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All sports involve great stress on the cardiovascular, respiratory, and skeletal systems. Athletes spend a lot of resources on maintaining body tone and developing their physiological capabilities to perform regular training and achievements. In athletic sports, the principal stresses are on the cardiovascular system because sprinting or running long distances requires a large blood volume in the bloodstream. The book in the vascular system depends on the diameter of the vessels, their ability to stretch, and the oxygen saturation of the blood. Therefore, processes such as angiogenesis and arteriogenesis are essential for athletic athletes, but they contribute differently to high performance. For high-level athletic performance, arteriogenesis is more critical than angiogenesis.
Angiogenesis and Arteriogenesis: Definition and Influence on Athletes Endurance
Angiogenesis is the formation of new blood vessels, during which the primary capillary network is reorganized. It becomes more straightforward and transparent, allowing more nutrients to reach organs or tissues (Hutchings et al., 2021). For athletes, the speed of transmission of these substances is essential, which many newly formed capillaries (Di Credico et al., 2020). In addition, veins contribute to the excellent oxygen exchange in the network, which significantly increases endurance during prolonged and robust exertion: sprinting and running.
Arteriogenesis refers to the growth of new arteries or arterioles by increasing their diameter, associated with endothelial cell proliferation and smooth muscle. This process allows significantly higher blood volumes per unit density than angiogenesis (Tianqi & Yong-Ping, 2020). As previously argued, large blood volumes are vital for athletic sports. Increased flow size is necessary for microcirculatory remodeling and, therefore, maintaining endurance (Vogel et al., 2020). Arteriogenesis depends on the hypoxia and inflammatory processes that often accompany athletic training.
Molecular Mechanisms of Angiogenesis and Arteriogenesis
Angiogenesis occurs naturally, predominantly after wound healing, and resulting activating growth factors, fibroblasts, smooth muscle cells, and the extracellular matrix. Hypoxia accompanies athletic training because athletes breathe sparingly during sprints or other types of running. Therefore, angiogenesis is stimulated by tissue hypoxia which leads to HIF activation. These factors move into the nucleus, activating the genes: VEGF-A, angiopoietins, and nitric oxide (Hutchings et al., 2021). The mature endothelial cells move to the tissue experiencing hypoxia and form new blood vessels. Cytokines released into the blood stimulate the genesis of proteolytic phagocytes, which facilitate cell migration (Di Credico et al., 2020). Other mechanisms that control genes are also crucial for vessel formation: for example, ATF3/4 boosts the uptake and metabolism of amino acids (Fan et al., 2021). ATF3/4 promotes the activation of red endothelial cells and prepares them for angiogenesis, thereby determining muscle potential.
Arteriogenesis occurs by a similar mechanism, but significant differences determine its advantages for athletes. In arteriogenesis, activation of VEGF-A kinases promotes endothelial cell proliferation and increases vascular lumen size, whereas, in angiogenesis, VEGF-A is responsible for the cell signaling pathway (Hutchings et al., 2021). Disruption of signaling leads to decreased arteriogenesis and blocks the release of chemokines such as monocyte chemoattractant protein-1 (MCP-1). Arteriogenesis requires a response from several cell types, providing coordinated transmission pathways. For example, lymphocytes, killer cells, and macrophages also affect arteriogenesis by stimulating VEGF-A. HIF-1 alpha, which provides transcriptional regulation of the cellular response to hypoxia, is also an essential factor. It promotes cell survival through energy metabolism and provides the higher hypoxia thresholds that an athlete can have.
Physiological Advantages of Arteriogenesis
Compared with angiogenesis, arteriogenesis activates ion channels to a greater extent, thereby ensuring the availability of nutrients. Increased physical activity contributes to increased shear stress, increasing vascular wall tension (Tianqi & Yong-Ping, 2020). This tension activates arteriogenesis, allowing an increase in bloodstream volume, which is helpful in hypoxemic exercise (Vogel et al., 2020). Bresler et al.s (2019) study showed that voluntary exercise capacity for forced running was significantly increased after ligation of the iliac artery (Bresler et al., 2019). Such results indicate that athletic performance is influenced by increasing channeling, which is accomplished by arteriogenesis.
An important physiological aspect of arteriogenesis is the relationship to reactive oxygen species (ROS) and the delivery of oxygen molecules to the arteries. ROS is both a positive and negative consequence of training for track and field athletes. In competition, athletes need to exceed their capacity, meaning that ROS accumulates significantly more, leading to soft tissue and vascular injury (Hutchings et al., 2021). Nevertheless, regular training before competition enhances antioxidant protection by pre-expanding the vascular lumen the adaptive capacity of athletes increases significantly (Pellegrin et al., 2020). Oxidative stress resulting from ROS accumulation does not lead to necrosis because arteriogenesis ensures the ability of vessels to dilate and maintain the tension of large volumes of blood.
Conclusion
Thus, arteriogenesis and angiogenesis are similar mechanisms regulating the vascular system through blood volume and vessel volume changes. Angiogenesis is carried out by activating HIFs, which trigger vascular proliferation. Arteriogenesis is more related to the increase in the vascular lumen due to VEGF-A and the coordinated action of several cell types. Arteriogenesis is advantageous for track and field athletes because it expands their adaptive capacity to ROS and supports vascular wall tension. It provides increased endurance and prevents the effects of hypoxia on the body.
References
Bresler, A., Vogel, J., Niederer, D., Gray, D., Schmitz-Rixen, T., & Troidl, K. (2019). Development of an exercise training protocol to investigate arteriogenesis in a murine model of peripheral artery disease. International journal of molecular sciences, 20(16), 39-56. Web.
Di Credico, A., Izzicupo, P., Gaggi, G., Di Baldassarre, A., & Ghinassi, B. (2020). Effect of physical exercise on the release of microparticles with angiogenic potential. Applied Sciences, 10(14). Web.
Fan, Z., Turiel, G., Ardicoglu, R., Ghobrial, M., Masscgelein, E., Kocijan, T., Zhang, J., Tan, G., Fitzgerald, G., Gorski, T., Alvarado-Diaz, A., Gilardoni, P., Adams, C. M., Chesquiere, B. & de Bock, K. (2021). Exercise-induced angiogenesis is dependent on metabolically primed ATF3/4+ endothelial cells. Cell Metabolism, 3(9), 1793-1807. Web.
Hutchings G., Kruszyna A., Nawrocki, M.J., Strauss, E., Bryl, R., SpaczyDska, J., Perek, B., Jemielity, M., Mozdziak, P., Kempisty, B., Nowicki, M. & KrasiDski, Z. (2021). Molecular mechanisms associated with ROS-dependent angiogenesis in lower extremity artery disease. Antioxidants, 10(5). Web.
Pellegrin, M., Bouzourène, K., Aubert, J.F., Bielmann, C., Gruetter, R., Rosenblatt-Velin, N., Poitry-Yamate, C. & Mazzolai, L. (2020). Impact of aerobic exercise type on blood flow, muscle energy metabolism, and mitochondrial biogenesis in experimental lower extremity artery disease. Scientific Reports, 10. Web.
Tianqi, M. &Yong-Ping, B. (2020). The hydromechanics in arteriogenesis. Aging Medicine, 3(3), 169-177. Web.
Vogel, J., Niederer, D., Jung, G., & Troidl, K. (2020). Exercise-induced vascular adaptations under artificially versus pathologically reduced blood flow: A focus review with special emphasis on arteriogenesis. Cells, 9(2). Web.
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