Our series of experiments in rats, and other data of the literature, indicate that the arterial baroreceptors are actively involved in the reflex control of circulation during acute and chronic exercise. Although heart rate increases simultaneously with arterial blood pressure during an acute bout of dynamic exercise, the gain of the baroreflex bradycardia remains unchanged. Moreover, the more pronounced increase in mean arterial pressure during all exercise period observed in sino-aortic denervated rats, compared to sham-operated rats, suggests that the arterial baroreflex restrains the increase in blood pressure during dynamic exercise. However, the arterial baroreflex seems to have no influence on the development of exercise tachycardia. Exercise training can affect baroreflex bradycardia and tachycardia in the opposite direction, since decreased baroreflex bradycardia is observed despite increased baroreflex tachycardia. Since the increased baroreflex tachycardia may be attributed to an increased sensitivity of the afferent pathway of the baroreceptors, the attenuation of the baroreflex bradycardia is probably due to an impairment of the efferent pathway of the reflex. Finally, the decreased tonic sympathetic nerve activity produced by exercise training can be considered as one of the mechanisms involved in the attenuation of hypertension induced by exercise training.