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All natural sports supplement VO2 BOOST® was scientifically engineered to significantly increase VO2 max (aerobic capacity) and running economy to enhance athletic endurance and performance. No other formula on the market is as complete as VO2-BOOST® for increasing VO2 max as demonstrated in the clinical study shown below. 

Koury MJ, Ponka P (2004). New insights into erythropoiesis: the roles of folate, vitamin B12, and iron. Annu Rev Nutr. 24:105-31.

Erythropoiesis is the process in which new erythrocytes are produced. These new erythrocytes replace the oldest erythrocytes (normally about one percent) that are phagocytosed and destroyed each day. Folate, vitamin B12, and iron have crucial roles in erythropoiesis. Erythroblasts require folate and vitamin B12 for proliferation during their differentiation. Deficiency of folate or vitamin B12 inhibits purine and thymidylate syntheses, impairs DNA synthesis, and causes erythroblast apoptosis, resulting in anemia from ineffective erythropoiesis. Erythroblasts require large amounts of iron for hemoglobin synthesis. Large amounts of iron are recycled daily with hemoglobin breakdown from destroyed old erythrocytes. Many recently identified proteins are involved in absorption, storage, and cellular export of nonheme iron and in erythroblast uptake and utilization of iron. Erythroblast heme levels regulate uptake of iron and globin synthesis such that iron deficiency causes anemia by retarded production rates with smaller, less hemoglobinized erythrocytes.

Newhouse IJ, Clement DB. (1988). Iron status in athletes. An update.Sports Med. 5(6):337-52.

As more studies are done on the iron status of athletes, the significance of apparent iron deficiency remains controversial. Do observed changes in iron status in athletes indicate an actual iron deficiency or a physiological response to exercise? Iron replacement would clearly be indicated if an iron deficiency was present but would not be necessary or effective if the observed changes were simply a physiological response. There is agreement that serum ferritin and haemoglobin decrease with some exercise conditions and that some indicators of haemolysis, such as serum haptoglobin and bilirubin, change in response to exercise. Expansion of plasma volume and the shift of iron storage from bone marrow to the liver could support the claim that the apparent reduced iron status parameters occurring with exercise are misleading. Countering this concept are studies in athletes which demonstrate dietary iron intake deficiencies and blood loss in the gastrointestinal and urinary tract. Iron deficiency is common in the general population, particularly in women. Therefore, continued monitoring of iron status in athletes appears justified in the face of present knowledge. Replacement therapy, when iron deficiency is apparent, is recommended.