Abstract
Endothelial vasodilatory function is dependent on the NO synthesis from L-arginine by endothelial NO-synthetase (eNOS). eNOS can be inhibited by asymmetric dimethylarginine (ADMA) by competitive inhibition on the binding site, and symmetric dimethylarginine (SDMA) can reduce the L-arginine availability intracellularly through competing for transport over the cellular membrane. To study the NO synthesis after prolonged exercise, we assessed circulatory L-arginine, the L-arginine/ADMA ratio, and SDMA before, after, and on the day after the Norseman Xtreme triathlon, an Ironman distance triathlon. We found significantly reduced levels of L-arginine and the L-arginine/ADMA ratio and increased levels of SDMA after the race (all p < 0.05). L-arginine rose toward baseline levels the day after the race, but ADMA increased beyond baseline levels, and SDMA remained above baseline the day after the race. The reduced levels of L-arginine and the L-arginine/ADMA ratio, and increased SDMA, after the race indicate a state of reduced capability of NO production. Increased levels of ADMA and SDMA, and reduced L-arginine/ADMA ratio, as seen the day after the race, are known risk markers of atherosclerosis and warrant further studies.
Highlights
Prolonged exercise is known to induce many physiological changes, including alteration of the circulatory inflammatory biomarkers [1,2,3,4] and plasma levels of essential nutrients [5]
Larginine and asymmetric dimethylarginine (ADMA) were significantly reduced at the end of the race, with a reduced L-arginine/ADMA ratio
Both plasma levels of L-arginine and ADMA inclined to the day after the race
Summary
Prolonged exercise is known to induce many physiological changes, including alteration of the circulatory inflammatory biomarkers [1,2,3,4] and plasma levels of essential nutrients [5]. Endothelial function was measured with flow-mediated dilation (FMD) [6]. FMD is measured by studying brachial artery dilatation in response to increased blood flow after a 5 min occlusion of the lower arm at rest [7]. Previous studies of amino acids after exercise have shown a generally reduced level of amino acid-bound nitrogen in prolonged exercise [13] and reduced L-arginine after marathons [14,15]. This reduction is believed to be due to increased gluconeogenesis and enhanced NO production during prolonged exercise [13,14]. Low levels of L-arginine could, in part, explain the reduced endothelial function after prolonged exercise, as described in our previous study [6]
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