The human vasculature is extremely plastic. This is clearly demonstrated by the broad-ranged adaptations seen in the vasculature in response to an exercise training period. However, the molecular mechanisms by which the vasculature communicates are largely unknown. Recent studies have demonstrated that substances are released into the circulation during exercise training. In addition, it has been shown that platelets carry and release Vascular Endothelial Growth Factor (VEGF) and Thrombospondin-1 (TSP-1) which are important for vascular plasticity, and it is further speculated that platelets are the main origin of extracellular vesicles in the circulation. Thus, we aimed to elucidate the angiogenic potential of human platelets and to study if platelets activate molecular pathways associated with angiogenesis in cultured endothelial cells. In this pilot study, platelets were isolated from four healthy male subjects at baseline and following an acute bout of exercise training on a bicycle ergometer (45 minutes at 80% HRmax). In brief, blood was drawn using Sodium Citrate as anticoagulant and centrifuged to obtain platelet-rich-plasma. Highly purified platelets were then isolated from the platelet-rich-plasma and platelet-free-plasma was collected. To study the effect on endothelial cells in culture, platelet releasate was prepared by activation of isolated platelets using Thrombin Receptor Activator Peptide 6 (TRAP-6) under stirring conditions. The releasate was collected and added to Human Umbilical Vein Endothelial Cells (HUVEC) in culture for 3- and 6 hours. Preliminary data demonstrate that platelets carry the pro- and antiangiogenic proteins VEGF and TSP-1, and exposure of isolated platelets to TRAP-6 leads to a release of these angiogenic proteins. VEGF levels in platelet releasate are ranging from 32 – 116 pg/mL. Furthermore, stimulation of cultured endothelial cells with platelet releasate upregulates mRNA expression of various angiogenesis-related genes up to 4-fold compared to control situation. Our preliminary data suggest that platelets mediate intercellular cross-talk in the vasculature by releasing angiogenic proteins consequently leading to an upregulation of molecular pathways related to angiogenesis in endothelial cells. Further studies are being conducted to verify the mechanism and analysis is ongoing.