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Published on: June 29, 2014
Combined effects of hypertension and chronic running program on rat heart
Insights
Chronic running did not improve cardiac function or contractile proteins in hypertensive rats, unlike swimming. This suggests other mechanisms maintain heart function under hypertension and exercise.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Cardiac Adaptation
Background:
- Hypertension often leads to cardiac hypertrophy and impaired cardiac function.
- Previous studies showed swimming exercise improved cardiac performance in hypertensive female rats.
- The effects of running exercise on hypertensive hearts remain less understood.
Purpose of the Study:
- To investigate the impact of chronic treadmill running on cardiac function and contractile proteins in a rat model of renal hypertension.
- To compare the effects of running versus swimming on cardiac adaptations in hypertensive hearts.
Main Methods:
- Induction of renal hypertension in female rats.
- Implementation of a chronic treadmill running program.
- Assessment of cardiac function, myosin adenosinetriphosphatase (ATPase) activity, and myosin isoenzyme distribution.
Main Results:
- Running alone enhanced cardiac function and myosin ATPase activity in normotensive rats.
- Hypertension caused cardiac hypertrophy with reduced myosin ATPase activity.
- Running did not improve cardiac function or myosin ATPase activity in hypertensive rats, despite diminished contractile protein activity.
Conclusions:
- Chronic running has minimal effects on cardiac performance and contractile proteins in hypertensive rats, contrasting with swimming.
- The dissociation between myocardial performance and contractile proteins suggests alternative biochemical pathways are involved in cardiac adaptation to running in hypertension.
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.
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