Key result
In the absence of overlying vasoconstriction, the contribution of beta-adrenergic mechanisms to augmented hypoxic vasodilatation is dependent on exercise intensity.
Why the study?
Does beta-adrenoceptor activation contribute to augmented hypoxic exercise vasodilatation in humans?
Population
14 human subjects, mean age 29 +/- 2 years
Comparison
Alpha-adrenoceptor inhibition and combined… vs Control under the same normoxic and hypoxic…
Design
Other
Authors
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Beta-adrenergic contribution to hypoxic vasodilatation may vary by intensity; hypothesis-generating for vascular control mechanisms without clinical implications yet.
Does beta-adrenoceptor activation contribute to augmented hypoxic exercise vasodilatation in humans?
p-value: p=<0.05
The contribution of beta-adrenergic mechanisms to augmented hypoxic vasodilatation is dependent on exercise intensity, playing a significant role at lower but not higher intensities.
Wilkins et al. (2007) studied this question. Combined alpha- and beta-adrenoceptor inhibition (phentolamine/propranolol) vs. Saline (control) and alpha-adrenoceptor inhibition (phentolamine) was evaluated on Change in forearm blood flow during 10% and 20% hypoxic exercise (p=<0.05). In the absence of overlying vasoconstriction, the contribution of beta-adrenergic mechanisms to augmented hypoxic vasodilatation is dependent on exercise intensity.
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