Effect Of A Two-week Exercise Intervention On Postprandial Extracellular Vesicles In Adults With Prediabetes: 2460 Board #124 May 31 11:00 AM - 12:30 PM

PURPOSE: Postprandial hyperglycemia is a stronger predictor of cardiovascular disease (CVD) compared to fasting glucose, but the mechanism remains unclear. Extracellular vesicles (EVs) are potential bio-effectors that impact CVD, and exercise is known to modify fasting EVs. However, the effect of exercise on EVs in the postprandial state in relation to CVD risk is unknown. METHODS: Twelve older (64.7±2.3 yrs), obese (BMI: 31.1±1.7 kg/m2) and sedentary (19.3 ml/kg/min) adults were screened for prediabetes using ADA criteria (75 g OGTT and/or HbA1c). Subjects underwent 12 bouts of supervised cycle ergometer training at 70%HRpeak for 60 min/d. Annexin V- total EVs, platelet EVs (CD31+/CD41+), endothelial EVs (CD105, CD31+/ CD41-) and leukocyte EVs (CD45+/CD41-) were collected at fasting and 2-hr during a 75g OGTT from fresh plasma. EVs were analyzed via imaging flow cytometry pre-/post- intervention. CVD risk factors including BMI, VO2peak, glucose, systolic (SBP), diastolic (DBP), arterial pressure (AP), and arterial stiffness (augmentation index; AIx) were assessed at fasting and 2-hr during the 75g OGTT. RESULTS: Exercise tended to decrease BMI (P=0.06) and postprandial AIx assessed at 2-hr (trend: P=0.08) and tAUC120 (trend: P=0.11), but had no significant effect on VO2peak (P=0.19) or 2-hr glucose (P=0.26). All AV- EVs except CD31+/CD41+ increased post-training (all P<0.001). However, when accounting for changes in fasted EVs following training, only AV-CD105 remained significantly elevated at 2-hr post-training (P=0.01). Increases in postprandial total AV- EVs correlated with reductions in postprandial AP (r=-0.73, P=0.03) and AIx (r=-0.75, P=0.02) while postprandial AV- CD31+/ CD41- was related to lowered SBP at 2-hr (r=-0.71, P=0.05). CONCLUSION: Although exercise training may modify the postprandial AV- EV response in adults with prediabetes, this response appears to be driven by alterations in fasted EVs. Future work should consider the physiological and clinical relevance of EVs in the fasted versus postprandial state to elucidate the physiologic underpinnings by which postprandial hyperglycemia confers CVD risk.