Cardiac mitochondria function in embryonic and 1-year old American alligators, Alligator mississippiensis, is not altered by hypoxic incubation or an acute anoxic challenge.

Hypoxic conditions naturally occur in nests of egg laying reptiles including the American alligator, Alligator mississippiensis. The effects of developmental hypoxia have been delineated in several studies of this species, with changes in cardiovascular function persisting into juvenile life. However, several questions regarding the effects of developmental hypoxia remain. In this study we designed a series of experiments to quantify the effects of developmental hypoxia on permeabilized cardiac muscle fiber mitochondrial respiration, reactive oxygen species production, and response to acute anoxia in American alligators. Alligator eggs were incubated in 21% O (normoxia) or 10% O (hypoxia) at 30 °C beginning on day 14 of a 72-day incubation period through hatching. Animals were studied at two ages, at 90% of incubation and 1-year post hatching. Mitochondrial respiration and ROS production under leak and oxidative phosphorylation states were measured in permeabilized cardiac muscle fibers with high-resolution respirometry coupled with fluorometry. To examine the response of mitochondria to acute anoxia and subsequent reoxygenation, permeabilized cardiac muscle fibers were exposed to 20 min of anoxia, followed by reoxygenation during measurement of mitochondria respiration and ROS production. Hypoxic incubation resulted in a decrease in embryos mass which was maintained through the first year of juvenile life. Hypoxic incubation had no effect on cardiac mitochondria respiration or ROS production at either 90% of incubation or 1-year post hatching. After exposure to anoxia for 20 min, the rate of mitochondria respiration did not differ between the pre-anoxia respiration levels for all animals tested. There was no change in ROS production observed upon reoxygenation of the permeabilized cardiac muscle. Our results suggest that hypoxic incubation has little influence on cardiac myocyte mitochondrial physiology in the developing alligator and the cardiac mitochondria are resistant to acute bouts of anoxic exposure.