Systemic hypoxia and vasoconstrictor responsiveness in exercising human muscle

Brad W. Wilkins, William G. Schrage, Zhong Liu, Kellie C. Hancock, Michael Joseph Joyner

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Exercise blunts sympathetic α-adrenergic vasoconstriction (functional sympatholysis). We hypothesized that sympatholysis would be augmented during hypoxic exercise compared with exercise alone. Fourteen subjects were monitored with ECG and pulse oximetry. Brachial artery and antecubital vein catheters were placed in the nondominant (exercising) arm. Subjects breathed hypoxic gas to titrate arterial O2 saturation to 80% while remaining normocapnic via a rebreath system. Baseline and two 8-min bouts of rhythmic forearm exercise (10 and 20% of maximum) were performed during normoxia and hypoxia. Forearm blood flow, blood pressure, heart rate, minute ventilation, and end-tidal CO2 were measured at rest and during exercise. Vasoconstrictor responsiveness was determined by responses to intraarterial tyramine during the final 3 min of rest and each exercise bout. Heart rate was higher during hypoxia (P < 0.01), whereas blood pressure was similar (P = 0.84). Hypoxic exercise potentiated minute ventilation compared with normoxic exercise (P < 0.01). Forearm blood flow was higher during hypoxia compared with normoxia at rest (85 ± 9 vs. 66 ± 7 ml/min), at 10% exercise (276 ± 33 vs. 217 ± 27 ml/min), and at 20% exercise (464 ± 32 vs. 386 ± 28 ml/min; P < 0.01). Arterial epinephrine was higher during hypoxia (P < 0.01); however, venoarterial norepinephrine difference was similar between hypoxia and normoxia before (P = 0.47) and during tyramine administration (P = 0.14). Vasoconstriction to tyramine (%decrease from pretyramine values) was blunted in a dose-dependent manner with increasing exercise intensity (P < 0.01). Interestingly, vasoconstrictor responsiveness tended to be greater (P = 0.06) at rest (-37 ± 6% vs. -33 ± 6%), at 10% exercise (-27 ± 5 vs. -22 ± 4%), and at 20% exercise (-22 ± 5 vs. -14 ± 4%) between hypoxia and normoxia, respectively. Thus sympatholysis is not augmented by moderate hypoxia nor does it contribute to the increased blood flow during hypoxic exercise.

Original languageEnglish (US)
Pages (from-to)1343-1350
Number of pages8
JournalJournal of Applied Physiology
Volume101
Issue number5
DOIs
StatePublished - 2006

Fingerprint

Vasoconstrictor Agents
Muscles
Tyramine
Forearm
Vasoconstriction
Ventilation
Heart Rate
Blood Pressure
Oximetry
Brachial Artery
Hypoxia
Adrenergic Agents
Epinephrine
Veins
Norepinephrine
Electrocardiography
Arm
Catheters
Gases

Keywords

  • Catecholamines
  • Doppler ultrasound
  • Exercise hyperemia

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Systemic hypoxia and vasoconstrictor responsiveness in exercising human muscle. / Wilkins, Brad W.; Schrage, William G.; Liu, Zhong; Hancock, Kellie C.; Joyner, Michael Joseph.

In: Journal of Applied Physiology, Vol. 101, No. 5, 2006, p. 1343-1350.

Research output: Contribution to journalArticle

Wilkins, Brad W. ; Schrage, William G. ; Liu, Zhong ; Hancock, Kellie C. ; Joyner, Michael Joseph. / Systemic hypoxia and vasoconstrictor responsiveness in exercising human muscle. In: Journal of Applied Physiology. 2006 ; Vol. 101, No. 5. pp. 1343-1350.
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abstract = "Exercise blunts sympathetic α-adrenergic vasoconstriction (functional sympatholysis). We hypothesized that sympatholysis would be augmented during hypoxic exercise compared with exercise alone. Fourteen subjects were monitored with ECG and pulse oximetry. Brachial artery and antecubital vein catheters were placed in the nondominant (exercising) arm. Subjects breathed hypoxic gas to titrate arterial O2 saturation to 80{\%} while remaining normocapnic via a rebreath system. Baseline and two 8-min bouts of rhythmic forearm exercise (10 and 20{\%} of maximum) were performed during normoxia and hypoxia. Forearm blood flow, blood pressure, heart rate, minute ventilation, and end-tidal CO2 were measured at rest and during exercise. Vasoconstrictor responsiveness was determined by responses to intraarterial tyramine during the final 3 min of rest and each exercise bout. Heart rate was higher during hypoxia (P < 0.01), whereas blood pressure was similar (P = 0.84). Hypoxic exercise potentiated minute ventilation compared with normoxic exercise (P < 0.01). Forearm blood flow was higher during hypoxia compared with normoxia at rest (85 ± 9 vs. 66 ± 7 ml/min), at 10{\%} exercise (276 ± 33 vs. 217 ± 27 ml/min), and at 20{\%} exercise (464 ± 32 vs. 386 ± 28 ml/min; P < 0.01). Arterial epinephrine was higher during hypoxia (P < 0.01); however, venoarterial norepinephrine difference was similar between hypoxia and normoxia before (P = 0.47) and during tyramine administration (P = 0.14). Vasoconstriction to tyramine ({\%}decrease from pretyramine values) was blunted in a dose-dependent manner with increasing exercise intensity (P < 0.01). Interestingly, vasoconstrictor responsiveness tended to be greater (P = 0.06) at rest (-37 ± 6{\%} vs. -33 ± 6{\%}), at 10{\%} exercise (-27 ± 5 vs. -22 ± 4{\%}), and at 20{\%} exercise (-22 ± 5 vs. -14 ± 4{\%}) between hypoxia and normoxia, respectively. Thus sympatholysis is not augmented by moderate hypoxia nor does it contribute to the increased blood flow during hypoxic exercise.",
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