Considering the role of redox homeostasis in exercise-induced signaling and adaptation, this study focuses on the exercise training-related intercellular communication of redox status mediated by circulating extracellular vesicles (EVs). 19 healthy young males were divided into trained (TG, 7) and untrained (UG, 12) subjects based on their VO 2MAX . The UG subjects were further randomly distributed in experimental (UG EX , N = 7) and control (UG CTRL , N = 5) groups. The steady state of plasma EVs in TG and UG EX have been characterized for total number and size, as well as cargo redox status (antioxidants, transcription factors, HSPs) before, 3 and 24 h after a single bout of aerobic exercise (30', 70% HRM). Plasma EVs from UG EX and UG CTRL have been further characterized after 24 h from the last session of a 5-day consecutive aerobic training or no training, respectively. No differences were detected in the EVs' size and distribution at baseline in TG and UG EX (p>0.05), while the EVs cargo of UG EX showed a significantly higher concentration of protein carbonyl, Catalase, SOD2, and HSF1 compared to TG (p<0.05). 5 days of consecutive aerobic training in UG EX did not determine major changes in the steady-state number and size of EVs. The post-training levels of protein carbonyl, HSF1, Catalase, and SOD2 in EVs cargo of UG EX resulted significantly lower compared with UG EX before training and UG CTRL , resembling the steady-state levels in circulating EVs of TG subjects. Altogether, these preliminary data indicate that individual aerobic capacity influences the redox status of circulating EVs, and that short-term aerobic training impacts the steady-state redox status of EVs. Taking this pilot study as a paradigm for physio-pathological stimuli impacting redox homeostasis, our results offer new insights into the utilization of circulating EVs as biomarkers of exercise efficacy and of early impairment of oxidative-stress related diseases.
Competing Interests: Declaration of competing interest The authors declare no conflict of interest.
(Copyright © 2023 Elsevier Inc. All rights reserved.)