# Chronic Hypoxia Reduced the Growth and Muscle Quality in Turbot, Scophthalmus maximus

**Authors:** Zhongmin Guo, Yuexing Zhang, Yuliang Wei, Chenchen Bian, Mengqing Liang, Zhenyu Du, Houguo Xu, Qiang Ma

PMC · DOI: 10.3390/ani16060861 · Animals : an Open Access Journal from MDPI · 2026-03-10

## TL;DR

Chronic low oxygen levels harm turbot growth and meat quality by affecting metabolism and muscle composition.

## Contribution

This study reveals how chronic hypoxia impacts turbot growth, energy metabolism, and meat quality in aquaculture.

## Key findings

- Chronic hypoxia reduced turbot growth, body indexes, and feed efficiency.
- Muscle quality declined due to lower amino acids, protein, and glycogen.
- Hypoxia activated the hif1α/vegfa pathway, increasing liver angiogenesis.

## Abstract

Flatfish are highly intolerant to hypoxia stress; thus, clarifying the adaptation mechanisms of flatfish to chronic hypoxia is of great significance for healthy aquaculture development. In this study, the turbot (Scophthalmus maximus) was reared under either normoxia or chronic hypoxia conditions for 8 weeks. The results suggested that chronic hypoxia significantly decreased growth, body indexes, feed efficiency, whole fish lipid content, and liver n-3 polyunsaturated fatty acid levels in the turbot. In addition, chronic hypoxia decreased meat hardness, springiness, and chewiness by reducing the muscle’s total amino acid, soluble protein, glycogen contents, and myofiber numbers. These results illustrated the mechanisms of adaptation to chronic hypoxia in flatfish.

Hypoxia is a common environmental stress in nature and aquaculture, but the adaptation mechanisms of flatfish to chronic hypoxia and its effects on flesh quality remain unclear. In this study, the turbot was cultured at control normoxia (CON, 6.5 ± 0.5 mg/L) or chronic hypoxia (CHO, 3.5 ± 0.5 mg/L) for 8 weeks; then, the growth, energy metabolism, meat quality, and the expression of related genes were measured. The CHO group significantly reduced the digestibility (p < 0.05), weight gain (p < 0.001), and body indexes (p < 0.01), but increased feed conversion ratio (p < 0.001) in turbot. Meanwhile, the CHO group decreased muscle texture, total amino acid, soluble protein (p < 0.001), glycogen contents, and myofiber numbers (p < 0.001), while increasing myofiber diameters and lactate content (p < 0.01). In addition, chronic hypoxia increased the hepatic angiogenesis by activating the hif1α/vegfa pathway (p < 0.05) and decreased the whole fish lipid content and liver n-3 polyunsaturated fatty acid levels (p < 0.05). In summary, chronic hypoxia reduced the growth, nutrient content, and flesh quality of turbot. This study provides important references for elucidating the adaptation mechanisms of flatfish to chronic hypoxia and for developing mitigation strategies.

## Linked entities

- **Genes:** HIF1A (hypoxia inducible factor 1 subunit alpha) [NCBI Gene 3091], VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422]
- **Chemicals:** lactate (PubChem CID 61503)
- **Species:** Scophthalmus maximus (taxon 52904)

## Full-text entities

- **Diseases:** Chronic Hypoxia (MESH:D000860)
- **Chemicals:** n-3 polyunsaturated fatty acid (MESH:D015525), glycogen (MESH:D006003), amino acid (MESH:D000596), lipid (MESH:D008055), CHO (-), lactate (MESH:D019344)
- **Species:** Scophthalmus maximus (turbot, species) [taxon 52904]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13023279/full.md

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13023279/full.md

## References

47 references — full list in the complete paper: https://tomesphere.com/paper/PMC13023279/full.md

---
Source: https://tomesphere.com/paper/PMC13023279