Abstract
Recently, we have shown that carotid chemoreceptor inhibition causes vasodilation in limb muscle via reduced sympathetic vasoconstrictor outflow in exercising dogs. The purpose of the present investigation was to determine if suppression of the carotid chemoreceptors reduced muscle sympathetic nervous activity (MSNA) in exercising humans. Experiments, whereby healthy subjects (N=7) breathed oxygen (FIO2, 1.0) for 60 secs, were conducted at rest and while subjects performed rhythmic double-handgrip exercise at 50% of maximal voluntary contraction for 10 min, using 1 sec contraction, 2 sec relaxation duty cycle. Microneurography was used to record MSNA in the peroneal nerve of the resting limb. End-tidal PCO2 was maintained at resting eupneic levels throughout, and using feedback, breathing rate was voluntarily fixed at 20 breaths/min, and tidal volume held constant. Exercise significantly increased heart rate (67 vs. 76 bpm), mean blood pressure (84 vs. 102 mmHg), MSNA burst frequency (28 vs 34 bursts/min) and MSNA total activity (5.72 vs. 8.76 units), but did not change blood lactate (0.67 vs. 0.66 mM). Transient hyperoxia had no significant effect on MSNA at rest. In contrast, a significant reduction in both MSNA burst frequency and total activity was observed during exercise beginning after 20 secs of transient hyperoxia, and reached an average nadir of −28 ± 2% and −39 ± 7%, respectively, below steady state normoxic control values. Blood pressure was unchanged with hyperoxia. Consistent with our animal work, these data suggest that the carotid chemoreceptors contribute significantly to sympathetic vasoconstrictor outflow during exercise in healthy humans. (NHLBI & AHA)
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