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(Hypertension. 2007;50:410.)
© 2007 American Heart Association, Inc.

Original Articles

Effects of Excessive Long-Term Exercise on Cardiac Function and Myocyte Remodeling in Hypertensive Heart Failure Rats

Rebecca L. Schultz; John G. Swallow; Robert P. Waters; James A. Kuzman; Rebecca A. Redetzke; Suleman Said; Gabriella Morreale de Escobar; Anthony M. Gerdes

From the Cardiovascular Research Institute (J.A.K., R.A.R., S.S., A.M.G.), Sanford Research/The University of South Dakota, Sioux Falls; the Department of Biology (R.L.S., J.G.S., R.P.W.), The University of South Dakota, Vermillion; the University of Sioux Falls (R.L.S.), Sioux Falls, SD; and Endocrinology, Instituto de investigaciones Biomédicas Alberto Sols (G.M.d.E.), Autonomous University of Madrid and Spanish Research Council, Madrid, Spain.

Correspondence to A Martin Gerdes, PhD, Cardiovascular Research Institute, Sanford Research/University of South Dakota, 1100 East 21st Street, 7th Floor, Sioux Falls, SD 57105. E-mailmgerdes{at}usd.edu

The long-term effects of exercise on cardiac function and myocyte remodeling in hypertension/progression of heart failure are poorly understood. We investigated whether exercise can attenuate pathological remodeling under hypertensive conditions. Fifteen female Spontaneously Hypertensive Heart Failure rats and 10 control rats were housed with running wheels beginning at 6 months of age. At 22 months of age, heart function of the trained rats was compared with heart function of age-matched sedentary hypertensive and control rats. Heart function was measured using echocardiography and left ventricular catheterization. Cardiac myocytes were isolated to measure cellular dimensions. Fetal gene expression was determined using Western blots. Exercise did not significantly impact myocyte remodeling or ventricular function in control animals. Sedentary hypertensive rats had significant chamber dilatation and cardiac hypertrophy. In exercised hypertensive rats, however, exercise time was excessive and resulted in a 21% increase in left ventricular diastolic dimension (P<0.001), a 24% increase in heart to body weight ratio (P<0.05), a 27% increase in left ventricular myocyte volume (P<0.01), a 13% reduction in ejection fraction (P<0.001), and a 22% reduction in fractional shortening (P<0.01) compared with sedentary hypertensive rats. Exercise resulted in greater fibrosis and did not prevent activation of the fetal gene program in hypertensive rats. We conclude that excessive exercise, in the untreated hypertensive state can have deleterious effects on cardiac remodeling and may actually accelerate the progression to heart failure.

Key Words: hypertension • heart failure • exercise • hypertrophy • myocytes • voluntary wheel running • SHHF

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