Contraction-induced inhibition of sympathetic vasoconstriction in humans: Evidence from Doppler and NIRS.
Research field:Cardiovascular physiology
Authors:Nilakantan JB, Hanada A, Hansen J
Address of presenting
author:		Jaya B. Nilakantan, MD
Copenhagen Muscle Research Center
Rigshospitalet Section 7652
Blegdamsvej 9,
DK-2100 Ø Copenhagen
Denmark
E-mail:jaya@dadlnet.dk
Phone:+45 35457614
Fax:+45 35457634
Text of abstract Introduction
Many of the circulatory adjustments to exercise are produced by activation of the sympathetic nervous system. In resting skeletal muscle, sympathetic activation produces vasoconstriction. In contracting muscle, it has been suggested that sympathetic vasoconstriction is largely negated by metabolic vasodilation thereby optimizing oxygen delivery to active muscle, a phenomenon termed functional sympatholysis (Remensnyder et al. 1962). However, this phenomenon has been difficult to demonstrate in humans. Using Near Infrared Spectroscopy (NIRS) measurements of muscle tissue oxygenation to estimate sympathetic vasoconstrictor responses, we have previously provided indirect evidence for functional sympatholysis in the human forearm (Hansen et al. 1996): reflex activation of sympathetic vasoconstrictor nerves with lower body negative pressure (LBNP) consistently decreased oxygenation in resting muscle, but had no effect on oxygenation when the same muscles were exercised. We now aimed to more directly test the hypothesis that muscle contraction attenuates sympathetic neural vasoconstriction in the human forearm.

Methods
In 11 healthy volunteers (25±2 years) we used image-guided Doppler velocimetry to measure blood flow in the brachial artery and NIRS to estimate changes in oxygenation in the flexor digitorum profundus muscle in response to reflex sympathetic activation with non-hypotensive LBNP (-20 mmHg for 2 min). Measurements were performed at rest and during a 5 min bout of ipsilateral rhythmic handgrip (RHG) at 25% of maximum. To further validate the ability of NIRS to detect vasoconstriction in resting vs. contracting muscle, we also examined the change in oxygenation produced by a given reduction in blood flow (by manual compression of the brachial artery) at rest and during handgrip.

Results
With the forearm at rest, LBNP reduced blood flow by 73±12 ml/min wich was accompanied by a fall in muscle oxygenation of 16±2% of the total labile signal (TLS, the maximal decrease with complete forearm occlusion), p less than 0.05. Handgrip alone produced steady state increases in brachial artery flow (from 125±20 to 227±26 ml/min, p less than 0.05) and decreased oxygenation by –29±5% TLS, p less than 0.05. The main finding is that the effect of LBNP on flow as well as oxygenation was greatly attenuated during handgrip: when superimposed during steady-state handgrip LBNP only reduced flow by -22±11 ml/min and oxygenation by -5±2% TLS (p less than 0.05 vs. response at rest). In addition, brachial artery compression performed to produce comparable reductions in blood flow at rest and during handgrip (-84±18 vs. -83±13 ml/min, p=ns) tended to produce a greater fall in oxygenation in exercising than in resting muscle (–29±5 vs. -12±3 %TLS, p=0.06).

Conclusions
These data in humans indicate that NIRS is a sensitive index of vasoconstrictor responses in the forearm, and provide direct evidence for contraction-induced inhibition of sympathetic vasoconstriction in skeletal muscle.

References
Hansen J et al. 1996. J Clin Invest 98,584-96.
Remensnyder JP et al. 1962. Circ Res 11, 370-80.

Keywords:skeletal muscle blood flow, exercise, sympathetic nervous system, skeletal muscle oxygenation

Created 2000-05-02