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

**Authors:** Ki-Woong Park, Yoonhwan Kim, Yuan Tan, Byung-Jun Ryu, Seung-Min Lee, Hanall Lee, Byunghun So, Jinhan Park, Junho Jang, Chounghun Kang, Taewan Kim, Jinkyung Cho, Moon-Hyon Hwang, Jae-Geun Kim, Yong Kyung Kim, Young-Min Park

PMC · DOI: 10.3390/nu18020332 · 2026-01-20

## TL;DR

This study explores how exercise and acetic acid affect muscle mitochondria in mice with estrogen deficiency, finding that the combination improves mitochondrial function.

## Contribution

The novel finding is that acetic acid supplementation during exercise rescues mitochondrial dysfunction in ovariectomized mice.

## Key findings

- OVX impaired whole-body metabolism and skeletal muscle mitochondrial function.
- Exercise alone did not mitigate OVX-induced mitochondrial dysfunction.
- Combined acetic acid supplementation and exercise rescued 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.

## Linked entities

- **Proteins:** PPARGC1A (PPARG coactivator 1 alpha)
- **Chemicals:** acetic acid (PubChem CID 176), sodium acetate (PubChem CID 517045)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Ppargc1a (peroxisome proliferative activated receptor, gamma, coactivator 1 alpha) [NCBI Gene 19017] {aka A830037N07Rik, Gm11133, PGC-1, PPARGC-1-alpha, Pgc-1alpha, Pgc1}
- **Diseases:** Estrogen (MESH:D056828), mitochondrial dysfunction (MESH:D028361)
- **Chemicals:** Acetic Acid (MESH:D019342), glucose (MESH:D005947), sodium acetate (MESH:D019346)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12845058/full.md

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Source: https://tomesphere.com/paper/PMC12845058