Exercise-induced hemolysis is caused by protein modification and most evident during the early phase of an ultraendurance race

Abstract

Whether structural changes of the erythrocyte membrane increase the susceptibility to hemolysis particularly of the relatively older cell population during the early phase of a 216-km ultrarace was tested in six male runners (age 53.6 ± 10.4 yr, height 175.8 ± 11.1 cm, body mass 75.9 ± 8.4 kg). Erythrocyte membrane spectrins were lowest ( P < 0.001) after 42 km (75.59 ± 5.25% of prerace) and increased ( P < 0.001) toward 216 km (88.27 ± 3.37%). Susceptibility to osmotic hemolysis was highest ( P < 0.01) after 42 km (107.34 ± 3.02 mOsm sodium phosphate buffer) with almost identical ( P > 0.05) values prerace (97.98 ± 3.41 mOsm) and postrace (98.61 ± 3.26 mOsm). Haptoglobin indicated intravascular hemolysis of 9.27 × 109cells/l ( P < 0.05) during the initial 84 km. Changes in hematocrit and plasma proteins indicated an estimated total net erythrocyte loss of 3.47 × 1011cells/l ( P < 0.05) after 21 km. This was compensated by a gain in erythrocytes ( P < 0.05) of 3.31 × 1011cells/l during the final 132 km. A main effect ( P < 0.05) on erythropoietin suggests increased erythropoiesis throughout the race. Exercise-induced hemolysis reflects alterations in erythrocyte membrane spectrins and occurs particularly in the early phase of an ultraendurance race because of a relative older cell population.