Exercise-Induced Hyperhomocysteinemia Is Not Related to Oxidative Damage or Impaired Vascular Function in Amateur Middle-Aged Runners under Controlled Nutritional Intake

• Published in: Nutrients 2021-08, Vol.13 (9), p.3033
• Main Authors: Iglesias-Gutiérrez, Eduardo, García-González, Ángela, Montero-Bravo, Ana, González-Medina, Antonio, Joglar, Judit, Tomás-Zapico, Cristina, Fernández-García, Benjamín, Fernández-Sanjurjo, Manuel, de Gonzalo-Calvo, David, Díaz-Martínez, Ángel Enrique, Úbeda, Natalia
• Format: Article
• Language: English
• Subjects: Aerobics; Biomarkers; Body composition; Body mass index; Cardiovascular disease; Cell adhesion; Cell adhesion molecules; E-selectin; Endothelial cells; endothelial function; Exercise; Fitness equipment; Food; Glutathione peroxidase; Heart rate; Homocysteine; Hyperhomocysteinemia; long-term acute exercise; Marathons; Markers; Medical screening; Oxidants; Oxidative stress; Oxidizing agents; Peroxidase; Physical fitness; Statistical correlation; Statistical methods; Strength training; Vascular cell adhesion molecule 1; Vascular endothelial growth factor
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu13093033

To determine the influence of different doses of maximal acute exercise on the kinetics of plasma homocysteine (tHcy) and its relationship with oxidative status and vascular function, nine recreational runners completed a 10 km race (10K) and a marathon (M). Blood samples were collected before (Basal), immediately post-exercise (Post0), and after 24 h (Post24). Nutritional intake was controlled at each sample point. A significant increase in tHcy was observed after both races, higher after M. Basal levels were recovered at Post24 after 10K, but remained elevated at Post 24 for M. A significant decrease in GSH/GSSG ratio was observed in Post0, especially marked after M. Furthermore, this increase in pro-oxidant status remained at Post24 only after M. Other oxidative status markers failed to confirm this exercise-induced pro-oxidant status except glutathione peroxidase activity that was lower in Post24 compared to Basal in 10K and in Post0 and Post24 in M. No statistical correlation was found between oxidative markers and tHcy. No significant changes were observed in the concentration of endothelial cell adhesion molecules (VCAM-1 and E-Selectin) and VEGF. In conclusion, tHcy increases in an exercise–dose–response fashion but is not related to endothelial dysfunction mediated by oxidative stress mechanisms.