Response of blood pressure and cardiac myosin polymorphism to swimming training in the spontaneously hypertensive rat

Abstract

Cardiac muscle can adapt to different functional demands, as evidenced by polymorphism of myosin. Pressure load in spontaneously hypertensive rats induced a shift of the myosin isoenzymes towards myosin V3 (18% V1, 27% V2, 55% V3) relative to normotensive Wistar rats (49% V1, 29% V2, 22% V3). A swimming routine with Wistar rats resulted in a shift towards myosin V1 (72% V1, 18% V2, 10% V3). The training effect is not restricted to normotensive rats, since spontaneously hypertensive rats subjected to the same swimming routine exhibited a myosin isoenzyme pattern (38% V1, 31% V2, 31% V3) approaching that of the sedentary Wistar rats. Swimming training can, therefore, prevent the myosin isoenzyme redistribution towards myosin V3 found in sedentary spontaneously hypertensive rats. Furthermore, systolic blood pressure was significantly reduced (130 ± 8 mmHg (1 mmHg = 133.322 Pa)) in the swim-trained compared with the sedentary spontaneously hypertensive rats (157 ± 12 mmHg). The training-induced changes in myosin polymorphism and systolic blood pressure are, at least partially, attributed to substantially normalized sympathetic activity. The functional relevance of swimming training in the spontaneously hypertensive rat is seen in the increased potential of coping with situations requiring fast contraction which may occur during sudden physical exertion or emotional stress.