# Influence of Neonatal Exposure to Hyperoxia on Skeletal Muscle in a Rat Model

**Authors:** Kentaro Awata, Irena Santosa, Yoshiteru Arai, Mayu Nakagawa, Hiroki Suganuma, Hiromichi Shoji

PMC · DOI: 10.3390/pediatric17060125 · Pediatric Reports · 2025-11-14

## TL;DR

Exposure to high oxygen levels in newborn rats leads to skeletal muscle changes that could affect them into adulthood.

## Contribution

The study reveals novel effects of early hyperoxia on skeletal muscle development in a rat model.

## Key findings

- Hyperoxia-exposed rats showed increased protein expression of Atrogin-1, adipophilin, myogenic differentiation factor 1, and myogenin.
- Myofiber size in the gastrocnemius muscle was reduced in hyperoxia-exposed rats compared to controls.
- No significant changes were observed in slow or fast myosin heavy chain protein expression.

## Abstract

Background/Objectives: Premature births below 32 weeks of gestation generally require respiratory oxygen support, leading to a relatively hyperoxic environment compared to in utero conditions. Transient hyperoxia exposure has been linked to an elevated risk of chronic lung disease and retinopathy of prematurity; however, its effects on skeletal muscles remain elusive. This study aimed to investigate the effects of hyperoxic exposure in rats as a model of premature infants receiving supplemental oxygen (30–60% O2 for several weeks). We hypothesized that rats exposed to postnatal hyperoxia would exhibit muscle fiber atrophy and alterations in fiber type. Methods: We used a rat model in which newborns were exposed to 80% oxygen from birth until postnatal day 12. We assessed the gastrocnemius muscles of rat legs at 12 weeks. Results: Rats exposed to hyperoxia showed substantially increased protein expression of Atrogin-1, along with elevated levels of adipophilin, myogenic differentiation factor 1, and myogenin. No significant changes were observed in the expression of slow or fast myosin heavy chain proteins. However, myofiber size in the gastrocnemius muscle was reduced in the hyperoxia-exposed group compared to the control group. Conclusions: Thus, transient hyperoxia exposure during early life can impede skeletal muscle development, potentially extending into adulthood.

## Linked entities

- **Genes:** Fbxo32 (F-box protein 32) [NCBI Gene 67731], myog.S (myogenin S homeolog) [NCBI Gene 373806]
- **Proteins:** Fbxo32 (F-box protein 32), plin2 (perilipin 2), myog.S (myogenin S homeolog)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Fbxo32 (F-box protein 32) [NCBI Gene 171043] {aka Atrogin1, MAFbx}, Myog (myogenin) [NCBI Gene 29148]
- **Diseases:** lung disease (MESH:D008171), retinopathy of prematurity (MESH:D012178), Hyperoxia (MESH:D018496), muscle fiber atrophy (MESH:D009133)
- **Chemicals:** O2 (MESH:D010100)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12641656/full.md

## References

16 references — full list in the complete paper: https://tomesphere.com/paper/PMC12641656/full.md

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Source: https://tomesphere.com/paper/PMC12641656