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Diverse Effects of Exercise on Myofilament Function in Pathologic Left Ventricular Hypertrophy and Dysfunction
Author(s) -
Deel Elza Dianne,
Boer Martine,
Boontje Nicky M,
Waard Monique,
Velden Jolanda,
Duncker Dirk J
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.619.15
Subject(s) - cardiology , myofilament , preload , medicine , muscle hypertrophy , pressure overload , diastole , fibrosis , concentric hypertrophy , ex vivo , heart failure , blood pressure , hemodynamics , myocyte , cardiac hypertrophy , chemistry , biochemistry , in vitro
Effects of exercise (EX) on pathologic left ventricular (LV) remodelling and dysfunction remain incompletely understood. Here we studied the effects of 8 weeks voluntary EX on LV and myofilament function in mice with myocardial infarction (MI) or pressure‐overload by transverse aortic constriction (TAC). Eight weeks after TAC or MI, LV geometry and function were measured and isometric force determined in single permeabilized cardiomyocytes. MI and TAC induced LV hypertrophy, interstitial fibrosis and LV dilation as well as systolic (fractional shortening, dP/dt P40 ) and diastolic (dP/dt min , end‐diastolic pressure [LVEDP]) dysfunction. Cardiomyocyte maximal force development (Fmax) was lower in MI, but unexpectedly elevated in TAC, coinciding with more pronounced LV systolic dysfunction in MI compared to TAC. Conversely, passive isometric myofilament force (Fpas) was elevated in TAC but unchanged in MI, coinciding with an elevated LVEDP in TAC. EX ameliorated LV dysfunction and fibrosis and increased Fmax after MI, without effecting Fpas. In contrast, EX had no effect on either LV dysfunction or Fmax in TAC mice. EX aggravated interstitial fibrosis, but did not further increase LVEDP, likely as a result of an EX‐induced decrease in Fpas. In conclusion, effects of EX on LV dysfunction depend critically on the underlying pathology which are in part explained by the diverse effects of EX on myofilament function.