Abstract

AbstractPrevious studies conducted at the Cle Elum Spring Chinook Salmon Supplementation Hatchery in Washington State demonstrated that 37–49% of the male Chinook salmon Oncorhynchus tshawytscha released from this facility in its first years of operation precociously matured at age 2 rather than the more typical age 4. We examined the effects of altering seasonal growth rate on the incidence of age‐2 male maturation in an experimental subset of that population and compared their physiological development (size, growth rate, condition factor, whole‐body lipid, gill Na+,K+‐ATPase activity, and plasma insulin‐like growth factor‐I [IGF‐I]) with that of both hatchery (production) and wild fish. Altering summer and autumn rations resulted in four growth trajectories with the following size and precocious male maturation rates: The high summer—high autumn growth trajectory produced fish averaging 25 g and 69% precocious maturation; the high summer—low autumn trajectory yielded fish that averaged 18 g and exhibited 58% precocious maturation; the low summer—high autumn trajectory produced 18‐g fish with 51% precocious maturation; and the low summer—low autumn trajectory yielded fish averaging 16 g and 42% precocious maturation. Production fish averaged 22 g and exhibited a 53% precocious maturation rate. The high summer growth treatments and production fish were largest among all groups and had higher plasma IGF‐I, adiposity levels, and precocious male maturation rates than did the low summer growth treatments. Wild fish were significantly smaller and leaner and had much lower plasma IGF‐I levels than all other groups. Gill Na+,K+‐ATPase activity was not different between groups, suggesting that there was no differential effect on smoltification. Growth modulation reduced the precocious male maturation rate by 39% among experimental treatments and by 21% between production fish and the low—low treatment. However, the maturation rate and adiposity of hatchery fish differed markedly from those of wild fish, suggesting that more dramatic alterations of rearing regime may be required to further reduce the prevalence of this phenotype in cultured fish.

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