1. Maternal hormones during embryogenesis act as a bridge between the maternal and the offspring environment and consequently may allow maternal pre-programming of offspring phenotype to the environment, assuming that maternal environment is a reliable predictor of offspring environment. 2. We use an orthogonal experimental design in which we increase plasma corticosterone concentration (vs. control) in placentotrophic gravid female spotted skinks (Niveoscincus ocellatus) and their offspring. We hypothesize that high concentrations of maternal corticosterone allow offspring phenotype to be pre-programmed to better cope with high concentrations of corticosterone after birth and, consequently, offspring would not suffer from its deleterious effects. We use growth as a measure of performance as corticosterone typically affects growth in reptiles. 3. High concentrations of maternal corticosterone had significant effects on offspring body condition at birth which could have resulted from corticosterone passing through the complex placenta and/or from the indirect effects of corticosterone on maternal body condition. 4. There was no indication of maternal pre-programming to high concentrations of corticosterone postpartum: growth rate of offspring placed in the same treatment (corticosterone vs. control) than their mother was not different to growth rate of offspring placed in a different treatment than their mother. 5. Maternal pre-programming to corticosterone may not have been selected for in this species either because maternal chronic stress is not a reliable predictor of offspring chronic stress or because maternal pre-programming does not outweigh the costs of having reduced sensitivity to the hormone, resulting in slower, less appropriate reactions in stressful conditions. This study further demonstrates the highly versatile and context-dependent nature of maternal effects and the trade-offs between costs and benefits of maternal pre-programming.