Regulation of Carotid Baroreflex Resetting During Arm Exercise

Date

1999-06-01

Authors

Querry, Ross G.

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Abstract

Querry, Ross G., Regulation of Carotid Baroreflex Resetting during Arm Exercise. Doctor of Philosophy (Biomedical Sciences), June 1999, 100 pp., 4 tables, 12 figures, bibliography, 56 titles. Cardiovascular responses to exercise are modulated by the integration of the central nervous system and afferent information from arterial baroreflexes and working skeletal muscle. Investigations have shown that during exercise, the carotid baroreflex (CBR) is reset in proportion to the exercise intensity. The role of the central nervous system contribution to the CBR resetting has not been elucidated. Investigations of CBR function in the animal model consistently report CBR variables such as maximal gain that are different than those reported in humans. These discrepancies may be due in part to methodological limitations in the neck pressure/neck suction (NP-NS) technique used to investigate the isolated CBR function in humans. To accurately examine the internal stimulus from the NP-NS maneuver, subjects were instrumented with a percutaneous catheter to record tissue pressure at the carotid sinus during five-second and rapid pulse NP-NS protocols. Carotid baroreflex function curves were analyzed with and without transmission correction of the carotid sinus pressure (CSP). Results indicated that positive pressure was more fully transmitted (~83%) than negative pressure (~65%) during the five-second-pulse, but not the rapid pulse protocol. Correction of the CSP in either protocol resulted in significant increases in CBR maximal gain and threshold and a reduced saturation pressure. These methodological refinements were then utilized to investigate the role of central command on CBR function during exercise. Subjects performed static and rhythmic handgrip exercise before and after regional anesthesia. Carotid baroreflex curves were analyzed at rest and during exercise before and after blockade at the same absolute workload. Muscle weakness from the blockade required an increased effort to maintain control tension. Heart rate, arterial pressure and perceived exertion during exercise were increased following blockade. During control exercise the CBR function curves were reset upward and rightward compared to rest with a further parallel shift during exercise with blockade. The operating point of the CBR was reset along with the centering point, but did not show the divergence toward the threshold pressure that had been previously described during dynamic exercise. The results support the proposal that central command was a primary mechanism for the resetting of the carotid baroreflex during exercise, but may not be the primary mechanism in the resetting of the operating point of the reflex.

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