Blood viscosity affects the transport and delivery of oxygen and nutrients to the body. This calculation is related to the flow of blood through the circulatory system. It's used in understanding conditions related to blood thickness or thinness, such as polycythemia, anemia, and various cardiovascular diseases. It's important for performance because high viscosity can impede blood flow, reducing the efficiency of oxygen delivery to muscles (source, source).
Blood viscosity is primarily determined by hematocrit, plasma protein concentration (especially fibrinogen), and red blood cell deformability. It increases with dehydration, polycythemia, or elevated acute-phase proteins during illness or overtraining. It decreases with overhydration or anemia. Both extremes compromise performance: high viscosity impairs capillary perfusion and cardiac output efficiency; low viscosity (hemodilution) reduces the oxygen-carrying capacity per unit volume (source).
Low blood viscosity is most often seen in athletes who are overhydrated, anemic, or experiencing plasma volume expansion from aerobic training adaptation. Aerobic conditioning naturally expands plasma volume, which can dilute hematocrit and reduce viscosity, this is a normal and often beneficial adaptation that enhances cardiac stroke volume and reduces cardiac work at submaximal intensities (source).
Pathological low viscosity occurs in iron deficiency anemia, B12/folate deficiency, or severe overhydration, where total hemoglobin mass is reduced. These states reduce oxygen delivery regardless of cardiac output, limiting VO2max and increasing perceived exertion at submaximal loads. Distinguishing training-adaptive plasma expansion (benign) from true anemia (pathological) requires examining hemoglobin concentration, reticulocyte count, and iron stores alongside viscosity (source).
Elevated blood viscosity is most commonly driven by dehydration, which concentrates red blood cells and plasma proteins, or by polycythemia (primary or secondary). Secondary polycythemia in athletes is most often driven by altitude adaptation, sleep apnea-induced hypoxia, or exogenous EPO use. Elevated hematocrit above 50% in males and 47% in females markedly increases viscosity and cardiovascular event risk (source).
High viscosity increases cardiac afterload, slows microvascular perfusion, and can promote thrombosis. In high-altitude endurance athletes, chronically elevated hematocrit is a major risk factor for stroke and pulmonary embolism. Dehydration-induced viscosity elevations are typically transient and resolve with rehydration, while polycythemia-driven elevations require medical evaluation (source).
Blood viscosity is a derived metric rather than a direct lab assay; it is typically calculated from hematocrit, hemoglobin, and plasma protein data. Use it as an integrative signal alongside hydration markers, hematocrit, hemoglobin, and iron studies rather than as a standalone value.
For athletes training at altitude or with known polycythemia risk, serial monitoring of hematocrit and hemoglobin provides a practical viscosity proxy. Ensure adequate hydration protocols before and during competition to prevent dehydration-driven viscosity spikes, particularly in hot and humid conditions where fluid losses are amplified (source).