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

Abstract

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% O2) would attenuate the cutaneous vasoconstrictor response to voluntary apnea. Second, activation of the peripheral chemoreceptors with 5 min of hypoxia (10% O2, 90% N2) would augment the cutaneous vasoconstrictor response to voluntary apnea. Third, activation of the central chemoreceptors with 5 min of hypercapnia (7% CO2, 30% O2, 63% N2) 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.

Keywords: Blood pressure; chemoreceptors; cutaneous vasoconstriction; heart rate; muscle blood flow; sympathetic activation.

Figure 1.

Procedure overview for Experiments 1, 2, and 3. The arrows indicate that trials were randomized. Please see text for details. Base, baseline; MVEEA, maximal voluntary end expiratory apnea.

Figure 2.

Hemodynamic and vascular changes in response to hyperoxic gas and room air apnea in Experiment 1. Absolute changes from Base 1 (room air) to Base 2 (at the end of hyperoxia or room air administration) are presented in the left panel. Room air is represented by a solid line, and hyperoxia is represented by a dashed line. Changes from Base 2 are presented in the right panel for both A1 (first three cardiac cycles after apnea begins) and A2 (last three cardiac cycles before breathing resumes). Room air A2 is represented as a black bar and hyperoxia time match is represented as a white bar. Base, baseline; MVEEA, maximal voluntary end expiratory apnea; MAP, mean arterial pressure; HR, heart rate; CVC, cutaneous vascular conductance; BBFV, brachial blood flow velocity. Data are presented as M ± SEM, *denotes significant difference between gases, P < 0.05.

Figure 3.

Hemodynamic and vascular changes in response to hypoxic gas and room air apnea in Experiment 2. Absolute changes from Base 1 (room air) to Base 2 (at the end of hypoxia or room air administration) are presented in the left panel. Room air is represented by a solid line, and hypoxia is represented by a dashed line. Changes from Base 2 are presented in the right panel for both A1 (first three cardiac cycles after apnea begins) and A2 (last three cardiac cycles before breathing resumes). Room air time match is represented as a black bar, and hypoxia A2 is represented as a white bar. Base, baseline; MVEEA, maximal voluntary end expiratory apnea; MAP, mean arterial pressure; HR, heart rate; CVC, cutaneous vascular conductance; BBFV, brachial blood flow velocity. Data are presented as M ± SEM, *denotes significant difference between gases, P < 0.05.

Figure 4.

Hemodynamic and vascular changes in response to hypercapnic gas and room air apnea in Experiment 3. Absolute changes from Base 1 (room air) to Base 2 (at the end of hypercapnia or room air administration) are presented in the left panel. Room air is represented by a solid line, and hypercapnia is represented by a dashed line. Changes from Base 2 are presented in the right panel for both A1 (first three cardiac cycles after apnea begins) and A2 (last three cardiac cycles before breathing resumes). Room air is represented as a black bar, and hypercapnia is represented as a white bar. Base, baseline; MVEEA, maximal voluntary end expiratory apnea; MAP, mean arterial pressure; HR, heart rate; CVC, cutaneous vascular conductance; BBFV, brachial blood flow velocity. Data are presented as M ± SEM, *denotes significant difference between gases, P < 0.05.