Excessive exercise in hypertension may speed heart failure progression

9 August 2007

MedWire News: Excessive exercise in untreated hypertension may, in the long term, worsen cardiac remodeling and accelerate progression to heart failure, preliminary study findings in rats indicate.

In the healthy heart, aerobic exercise leads to increased myocardial mass, left ventricle chamber dimensions, and stroke volume. However, the long-term effects of exercise on cardiac function and myocyte remodeling in hypertension and progression of heart failure are unclear.

To investigate further, A Martin Gerdes, from the University of South Dakota, and colleagues studied 15 female rats with spontaneous hypertensive heart failure and six healthy controls. The animals were housed with running wheels at 6 months of age, and the heart function of the two groups of rats was compared at 22 months. The team also compared heart function at 22 months in these groups with that of 14 rats with spontaneous hypertensive heart failure and 10 control rats without access to running wheels.

Echocardiography and left ventricular catheterization was used to measure heart function, and cardiac myocytes were extracted to determine cellular dimensions. Western blots were used to examine fetal gene expression.

Writing in the journal Hypertension, the team reports that myocyte remodeling and ventricular function were not significantly affected by exercise in the control rats, while sedentary hypertensive rats had significant chamber dilatation and cardiac hypertrophy in comparison with sedentary controls.

Exercised hypertensive rats had excessive exercise times, which led to a 21% increase in the volume of left ventricular myocytes compared with sedentary hypertensive rats, along with a reduction in ejection fraction of 13% and a 22% reduction in fractional shortening. Exercised hypertensive rats also had increased fibrosis, and expression of fetal genes was not prevented by exercise.

The team says: "Although the mechanisms of such findings are unclear, it is likely that the spontaneous hypertensive heart failure rats simply exercised too much. Perhaps the frequent acute stress of repeated bouts of high-intensity exercise, in their already chronically stressed, hypertensive condition, only served to exacerbate left ventricular dilatation and, thus, the decline in function and progression to failure.

"This model may prove useful in defining the optimum level of exercise in hypertension-induced heart failure by establishing the threshold between beneficial and detrimental levels of exercise."

Hypertension 2007; 50: 410-416