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Themed Issue Papers |
Departments of 1 Internal Medicine2 Health Care Sciences3 Physical Therapy, University of Texas Southwestern Medical Center, Dallas, TX, USA4 Department of Anaesthesia, Copenhagen Muscle Research Centre, Rigshospitalet, Copenhagen, Denmark 5 Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX, USA
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.
(Received 2 September 2005;
accepted after revision 27 October 2005; first published online 1 November 2005)
Corresponding author K. M. Gallagher: Department of Internal Medicine, Division of Cardiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9034, USA. Email: kevin.gallagher{at}utsouthwestern.edu
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