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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.