title: Vasoconstrictor responsiveness during hyperbaric hyperoxia in contracting human muscle.
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 < 0.01). At rest, vasoconstriction to tyramine (% decrease from pretyramine values) did not differ between normoxia and hyperoxia (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.
authors.affiliation: Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905, USA. casey.darren@mayo.edu
authors.forename: Darren P
authors.initials: DP
authors.lastname: Casey
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Joyner
authors.forename: Paul L
authors.initials: PL
authors.lastname: Claus
authors.forename: Timothy B
authors.initials: TB
authors.lastname: Curry
mesh_terms: D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D015444:Exercise / Q000502:physiology; D005542:Forearm / Q000098:blood supply*; D006801:Humans; D006931:Hyperbaric Oxygenation; D018496:Hyperoxia / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000502:physiology*; D010646:Phentolamine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology*; D014439:Tyramine / Q000494:pharmacology; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D018759:Adrenergic Uptake Inhibitors; D000317:Adrenergic alpha-Antagonists; D011942:Receptors, Adrenergic, alpha; D014439:Tyramine; D010646:Phentolamine