Do peripheral and/or central chemoreflexes influence skin blood flow in humans?

Voluntary apnea activates the central and peripheral chemoreceptors, leading to a rise in sympathetic nerve activity and limb vasoconstriction (i.e., brachial blood flow velocity and forearm cutaneous vascular conductance decrease to a similar extent). Whether peripheral and/or central chemoreceptors contribute to the cutaneous vasoconstrictor response remains unknown. We performed three separate experiments in healthy young men to test the following three hypotheses. First, inhibition of peripheral chemoreceptors with brief hyperoxia inhalation (100% O(2)) would attenuate the cutaneous vasoconstrictor response to voluntary apnea. Second, activation of the peripheral chemoreceptors with 5 min of hypoxia (10% O(2), 90% N(2)) would augment the cutaneous vasoconstrictor response to voluntary apnea. Third, activation of the central chemoreceptors with 5 min of hypercapnia (7% CO2, 30% O(2), 63% N(2)) would have no influence on cutaneous responses to voluntary apnea. Studies were performed in the supine posture with skin temperature maintained at thermoneutral levels. Beat‐by‐beat blood pressure, heart rate, brachial blood flow velocity, and cutaneous vascular conductance were measured and changes from baseline were compared between treatments. Relative to room air, hyperoxia attenuated the vasoconstrictor response to voluntary apnea in both muscle (−16 ± 10 vs. −40 ± 12%, P = 0.023) and skin (−14 ± 6 vs. −24 ± 5%, P = 0.033). Neither hypoxia nor hypercapnia had significant effects on cutaneous responses to apnea. These data indicate that skin blood flow is controlled by the peripheral chemoreceptors but not the central chemoreceptors.