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Simple Summary: Otoliths, which are calcium carbonate structures found in the inner ears of fish, can be used to describe the use of freshwater and saltwater habitats during the lifespan of fish. This is performed by looking at the ratio of strontium to calcium along the radius of an otolith, where a high ratio indicates the use of saltwater and a low ratio indicates the use of freshwater. We studied brown trout (Salmo trutta L.) from the Swedish River Emån. We found that most brown trout, as expected, spent the first 1–2 years of their lives in freshwater before migrating to the Baltic Sea. We also found that 13% spent considerably less than one year in the river, which was not expected based on classical life history patterns for brown trout. In addition, we found that brown trout, which ranged from 3 to 6 years of age, returned to freshwater 2.3 times, and the amount of time spent in freshwater after hatching was negatively related to the number of visits to freshwater. Previous studies have explained that precocial migration occurs when there is a risk of drought. This explanation cannot apply to the permanently flowing River Emån. By analyzing otolith microchemistry, we examined the use of freshwater and marine environments by brown trout Salmo trutta L. that spawn in the Swedish River Emån and migrate to the Baltic Sea. We estimated the time juveniles spent in freshwater and the number of times the fish returned to freshwater, presumably to spawn. Twenty-six percent of the fish migrated to sea by 1 year of age. However, 13% spent less than one year in the river. Most brown trout (48%) migrated to the sea between 1 and 2 years of age. On average, brown trout, which averaged 4.4 years in age (range 3–6 years), returned to freshwater 2.3 times, and there was an inverse relationship between time spent in freshwater after hatching and the number of visits to freshwater. Our results do not support the classical life history pattern, where brown trout spend one or more years in freshwater before migrating to the sea. Here, we found evidence that part of the population leaves freshwater during their first year. While the cause for precocial migration in the River Emån is not known, our results from this permanently flowing river do not support the idea proposed for other Baltic Sea populations, where the risk of drought has been suggested to be the cause. [ABSTRACT FROM AUTHOR]

Changes in the number, structure, and function of mitochondria during the early life stages of animals can play an important role for an organism's metabolic rate, growth, and health. Previous studies have shown that juvenile brown trout (Salmo trutta) subjected to elevated temperatures during the embryonic stage respond phenotypically with a reduced metabolic rate. The aim of this study was to explore if embryonic temperature affects the mitochondria content of young brown trout and as such explains the previously found differences in metabolic rates. Here, we optimize a quantitative PCR (qPCR) method for the mitochondria cytochrome c oxidase subunit I gene, and then use the method as a proxy for mitochondrial DNA content. We hypothesize that young trout subjected to elevated temperatures during the embryonic stage respond phenotypically with a reduced mitochondrial DNA content. To test this hypothesis, we subjected brown trout to either control ambient (4.4 ± 1.5 °C) or elevated temperatures (7.1 ± 0.6 °C) during embryogenesis. Subsequently, we extracted DNA from liver and white muscle tissue of juvenile brown trout from the two different incubation temperature treatments and successively optimized qPCR for mitochondrial DNA. We found that the amount of mitochondria DNA in liver tissue was 18 times higher than in white muscle tissue, but there was no significant difference in mitochondria content in liver or muscle tissue between brown trout exposed to elevated and ambient control temperatures during embryogenesis. We conclude that reduced metabolic rate is not likely associated with mitochondria DNA content. We also suggest that qPCR is a simple and cost-effective method to quantify mitochondria DNA in frozen and partly degraded tissue from different treatment groups and a useful proxy for identification of differences in mitochondria number. [ABSTRACT FROM AUTHOR]