SUMMARYThis study evaluated the link between swimming endurance and condition of Atlantic cod Gadus morhua that had been fed or starved during the 16 weeks preceding the tests, and assessed whether muscle metabolic capacities explain such links. The condition factor [(somatic mass × fork length-3)×100] of starved cod was 0.54±0.1 whereas that of fed cod was 0.81±0.1. In white and red muscle, we measured four glycolytic enzymes: phosphofructokinase (PFK), pyruvate kinase (PK), creatine kinase (CK) and lactate dehydrogenase (LDH), two mitochondrial enzymes:cytochrome c oxidase (CCO) and citrate synthase (CS), a biosynthetic enzyme, nucleoside diphosphate kinase (NDPK), glycogen and protein levels and water content. Muscle samples were taken at three positions along the length of the fish; starvation affected the metabolic capacities of white muscle more than those of red muscle. The levels of glycolytic enzymes and glycogen changed more in white than red muscle during starvation. Both in fed and starved cod, muscle metabolic capacities varied with position along the fish;starvation reduced this longitudinal variation more in white than red muscle. In white muscle of fed cod, the glycolytic enzyme levels increased from head to tail, while in starved cod this longitudinal variation disappeared. In red muscle mitochondrial enzyme levels were highest in the caudal sample, but fewer differences were found for glycolytic enzymes. Swimming endurance was markedly affected by fish condition, with starved fish swimming only 30% of the time (and distance) of fed fish. This endurance was closely linked with the number of burst—coast movements during the test and the activity of CCO and LDH in white muscle. The number of burst—coast movements was significantly linked with condition factor and PFK activity in caudal red muscle and gill arch mass. Our data indicated that cod use both glycolytic and oxidative capacities to support endurance swimming. Furthermore, swimming endurance is linked with the metabolic capacities of red and white muscle.

SUMMARY The goal of the current study was to generate a comprehensive, multi-tissue perspective of the effects of chronic hypoxic exposure on carbohydrate metabolism in the Gulf killifish Fundulus grandis. Fish were held at approximately 1.3 mg l-1 dissolved oxygen (∼3.6 kPa) for 4 weeks, after which maximal activities were measured for all glycolytic enzymes in four tissues (white skeletal muscle, liver, heart and brain), as well as for enzymes of glycogen metabolism (in muscle and liver) and gluconeogenesis(in liver). The specific activities of enzymes of glycolysis and glycogen metabolism were strongly suppressed by hypoxia in white skeletal muscle, which may reflect decreased energy demand in this tissue during chronic hypoxia. In contrast, several enzyme specific activities were higher in liver tissue after hypoxic exposure, suggesting increased capacity for carbohydrate metabolism. Hypoxic exposure affected fewer enzymes in heart and brain than in skeletal muscle and liver, and the changes were smaller in magnitude, perhaps due to preferential perfusion of heart and brain during hypoxia. The specific activities of some gluconeogenic enzymes increased in liver during long-term hypoxic exposure, which may be coupled to increased protein catabolism in skeletal muscle. These results demonstrate that when intact fish are subjected to prolonged hypoxia, enzyme activities respond in a tissue-specific fashion reflecting the balance of energetic demands, metabolic role and oxygen supply of particular tissues. Furthermore, within glycolysis, the effects of hypoxia varied among enzymes, rather than being uniformly distributed among pathway enzymes.

the Ucrit tests, white muscle lactate levels and lactate accumulation per burst-coast movement were considerably higher in fed than starved cod, suggesting more intensive use of fast muscle fibres in cod in good condition. Multiple regression analysis indicated strong correlations between U crit, the speed at which regular burst-coasting began and the activity of pyruvate dehydrogenase (PDH) in red muscle (both caudal and central positions). PDH activity may limit the rate of oxidative ATP production by red muscle. The activity of cytochrome c oxidase in rostral white muscle was the strongest correlate of sprint swimming, suggesting that aerobic preparation of white muscle facilitates rapid contraction. The correlation between Ucrit and sprint swimming was weak, perhaps due to inter-individual differences in sensitivity during sprint tests.

To examine whether Atlantic cod maintain constant hierarchies of sprint speeds and muscle metabolic capacities under different feeding regimes, the physiological capacities of individual cod were followed through a starvation-feeding-starvation cycle. We examined sprint speeds and maximal enzyme activities in white-muscle biopsies at each period. We measured the glycolytic enzymes, phosphofructokinase (PFK) and lactate dehydrogenase (LDH), the mitochondrial enzyme, cytochrome C oxidase (CCO), and the biosynthetic enzyme, nucleotide diphosphate kinase (NDPK). Sprint speeds were measured in a laser diode/photocell-timed raceway. As expected, the feeding regime had a marked impact on the physiological capacities of cod, but the responses differed for sprint-swimming and muscle metabolic capacities. The different enzyme activities as well the condition index generally decreased during the first starvation, improved with feeding, and fell again during the second starvation. In contrast, sprint performance improved after feeding but did not fall with the second starvation. Although both the enzyme activities and the sprint speeds showed considerable interindividual variation, sprint speeds were not significantly correlated with the enzyme activities. The hierarchy of sprint performance of the cod was maintained, regardless of the preceding feeding regime, whereas those of muscle metabolic capacities were not.

The antipredator responses of adult and larval fathead minnows Pimephales promelas to chemical alarm cues prepared throughout ontogeny were tested using various behavioural assays. Larval epidermis was also examined during ontogeny using standard haematoxylin and eosin staining techniques. Adults elicited an antipredator response to chemical alarm cue made from larvae as young as 8-17 days post-hatch. Interestingly, larvae did not possess visible club cells until 28-37 days post-hatch and did not respond to conspecific chemical alarm cue until 48-57 days post-hatch. These results suggest that chemical alarm cue may not be contained within club cells and that the components of larval and adult chemical alarm cue may be similar throughout ontogeny.