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.

Objective. Asthma is a common problem among elite athletes and represents a health risk interfering with the athlete’s performance status. This study aimed to evaluate the asthma prevalence among Norwegian summer and winter elite athletes and asthma prevalence across sport categories. We also aimed to examine whether bronchial hyperresponsiveness (BHR), lung function, fraction of exhaled nitric oxide (FE_NO), and allergy status differed between asthmatic and non-asthmatic elite athletes. Methods. Norwegian athletes qualifying for the Beijing Olympic Summer Games 2008 (n = 80) and the Vancouver Olympic Winter Games 2010 (n = 55) were included. The athletes underwent clinical respiratory examination including lung function measurement, methacholine bronchial challenge for assessment of BHR, FE_NO, and skin prick testing. Asthma was diagnosed based on respiratory symptoms and clinical examination including objective measurements. Results. Asthma was more prevalent among winter athletes (50%) than summer athletes (20%). Thirty-three (52%) endurance athletes, 3 (6%) team sport athletes, and 7 (33%) technical sport athletes had medically diagnosed asthma. Significantly lower lung function ( ) and higher prevalence of severe BHR ( ) were found in asthmatic athletes compared with non-asthmatic athletes. Conclusion. Asthma is common among Norwegian elite athletes, with winter and endurance athletes showing the highest prevalence. Asthmatic athletes were characterized by lower lung function and more severe BHR compared with non-asthmatic counterparts. The high prevalence among winter and endurance athletes demonstrates a need for increased attention to prevent and reduce the prevalence of asthma among those athletes.

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.

Anabolic-androgenic steroids (AAS) are commonly used by recreational weightlifters for performance enhancement, despite associated health risks, including cardiovascular and brain effects. This study investigates the cerebrovascular effects of prolonged AAS use in male weightlifters, focusing on cerebral blood flow (CBF) and other indicators of cerebrovascular health. Eighty-six males were included, with 41 current consumers of AAS and 45 non-using weightlifting controls. Cerebrovascular health was evaluated using magnetic resonance imaging (MRI) pseudo-continuous arterial spin labeling (PCASL) derivatives to measure CBF and spatial coefficient of variation (sCoV) of CBF in gray matter. Additionally, MRI T2-weighted fluid-attenuated inversion recovery (FLAIR) sequences were used to analyze white matter hyperintensities as a marker of small-vessel disease. AAS consumers had significantly higher sCoV than weightlifting controls (p = 0.001). Further, sCoV in total gray matter correlated with testosterone/epitestosterone ratio and total years of AAS use. No significant differences were found in CBF or white matter hyperintensity volume. These findings indicate that long-term AAS use may impact cerebrovascular health, evidenced by increased sCoV. Although cerebral perfusion was unaffected, elevated sCoV suggest that AAS use may pose a risk for cerebrovascular pathology later in life.