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January 22, 2026Nutrients1 citationsOpen Access

Effects of Voluntary Exercise and Acetic Acid Supplementation on Skeletal Muscle Mitochondrial Function in Ovariectomized Mice

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KPK. ParkYKYoonhwan KIMYTYuan Tan

Key Points

  • This research aims to explore how voluntary exercise and acetic acid supplementation affect mitochondrial function in ovariectomized mice.
  • Used female C57BL/6J mice, assigned to sham, OVX, OVX with exercise, OVX with acetic acid, and OVX with both interventions groups.
  • Administered 5% sodium acetate-supplemented chow and/or voluntary exercise for 13 weeks post-recovery from OVX.
  • Assessed body composition, glucose tolerance, total energy expenditure, and mitochondrial function in skeletal muscle.
  • OVX led to impaired metabolism and reduced mitochondrial function, particularly in the gastrocnemius muscle.
  • Neither exercise nor acetic acid alone reversed mitochondrial dysfunction.
  • The combination of exercise and acetic acid significantly improved mitochondrial function in OVX mice.

Abstract

Background: Estrogen deficiency following human menopause or rodent ovariectomy (OVX) induces adverse alterations in body composition and metabolic function. This study investigated the combined effects of acetic acid supplementation and voluntary exercise on metabolic health and skeletal muscle mitochondrial function using an OVX mouse model. Methods: Forty female C57BL/6J mice (8 weeks old) were randomly assigned to 5 groups: sham (SHM), ovariectomized control (OVX), OVX with exercise (OVX-E), OVX with acetic acid (OVX-A), and OVX with both interventions (OVX-AE). Following a 1-week recovery from OVX, a 13-week intervention was initiated: 5% sodium acetate-supplemented chow and/or voluntary wheel running. Body composition, glucose tolerance, total energy expenditure, skeletal muscle mitochondrial function, and the contents of AMPKα, PGC-1α, and carbonyl protein were assessed. Results: OVX impaired whole-body metabolism and skeletal muscle mitochondrial function, specifically in the gastrocnemius muscle. While the exercise alone failed to mitigate the OVX-induced mitochondrial dysfunction, the combined treatment of exercise and acetic acid supplementation significantly rescued from the OVX-induced mitochondrial dysfunction. Conclusions: OVX resulted in detrimental changes in whole-body metabolism, but voluntary exercise and/or acetic acid supplementation had no rescuing effects on those parameters. In gastrocnemius muscle, acetic acid supplementation during exercise enhanced mitochondrial function in OVX mice.

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Cite This Study

Park et al. (2026) studied this question.

synapsesocial.com/papers/6971bd4c642b1836717e1f24https://doi.org/10.3390/nu18020332
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