The interaction of central command and the exercise pressor reflex in mediating baroreflex resetting during exercise in humans

• Published in: Experimental physiology 2006-01, Vol.91 (1), p.79-87
• Main Authors: Gallagher, Kevin M., Fadel, Paul J., Smith, Scott A., Strømstad, Morten, Ide, Kojiro, Secher, Niels H., Raven, Peter B.
• Format: Article
• Language: English
• Subjects: Adult; Afferent Pathways - physiology; Baroreflex - drug effects; Baroreflex - physiology; Blood Pressure - drug effects; Carotid Body - drug effects; Central Nervous System - physiology; Exercise - physiology; Exercise Test; Gravity Suits; Heart Rate - drug effects; Humans; Male; Muscle Contraction; Muscle, Skeletal - blood supply; Muscle, Skeletal - innervation; Muscle, Skeletal - physiology; Neuromuscular Nondepolarizing Agents - administration & dosage; Neuromuscular Nondepolarizing Agents - pharmacology; Vascular Resistance - physiology; Vasomotor System - drug effects; Vasomotor System - physiology; Vecuronium Bromide - administration & dosage; Vecuronium Bromide - pharmacology
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/expphysiol.2005.032110

Central command and the exercise pressor reflex can independently reset the carotid baroreflex (CBR) during exercise. The present investigation assessed the interactive relationship between these two neural mechanisms in mediating baroreflex resetting during exercise. Six men performed static leg exercise at 20% maximal voluntary contraction under four conditions: control, no perturbation; neuromuscular blockade (NMB) induced by administration of the neuromuscular blocking agent Norcuron (central command activation); MAST, application of medical antishock trousers inflated to 100 mmHg (exercise pressor reflex activation); and Combo, NMB plus MAST (concomitant central command and exercise pressor reflex activation). With regard to CBR control of heart rate (HR), both NMB and Combo conditions resulted in a further resetting of the carotid–cardiac stimulus–response curve compared to control conditions, suggesting that CBR–HR resetting is predominately mediated by central command. In contrast, it appears that CBR control of blood pressure can be mediated by signals from either central command or the exercise pressor reflex, since both NMB and MAST conditions equally augmented the resetting of the carotid–vasomotor stimulus–response curve. With regard to the regulation of both HR and blood pressure, the extent of CBR resetting was greater during the Combo condition than during overactivation of either central command or the exercise pressor reflex alone. Therefore, we suggest that central command and the exercise pressor reflex interact such that signals from one input facilitate signals from the other, resulting in an enhanced resetting of the baroreflex during exercise.