Effects of exercise on blood flow in the hypertrophied heart

Robert J Bache, Thomas R. Vrobel

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


This study was carried out to examine the response of regional myocardial blood flow to exercise in normal dogs and in dogs with left ventricular hypertrophy. Left ventricular hypertrophy, with an approximately 50 percent increase in left ventricular mass, was produced by means of perinephritic hypertension. The animals were studied approximately 5 months after the induction of hypertension. Myocardial blood flow to four transmural layers of the left ventricular wall was measured using left atrial injections of 15 μ radioactive microspheres at rest and during two levels of treadmill exercise to increase heart rates to 200 and 260 beats/min, respectively. Mean left ventricular blood flow during resting control conditions was similar in the two groups of dogs. In addition, blood flow increased similarly during exercise so that heart rate or the product of heart rate and systolic blood pressure predicted myocardial blood flow equally well in normal dogs and in those with left ventricular hypertrophy. During resting conditions, subendocardial blood flow significantly exceeded subepicardial blood flow in normal dogs, but exertion abolished this perfusion gradient, resulting in uniform transmural myocardial blood flow during exercise. In contrast, in dogs with left ventricular hypertrophy, blood flow to the subendocardium of the left ventricle significantly exceeded subepicardial blood flow both at rest and during exercise. Nevertheless, this study failed to demonstrate any exercise-induced perfusion deficit within the hypertrophied left ventricle.

Original languageEnglish (US)
Pages (from-to)1029-1033
Number of pages5
JournalThe American Journal of Cardiology
Issue number5
StatePublished - Oct 22 1979

Bibliographical note

Funding Information:
From the Department of Medicine (Division of Cardiology), University of Minnesota School of Medicine, Minneapolis, Minnesota. This study was supported by U. S. Public Health Service Grants HL-20598 and HL-2 1872 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Dr. Bathe is the recipient of Research Career Development Award l-K04-HL00367 from the U. S. Public Health Service. Manuscript received June 8, 1979. accepted June 15, 1979. Address for reprints: Robert J. Bathe, MD, University of Minnesota Hospitals, Department of Medicine, Box 338-Mayo Memorial Bldg, Minneapolis, Minnesota 55455.


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