The impact of adult and lifelong hypoxia on ventricle phenotype in zebrafish ().

Hypoxia occurs naturally in a wide range of aquatic ecosystems. However, the physiological and morphological effects of prolonged hypoxia on organ systems remain poorly understood, especially in the cardiovascular system of fishes. We assessed the contractile force of isolated hearts from adult zebrafish from control conditions (Po = 21 kPa), from adults after a 4-wk exposure to hypoxia (Po = 10 kPa), or adults exposed to lifelong hypoxia (Po = 10 kPa) throughout development, from egg to adult. Isolated ventricle contractility measurements were conducted during two challenges: increasing stimulation frequency (force-frequency) and during acute hypoxia exposure. All contractile parameters were at least 35% greater in lifelong hypoxic fish compared with control fish, whereas heart mass was significantly smaller in lifelong hypoxic fish compared with controls. However, there were no differences in response to the force-frequency protocol or graded acute hypoxia. The thickness of the ventricle's compact myocardium was increased ∼35% by lifelong hypoxia but not by 4 wk of hypoxia as adults compared with the control fish. Furthermore, mitochondrial abundance did not significantly change. Collectively, these data suggest that early-life hypoxia has major effects on remodeling cardiac tissue and performance in zebrafish. In adult zebrafish, morphological and functional changes in the ventricle phenotype are dependent on the timing of the hypoxic exposure. Exposure to hypoxia as an adult did not alter the ventricle phenotype, unlike the changes caused by continuous hypoxic exposure from the embryonic to adult phase. Thus, exposure to hypoxia before the adult phase life results in changes in the zebrafish ventricle. However, adults may lack the plasticity needed to respond to hypoxic environments.