Journal article
Nitric oxide-mediated vasodilation becomes independent of β-adrenergic receptor activation with increased intensity of hypoxic exercise
Journal of applied physiology (1985), Vol.110(3), pp.687-694
03/2011
DOI: 10.1152/japplphysiol.00787.2010
PMCID: PMC3069624
PMID: 21193565
Abstract
Hypoxic vasodilation in skeletal muscle at rest is known to include β-adrenergic receptor-stimulated nitric oxide (NO) release. We previously reported that the augmented skeletal muscle vasodilation during mild hypoxic forearm exercise includes β-adrenergic mechanisms. However, it is unclear whether a β-adrenergic receptor-stimulated NO component exists during hypoxic exercise. We hypothesized that NO-mediated vasodilation becomes independent of β-adrenergic receptor activation with increased exercise intensity during hypoxic exercise. Ten subjects (7 men, 3 women; 23 ± 1 yr) breathed hypoxic gas to titrate arterial O
2
saturation to 80% while remaining normocapnic. Subjects performed two consecutive bouts of incremental rhythmic forearm exercise (10% and 20% of maximum) with local administration (via a brachial artery catheter) of propranolol (β-adrenergic receptor inhibition) alone and with the combination of propranolol and nitric oxide synthase inhibition [
N
G
-monomethyl-
l
-arginine (
l
-NMMA)] under normoxic and hypoxic conditions. Forearm blood flow (FBF, ml/min; Doppler ultrasound) and blood pressure [mean arterial pressure (MAP), mmHg; brachial artery catheter] were assessed, and forearm vascular conductance (FVC, ml·min
−1
·100 mmHg
−1
) was calculated (FBF/MAP). During propranolol alone, the rise in FVC (Δ from normoxic baseline) due to hypoxic exercise was 217 ± 29 and 415 ± 41 ml·min
−1
·100 mmHg
−1
(10% and 20% of maximum, respectively). Combined propranolol-
l
-NMMA infusion during hypoxic exercise attenuated ΔFVC at 20% (352 ± 44 ml·min
−1
·100 mmHg
−1
;
P
< 0.001) but not at 10% (202 ± 28 ml·min
−1
·100 mmHg
−1
;
P
= 0.08) of maximum compared with propranolol alone. These data, when integrated with earlier findings, demonstrate that NO contributes to the compensatory vasodilation during mild and moderate hypoxic exercise; a β-adrenergic receptor-stimulated NO component exists during low-intensity hypoxic exercise. However, the source of the NO becomes less dependent on β-adrenergic mechanisms as exercise intensity increases.
Details
- Title: Subtitle
- Nitric oxide-mediated vasodilation becomes independent of β-adrenergic receptor activation with increased intensity of hypoxic exercise
- Creators
- Darren P Casey - Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota; andTimothy B Curry - Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota; andBrad W Wilkins - Nike Sport Research Laboratory, Nike Incorporated, Beaverton, OregonMichael J Joyner - Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota; and
- Resource Type
- Journal article
- Publication Details
- Journal of applied physiology (1985), Vol.110(3), pp.687-694
- DOI
- 10.1152/japplphysiol.00787.2010
- PMID
- 21193565
- PMCID
- PMC3069624
- NLM abbreviation
- J Appl Physiol (1985)
- ISSN
- 8750-7587
- eISSN
- 1522-1601
- Publisher
- American Physiological Society; Bethesda, MD
- Language
- English
- Date published
- 03/2011
- Academic Unit
- Physical Therapy and Rehabilitation Science; Fraternal Order of Eagles Diabetes Research Center
- Record Identifier
- 9984046820402771
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