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Early exercise training normalizes myofilament function and attenuates left ventricular pump dysfunction in mice with
Monique C de Waard1, Jolanda van der Velden, Virginie Bito
1Experimental Cardiology, Department of Cardiology, Thoraxcenter, Erasmus MC, University Medical Center Rotterdam, The Netherlands.
Circulation Research
|March 10, 2007
Summary
Early exercise after myocardial infarction (MI) in mice improves cardiac function by enhancing myofilament function, not by altering cardiac remodeling. This intervention attenuates left ventricular (LV) dysfunction.
Area of Science:
- Cardiovascular Physiology
- Exercise Science
- Cardiac Rehabilitation
Background:
- Myocardial infarction (MI) often leads to left ventricular (LV) remodeling and dysfunction.
- Early exercise training post-MI may offer cardiac benefits, potentially by addressing calcium (Ca2+) handling and myofilament abnormalities.
Purpose of the Study:
- To investigate the effects of early voluntary exercise on LV remodeling and dysfunction following a large MI in mice.
- To elucidate the underlying mechanisms, focusing on Ca2+-handling and myofilament function.
Main Methods:
- Mice underwent 8 weeks of voluntary exercise initiated early after a large MI.
- Evaluated LV remodeling (dimensions), function (fractional shortening, LVdP/dt), pulmonary congestion, myofilament Ca2+-sensitivity, beta-adrenergic signaling (receptor protein, cAMP), and cardiomyocyte contractility.
- Assessed Ca2+ handling proteins (SERCA2a, PLB) and phosphorylation status.
Main Results:
- Exercise did not improve survival, MI size, or LV dimensions but improved LV fractional shortening and LVdP/dt, reducing pulmonary congestion.
- Exercise normalized MI-induced increases in myofilament Ca2+-sensitivity, mediated by PKA and enhanced beta(1)-adrenergic signaling.
- Prevented decreased myocyte force generation and enhanced cardiomyocyte shortening, primarily due to improved myofilament function rather than altered Ca2+-transient amplitude.
Conclusions:
- Early exercise post-MI in mice attenuates global LV dysfunction without affecting LV remodeling.
- The cardiac benefits are attributed to exercise-induced improvements in myofilament function, likely via enhanced beta(1)-adrenergic signaling and PKA activity.
