Moser Samantha E, Brown Austin M, Ganjayi Muni Swamy, Otis Jeffrey S, Baumann Cory W
Department of Kinesiology and Health, Georgia State University, GA.
Med Sci Sports Exerc. 2023 May 1;55(5):873-883. doi: 10.1249/MSS.0000000000003118. Epub 2023 Jan 5.
Alcoholics develop muscle atrophy and weakness from excessive ethanol (EtOH) intake. To date, most research has examined outcomes of alcohol-induced atrophy and weakness under basal or unstressed conditions despite physical stress being a normal occurrence in a physiological setting. Therefore, this study set out to determine if recovery of torque is impaired after repetitive bouts of physical stress in skeletal muscle during excessive short-term (experiment 1) and long-term (experiment 2) EtOH consumption.
Twenty male and female mice were assigned to receive either 20% EtOH in their drinking water or 100% water. Short- and long-term consumption was predetermined to be EtOH intake starting at 4 and 26 wk, respectively. Anterior crural muscles performed repeated bouts of physical stress using in vivo eccentric contractions, with tetanic isometric torque being measured immediately pre- and postinjury. A total of 10 bouts were completed with 14 d between each bout within bouts 1-5 (experiment 1) and bouts 6-10 (experiment 2), and 12 wk between bouts 5 and 6.
Mice consuming EtOH had blood alcohol concentrations up to 270 mg·dL -1 . In experiment 1, five bouts of eccentric contractions did not reduce recovery of torque, regardless of sex or EtOH treatment ( P ≥ 0.173). Similarly, in experiment 2, preinjury torques did not differ from day 14 values regardless of sex or treatment ( P ≥ 0.322). However, there was a group effect in female mice for bouts 6 and 10 during experiment 2, with female EtOH mice being weaker than controls ( P ≤ 0.002).
Excessive short- or long-term EtOH misuse in a mouse model did not affect the muscle's ability to regain strength after repeated bouts of eccentric contractions, suggesting that EtOH may not be as detrimental to recovery as once predicted.
酗酒者因过量摄入乙醇（EtOH）而出现肌肉萎缩和无力。迄今为止，尽管身体应激在生理环境中是正常现象，但大多数研究都考察了在基础或无应激条件下酒精诱导的萎缩和无力的结果。因此，本研究旨在确定在短期（实验1）和长期（实验2）过量摄入EtOH期间，骨骼肌在反复遭受身体应激后扭矩恢复是否受损。
将20只雄性和雌性小鼠分为两组，分别给予含20% EtOH的饮用水或100%的水。短期和长期摄入的EtOH量分别预先设定为从第4周和第26周开始。使用体内离心收缩对股前肌进行反复的身体应激，在损伤前后立即测量强直等长扭矩。在第1 - 5次（实验1）和第6 - 10次（实验2）应激期间，每次应激之间间隔14天，共完成10次应激，第5次和第6次应激之间间隔12周。
摄入EtOH的小鼠血液酒精浓度高达270 mg·dL -1 。在实验1中，五次离心收缩应激并未降低扭矩恢复，无论性别或EtOH处理如何（P≥0.173）。同样，在实验2中，无论性别或处理如何，损伤前的扭矩与第14天的值无差异（P≥0.322）。然而，在实验2的第6次和第10次应激中，雌性小鼠存在组效应；摄入EtOH的雌性小鼠比对照组弱（P≤0.002）。
在小鼠模型中，短期或长期过量滥用EtOH并不影响肌肉在反复离心收缩应激后恢复力量的能力，这表明EtOH对恢复的损害可能不像曾经预测的那么严重。
