PMID: 11927694Apr 3, 2002Paper

Nitric oxide-dependent modulation of sympathetic neural control of oxygenation in exercising human skeletal muscle

The Journal of Physiology
Bahman ChavoshanGail D Thomas

Abstract

Nitric oxide (NO) attenuates alpha-adrenergic vasoconstriction in contracting rodent skeletal muscle, but it is unclear if NO plays a similar role in human muscle. We therefore hypothesized that in humans, NO produced in exercising skeletal muscle blunts the vasoconstrictor response to sympathetic activation. We assessed vasoconstrictor responses in the microcirculation of human forearm muscle using near-infrared spectroscopy to measure decreases in muscle oxygenation during reflex sympathetic activation evoked by lower body negative pressure (LBNP). Experiments were performed before and after NO synthase inhibition produced by systemic infusion of N(G)-nitro-L-arginine methyl ester (L-NAME). Before L-NAME, LBNP at -20 mmHg decreased muscle oxygenation by 20 +/- 2 % in resting forearm and by 2 +/- 3 % in exercising forearm (n = 20), demonstrating metabolic modulation of sympathetic vasoconstriction. As expected, L-NAME increased mean arterial pressure by 17 +/- 3 mmHg, leading to baroreflex-mediated suppression of baseline muscle sympathetic nerve activity (SNA). The increment in muscle SNA in response to LBNP at -20 mmHg also was attenuated after L-NAME (before, +14 +/- 2; after, +8 +/- 1 bursts min(-1); n = 6), but this effec...Continue Reading

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Citations

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