Post-exercise endothelial function is not associated with extracellular vesicle release in healthy young males

Abstract

Acute exercise can result in temporary decrease in endothelial function, which may represent a transient period of risk. Numerous mechanisms underpin these responses included release of extracellular vesicles (EVs) derived from apoptotic or activated endothelial cells and platelets. This study aimed to compare the time-course of endothelial responses to two exercise protocols: moderate-intensity-continuous-exercise (MICE) and high-intensity-interval-exercise (HIIE) and the associations with EV release. Eighteen young healthy males (age: 22.6±3.7y, BMI: 25.6±2.5m2/kg, VO2peak: 38.6±6.5ml/kg/min) completed two randomly assigned exercises; HIIE (10x1min-@-90% heart rate reserve (HRR), 1min passive recovery) or MICE (30min-@-70% HRR) on a cycle ergometer. FMD was used to assess endothelial function and blood samples were collected to evaluate endothelial cell-derived EV (CD62E+) and platelet-derived EV (CD41a+), prior- and 10, 60, and 120min post-exercise. There were similar increases, but different time-courses (P=0.017) in FMD (increased 10min post-HIIE, P<0.0001 and 60min post-MICE, P=0.038). CD62E+ remained unchanged (P=0.530), whereas overall CD41a+ release was reduced 60min post-exercise (P=0.040). FMD was not associated with EV absolute release or change (P>0.05). Acute exercise resulted in similar improvements, but different time-course in FMD following either exercise. Whilst EVs were not associated with FMD, the reduction in platelet-derived EVs may represent a protective mechanism following acute exercise.