Mechanisms to explain purse seine bycatch mortality of coho salmon.

Research on fisheries bycatch and discards frequently involves the assessment of reflex impairment, injury, or blood physiology as means of quantifying vitality and predicting post-release mortality, but exceptionally few studies have used all three metrics concurrently. We conducted an experimental purse seine fishery for Pacific salmon in the Juan de Fuca Strait, with a focus on understanding the relationships between different sublethal indicators and whether mortality could be predicted in coho salmon (Oncorhynchus kisutch) bycatch. We monitored mortality using a ~24-h net pen experiment (N = 118) and acoustic telemetry (N = 50), two approaches commonly used to assess bycatch mortality that have rarely been directly compared. Short-term mortality was 21% in the net pen experiment (~24 h) and estimated at 20% for telemetry-tagged fish (~48-96 h). Mortality was predicted by injury and reflex impairment, but only in the net pen experiment. Higher reflex impairment was mirrored by perturbations to plasma ions and lactate, supporting the notion that reflex impairment can be used as a proxy for departure from physiological homeostasis. Reflex impairment also significantly correlated with injury scores, while injury scores were significantly correlated with plasma ion concentrations. The higher time-specific mortality rate in the net pen and the fact that reflexes and injury corresponded with mortality in that experiment, but not in the telemetry-tagged fish released into the wild could be explained partly by confinement stress. While holding experiments offer the potential to provide insights into the underlying causes of mortality, chronic confinement stress can complicate the interpretation of patterns and ultimately affect mortality rates. Collectively, these results help refine our understanding of the different sublethal metrics used to assess bycatch and the mechanisms that can lead to mortality.

Genomic and metabolic preparation of muscle in sockeye salmon Oncorhynchus nerka for spawning migration.

Prolonged endurance exercise and fasting are two major metabolic challenges facing Pacific salmon during spawning migrations that often occur over 1,000 km. Because both prolonged exercise and fasting stimulate the oxidation of lipids, particularly in heavily recruited tissues such as muscle, we sought to investigate the regulatory mechanisms that establish and maintain the capacity for substrate oxidation at four separate locations during the final 750 km of nonfeeding migration in sockeye salmon Oncorhynchus nerka. Transcript levels of multiple genes encoding for important regulators of lipid, carbohydrate, and protein oxidation as well as the activity of several important enzymes involved in lipid and carbohydrate oxidation were examined in red and white muscle. We found in both muscle types that the messenger RNA (mRNA) expression of carnitine palmitoyltransferase I isoforms, peroxisome proliferator-activated receptors α and ß, and adenosine monophosphate-activated protein kinase ß1 were all significantly higher at the onset compared to later stages of nonfeeding migration. However, the activities of ß-hydroxyacyl-CoA dehydrogenase and citrate synthase were higher only early in migration and only in red muscle. Later in the migration and as muscle lipid stores were greatly depleted, the mRNA levels of hexokinase I and aspartate aminotransferase increased in white muscle. Overall, at the onset of migration, high transcript and metabolic enzyme activity levels in skeletal muscle of sockeye salmon may help support the high rates of lipid oxidation needed for endurance swimming. Furthermore, we suggest that the muscle capacity to use carbohydrates and proteins may be adjusted throughout migration on an as-needed basis to fuel burst exercise through very difficult hydraulic passages in the river and perhaps during mating activities.