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Left ventricular functional capacity in the endurance-trained rodent.
D P Fitzsimons1, P W Bodell, R E Herrick
1Department of Physiology and Biophysics, University of California, Irvine 92717.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|July 1, 1990
Summary
Endurance training enhances rodent cardiac function by increasing cardiac myosin phosphorylation (P-LC(P)) at equivalent heart rates, augmenting myocardial force production and systolic pressure.
Area of Science:
- Cardiovascular Physiology
- Exercise Science
- Molecular Cardiology
Background:
- Cardiac myosin phosphorylation (P-LC(P)) is theorized to increase myocardial force.
- Understanding P-LC(P) regulation in trained vs. untrained states is crucial for exercise physiology.
Purpose of the Study:
- To investigate the role of cardiac myosin P-LC(P) in trained and untrained rodents.
- To compare P-LC(P) responses at equivalent heart rates and workloads during exercise.
Main Methods:
- Utilized a 10-wk endurance training protocol in rodents.
- Measured submaximal and peak oxygen uptake, and left ventricular pressure (LVP) using a high-fidelity transducer.
- Assessed cardiac myosin P-LC(P) levels under controlled exercise conditions.
Main Results:
- Trained rodents showed reduced submaximal O2 uptake and heart rate, but maintained peak LVP.
- At equivalent workloads, both groups had similar increases in P-LC(P) and systolic pressure.
- At equivalent heart rates, training significantly increased systolic pressure and P-LC(P).
Conclusions:
- Endurance training augments cardiac function, partly through increased P-LC(P) at equivalent heart rates.
- This suggests P-LC(P) plays a role in enhanced myocardial contractility in trained individuals.
- Training alters cardiac myosin properties, potentially impacting force generation.