Combined effects of hypertension and chronic running program on rat heart

Abstract

Previous studies in hearts of female rats have demonstrated that ventricular hypertrophy due to systolic overload, when combined with hypertrophy induced by a chronic swimming program, results in increased cardiac performance and enhanced contractile protein activity compared with the effects of hypertension alone. To explore how a chronic running program affects the function of hypertensive hearts, renal hypertension was created in female rats, and the animals were subjected to a program of chronic treadmill running. Running alone caused enhanced cardiac function, an increase in myosin adenosinetriphosphatase (ATPase) activity, and an increase in the percent of the V1 myosin isoenzyme. Hypertension alone caused cardiac hypertrophy with a depression in myosin ATPase activity and a decrease in the percent of the V1 isoenzyme. Running improved cardiac function in hearts of normotensive rats but had no effect in hearts of hypertensive rats. Despite the diminished myosin ATPase activity in hearts of hypertensive runners and the decrease in percent of the V1 isoenzyme, cardiac function was well maintained. The results demonstrate that a chronic running program in hypertensive rats, in contrast to a chronic swimming program, had virtually no effect on cardiac performance or contractile proteins. The dissociation between myocardial performance and the contractile proteins implicates other biochemical mechanisms in the adaptations observed.

Exercise training and detraining modify the morphological and mechanical properties of single cardiac myocytes obtained from spontaneously hypertensive rats

“…Our findings give support to the improvement of left ventricular performance demonstrated in exercised SHR isolated heart (5,17,19). Although we did not measure cardiac function in the present study, the morphological and mechanical cellular adaptations reported here may contribute to our understanding of the mechanisms underlying the benefits of exercise training on the cardiac function of SHR (i.e., improved left ventricular performance).…”

“…There is evidence at the whole heart level that exercise training provides beneficial adaptations to cardiac contractile function and morphology in hypertensive rats (5). Nevertheless, to date the effects of exercise training and detraining on the left ventricular single myocyte morphological and mechanical properties of SHR are not known.…”

Calcineurin Is Activated in Rat Hearts With Physiological Left Ventricular Hypertrophy Induced by Voluntary Exercise Training

“…The LVW/BW, LV end-diastolic dimension, and velocity-time integral of aortic ejection flow increased, without an increase in cardiomyocytes width as previously reported. 12,13 This is the first report that shows the involvement of calcineurin in physiological adaptive hypertrophy. The role of calcineurin in cardiac hypertrophy had not yet been elucidated.…”

Exercise training increases the Ca2+sensitivity of tension in rat cardiac myocytes

“…myocardium; tension-pCa; endurance training; contractility CHRONIC ENDURANCE EXERCISE training has been shown to elicit positive adaptations in the cardiovascular system that result in improved performance at maximal and submaximal work levels. Among these adaptations is a training-induced increase in peak left ventricular pressure development (5,10,27,28). Because pressure development in the ventricle is driven by the capacity of the myocardium to generate tension or force, much work has been focused on the effect of exercise training on myocardial force generation.…”