This paper reviews a series of recent studies on the effect of adaptation to chronic stress on pubertal development in the common carp. In pre-pubertal male common carp adaptation to temperature stress caused a retardation of testicular development. Stress-induced delay of the first wave of spermatogenesis could be prevented by treatment with a cortisol antagonist, indicating that the stress effect is mediated by cortisol. Chronically elevated cortisol levels affected all parts of the brain-pituitary-gonad (BPG)-axis. In the hypothalamus lower levels of sGnRH were observed, in the pituitary the steady state levels of FSHbeta-m RNA were decreased, while the testicular production of especially the 11-oxygenated androgens 11-ketoandrostenedione (OA) and 11keto-testosterone (11KT) was strongly diminished. OA and 11KT have been shown to promote testicular development in fish. The LH-induced androgen synthesis in vitro was strongly inhibited by cortisol and its agonist dexamethasone. Although cortisol was shown also to interfere with the synthesis of the 11-oxygenated androgens in vivo, the lower androgen levels induced by cortisol were mainly due to the reduced testicular mass. Restoration of the plasma concentrations of these androgens by implantation could not prevent the cortisol-induced retardation of testicular growth and the first wave of spermatogenesis. Therefore, it is suggested that cortisol acts directly on Sertoli cells and/or on germ cells, which is supported by the demonstration of GRs on germ cells. We have little indication that the cortisol-induced retardation of testicular development is mediated by a decreased secretion of LH, but a crucial role for FSH can not be excluded.