News Release

Why nitrate supplementation may increase athletic performance

New research in The FASEB Journal suggests that nitrate -- a nitric oxide metabolite -- meets tissue oxygen demands without the side effects of increasing red blood cells or blood viscosity

Peer-Reviewed Publication

Federation of American Societies for Experimental Biology

Walk down the aisles of any food supplement store and you'll see that the use of nitrate supplements by athletes and fitness buffs has been popular for years. The hope is that these supplements will increase endurance (and possibly other performance/health benefits) by improving the efficiency at which muscles use oxygen. Now, a research study published in the March 2015 issue of The FASEB Journal helps explain how some of these supplements may work and why they may increase performance--they decrease the viscosity of blood, aiding in blood flow, while at the same time ensuring that tissue oxygen requirements are not compromised.

"Our research sheds new light on how oxygen delivery to bodily tissues is controlled to support mammalian life, and what role the kidneys and the liver play in achieving this," said Andrew Murray, Ph.D., a researcher involved in the work from the Department of Physiology, Development and Neuroscience at the University of Cambridge in Cambridge, United Kingdom. "These findings offer potential therapeutic avenues for dietary intervention in polycythemia and other conditions that warrant a reduction in red cell mass, but may have broader implications related to the way that supply and demand of oxygen are matched."

Scientists investigated the effects of nitrate supplementation on hemoglobin in four groups of rats, which were housed in either normoxic or hypoxic (low oxygen) conditions and supplemented with sodium nitrate (or sodium chloride, ordinary table salt, as a control). Intake of nitrate via diet and drinking water was carefully monitored. Hypoxia is known to elevate hemoglobin levels, but nitrate supplementation at a moderate dose largely suppressed this effect. Unexpectedly, nitrate also lowered hemoglobin levels in normoxic animals. They found that at higher doses of nitrate, hemoglobin levels began to rise again. Researchers investigated the mechanisms underlying these effects and found that the suppression of hemoglobin was due to nitrate enhancing liver oxygenation and suppressing its expression of the hormone, erythropoietin. Conversely, as hemoglobin levels fell, the kidney became less well supplied with oxygen and at higher doses of nitrate it expressed more erythropoietin, reversing the effect.

"This doesn't mean that taking a nitrate supplement will transform you into the next Marshawn Lynch," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "What it does mean, however, is that we're beginning to understand the science behind why some people feel they turn into the Seahawk's 'Beast Mode' when taking these supplements."

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Receive monthly highlights from The FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx. The FASEB Journal is published by the Federation of the American Societies for Experimental Biology (FASEB). It is the world's most cited biology journal according to the Institute for Scientific Information and has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century.

FASEB is composed of 27 societies with more than 120,000 members, making it the largest coalition of biomedical research associations in the United States. Our mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

Details: Tom Ashmore, Bernadette O. Fernandez, Colin E. Evans, Yun Huang, Cristina Branco-Price, Julian L. Griffin, Randall S. Johnson, Martin Feelisch, and Andrew J. Murray. Suppression of erythropoiesis by dietary nitrate. FASEB J. March 2015 29:1102-1112; doi:10.1096/fj.14-263004 ; http://www.fasebj.org/content/29/3/1102.abstract


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