Hypoxia augments apnea-induced peripheral vasoconstriction in humans

Urs A. Leuenberger, J. Cullen Hardy, Michael D. Herr, Kristen S. Gray, Lawrence I. Sinoway

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Abstract

Obstructive apnea and voluntary breath holding are associated with transient increases in muscle sympathetic nerve activity (MSNA) and arterial pressure. The contribution of changes in blood flow relative to the contribution of changes in vascular resistance to the apnea-induced transient rise in arterial pressure is unclear. We measured heart rate, mean arterial blood pressure (MAP), MSNA (peroneal microneurography), and femoral artery blood velocity (VFA, Doppler) in humans during voluntary end-expiratory apnea while they were exposed to room air, hypoxia (10.5% inspiratory fraction of O2), and hyperoxia (100% inspiratory fraction of O2). Changes from baseline of leg blood flow (Q̇) and vascular resistance (R) were estimated from the following relationships: Q̇ ∝ VFA, corrected for the heart rate, and R ∝ MAP/Q̇. During apnea, MSNA rose; this rise in MSNA was followed by a rise in MAP, which peaked a few seconds after resumption of breathing. Responses of MSNA and MAP to apnea were greatest during hypoxia and smallest during hyperoxia (P < 0.05 for both compared with room air breathing). Similarly, apnea was associated with a decrease in Q̇ and an increase in R. The decrease in Q̇ was greatest during hypoxia and smallest during hyperoxia (-25 ± 3 vs. -6 ± 4%, P < 0.05), and the increase in R was the greatest during hypoxia and the least during hyperoxia (60 ± 8 vs. 21 ± 6%, P < 0.05). Thus voluntary apnea is associated with vasoconstriction, which is in part mediated by the sympathetic nervous system. Because apnea-induced vasoconstriction is most intense during hypoxia and attenuated during hyperoxia, it appears to depend at least in part on stimulation of arterial chemoreceptors.

Original languageEnglish (US)
Pages (from-to)1516-1522
Number of pages7
JournalJournal of applied physiology
Volume90
Issue number4
StatePublished - Mar 28 2001

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Apnea
Vasoconstriction
Arterial Pressure
Hyperoxia
Muscles
Vascular Resistance
Respiration
Heart Rate
Air
Hypoxia
Breath Holding
Peroneal Nerve
Sympathetic Nervous System
Femoral Artery
Leg

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Leuenberger, Urs A. ; Hardy, J. Cullen ; Herr, Michael D. ; Gray, Kristen S. ; Sinoway, Lawrence I. / Hypoxia augments apnea-induced peripheral vasoconstriction in humans. In: Journal of applied physiology. 2001 ; Vol. 90, No. 4. pp. 1516-1522.
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abstract = "Obstructive apnea and voluntary breath holding are associated with transient increases in muscle sympathetic nerve activity (MSNA) and arterial pressure. The contribution of changes in blood flow relative to the contribution of changes in vascular resistance to the apnea-induced transient rise in arterial pressure is unclear. We measured heart rate, mean arterial blood pressure (MAP), MSNA (peroneal microneurography), and femoral artery blood velocity (VFA, Doppler) in humans during voluntary end-expiratory apnea while they were exposed to room air, hypoxia (10.5{\%} inspiratory fraction of O2), and hyperoxia (100{\%} inspiratory fraction of O2). Changes from baseline of leg blood flow (Q̇) and vascular resistance (R) were estimated from the following relationships: Q̇ ∝ VFA, corrected for the heart rate, and R ∝ MAP/Q̇. During apnea, MSNA rose; this rise in MSNA was followed by a rise in MAP, which peaked a few seconds after resumption of breathing. Responses of MSNA and MAP to apnea were greatest during hypoxia and smallest during hyperoxia (P < 0.05 for both compared with room air breathing). Similarly, apnea was associated with a decrease in Q̇ and an increase in R. The decrease in Q̇ was greatest during hypoxia and smallest during hyperoxia (-25 ± 3 vs. -6 ± 4{\%}, P < 0.05), and the increase in R was the greatest during hypoxia and the least during hyperoxia (60 ± 8 vs. 21 ± 6{\%}, P < 0.05). Thus voluntary apnea is associated with vasoconstriction, which is in part mediated by the sympathetic nervous system. Because apnea-induced vasoconstriction is most intense during hypoxia and attenuated during hyperoxia, it appears to depend at least in part on stimulation of arterial chemoreceptors.",
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Hypoxia augments apnea-induced peripheral vasoconstriction in humans. / Leuenberger, Urs A.; Hardy, J. Cullen; Herr, Michael D.; Gray, Kristen S.; Sinoway, Lawrence I.

In: Journal of applied physiology, Vol. 90, No. 4, 28.03.2001, p. 1516-1522.

Research output: Contribution to journalArticle

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N2 - Obstructive apnea and voluntary breath holding are associated with transient increases in muscle sympathetic nerve activity (MSNA) and arterial pressure. The contribution of changes in blood flow relative to the contribution of changes in vascular resistance to the apnea-induced transient rise in arterial pressure is unclear. We measured heart rate, mean arterial blood pressure (MAP), MSNA (peroneal microneurography), and femoral artery blood velocity (VFA, Doppler) in humans during voluntary end-expiratory apnea while they were exposed to room air, hypoxia (10.5% inspiratory fraction of O2), and hyperoxia (100% inspiratory fraction of O2). Changes from baseline of leg blood flow (Q̇) and vascular resistance (R) were estimated from the following relationships: Q̇ ∝ VFA, corrected for the heart rate, and R ∝ MAP/Q̇. During apnea, MSNA rose; this rise in MSNA was followed by a rise in MAP, which peaked a few seconds after resumption of breathing. Responses of MSNA and MAP to apnea were greatest during hypoxia and smallest during hyperoxia (P < 0.05 for both compared with room air breathing). Similarly, apnea was associated with a decrease in Q̇ and an increase in R. The decrease in Q̇ was greatest during hypoxia and smallest during hyperoxia (-25 ± 3 vs. -6 ± 4%, P < 0.05), and the increase in R was the greatest during hypoxia and the least during hyperoxia (60 ± 8 vs. 21 ± 6%, P < 0.05). Thus voluntary apnea is associated with vasoconstriction, which is in part mediated by the sympathetic nervous system. Because apnea-induced vasoconstriction is most intense during hypoxia and attenuated during hyperoxia, it appears to depend at least in part on stimulation of arterial chemoreceptors.

AB - Obstructive apnea and voluntary breath holding are associated with transient increases in muscle sympathetic nerve activity (MSNA) and arterial pressure. The contribution of changes in blood flow relative to the contribution of changes in vascular resistance to the apnea-induced transient rise in arterial pressure is unclear. We measured heart rate, mean arterial blood pressure (MAP), MSNA (peroneal microneurography), and femoral artery blood velocity (VFA, Doppler) in humans during voluntary end-expiratory apnea while they were exposed to room air, hypoxia (10.5% inspiratory fraction of O2), and hyperoxia (100% inspiratory fraction of O2). Changes from baseline of leg blood flow (Q̇) and vascular resistance (R) were estimated from the following relationships: Q̇ ∝ VFA, corrected for the heart rate, and R ∝ MAP/Q̇. During apnea, MSNA rose; this rise in MSNA was followed by a rise in MAP, which peaked a few seconds after resumption of breathing. Responses of MSNA and MAP to apnea were greatest during hypoxia and smallest during hyperoxia (P < 0.05 for both compared with room air breathing). Similarly, apnea was associated with a decrease in Q̇ and an increase in R. The decrease in Q̇ was greatest during hypoxia and smallest during hyperoxia (-25 ± 3 vs. -6 ± 4%, P < 0.05), and the increase in R was the greatest during hypoxia and the least during hyperoxia (60 ± 8 vs. 21 ± 6%, P < 0.05). Thus voluntary apnea is associated with vasoconstriction, which is in part mediated by the sympathetic nervous system. Because apnea-induced vasoconstriction is most intense during hypoxia and attenuated during hyperoxia, it appears to depend at least in part on stimulation of arterial chemoreceptors.

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