Abstract
Exercise causes parallel increases in systemic arterial pressure (AP), heart rate (HR) and renal sympathetic nerve activity (RSNA). This review focused on the potential role of the acute shift in the baroreflex control of RSNA in both increasing and stabilizing AP during exercise, and causing hypotension afterwards. Treadmill exercise shifted the baroreflex curve for RSNA acutely to the right and upward, characterized by a significant increase in the maximum response, about 170%, which could well explain the parallel increases in AP, HR, and RSNA. In contrast, exercise shifted the baroreflex stimulus-response curve for HR upwards in rats, differing from the shift shown for RSNA, suggesting that the dependent variable of baroreflex control has to be specified when shifts in baroreflex stimulus response curves are discussed. During the post-exercise period, the AP-RSNA baroreflex curve was suppressed vertically, with a significant reduction of about 50% shown in the upper plateau without any alteration in the minimum response, which may be the reason for the post exercise hypotension. The loading of cardiopulmonary baroreceptors modulated the baroreflex control of RSNA in a way resembling “Flip-Flop” or “On-Off” type regulation. In part, this may explain the orthostatic intolerance caused by endurance training.
