The Disparate Roles of Cobalt in Erythropoiesis, and Doping Relevance

Abstract

Some athletes seek to increase their red blood cells, because the aerobic capacity correlates with the mass of hemoglobin. Cobalt as part of dietary supplements is proclaimed to increase erythropoiesis and physical performance. However, the knowledge of the disparate mechanisms of cobalt s actions in erythropoiesis is generally insufficient. First, there are cobalt-containing corrinoids, termed cobalamin or vitamin B12. These are naturally present only in animal-derived foods. The active forms in the human body are methylcobalamin and deoxyadenosylcobalamin, which are essential cofactors for the methionine synthase and the L-methylmalonylcoenzyme A mutase. Cobalamin deficiency can result in anemia. However, supplemental cobalamin does not benefit performance unless a nutritional deficit is present. Second, inorganic cobalt ions (Co 2+ ) stimulate erythropoiesis, even in non-anemic subjects. Co 2+ stabilizes the hypoxia-inducible transcription factors (HIFs) which increase the expression of the erythropoietin gene (EPO). Cobaltous salts are orally active, easy to obtain and inexpensive. Typical side effects associated with chronic Co 2+ exposure include nausea, vomiting, heart failure, hypothyroidism and goiter. The potential misuse of inorganic cobalt deserves attention in anti-doping