No abstract

The purpose of this study was to assess the compensatory responses to food restriction and subsequent increased food availability in juvenile green turtles (Chelonia mydas). Turtles were fed an ad libitum ration for 12 weeks (AL), a restricted ration for 12 weeks (R), or a restricted ration for 5 weeks and an ad libitum ration for 7 weeks (R-AL). Analysis of covariance was used to test the relationships between (1) growth and body size, (2) intake and body size, and (3) growth and intake for each of the three treatment groups. Body composition of turtles in each group was also evaluated at the beginning of the study and after weeks 5 and 12. After the switch to ad libitum feeding, R-AL turtles consumed comparable amounts of food and grew faster than AL turtles on a size-adjusted basis, but mean body sizes did not converge, although the overlap in their size ranges increased with time. The R-AL turtles also converted food to growth more efficiently and allocated proportionally more nutrients to protein accretion, thereby restoring body composition (except mineral content) to AL levels by the end of the study. Thus, accelerated size-specific growth without hyperphagia restored body condition but not size. These results indicate that (1) intake in juvenile green turtles is maximal when food is readily available and cannot be increased to compensate for a previous period of food limitation, (2) growth rates of ad libitum-fed turtles are only mildly plastic in response to past nutritional history, and (3) priority rules for nutrient allocation favor the attainment of an optimal condition rather than an optimal size. Nutritional setbacks experienced during the vulnerable juvenile stage could therefore have long-lasting consequences for wild turtles in terms of size-specific mortality risk, but these risks may be mitigated by the potential benefits of maintaining sufficient body stores.

No abstract

Developing organisms interpret and integrate environmental signals to produce adaptive phenotypes that are prospectively suited for probable demands in later life. This plasticity can be disrupted when embryos are impacted by exogenous contaminants, such as environmental pollutants, producing potentially deleterious and long-lasting mismatches between phenotype and the future environment. We investigated the ability for in ovo environmental contaminant exposure to alter the growth trajectory and ovarian function of alligators at five months after hatching. Alligators collected as eggs from polluted Lake Apopka, FL, hatched with smaller body masses but grew faster during the first five months after hatching, as compared to reference-site alligators. Further, ovaries from Lake Apopka alligators displayed lower basal expression levels of inhibin beta A mRNA as well as decreased responsiveness of aromatase and follistatin mRNA expression levels to treatment with follicle stimulating hormone. We posit that these differences predispose these animals to increased risks of disease and reproductive dysfunction at adulthood.