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Thermal acclimation can enhance heat tolerance in cold-water fish, but the associated multi-tissue histological changes, energy-metabolism indices, and cellular stress-response gene expression patterns in Atlantic salmon ( Salmo salar ) remain unclear. Juvenile Atlantic salmon initially maintained at 16 °C were acclimated at 23 °C for 45 d, returned to 16 °C for 48 h, and then exposed acutely to 23 or 26 °C. Thermal acclimation significantly increased the critical thermal maximum ( CT max ) by about 2 °C, and the elevated CT max persisted after 48 h at 16 °C. Histological analysis revealed gill lamellar thickening, lamellar bending and shortening, epithelial lifting, epithelial vacuolization, and mucous cell hypertrophy. In skeletal muscle, acclimation enhanced the proportion of smaller fibers but reduced that of large fibers. Glycogen and triglyceride contents declined significantly in both liver and skeletal muscle, while lactate dehydrogenase (LDH) and malate dehydrogenase (MDH) activities were markedly elevated only in the liver. After acclimated fish were returned to 16 °C for 48 h, the expression of selected stress-response genes, including hsp10, hsp70, gpx , and gr , was remarkably higher in the intestine and skeletal muscle than in non-acclimated fish. During acute heat exposure, acclimated fish showed tissue- and temperature-specific transcriptional responses. At 23 °C, several heat-shock protein-encoding genes were suppressed in acclimated fish, whereas antioxidant defense-related genes were selectively upregulated. At 26 °C, intestinal stress-response genes were broadly upregulated; hepatic responses mainly involved gclc and gr , and the skeletal muscle transcription of hsp30 and gclc was enhanced. Overall, prolonged warm acclimation induced persistent changes in thermal tolerance, tissue morphology, energy metabolism, and stress-response gene expression in juvenile Atlantic salmon.
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Song et al. (2026) studied this question.
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