Chronic hypoxia exposure of trout embryos alters swimming performance and cardiac gene expression in larvae.

Hypoxia exposure during embryonic development of rainbow trout causes developmental delay and bradycardia and alters the ontogeny of cardiac regulatory control mechanisms. The purpose of this study was to characterize how hypoxia exposure from the day of fertilization until stage 34 (57 d postfertilization) affects the aerobic fitness and growth of the hatched fish at multiple stages. In addition, we characterized the expression of gene transcripts for seven troponin I (TnI) isoforms to examine the effect of hypoxia treatment on cardiac muscle development. Results demonstrate that the critical swimming speed of the hypoxia-exposed fish was significantly less than that of the control group at stage 35 and the fry stage. Growth was reduced in the hypoxia-treated fish between stages 35 and 37, as was the relative lipid content at stage 37. Finally, six TnI isoforms were found in all hearts. One of these isoforms, RTcTnI, decreased in abundance between stage 35 and the fry stage, but hypoxia-exposed fish had higher levels than did controls at the fry stage. The abundance of AScTnI2 was significantly lower in hypoxia-exposed fry fish than in controls. These results indicate that chronic hypoxia exposure during embryonic development has long-term consequences on aerobic fitness, growth, and cardiac gene expression following hatch.