia / therapy
  • Myocardium / metabolism
  • Myocardium / pathology
  • Myosin Light Chains / metabolism
  • Phosphorylation
  • Rats
  • Rats, Wistar
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism
  • Time Factors
  • Ventricular Function, Left*
  • Ventricular Remodeling*


  • Atp2a2 protein, rat
  • Muscle Proteins
  • Myosin Light Chains
  • myosin light chain 2
  • Cardiac Myosins
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases