Study of energy metabolism of skeletal muscles in alcoholic liver disease--expired gas analysis during exercise.

BACKGROUND: The effects of chronic alcohol intake on skeletal muscle are clinically observed as muscle cramps with decrease in the amount of muscle. It was clarified by expired gas analysis that acute alcohol load affects disturbed energy metabolism of skeletal muscle. We studied abnormal energy metabolism of skeletal muscles in alcoholic liver diseases using expired gas analysis. METHODS: Subjects of the study were five inpatients with alcoholic liver disease (fatty liver: one case, hepatic fibrosis: one case, liver cirrhosis: three case). Expired gas analysis during exercise was performed using AEROMONITOR. Minute ventilation, oxygen consumption and carbon dioxide output were monitored, and anaerobic threshold (AT) and respiratory compensation point (RCP) were calculated. RESULTS: The anaerobic threshold, which is the limit of the aerobic exercise, was significantly reduced in patients with alcoholic disease (p < 0.01). The respiratory compensation point, which is the limit of the metabolic compensation of intracellular lactic acidosis, was decreased (p < 0.01). CONCLUSIONS: The results of expired gas analysis during exercise indicate that the aerobic energy metabolism of skeletal muscle had been disturbed in alcoholic liver disease. The reduced RCP suggests that the lactate metabolism in skeletal muscle is also disturbed in alcoholic liver disease. Expired gas analysis during exercise allows determination of the amount of exercise required to treat liver diseases through analysis of AT.

[Analysis of medical care costs for gastroenterological inpatients with alcohol-related disease].

Current estimates suggest that approximately 2.3-2.5 million people in Japan are alcoholics. Of these patients, less than 1% visit alcohol outpatient clinics; most patients visit general clinics. Alcohol is associated with disorders of the gastrointestinal system, circulatory system, nervous system, and other organs. The costs for medical care impose a heavy burden on healthcare financing. Among all, the costs for alcohol-related gastrointestinal diseases are enormous. Reports show that the percentages of medical care costs for alcohol-related gastrointestinal diseases is as high as about 29% of the costs for all gastrointestinal diseases. Our analysis has found that hospital and treatment costs for alcohol-related liver and pancreatic diseases amounted to 35.2% of the costs for all liver and pancreatic diseases. Furthermore, results indicated that the average daily hospital and treatment costs for patients with alcohol-related liver diseases were significantly higher than the costs for patients with non-alcohol-related liver diseases. To reduce medical care costs for alcohol-related diseases, not only treatment of such diseases but also preventive care for pre-alcoholics is crucial. In this context, close contact between general clinics and alcohol outpatient clinics are important, and a network system of support for patients with alcohol-related diseases should be established.

Influence of acute alcohol load on metabolism of skeletal muscles--expired gas analysis during exercise.

BACKGROUND: The chronic intake of alcohol affects the function of skeletal muscles. To elucidate the influence of acute alcoholic load on muscular metabolism during exercise, we analyzed expired gases to measure the volume of consumed oxygen and the volume of exhaled CO2. METHODS: Healthy volunteers were enrolled for the study. For the exercise test, they were asked to rest for 5 min, warm up on an aerobike at 20 W for 2 min, and then gradually increase the load by 2 W every 6 sec. On another day, they were asked to drink 0.5 to 0.6 g/kg ethanol in 30 min, rest for 30 min, and then do the test. The expired gas analysis was used to measure changes in the anaerobic threshold and the respiratory compensation point. The blood concentrations of lactate, ethanol, and acetate also were measured. RESULTS: The anaerobic threshold showed no significant change in the case of exercise without alcoholic load. The respiratory compensation point decreased significantly in the case of alcoholic load (p < 0.001), and the interval from the anaerobic threshold to the respiratory compensation point decreased (p < 0.02). The blood concentration of lactate increased, after alcoholic load, to a level significantly higher than the level measured before the alcoholic load (p < 0.001). It showed a marked increase immediately after exercise stress (p < 0.001). The blood concentration of acetate tended to decrease after exercise load, but no significant change was noted. CONCLUSIONS: The anaerobic threshold, which is the limit of the aerobic glycolytic system (i.e., the so-called aerobic exercise limit) was not influenced by exercise under an acute alcoholic load. However, after the production of lactate started, the respiratory compensation point, which is the limit of the metabolic compensatory action, appeared earlier. This suggested that the intake of alcohol would influence the energy metabolism of skeletal muscles by a mechanism in which the disturbed metabolism of lactate in skeletal muscles was mainly involved.