Abstract

We assessed endothelial function by flow-mediated dilatation (FMD), levels of the NO-precursor L-arginine, and markers of endothelial inflammation before, at the finish line, and one week after the Norseman Xtreme triathlon. The race is an Ironman distance triathlon with a total elevation of 5200 m. Nine male participants were included. They completed the race in 14.5 (13.4–15.3) h. FMD was significantly reduced to 3.1 (2.1–5.0)% dilatation compared to 8.7 (8.2–9.3)% dilatation before the race (p < 0.05) and was normalized one week after the race. L-arginine showed significantly reduced levels at the finish line (p < 0.05) but was normalized one week after the race. Markers of endothelial inflammation E-Selectin, VCAM-1, and ICAM-1 all showed a pattern with increased values at the finish line compared to before the race (all p < 0.05), with normalization one week after the race. In conclusion, we found acutely reduced FMD with reduced L-arginine levels and increased E-Selectin, VCAM-1, and ICAM-1 immediately after the Norseman Xtreme triathlon. Our findings indicate a transient reduced endothelial function, measured by the FMD-response, after prolonged strenuous exercise that could be explained by reduced NO-precursor L-arginine levels and increased endothelial inflammation.

Highlights

  • There are few studies of how prolonged exercise affects the flow-mediated dilatation (FMD)-response [6,16,17] and as far as we are aware there are no studies of FMD after any Ironman distance triathlon

  • Nine male participants of the Norseman Xtreme Triathlon were included in this study

  • We found increased levels of the endothelial adhesion molecules E-selectin, ICAM-1, and VCAM-1 after the Ironman distance triathlon, along with reduced FMD

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Summary

Introduction

Flow-mediated dilatation (FMD) refers to the non-invasive assessment of endothelial function by studying the brachial artery’s dilatation in response to increased blood flow [1]. The dilatation is endothelial-dependent [2] as increased shear forces from the blood activate mechanoreceptors in the endothelium [3], causing a predominantly NO-mediated relaxation of the arterial smooth muscles [4]. A biphasic response has been proposed with an initial reduction in FMD after exercise with normalization within 24–48 h [17]. There are few studies of how prolonged exercise affects the FMD-response [6,16,17] and as far as we are aware there are no studies of FMD after any Ironman distance triathlon

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