(Hypertension. 2001;37:204.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Exercise Intolerance in Rats With Hypertensive Heart Disease Is Associated With Impaired Diastolic Relaxation
From the Institute of Cardiology (M.G.), University of Milan, Milan, Italy, and the Cardiac Muscle Research Laboratory (D.A.B., C.S.A., K.W.S.), Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass.
Correspondence to Kurt W. Saupe, PhD, Cardiac Muscle Research Laboratory, X-720, Boston University School of Medicine, 650 Albany St, Boston, MA 02118. E-mail ksaupe{at}aol.com
Abstract—A decrease in functional
capacity is one of the most important clinical manifestations of
hypertensive heart disease, but its cause is poorly understood. Our
purpose was to evaluate potential causes of hypertension-induced
exercise intolerance, focusing on identifying the type(s) of cardiac
dysfunction associated with the first signs of exercise intolerance
during the course of hypertensive heart disease. Exercise capacity was
measured weekly in Dahl salt-sensitive rats as they developed
hypertension as well as in Dahl salt-resistant control rats.
Exercise capacity was unchanged from baseline during the first 8 weeks
of hypertension, suggesting that hypertension itself did not cause
exercise intolerance. After 9 to 12 weeks of hypertension, exercise
capacity decreased in salt-sensitive rats but not in control rats.
After 10 weeks of hypertension, indices of diastolic
function (early truncation of the E wave), as assessed by
echocardiography at rest, were decreased in the
salt-sensitive rats. When exercise capacity had decreased by 
25% in
a rat, the heart was isolated, and left ventricular (LV)
compliance and systolic function were measured. At that time
point, LV hypertrophy was modest (an 20% increase in LV
mass), and systolic function was normal or supernormal,
indicating that exercise intolerance began during "compensated" LV
hypertrophy. Passive LV compliance remained normal in
salt-sensitive rats. Thus, in this model of hypertensive heart disease,
exercise intolerance develops during the compensated stage of LV
hypertrophy and appears to be due to changes in
diastolic rather than systolic function. However,
studies in which LV function is assessed during exercise are needed to
conclusively define the roles of systolic and
diastolic dysfunction in causing exercise intolerance.
Key Words: exercise • hypertension, experimental • hypertrophy • echocardiography • heart • rats
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