The NCAA has also recently encouraged athletes to become aware of their sickle cell trait status, as the trait itself does not typically result in symptoms under normal conditions but can become dangerous during extreme physical activity similar to the daily training that athletes undergo.Normal hemoglobin (and hemoglobin S in the presence of oxygen) contains a deformability characteristic that allows erythrocytes to essentially squeeze their way into smaller vessels, including those involved in microcirculation to the capillaries within muscle tissue as well as blood supply embedded within organ tissues. When hemoglobin S is deprived of oxygen, it can polymerize, which is what is proposed to cause the "sickled" cells. The sickled erythrocytes present a decreased deformability when compared to normal erythrocytes, leading to distress in circulation into the smaller vessels involved in microcirculation, particularly, in this case, the capillaries embedded in muscle tissue.The resulting microvasculatory distress in capillaries specific to muscle tissue can cause acute rhabdomyolysis and necrosis within the muscle cells. The inflammation and leakage of intracellular material resulting from muscle cell necrosis releases a particular protein, myoglobin, into the blood stream. While necessary in muscle tissue to bind iron and oxygen, myoglobin circulating through the bloodstream can break down into smaller compounds that damage kidney cells, leading to various complications, such as those seen in sickle cell trait athletes during high levels of physical exertion.Because of the link between deformability and sickled cells, deformability can be used to evaluate the amount of sickled cells in the blood.
Sudden deaths during physical exertion in African-American US army recruits, and athletes
Urinary tract infection

Suggested
Probable: complicated hyphema, venous thromboembolic events, fetal loss, neonatal deaths, and preeclampsia
Possible: acute chest syndrome, asymptomatic bacteriuria, and anemia in pregnancy
Insufficient evidence: retinopathy, cholelithiasis, priapism, leg ulcers, liver necrosis, avascular necrosis of the femoral head, and stroke. An association with complicated migraines has been suggested.There have been reports of pulmonary venous thromboembolism in pregnant women with sickle cell trait, or men during prolonged airflight, and mild strokes and abnormalities on PET scans in children with the trait.Sickle cell trait appears to worsen the complications seen in diabetes mellitus type 2 (retinopathy, nephropathy and proteinuria) and provoke hyperosmolar diabetic coma nephropathy, especially in male patients. Genetics
Normally, a person inherits two copies of the gene that produces beta-globin, a protein needed to produce normal hemoglobin (hemoglobin A, genotype AA). A person with sickle cell trait inherits one normal allele and one abnormal allele encoding hemoglobin S (hemoglobin genotype AS).The sickle cell trait can be used to demonstrate the concepts of co-dominance and incomplete dominance. An individual with the sickle cell trait shows incomplete dominance when the shape of the red blood cell is considered. This is because the sickling happens only at low oxygen concentrations. With regards to the actual concentration of hemoglobin in the circulating cells, the alleles demonstrate co-dominance as both normal and mutant forms co-exist in the bloodstream. Thus it is an ambiguous condition showing both incomplete dominance and co-dominance.Unlike the sickle-cell trait, sickle-cell disease is passed on in a recessive manner.