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Transient Reduction of FMD-Response and L-Arginine Accompanied by Increased Levels of E-Selectin, VCAM, and ICAM after Prolonged Strenuous Exercise.

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.

SUBMITTER: Nyborg C

PROVIDER: S-EPMC8234080 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Atherosclerosis (AS) is a chronic pathophysiological process that causes high mortality and morbidity. It has previously been reported that homeobox A9 (HOXA9) may participate in regulation of the cardiovascular system and the pathology of AS by upregulating E-selectin and vascular cell adhesion molecule-1 (VCAM-1). Thus, inhibiting HOXA9 could promote microcirculation of coronary arteries and could act as a potential therapy for AS treatment. Sprague-Dawley rats were randomly divided into four groups, as follows: i) AS; ii) AS + HOXA9 inhibitor; iii) AS + small interfering RNA-HOXA9 and iv) normal control. ELISA was used to measure the levels of TNF-α, IL-1β, IL-12, C-C motif chemokine ligand 25 (CCL25), low-density lipoprotein (LDL), high-density lipoprotein (HDL) and very-low-density lipoprotein (VLDL). Flow cytometry was employed to detect the content of M1 macrophages. Hematoxylin & eosin (H&E) staining was performed to observe the morphology of the coronary arteries. Oil red O staining was conducted for the evaluation of lipid accumulation. Immunohistochemistry was used to visualize the protein expression levels of HOXA9 in the coronary arteries. Western blotting was utilized to determine the protein expression levels of HOXA9, platelet factor-4 (PF4), E-selectin and VCAM-1. HOXA9 inhibitors were found to downregulate the levels of TNF-α, IL-1β, IL-12, CCL25, LDL and VLDL, and upregulate HDL levels in the blood of AS rats. The content of M1 macrophages was also decreased following injection of HOXA9 inhibitors in the AS group. H&E and oil red O staining analysis indicated that HOXA9 inhibitors attenuated vascular symptoms and lipid formation in AS rats. Furthermore, western blotting suggested that inhibition of HOXA9 reduced the expression levels of PF4, E-selectin and VCAM-1, while overexpression of PF4 resulted in the opposite effects. The present study revealed that inhibiting HOXA9 alleviated the symptoms of AS via downregulation of the PF4 and E-selectin/VCAM-1 pathway to promote microcirculation in the coronary arteries of AS rats. These findings indicated that HOXA9 inhibitors may have the potential to succeed in the treatment of AS.

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Transient Reduction of FMD-Response and L-Arginine Accompanied by Increased Levels of E-Selectin, VCAM, and ICAM after Prolonged Strenuous Exercise.

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