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Ultra-long-distance running and the liver
1Institut für Klinische Chemie, Klinikum Ludwigshafen, Universität Mainz.
International Journal of Sports Medicine
|December 1, 1990
Summary
Ultra-long-distance running impacts liver enzymes. Significant increases in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were observed, alongside potential liver cell injuries indicated by glutamate dehydrogenase (GLDH) and gamma-glutamyl-transferase (GGT) elevations.
Area of Science:
- Sports Medicine
- Biochemistry
- Physiology
Background:
- Ultra-long-distance running presents unique physiological challenges.
- Liver enzymes are sensitive indicators of cellular stress and damage.
- Assessing liver function during extreme endurance events is crucial for understanding athlete health.
Purpose of the Study:
- To investigate the impact of an ultra-long-distance race (1000 km in 20 days) on key liver enzymes.
- To evaluate the liver's synthetic capacity during prolonged strenuous exercise.
- To identify potential liver cell injuries or functional changes in endurance athletes.
Main Methods:
- Blood samples were collected from finishers of a 1000 km race over 20 days.
- Activities of liver enzymes including AST, ALT, AP, GGT, and GLDH were measured.
- Cholinesterase (CHE) activity and serum albumin concentration were assessed to gauge liver synthetic function.
Main Results:
- Alkaline phosphatase (AP) showed a continuous increase throughout the race.
- Aspartate aminotransferase (AST) and creatine kinase (CK) levels peaked early and then decreased.
- Alanine aminotransferase (ALT) increased and stabilized, while GLDH and GGT showed significant individual elevations, suggesting liver cell injury in over half of finishers.
- Cholinesterase (CHE) activity and serum albumin levels decreased, correlating significantly.
Conclusions:
- Ultra-long-distance running significantly affects liver enzyme profiles.
- Elevated GLDH and GGT indicate potential liver cell damage during extreme endurance events.
- Reduced CHE and albumin suggest a compromised liver synthetic capacity under prolonged stress.