Chui L A, Munsat T L, Craig J R
Muscle Nerve. 1978 Jan-Feb;1(1):57-61. doi: 10.1002/mus.880010108.
Several studies have suggested that muscle lactic acid production is defective in alcoholic myopathy. However, normal controls have not been evaluated. To study the effects of ethanol on the production of lactic acid in normal exercised muscle, oral ethanol (1 g per kg body weight, 20% v/v) was given to eight nonalcoholic subjects. Forearm ischemic exercise with a total work load of 7.2 kg-m/min was performed just before and 90 min after ingestion of ethanol. At the time of exercise, the serum ethanol level was 95.7 +/- 15.1 mg% (mean +/- SD). Resting serum lactic acid was significantly higher after ingestion of ethanol (15.7 +/- 4.5 mg%) than before (8.5 +/- 4.7 mg%). Lactic acid generation with ischemic exercise was significantly lower after ethanol ingestion. The mean peak serum lactic acid level (expressed as percentage elevation above resting) was 330.5 +/- 118.2% before and 127.9 +/- 75.1% after (p less than .05). These results indicate that a single oral dose of ethanol decreases lactic acid production by exercised muscle in normal subjects.
多项研究表明，酒精性肌病患者的肌肉乳酸生成存在缺陷。然而，尚未对正常对照组进行评估。为了研究乙醇对正常运动肌肉中乳酸生成的影响，对8名非酒精依赖受试者口服乙醇（每千克体重1克，体积分数20%）。在摄入乙醇前及摄入后90分钟进行前臂缺血性运动，总工作量为7.2千克-米/分钟。运动时，血清乙醇水平为95.7±15.1毫克%（均值±标准差）。摄入乙醇后静息血清乳酸（15.7±4.5毫克%）显著高于摄入前（8.5±4.7毫克%）。乙醇摄入后缺血性运动时的乳酸生成显著降低。血清乳酸峰值水平均值（以高于静息水平的百分比表示）在摄入乙醇前为330.5±118.2%，摄入后为127.9±75.1%（p<0.05）。这些结果表明，单次口服乙醇会降低正常受试者运动肌肉的乳酸生成。
