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Cardiac and vasomotor components of the carotid baroreflex control of arterial blood pressure during isometric exercise in humans
Authors:James P Fisher  Shigehiko Ogoh  Ellen A Dawson  Paul J Fadel  Niels H Secher  Peter B Raven  Michael J White
Institution:School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK;Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, TX 76107, USA;Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, USA;Copenhagen Muscle Research Center, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2100, Copenhagen, Denmark
Abstract:We sought to examine the importance of the cardiac component of the carotid baroreflex (CBR) in control of blood pressure during isometric exercise. Nine subjects performed 4 min of ischaemic isometric calf exercise at 20% of maximum voluntary contraction. Trials were repeated with β1-adrenergic blockade (metoprolol, 0.15 ± 0.003 mg kg?1) or parasympathetic blockade (glycopyrrolate, 13.6 ± 1.5 μg kg?1). CBR function was determined using rapid pulses of neck pressure and neck suction from +40 to ?80 mmHg, while heart rate (HR), mean arterial pressure (MAP) and changes in stroke volume (SV, Modelflow method) were measured. Metoprolol decreased and glycopyrrolate increased HR and cardiac output both at rest and during exercise ( P < 0.05), while resting and exercising blood pressure were unchanged. Glycopyrrolate reduced the maximal gain ( G max) of the CBR-HR function curve (?0.58 ± 0.10 to ?0.06 ± 0.01 beats min?1 mmHg?1, P < 0.05), but had no effect on the G max of the CBR-MAP function curve. During isometric exercise the CBR-HR curve was shifted upward and rightward in the metoprolol and no drug conditions, while the control of HR was significantly attenuated with glycopyrrolate ( P < 0.05). Regardless of drug administration isometric exercise produced an upward and rightward resetting of the CBR control of MAP with no change in G max. Thus, despite marked reductions in CBR control of HR following parasympathetic blockade, CBR control of blood pressure was well maintained. These data suggest that alterations in vasomotor tone are the primary mechanism by which the CBR modulates blood pressure during low intensity isometric exercise.
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