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Chronic swimming reverses cardiac dysfunction and myosin abnormalities in hypertensive rats
Insights
A chronic swimming program reversed cardiac dysfunction in hypertensive rats by normalizing heart function and myosin biochemistry, despite unchanged blood pressure. This exercise intervention offers potential therapeutic benefits for renal hypertension-induced heart disease.
Area of Science:
- Cardiovascular Physiology
- Exercise Physiology
- Biochemistry
Background:
- Renal hypertension leads to decreased cardiac function and altered myosin biochemistry.
- Understanding the effects of exercise on hypertensive heart disease is crucial.
Purpose of the Study:
- To investigate if a chronic swimming program can reverse cardiac dysfunction and myosin alterations in rats with renal hypertension.
Main Methods:
- Isolated working heart apparatus used to assess cardiac function.
- Myosin biochemistry analyzed, including actin-activated myosin adenosinetriphosphatase (ATPase) activity and myosin isoenzyme content.
- Comparison of sedentary and swimming-trained normotensive and hypertensive rats.
Main Results:
- Hypertension increased dry heart weight and decreased coronary flow, stroke work, ejection fraction, and fractional shortening.
- Actin-activated myosin ATPase activity decreased, and V3 myosin isoenzyme content increased in hypertensive hearts.
- Swimming normalized stroke work, ejection fraction, and fractional shortening in hypertensive rats, despite no improvement in coronary flow.
Conclusions:
- Chronic swimming exercise can restore cardiac function in renal hypertension.
- Exercise normalizes myosin ATPase activity and isoenzyme distribution in hypertensive hearts.
- Exercise demonstrates therapeutic potential for mitigating cardiac complications of renal hypertension.
Abstract:
The purpose of this study was to determine whether a chronic swimming program could reverse the decreased cardiac function and altered myosin biochemistry found in hearts of rats with established renal hypertension. Ten wk after the onset of hypertension [midpoint (m)], hearts from normotensive controls (C) and hypertensives (H) were studied in an isolated working heart apparatus, and myosin biochemistry was analyzed. Half of the control and hypertensive animals were then subjected to a 10-wk swimming program (Sw) and their hearts were compared with those from age-matched sedentary rats. Body weight was no different at the midpoint of the study between Cm and Hm or at the end point (e) of the study among Ce, Swe, He, or H-Swe. Swimming had no effect on blood pressure in either normotensive or hypertensive rats. Dry heart weight was increased by 46% in Hm compared with Cm and by 36% in He, 21% in Swe, and 61% in H-Swe when compared with Ce. Hypertension was associated in both the mid- and end-point studies, with decreases in coronary flow, stroke work (both per gram left ventricle), ejection fraction, and midwall fractional shortening. In addition, actin-activated myosin adenosinetriphosphatase (ATPase) activity was decreased in Hm and He associated with an increase in the content of the V3 myosin isoenzyme. Although the coronary deficit was not corrected in H-Swe, stroke work, ejection fraction, and fractional midwall shortening were normalized compared with control hearts. Myosin ATPase activity and the myosin isoenzyme distribution were similarly restored in H-Swe.(ABSTRACT TRUNCATED AT 250 WORDS)