Intermittent hypoxia promotes largemouth bassheart adaptation through increasing angiogenesis, reprogramming calcium signaling, and upregulating mitochondrial turnover

Intermittent hypoxia (IH) is a common phenomenon in ecological environment. At present, researchers have shown that fish can adapt to hypoxia through various ways as improve respiratory efficiency, promote angiogenesis, and reduce metabolism, but different tissues have different coping strategies. The heart is the key organ for coping with environmental pressure such as hypoxia and has physiological plasticity. However, the changes in the fish heart under hypoxia are still opaque. Here we used multi-level techniques such as western blot, immunohistochemistry and transmission electron microscopy to explore the effects of IH on heart. First, we found that IH induced a significant increase in the ratios of heart weight/ body weight (the HW/BW of IH group is approximately 1.24 times that of C group at D16) and more collagen deposition, accompanied by higher levels of plasma catenine (CA), heart myoglobin (Mb), and nitric oxide (NO). Second, IH promoted angiogenesis through increasing the content of hemoglobin (Hb) and Erythropoietin (EPO), and the expression of related genes and protein that regulated angiogenesis, the EPO concentration increased 0.61-fold after IH. Third, IH exposure altered calcium signals, the content of cytoplasmic and mitochondrial Ca2+ increased 0.67-fold and 0.63-fold respectively, the expression of calcium channels has also been altered. Finally, IH induced the enhancement of the mitochondrial function, the dynamic changes of fusion, division, biogenesis, and autophagy in mitochondria, and ultimately lead to the enhancement of the mitochondrial function. In conclusion, our study demonstrated that changing the structure, promoting angiogenesis, reprogramming Ca2+ signaling, and up-regulating mitochondrial turnover were the compensatory mechanisms of heart remodeling in the hypoxia adaptation of the largemouth bass.