Skip Navigation LinksHome > May 2003 - Volume 35 - Issue 5 > BLUNTED SYMPATHETIC NEURAL VASOCONSTRICTION DURING HANDGRIP...
Medicine & Science in Sports & Exercise:
Functional Sympatholysis: Integrated Vascular Regulation in Active Skeletal Muscle

BLUNTED SYMPATHETIC NEURAL VASOCONSTRICTION DURING HANDGRIP EXERCISE IN HUMANS: ROLE FOR NITRIC OXIDE?

Dinenno, F A.1; Joyner, M J.1

Free Access
Article Outline
Collapse Box

Author Information

1Mayo Clinic and Foundation, Rochester, Minnesota 55905

In experimental animals, sympathetic neural vasoconstriction is blunted in the vascular beds of contracting compared with resting skeletal muscle, and nitric oxide (NO) is thought to be the primary factor involved. To date, the only data in humans are derived from vasoconstrictor responses obtained via indirect measurements of muscle oxygenation during reflex increases in sympathetic nerve activity, and have supported a role for NO in mediating this blunted vasoconstriction during exercise.

Back to Top | Article Outline

PURPOSE

To determine the role of NO in the blunted vasoconstrictor responses to endogenous norepinephrine release in contracting human muscle.

Back to Top | Article Outline

METHODS

Forearm blood flow (FBF; doppler Ultrasound) and mean arterial blood pressure (MAP; brachial artery catheter) were measured, and forearm vascular conductance (FVC) calculated (FBF/MAP*100) during steady-state rhythmic handgrip exercise (10–15% MVC) and steady-state control non-exercise vasodilator infusions (adenosine). The vasoconstrictor responses to 2 doses of tyramine were determined during exercise and adenosine administration, before and after NO synthase (NOS) inhibition with L-NMMA (n = 6) or L-NAME (n = 4).

Back to Top | Article Outline

RESULTS

The percentage reductions in FVC to tyramine were significantly less during exercise (−21 ± 4 and −22 ± 3%) compared with adenosine (−53 ± 5 and −69 ± 5%; P < 0.001), despite similar steady-state FVC. The vasoconstrictor responses to tyramine were still significantly less during exercise after L-NMMA (−20 ± 2 and −22 ± 2%) and L-NAME (−15 ± 5 and −28 ± 2%) compared with adenosine (−42 ± 5 and −62 ± 5%). Importantly, local NOS inhibition did not reverse the blunted vasoconstrictor responses to tyramine observed during exercise.

Back to Top | Article Outline

CONCLUSION

Our preliminary results challenge the hypothesis that NO plays an obligatory role in the blunted sympathetic vasoconstrictor responses during rhythmic handgrip exercise in humans.

©2003The American College of Sports Medicine

Login

Article Tools

Share

Connect With Us