Christoffer Nyborg

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.

Triathlon and other endurance races have grown in popularity. Although participants are generally fit and presumably healthy, there is measurable morbidity and mortality associated with participation. In triathlon, most deaths occur during the swim leg, and more insight into risk factors, such as hypothermia, is warranted. In this study, we measured the core temperature of 51 participants who ingested temperature sensor capsules before the swim leg of a full-distance triathlon. The water temperature was 14.4–16.4 °C, and the subjects wore wetsuits. One subject with a low body mass index and a long swim time experienced hypothermia (<35 °C). Among the remaining subjects, we found no association between core temperature and swim time, body mass index, or sex. To conclude, the present study indicates that during the swim leg of a full-distance triathlon in water temperatures ≈ 15–16 °C, subjects with a low body mass index and long swim times may be at risk of hypothermia even when wearing wetsuits.

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.

Prolonged exercise is known to cause changes in common biomarkers. Occasionally, competition athletes need medical assistance and hospitalisation during prolonged exercise events. To aid clinicians treating patients and medical teams in such events we have studied common biomarkers after at The Norseman Xtreme Triathlon (Norseman), an Ironman distance triathlon with an accumulated climb of 5200 m, and an Olympic triathlon for comparison. Blood samples were collected before, immediately after, and the day following the Norseman Xtreme Triatlon (n = 98) and Oslo Olympic Triathlon (n = 15). Increased levels of clinical significance were seen at the finish line of the Norseman in white blood cells count (WBC) (14.2 [13.5–14.9] 109/L, p < 0.001), creatinine kinase (CK) (2450 [1620–3950] U/L, p < 0.001) and NT-proBNP (576 [331–856] ng/L, p < 0.001). The following day there were clinically significant changes in CRP (39 [27–56] mg/L, p < 0.001) and Aspartate Aminotransferase (AST) (142 [99–191] U/L, p < 0.001). In comparison, after the Olympic triathlon distance, there were statistically significant, but less clinically important, changes in WBC (7.8 [6.7–9.6] 109/L, p < 0.001), CK (303 [182–393] U/L, p < 0.001) and NT-proBNP (77 [49–88] ng/L, p < 0.01) immediately after the race, and in CRP (2 [1–3] mg/L, p < 0.001) and AST (31 [26–41] U/L, p < 0.01) the following day. Subclinical changes were also observed in Hemoglobin, Thrombocytes, K+, Ca2+, Mg2+, Creatinine, Alanine Aminotransferase and Thyroxine after the Norseman. In conclusion, there were significant changes in biomarkers used in a clinical setting after the Norseman. Of largest clinical importance were clinically significant increased WBC, CRP, AST, CK and NT-proBNP after the Norseman. This is important to be aware of when athletes engaging in prolonged exercise events receive medical assistance or are hospitalised.