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Effects of chronic alcohol intoxication on aerobic exercise-induced adaptations in female mice.

Abigail L Tice,Bradley S. Gordon,Emma Fletcher,Addison McNeill,Grant R. Laskin,Joseph A. Laudato,Michael L. Rossetti,Panagiotis Koutakis,Jennifer L. Steiner

Published 2024 in Journal of applied physiology

ABSTRACT

Chronic alcohol intoxication decreases muscle strength/function and causes mitochondrial dysfunction. Aerobic exercise training improves mitochondrial oxidative capacity and increases muscle mass and strength. Presently, the impact of chronic alcohol on aerobic exercise-induced adaptations was investigated. Female C57BL/6Hsd mice were randomly assigned to one of 4 groups: control sedentary (CON SED; n=26), alcohol sedentary (ETOH SED; n=27), control exercise (CON EX; n=28), and alcohol exercise (ETOH EX; n=25). Exercise mice had running wheel access for 2hrs a day, 7 days a week. All mice were fed either control or alcohol-containing liquid diet. Grip strength testing and EchoMRI were performed before and after the interventions. After 6 weeks, hindlimb muscles were collected for molecular analyses. A subset of mice performed a treadmill run to fatigue (RTF), then abstained from alcohol for 2 weeks and repeated the RTF. Alcohol decreased lean mass and forelimb grip strength compared to control-fed mice. Alcohol blunted the exercise induced increase in muscle mass (plantaris and soleus), type IIa fiber percentage in the plantaris and run time to fatigue. Mitochondrial markers (Citrate synthase activity and Complex I-IV, COXIV and Cytochrome C protein expression), were increased with exercise regardless of ETOH in the gastrocnemius but not tibialis anterior muscle. Two-weeks of alcohol abstinence improved RTF time in ETOH EX but not in ETOH SED. While these data suggest alcohol impairs some exercise-induced adaptations in skeletal muscle, not all were negatively affected, indicating exercise may be a beneficial behavior even while consuming alcohol.

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