Endurance Exercise Training Attenuates The Sympathetic-nerve Response To Exercise, In Part, By Enhanced Cardiac Afferents
Biochemistry & Molecular Biology; Cell Biology; Life Sciences & Biomedicine - Other; Topics
DiCarlo S E; Stahl L K; Bishop V S
Faseb Journal
1995
1995-03
Journal Article or Conference Abstract Publication
n/a
Daily exercise attenuates the sympathetic nerve response to exercise by enhancing cardiac afferents.
Afferent Pathways; Animal/*physiology; Animals; Baroreflex; Blood Pressure; Femoral Artery/physiology; Femoral Vein/physiology; Heart Rate; Heart/innervation/*physiology; Kidney/innervation; Physical Conditioning; Rabbits; Sympathetic Nervous System/*physiology
"Central command" may initiate the sympathoexcitatory responses at the onset of exercise by shifting the operating point of the arterial baroreflex toward higher pressures. Daily exercise (DE) attenuates the sympathoexcitatory responses to submaximal exercise. This DE-induced adaptation may be due, in part, to an enhanced inhibitory influence of cardiac afferents. This is suggested because cardiac afferents exert a tonic inhibitory influence on the arterial baroreflex which is enhanced by DE. Therefore, the influence of cardiac afferents on the regulation of renal sympathetic nerve activity (RSNA) during exercise was examined in a group of sedentary and age-matched DE rabbits. The rabbits were instrumented with a Silastic catheter inserted into the pericardial sac, electrodes around the renal sympathetic nerves, and catheters in the femoral artery and vein. In the sedentary rabbits, treadmill exercise (12 m/min, 20% grade) significantly increased mean arterial pressure (delta 18 +/- 3 mmHg), heart rate (delta 36 +/- 3 beats/min), and RSNA (delta 295 +/- 23%). More importantly, cardiac afferent blockade (2% intrapericardial procainamide) did not significantly alter the RSNA response to exercise in the sedentary rabbits. DE did not alter the mean arterial pressure (delta 15 +/- 1 mmHg) or heart rate (delta 55 +/- 8 beats/min) response to exercise; however, RSNA (delta 252 +/- 9%) was significantly reduced. In contrast to the sedentary rabbits, cardiac afferent blockade in the DE rabbits significantly increased the RSNA response to exercise (delta 417 +/- 30%). These results suggest that DE attenuates the RSNA response to dynamic exercise due, in part, to an enhanced inhibitory influence of cardiac afferents.
DiCarlo S E; Stahl L K; Bishop V S
The American journal of physiology
1997
1997-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.1997.273.3.H1606" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1997.273.3.H1606</a>
Onset of exercise shifts operating point of arterial baroreflex to higher pressures.
*Blood Pressure; *Physical Exertion; Animals; Arteries/*physiology; Denervation; Heart Rate; Kidney/physiology; Pressoreceptors/*physiology; Rabbits; Reflex/*physiology; Sinus of Valsalva/physiology; Sympathetic Nervous System/physiology
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.(ABSTRACT TRUNCATED AT 250 WORDS)
DiCarlo S E; Bishop V S
The American journal of physiology
1992
1992-01
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.1992.262.1.H303" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1992.262.1.H303</a>