The catecholamines strike back. What NO does not do.

**Will Brink** · 08-19-2010, 11:17 AM

In the 90s, a number of studies suggested that exercised induced hyperemia may be mediated by Nitric Oxide (NO). This lead in large part to the whole NO supplement category craze as the angle was increased NO (using arginine and other NO precursors) would lead to improved blood flow to muscle with an improved "pump" and more muscle growth, etc, etc. Recent studies however suggest NO plays a minor role in exercise induced vasodilation to muscles. This is not the end of NO by any means as it's an extremely complex - and yet to be fully understood - system, but it seems research is starting to put the breaks on the effects of NO as a vasodilator during exercise specifically:

Circ J. 2009 Oct;73(10):1783-92. Epub 2009 Sep 4.
The catecholamines strike back. What NO does not do.

Joyner MJ, Casey DP.

Department of Anesthesiology, Mayo Clinic,Rochester, MN 55905, USA. [email protected]
Abstract

The discovery of endothelial-derived relaxing factor, and later nitric oxide (NO), as a biologically active substance led to intense focus on the vascular endothelium as a major site of physiological regulation and pathophysiological dysfunction. NO is clearly a potent vasodilator and plays a key role in establishing both whole body and regional "vascular tone". In this context, skeletal muscle and human skin have the remarkable capacity to increase their blood flow 50-100-fold and this increase is caused almost exclusively by local vasodilation.

In general, the mechanisms responsible for these vasodilator phenomena have been poorly understood. In the early 1990s, investigators started to ask if NO might explain the "unexplained" vasodilator responses seen in skeletal muscle and skin. They also asked how "NO tone" interacted with "sympathetic tone" and whether NO can override the vasoconstrictor responses normally generated when sympathetic nerves release norepinephrine.

Surprisingly, it was found that NO plays only a modest (non-obligatory) role in exercise hyperemia, reactive hyperemia and the neurally mediated rise in skin blood flow during whole body heat stress. By contrast, NO plays a major role in the skeletal muscle vasodilator responses to mental stress and the skin dilator responses to local heating. In animals, but not humans, NO can limit the ability of the sympathetic nerves to cause vasoconstriction in exercising muscles.

Thus the role of NO in two of the most extreme dilator responses seen in nature is limited and in muscle the sympathetic nerves can restrain the dilation to defend arterial blood pressure.