Foot strike hemolysis, also known as exercise-induced hemolysis, occurs due to the destruction of erythrocytes in the capillaries of the foot due to repetitive contact with the ground (3). This process was first identified in 1881 when a German soldier was found to have multiple episodes of hemoglobinuria after marching (5). There are other theories as to why athletes develop an intravascular hemolysis and develop what is called “sports anemia”. One process is that repetitive large muscle contractions can cause destruction of red blood cells and cause an anemia (1). Another cause of a sports anemia is the development of a hemodilution anemia secondary to an increase in plasma volume with exercise (3). Increased levels of hemolysis have been found in runners compared to swimmers and cyclists, suggesting foot strike hemolysis as the primary source of exercise-induced hemolysis (4).
Foot strike hemolysis can be diagnosed with serum lab findings that occur during and after exercise. Hemolysis of the erythrocytes will cause hemoglobin and iron to be released (3). Haptoglobin is an acute phase reactant whose job is to bind to free hemoglobin (2). During hemolysis free hemoglobin is released and the haptoglobin levels are decreased due to their binding with hemoglobin (2). Elevated MCV levels can also be seen because of the selective destruction of older RBCs (5). A urinalysis may also show a hemoglobinuria due to the intra-vascular release of hemoglobin during the destruction of the erythrocyte (5). Another level that can be elevated with hemolysis is lactate dehydrogenase, which has been found to be elevated with foot strike hemolysis (6). Finally, elevated unconjugated bilirubin levels can be seen due to the destruction of hemoglobin (7). Other causes of hemolytic anemia must be ruled out in patients who are being evaluated for foot strike hemolysis (6).
Due to the repetitive loss of iron from the red blood cells with foot strike hemolysis, studies have looked at ultramarathon runners to see if they develop an anemia. In a group of ultramarathon runners, they did find an immediate decrease of haptoglobin levels, but they did not find significant anemia in this population (3).
The advent of better running shoe material has potentially led to an attenuation of anemia in runners in more recent studies (3). It has also been hypothesized that most of the hemolysis occurs during heel strike. As a result, a study was performed looking at hindfoot verse forefoot runners and the effects on intravascular hemolysis (4). However, a study published in the Journal of Sports Sciences failed to find a statistically significant difference in haptoglobin levels in the rearstrike and forefoot strike groups (4). There is also no clear consensus if athletes wearing firm or soft insoles can decrease intravascular hemolysis (7). Oral iron intake is typically not necessary to prevent the development of a significant anemia in patients suspected to have foot strike hemolysis (6).
Overall, foot strike hemolysis leads to the intravascular destruction of red blood cells in the capillaries of the heel. This can lead to a decrease in serum haptologin, as it binds to free hemoglobin. This process also causes the release of free iron and LDH. However, despite the hemolysis, clinically significant anemia is rarely identified.
By Gregory Rubin, DO
– Read More @ Wiki Sports Medicine: https://wikism.org/Foot_Strike_Hemolysis
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2) Long, Brit, and Alex Koyfman. “Emergency Medicine Evaluation and Management of Anemia.” Emergency Medicine Clinics of North America, vol. 36, no. 3, Aug. 2018, pp. 609–30. PubMed, https://doi.org/10.1016/j.emc.2018.04.009.
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6) Fazal, Abid A., et al. “Foot-Strike Haemolysis in an Ultramarathon Runner.” BMJ Case Reports, vol. 2017, Dec. 2017, pp. bcr2017220661, bcr-2017–220661. PubMed, https://doi.org/10.1136/bcr-2017-220661.
7) Janakiraman, Kamal, et al. “Firm Insoles Effectively Reduce Hemolysis in Runners during Long Distance Running – a Comparative Study.” Sports Medicine, Arthroscopy, Rehabilitation, Therapy & Technology: SMARTT, vol. 3, no. 1, June 2011, p. 12. PubMed, https://doi.org/10.1186/1758-2555-3-12.