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(Circulation Research. 2007;100:937.)
© 2007 American Heart Association, Inc.

Editorials

Exercise After Myocardial Infarction Improves Contractility and Decreases Myofilament Ca²⁺ Sensitivity

Tilmann Schober, Björn C. Knollmann

From the Oates Institute for Experimental Therapeutics and Division of Clinical Pharmacology, Departmentsts of Medicine and Pharmacology (T.S., B.C.K.), Medical Center, Nashville, Tenn.

Correspondence to Björn C. Knollmann, MD, PhD, Associate Professor of Medicine and Pharmacology, Oates Institute for Experimental Therapeutics, Division of Clinical Pharmacology, Vanderbilt University Medical Center, 1265 Medical Research Building IV, Nashville, TN 37232-0575. E-mail bjorn.knollmann@vanderbilt.edu

See related article, pages 1079–1088

Key Words: exercise training • myocardial infarction • Ca²⁺ handling • myofilament Ca²⁺ sensitivity • cardiac arrhythmias

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Impaired Myofilament Function After Myocardial Infarction

 
While myocardial infarction (MI) is the major cause of heart failure, there are conflicting data over the roles of abnormal calcium handling and myofilament function. The acute injury leads to the activation of neurohormones and cytokines, subsequent myocardial remodelling, further decline in heart function, and finally overt heart failure. Depressed myocyte contractility in the remodelled myocardium can largely be explained by Ca²⁺ handling abnormalities.¹ Abnormalities in myofilament function are less well understood. A seminal study in pigs demonstrated that impaired pump function three weeks after MI can also be attributed to decreased maximal isometric tension in skinned cardiomyocytes in areas remote from the ischemic border zone.² Somewhat paradoxically, the impairment occurred in the context of increased Ca²⁺ sensitivity of the myofilaments. The authors attributed the increased Ca²⁺ sensitivity following MI to reduced protein kinase A-mediated troponin I (TnI) phosphorylation.² Increased myofilament Ca²⁺ sensitivity has also been reported for end-stage human heart failure, apparently largely because of a reduction of TnI phosphorylation.³

	Benefit of Exercise Training Post MI

 
One of the most effective and least expensive therapies for cardiovascular disease is exercise. Clinical studies generally show a benefit of exercise training and a reduction of cardiac mortality after MI by 26%.⁴ The question remains of how soon to start exercising, especially after a large MI. In several clinical⁵ and animal^6,7 studies, there were detrimental consequences when exercise began immediately after an MI.

In the current issue of Circulation Research, de Waard et al⁸ present remarkable data addressing the question of exercise training early post MI. After . . . [Full Text of this Article]

Related Article:

Early Exercise Training Normalizes Myofilament Function and Attenuates Left Ventricular Pump Dysfunction in Mice With a Large Myocardial Infarction

Monique C. de Waard, Jolanda van der Velden, Virginie Bito, Semir Ozdemir, Liesbeth Biesmans, Nicky M. Boontje, Dick H.W. Dekkers, Kees Schoonderwoerd, Hans C.H. Schuurbiers, Rini de Crom, Ger J.M. Stienen, Karin R. Sipido, Jos M.J. Lamers, and Dirk J. Duncker
Circ. Res. 2007 100: 1079-1088. [Abstract] [Full Text] [PDF]