What is the clinical evidence from this study?

Study design: Other. Population: Healthy (n=9). Intervention: Hyperbaric hyperoxia vs. Normoxia (1 ATA while breathing 21% O2). Primary outcome: Vasoconstrictor responsiveness to tyramine during exercise (% decrease in forearm blood flow) (p=<0.05).

November 16, 2012

Vasoconstrictor responsiveness during hyperbaric hyperoxia in contracting human muscle

Q: What are the key findings of this study?

Hyperbaric hyperoxia slightly increased vasoconstrictor responsiveness during exercise compared to normoxia (-22% vs -17%), but this did not fully explain the 20-25% reduction in forearm blood flow.

Key Result

Hyperbaric hyperoxia slightly increased vasoconstrictor responsiveness during exercise compared to normoxia (-22% vs -17%), but this did not fully explain the 20-25% reduction in forearm blood flow.

Structured PICO

Does hyperbaric hyperoxia alter functional sympatholysis and vasoconstrictor responsiveness during forearm exercise in healthy young men?

Population

9 healthy young male subjects, mean age 28 ± 1 yr, non-obese (BMI 25 ± 1 kg/m2), non-smokers, taking no medications.

Intervention

Hyperbaric hyperoxia (2.82 atmospheres absolute while breathing 100% O2) during rhythmic forearm exercise at 20% maximal voluntary contraction, with and without intra-arterial tyramine or phentolamine.

Comparator

Normobaric normoxia (1 atmosphere absolute while breathing 21% O2) during the same exercise protocol.

Outcome

Forearm blood flow (FBF), forearm vascular conductance (FVC), and vasoconstrictor responsiveness to intra-arterial tyramine.surrogate

The substantial reductions in skeletal muscle blood flow during hyperbaric hyperoxic exercise are not primarily explained by an attenuation of functional sympatholysis or greater alpha-adrenergic vasoconstriction.

Main Result

Absolute Event Rate: -22% vs -17%

p-value: p=<0.05

Limitations

Findings are limited to data derived from young men, so sex-specific differences cannot be excluded.
Unable to directly measure arterial and venous blood gases due to maximal PO2 limits of commercially available analyzers.
Unable to calculate or determine whether oxygen consumption in the active forearm was different between trials.
Tyramine infusion method cannot exclude the possibility that attenuated blood flow is due to enhanced sympathetic outflow.

Abstract

Large increases in systemic oxygen content cause substantial reductions in exercising forearm blood flow (FBF) due to increased vascular resistance. We hypothesized that 1) functional sympatholysis (blunting of sympathetic α-adrenergic vasoconstriction) would be attenuated during hyperoxic exercise and 2) α-adrenergic blockade would limit vasoconstriction during hyperoxia and increase FBF to levels observed under normoxic conditions. Nine male subjects (age 28 ± 1 yr) performed forearm exercise (20% of maximum) under normoxic and hyperoxic conditions. Studies were performed in a hyperbaric chamber at 1 atmosphere absolute (ATA; sea level) while breathing 21% O(2) and at 2.82 ATA while breathing 100% O(2) (estimated change in arterial O(2) content ∼6 ml O(2)/100 ml). FBF (ml/min) was measured using Doppler ultrasound. Forearm vascular conductance (FVC) was calculated from FBF and blood pressure (arterial catheter). Vasoconstrictor responsiveness was determined using intra-arterial tyramine. FBF and FVC were substantially lower during hyperoxic exercise than normoxic exercise (∼20-25%; P 0.05). During exercise, vasoconstrictor responsiveness was slightly greater during hyperoxia than normoxia (-22 ± 3 vs. -17 ± 2%; P < 0.05). However, during α-adrenergic blockade, hyperoxic exercise FBF and FVC remained lower than during normoxia (P < 0.01). Therefore, our data suggest that although the vasoconstrictor responsiveness during hyperoxic exercise was slightly greater, it likely does not explain the majority of the large reductions in FBF and FVC (∼20-25%) during hyperbaric hyperoxic exercise.

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