Physical training by a chronic swimming program prevented the depression of cardiac actomyosin ATPase activity and the shift in myosin isoenzymes induced by hypertension in rats.
Absolute Event Rate: 0.6% vs 0.52%
p-value: p=<0.05
To evaluate the combined effects of cardiac overload imposed by hypertension and by chronic exercise, male and female rats were made hypertensive by unilateral renal artery stenoses and made to exercise in an 8-10-wk swimming program. Sedentary normotensive animals, sedentary hypertensive animals and normotensive animals exposed to the swimming program were also studied. Hypertension was associated with the development of cardiac hypertrophy, and this was exaggerated in hypertensive swimmers. Actomyosin, Ca2+-myosin, and actin-activated Mg2+-myosin ATPase activities were enhanced in normotensive swimmers, depressed in hypertensives and were normal or increased in hypertensive swimmers. Myosin isoenzyme analysis showed a predominant V1 pattern in normals; an increase in percent V1 isoenzyme is swimmers; a predominant V3 pattern in hypertensives; and a return to the predominant V1 pattern in hypertensive swimmers. These findings suggest that the hypertrophy imposed by hypertension and hypertrophy imposed by physical training using a chronic swimming program are distinctly different biological phenomena. Physical training by swimming prevents the changes in cardiac myosin induced by hypertension despite the exaggeration of hypertrophy.
Scheuer et al. (Wed,) conducted a other in Hypertension and cardiac hypertrophy (n=52). Physical training by swimming vs. Sedentary lifestyle was evaluated on Actomyosin ATPase activity in female hypertensive rats (micromoles Pi/mg protein/min) (p=<0.05). Physical training by a chronic swimming program prevented the depression of cardiac actomyosin ATPase activity and the shift in myosin isoenzymes induced by hypertension in rats.