While moderate exercise improves cardiovascular health, marathons and ultra-long-distance running may damage RBCs, cause premature “aging,” and lower hematocrits. A recently published study collected pre- and post-blood samples from 23 long distance runners—11 (5 female; median age, 36 years) from a 40 km marathon and 12 (4 female; median age, 38 years) from an ultra-marathon 171 km in length. Based on analysis of plasma and RBCs—covering 440/1105 proteins, 659/647 lipids, 197/271 metabolites, and 8/6 trace elements—the molecular responses differed between marathon and ultramarathon runners. All runners, however, showed increased inflammation and oxidative stress in post-run RBCs. In plasma, marathon runners had elevated levels of IL-6, acute phase protein induction, and kynurenine (a marker of RBC hemolytic fragility), with even higher levels observed in ultra-marathon runners. Elevated levels of acylcarnitine and fatty acids were observed in all plasma samples post-run suggestive of ongoing RBC membrane repair, but again, levels were higher in the ultra-marathon runners. Ultra-marathon runners also accumulated more RBC damage than marathon runners with an increased number of extracellular vesicles and significantly decreased hematocrit. Levels of acetoacetate, hypoxanthine, and bilirubin were also higher in ultra-runners, as compared to marathon runners, and inversely correlated to hematocrit—suggesting extravascular clearance of RBCs instead of intravascular hemolysis. These findings could help improve the understanding of cardiovascular health and recovery in athletes and inform strategies for the storage of RBCs, but further studies are needed.
Reference:
Leave a Reply