Are hepatitis B carriers more vulnerable to exercise-related liver injury? Recent evidence from a 7-day ultramarathon.

Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are the most well-known liver enzyme tests used to diagnose hepatocyte injury. Besides, these two enzymes are localized in the liver at high concentrations. AST is also present in the heart, skeletal muscle, kidneys, pancreas, brain, and red blood cells in considerable amounts. However, ALT is present in low concentrations in skeletal muscle and other extrahepatic organs. Therefore, ALT is an indicator of liver damage in most situations, and AST is a less specific marker of liver injury. The presence of these enzymes in the blood is due to changes in membrane permeability as well as cellular disruption, damage, and death. These enzymes are also observed in blood in response to exercise. Many previous studies have revealed that endurance exercise, especially marathon race, may increase the serum level of ALT, AST, bilirubin, alkaline phosphatase (ALP), lactate dehydrogenase, and creatine kinase, and decrease serum albumin and protein. During aerobic energy production, aminotransferases can catabolize amino acids, allowing them to enter the citric acid cycle, and thus generating adenosine triphosphate to maintain muscle contraction and substantial physiologic response, such as increased heart and respiratory rates and thermoregulation. It is generally believed that the elevation of ALT and AST levels after exercise originates mainly from muscle, and that only small amounts originate from the liver. The increase in bilirubin may be caused by foot-strike intravascular hemolysis, intramuscular destruction of red blood cells due to osmotic stress, and membrane lipid peroxidation caused by free radicals released by activated white cells. ALP is an enzyme that can transport metabolites across cell membranes including lipids for oxidative energy production. Liver and bone diseases are the most common causes of pathological elevation of ALP, followed by intestinal problems. The origin of exercise-related elevation of ALP was believed to arise mainly from osteoblasts in the bone by the stress and stimulation from exercise, although little data regarding the isoenzyme of ALP have been reported in the