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This Article Full Text Full Text (PDF) All Versions of this Article: 586/6/1743    most recent jphysiol.2007.147421v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Stickland, M. K. Articles by Dempsey, J. A. PubMed PubMed Citation Articles by Stickland, M. K. Articles by Dempsey, J. A. Related Collections Integrative

¹ John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison and the William S. Middleton Memorial Veterans Hospital, Madison, WI 53705, USA

Recently, we have shown that specific, transient carotid chemoreceptor (CC) inhibition in exercising dogs causes vasodilatation in limb muscle. The purpose of the present investigation was to determine if CC suppression reduces muscle sympathetic nerve activity (MSNA) in exercising humans. Healthy subjects (N = 7) breathed hyperoxic gas (F_IO2 1.0) for 60 s at rest and during rhythmic handgrip exercise (50% maximal voluntary contraction, 20 r.p.m.). Microneurography was used to record MSNA in the peroneal nerve. End-tidal P_CO2 was maintained at resting eupnoeic levels throughout and breathing rate was voluntarily fixed. Exercise increased heart rate (67 versus 77 beats min^–1), mean blood pressure (81 versus 97 mmHg), MSNA burst frequency (28 versus 37 bursts min^–1) and MSNA total minute activity (5.7 versus 9.3 units), but did not change blood lactate (0.7 versus 0.7 mM). Transient hyperoxia had no significant effect on MSNA at rest. In contrast, during exercise both MSNA burst frequency and total minute activity were significantly reduced with hyperoxia. MSNA burst frequency was reduced within 9–23 s of end-tidal P_O2 exceeding 250 mmHg. The average nadir in MSNA burst frequency and total minute activity was –28 ± 2% and –39 ± 7%, respectively, below steady state normoxic values. Blood pressure was unchanged with hyperoxia at rest or during exercise. CC stimulation with transient hypoxia increased MSNA with a similar time delay to that obtained with CC inhibition via hyperoxia. Consistent with previous animal work, these data indicate that the CC contributes to exercise-induced increases in sympathetic vasoconstrictor outflow.

(Received 29 October 2007; accepted after revision 11 January 2008; first published online 17 January 2008)
Corresponding author M. K. Stickland: Division of Pulmonary Medicine, Department of Medicine, 2E4.42 Walter C Mackenzie, Health Sciences Centre, University of Alberta, Edmonton, Alberta, Canada T6G 2B7. Email: michael.stickland{at}ualberta.ca