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  • Sports such as swimming, cycling and running cause RBC damage, according to J. A. Smith in a "Sports Medicine" article. Physicians can track RBC damage by measuring indices of haemolysis, or breakdown RBCs by normal processes in the liver, spleen and lymph nodes. Smith suggests that most exercise-related RBC destruction takes place within the circulatory system and should be measured by tracking antioxidant depletion or damage to lipids and proteins. Red blood cells have constant exposure to oxygen, polyunsaturated fats and blood iron, which makes them vulnerable to oxidative damage. As oxygen uptake increases in exercise, antioxidants in muscles and red blood cells can run low, causing increased damage. Oxidative damage dehydrates RBCs, which deforms them and makes it more difficult for them to pass through narrow vessels. This deprives some tissues of oxygen, giving rise to further RBC damage during prolonged exercise. If the bone marrow can't produce enough new RBCs to keep up with losses, the athlete may develop a low RBC count. RBCs have no nuclei and can't divide, so they have a finite lifespan. Normally, a RBC has a lifespan of 120 days. The rate of RBC aging can increase during exercise, resulting in more rapid turnover. This may be an advantage because younger RBCs carry oxygen more efficiently. However, new RBC generation has to be able to keep up with the increased demand.
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