# Blood, sweat, tears and fibrosis: when overtraining injures the liver

**Authors:** Enis Kostallari

PMC · DOI: 10.20517/evcna.2025.56 · Extracellular Vesicles and Circulating Nucleic Acids · 2025-11-10

## TL;DR

Excessive exercise can harm the liver by promoting fibrosis through signals from muscle cells, according to a new study.

## Contribution

The study reveals that overtraining causes liver fibrosis via myocyte-derived small extracellular vesicles.

## Key findings

- Overtraining promotes liver fibrosis through myocyte-derived small extracellular vesicles.
- Excessive exercise may impair mitochondrial function and liver health.
- Physical exercise can improve insulin sensitivity and hepatic steatosis in some liver disease patients.

## Abstract

The crosstalk between the skeletal muscles and the liver is receiving growing attention, as patients with chronic liver disease often develop a loss of skeletal muscle mass. In these patients, particularly those with metabolic dysfunction-associated steatotic liver disease, physical exercise improves insulin sensitivity and hepatic steatosis. However, excessive exercise may impair mitochondrial function, inflammation, and liver health. The study by Liu et al. demonstrates that overtraining promotes liver fibrosis through myocyte-derived small extracellular vesicles. Here, we comment on the novelty of these findings and areas to be developed in the future.

## Linked entities

- **Diseases:** metabolic dysfunction-associated steatotic liver disease (MONDO:0013209)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** hepatic steatosis (MESH:D005234), metabolic dysfunction (MESH:D008659), inflammation (MESH:D007249), liver disease (MESH:D008107), liver fibrosis (MESH:D008103), fibrosis (MESH:D005355), loss of skeletal muscle mass (MESH:C536030)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

14 references — full list in the complete paper: https://tomesphere.com/paper/PMC12809390/full.md

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Source: https://tomesphere.com/paper/PMC12809390