Twenty male athletes, mean age 26 years, were studied by a work load test with cycle-ergometer, with increasing power output for 60 minutes until an intensity corresponding to 70% of the individual maximal heart rate was achieved. Ten of them had familial hyperbilirubinemia (Gilbert's syndrome) and ten had been considered as healthy controls. The diagnosis of Gilbert's syndrome was made using the following criteria: unconjugated hyperbilirubinemia, no systemic symptoms, no overt or clinically recognizable haemolysis, normal liver function tests. Blood levels of free fatty acids (FFA) showed a progressive significant increase after muscular exercise in both healthy and Gilbert's syndrome subjects (p < 0.001). The increase was more evident in controls compared to Gilbert's syndrome subjects (p < 0.05). Total and fractionated bilirubin showed no change in both groups. In conclusion, a competitive mechanism between bilirubin and FFA is probably responsible for the lower increase in plasma FFA in Gilbert's syndrome.

No effect of endurance exercise on serum bilirubin in healthy athletes and with congenital hyperbilirubinemia (Gilbert's syndrome).

FLOREANI, ANNAROSA;MARTINES, DIEGO;NACCARATO, REMO
1993

Abstract

Twenty male athletes, mean age 26 years, were studied by a work load test with cycle-ergometer, with increasing power output for 60 minutes until an intensity corresponding to 70% of the individual maximal heart rate was achieved. Ten of them had familial hyperbilirubinemia (Gilbert's syndrome) and ten had been considered as healthy controls. The diagnosis of Gilbert's syndrome was made using the following criteria: unconjugated hyperbilirubinemia, no systemic symptoms, no overt or clinically recognizable haemolysis, normal liver function tests. Blood levels of free fatty acids (FFA) showed a progressive significant increase after muscular exercise in both healthy and Gilbert's syndrome subjects (p < 0.001). The increase was more evident in controls compared to Gilbert's syndrome subjects (p < 0.05). Total and fractionated bilirubin showed no change in both groups. In conclusion, a competitive mechanism between bilirubin and FFA is probably responsible for the lower increase in plasma FFA in Gilbert's syndrome.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2505739
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