Abstract
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.