Epidemiological, biological and clinical update on exercise-induced hemolysis
Exercise-induced hemolysis can be conventionally defined as rupture and destruction of erythrocytes during physical exercise. The currently available epidemiologic information attests that a substantial degree of exercise-induced hemolysis is commonplace after short-, medium-, long- and ultra-long distance running, as reflected by significant decrease of serum or plasma haptoglobin and significant increase of plasma concentration (or overall blood content) of free hemoglobin. This paraphysiological intravascular hemolysis is typically mild (average variations of hemolysis biomarkers are usually comprised between 1.2- and 1.8-fold), almost self-limiting (completely resolving within 24–48 hours), with severity depending on athlete population, analytical technique used for detecting intravascular hemolysis, as well as on number, frequency and intensity of ground contacts, but not on running technique. Additional lines of evidence support the notion that both osmotic fragility and membrane structure of erythrocytes are considerably modified during endurance exercise. This fact goes hand in hand with findings that erythrocyte lifespan in runners is approximately 40% shorter than in sedentary controls. Direct mechanical injury caused by forceful ground contacts, repeated muscle contractile activity or vasoconstriction in internal organs are three potential sources of exercise-induced hemolysis, whilst metabolic abnormalities developing while exercising (e.g., hyperthermia, dehydration, hypotonic shock, hypoxia, lactic acidosis, shear stress, oxidative damage, proteolysis, increased concentration of catecholamines and lysolecithin) may actively contribute to trigger, accelerate or amplify this phenomenon. Although no systematic evidence is available, it seems also reasonable to hypothesize that patients bearing erythrocyte disorders may be particularly vulnerable to developing exercise-induced hemolysis.