The environment under which fish are maintained as broodstock before reproduction is often stressful; however, the impact of stress on broodstock and gamete quality is not well known. We investigated the effects of stress over the final stages (i.e. the 3 months preceding ovulation) of sexual maturation of female rainbow trout, Oncorhynchus mykiss, on their reproductive performance and physiology and that of their progeny. Stress was administered over the period of early vitellogenesis (one and a half months), late vitellogenesis-final maturation (one and a half months), or during both periods (three months). Each stress treatment and control was triplicated with eight females in each replicate (n=24 fish per treatment). The eggs and progeny of each female were kept separate and observations made for four months after transfer to rearing tanks. Cortisol levels were measured in plasma, ovarian fluid and eggs by radioimmunoassay. Fish that experienced stress during final maturation and those that were under stress during the whole experiment spawned on average two weeks earlier than the control group. In contrast, fish stressed during the period of early vitellogenesis spawned at the same time as the controls. Absolute fecundity and fertilization were not significantly affected in any treatment group; however, significant differences were found in relative fecundity. Stress applied early in vitellogenesis resulted in smaller eggs and swim-up fry; but, these differences were not found in juveniles 8 weeks after hatching. Furthermore, we found no differences in survival of the progeny or resistance to the fish pathogen Vibrio anguillarum. Circulating levels of cortisol were high at ovulation in all groups, but significantly less cortisol was observed in the ovarian fluid and eggs. Sex hormone concentrations were high in plasma; however, they were several orders of magnitude lower in the ovarian fluid. These differences were not as extreme as those observed for cortisol. Lower levels of cortisol and sex steroids in ovarian fluid and eggs compared to that which is available from plasma suggests that there is a mechanism by which the female protects the eggs from potentially deleterious effects of prolonged exposure to elevated concentrations of steroids.

Sustainable, "aerobic" exercise at 30 and 60% Ucrit is characterized by an initial (2 min) oxidative utilization of carbohydrate for ATP production. Within 15 min swimming at 30 and 60% Ucrit, PDH activation returns to resting values, and at 240 min increases in LCFA-carnitine and decreases in malonyl-CoA indicate an overall enhancement of lipid oxidation. (Abstract shortened by UMI.).

The metabolic role of chronically elevated cortisol in otherwise unstressed rainbow trout, Oncorhynchus mykiss, was examined. Fish were fitted with mini-osmotic pumps which maintained plasma cortisol levels at approximately 100 or 200 ng $\cdot$ mL$\sp{-1}$ for ten days. Plasma metabolites, liver enzyme activities, liver glycogen content, metabolic flux in isolated hepatocytes and alanine turnover were investigated. Plasma glucose, lactate and protein levels were unaffected by ten days of cortisol administration, despite a significant elevation in plasma cortisol. Plasma amino acids in cortisol treated fish (1023.8 $\pm$ 90.7 $\rm\mu g\cdot mL\sp{-1})$ were significantly elevated compared to shams $\rm(716.7\pm68.5\ \mu g\cdot mL\sp{-1})$ after nine days. Liver glycogen content was significantly reduced by cortisol treatment. The activities of the liver enzymes assayed were unchanged; likewise the fluxes of radioactive substrates to radiolabelled CO$\sb2,$ glucose, and protein in isolated hepatocytes were unaffected in trout with chronically elevated cortisol compared to shams. Both the caloric and water contents of white muscle were unaffected by chronically elevated circulating cortisol levels. The cortisol treatment did not alter the turnover of alanine. These data do not support the purported role of cortisol as a glucocorticoid in rainbow trout. While chronically elevated cortisol may increase the supply of plasma amino acids, the hormone does not appear to alter the manner in which these potential gluconeogenic substrates are metabolized. The absence of other stressors may be partially responsible for the differences between this study and others in the literature.