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Department of Anesthesiology and General Clinical Research Center, Mayo Clinic and Foundation, Rochester, Minnesota 55905
An acute bout of aerobic exercise
results in a reduced blood pressure that lasts several hours. Animal
studies suggest this response is mediated by increased production of
nitric oxide. We tested the extent to which systemic nitric oxide
synthase inhibition [NG-monomethyl-L-arginine
(L-NMMA)] can reverse the drop in blood pressure that
occurs after exercise in humans. Eight healthy subjects underwent parallel experiments on 2 separate days. The order of the
experiments was randomized between sham (60 min of seated upright rest)
and exercise (60 min of upright cycling at 60% peak aerobic capacity).
After both sham and exercise, subjects received, in sequence, systemic
-adrenergic blockade (phentolamine) and L-NMMA.
Phentolamine was given first to isolate the contribution of nitric
oxide to postexercise hypotension by preventing reflex changes in
sympathetic tone that result from systemic nitric oxide synthase
inhibition and to control for alterations in resting sympathetic
activity after exercise. During each condition, systemic and regional
hemodynamics were measured. Throughout the study, arterial pressure and
vascular resistances remained lower postexercise vs. postsham despite
nitric oxide synthase inhibition (e.g., mean arterial pressure after
L-NMMA was 108.0 ± 2.4 mmHg postsham vs. 102.1 ± 3.3 mmHg postexercise; P < 0.05). Thus it does not
appear that postexercise hypotension is dependent on increased
production of nitric oxide in humans.
exercise; vasodilator agents; blood pressure; sympathetic nervous system; vascular resistance
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