The influence of the adrenergic system on the population of ventricular myosin isoenzymes under physiological conditions was assessed by subjection of normotensive and spontaneously hypertensive rats (SHR) to different types of physical exercise that increased the activity of the peripheral adrenergic system to varying degrees. The routines, which were 5-6 weeks in duration, involved the mild exercise of enforced swimming (2 x 90 min/day), spontaneous running (daily, about 15 km/10-12 hr) that resulted in absolute ventricular hypertrophy, and enforced running of low intensity (daily, 2 x 1.8 km/3 hr) but associated with marked stressors. Swimming and spontaneous running reduced the high blood pressure of SHR, whereas enforced running increased it. In both strains, the myosin isoenzymes were redistributed in the direction of V1 after swimming but not after running. In SHR, therefore, reduction of pressure load seems insufficient for induction of a higher proportion of V1. The unique and, until now, unexplained effect of swimming was attributed to the pronounced activation of the peripheral adrenergic system as judged from catecholamine stores of ventricles and adrenal glands. Only swimming increased the norepinephrine content of ventricles and adrenal glands in normotensive rats. Swimming also had the strongest influence in SHR. Further evidence for the influence of the adrenergic system came from the effect of selective cardiac beta-blockade with atenolol (50 mg/kg/day). The diminished adrenergic drive of the heart reduced the proportion of V1 to a greater extent in the swimming rats than in the sedentary rats. Taken together, the data demonstrate that substantial changes in adrenergic activity occur under physiological conditions associated with an altered myosin heavy-chain expression.