ONSET OF EXERCISE SHIFTS OPERATING POINT OF ARTERIAL BAROREFLEX TO HIGHER PRESSURES

This study was designed to test the hypothesis that the increase in sympathetic nerve activity (SNA) and mean arterial pressure (MAP) at the onset of exercise is dependent on a rapid upward shift of the operating point of the arterial baroreflex. To test this hypothesis, we recorded renal sympathetic nerve activity (RSNA) in 16 New Zealand White rabbits during treadmill running (12.6 m/min, 20% grade) under control conditions and during concomitant intravenous infusions of nitroglycerin (NTG) to attenuate the exercise pressor response. In the control condition, MAP increased 18 +/- 2 mmHg. This was associated with an increase in heart rate (HR) (104 +/- 4 beats/min) and RSNA (414 +/- 20%). The increases in RSNA (848 +/- 32%) and HR (155 +/- 5 beats/min) at the onset of exercise were significantly augmented when the rate of development of the exercise pressor response (0.3 +/- 0.03 to 0.12 +/- 0.01 mmHg/s) and the magnitudes of the pressor response (91 +/- 2 to 79 +/- 1 mmHg) were attenuated by infusions of NTG. These data suggest that at the onset of exercise the operating point of the arterial baroreflex is reset toward higher pressures. The MAP, RSNA, and HR responses to exercise were also determined in eight sinoaortic-denervated (SAD) rabbits. In the absence of a functional baroreflex, MAP (-46 +/- 2 mmHg), RSNA (-19 +/- 1%), and HR (-62 +/- 3 beats/min) decreased at the onset of exercise and recovered 1 min to -42 +/- 2, +13 +/- 1, and +9 +/- 1% of control, respectively. These data suggest that the normal MAP, RSNA, and HR responses to exercise require a functional arterial baroreflex.