In the last years there has been a lively discussion about the potential of HIT and HVT to improve performance and health. Although past research revealed better insights into the molecular mechanisms, there is still a lack of knowledge on the influence different protocols and protocol arrangements on cellular mechanisms. Therefore, the aim of this fundamental research project was to investigate the hormonal, cellular and genetic responses and training adaptations in adults and children to different training intensities and different recovery modalities in endurance training. Thereby we mainly focused on angiogenesis.
Within this research project different training intensities and training volumes like high-volume training (HVT), high-intensity training (HIT) and sprint-interval training (SIT) were compared. Before and after each intervention, anabolic and angiogenic growth factors, endothelial microparticles or miRNAs were analyzed. In the case of training interventions, various performance tests were conducted.
The major findings of this project are, that based on the data of angiogenic and anabolic growth factors and endothelial microparticles (EMP) it appears that especially intense training protocols may promote pro-angiogenic conditions. We could show that strenuous physical activity leads to decreased EMP levels and promotes a phosphatidylserin-dependent uptake of EMP into target endothelial cells, which is associated with a protection of target cells against apoptosis. Intense training protocols caused the highest increases in angiogenic and anabolic growth factors and hormones. Furthermore, we found that HVT and SIT are associated with the release of endothelial miRNAs into the circulation in children and adults, which can function as intercellular communication devices regulating vascular biology. Finally, we showed that the mode of recovery (active vs. passive) between intervals has an influence on the hormonal response and the long term training adaptations.
Status | Finished |
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Effective start/end date | 31.05.12 → 31.01.16 |
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