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Incorporating host-pathogen(s)-environment axes into management and conservation planning is critical to preserving species in a warming climate. However, the role pathogens play in host stress resilience remains largely unexplored in wild animal populations. We experimentally characterized how independent and cumulative stressors (fisheries handling, high water temperature) and natural infections affected the health and longevity of released wild adult sockeye salmon (Oncorhynchus nerka) in British Columbia, Canada. Returning adults were collected before and after entering the Fraser River, yielding marine- and river-collected groups, respectively (N = 185). Fish were exposed to a mild (seine) or severe (gill net) fishery treatment at collection, and then held in flow-through freshwater tanks for up to four weeks at historical (14°C) or projected migration temperatures (18°C). Using weekly nonlethal gill biopsies and high-throughput qPCR, we quantified loads of up to 46 pathogens with host stress and immune gene expression. Marine-collected fish had less severe infections than river-collected fish, a short migration distance (100 km, 5-7 days) that produced profound infection differences. At 14°C, river-collected fish survived 1-2 weeks less than marine-collected fish. All fish held at 18°C died within 4 weeks unless they experienced minimal handling. Gene expression correlated with infections in river-collected fish, while marine-collected fish were more stressor-responsive. Cumulative stressors were detrimental regardless of infections or collection location, probably due to extreme physiological disturbance. Because river-derived infections correlated with single stressor responses, river entry probably decreases stressor resilience of adult salmon by altering both physiology and pathogen burdens, which redirect host responses toward disease resistance.

With regional hypoxic episodes in the world’s oceans becoming more severe and more frequent, a valuable management need will be a screening protocol to characterize the full diversity of hypoxic robustness among fishes (defined here as their tolerance and performance). Yet, high-throughput screening protocols to deal with the almost 33,000 fish species have the potential to trade off convenience with the information depth normally provided with comprehensive but more time-consuming phenotyping protocols. As a solution, we propose a two-tier testing approach, one that combines a simple, rapid, cost-effective, and well-established hypoxia challenge test (a measure of hypoxic tolerance) with an individual-based hypoxic performance test that defines maximum aerobic capacity over a wide range of ambient water oxygen levels (a hypoxic performance curve). The later test would be performed on selected indicator species identified from the tolerance screening test. Here we describe the two methodological approaches for this two-tier approach using some existing data to illustrate the potential for their applications in marine science.

Migratory fishes commonly encounter large and rapid thermal variation, which has the potential to disrupt essential physiological functions. Thus, we acclimated wild, migratory Arctic char to 13°C (∼7°C above a summer average) for an ecologically relevant period (3 days) and measured maximum heart rate (ƒH,max) during acute warming to determine their ability to rapidly improve cardiac function at high temperatures. Arctic char exhibited rapid compensatory cardiac plasticity similar to past observations following prolonged warm acclimation: they reduced ƒH,max over intermediate temperatures (−8%), improved their ability to increase ƒH,max during warming (+10%), and increased (+1.3°C) the temperature at the onset of an arrhythmic heartbeat, a sign of cardiac failure. This rapid cardiac plasticity may help migrating fishes such as Arctic char mitigate short-term thermal challenges. Furthermore, by using mobile Arctic research infrastructure in a remote field location, the present study illustrates the potential for field-based, experimental physiology in such locations.

Background Viruses can impose energetic demands on organisms they infect, in part by hosts mounting resistance. Recognizing that oxygen uptake reliably indicates steady-state energy consumption in all vertebrates, we comprehensively evaluated oxygen uptake and select transcriptomic messaging in sockeye salmon challenged with either a virulent rhabdovirus (IHNV) or a low-virulent reovirus (PRV). We tested three hypotheses relating to the energetic costs of viral resistance and tolerance in this vertebrate system: (1) mounting resistance incurs a metabolic cost or limitation, (2) induction of the innate antiviral interferon system compromises homeostasis, and (3) antiviral defenses are weakened by acute stress. Results IHNV infections either produced mortality within 1–4 weeks or the survivors cleared infections within 1–9 weeks. Transcription of three interferon-stimulated genes (ISGs) was strongly correlated with IHNV load but not respiratory performance. Instead, early IHNV resistance was associated with a mean 19% (95% CI = 7–31%; p = 0.003) reduction in standard metabolic rate. The stress of exhaustive exercise did not increase IHNV transcript loads, but elevated host inflammatory transcriptional signaling up to sevenfold. For PRV, sockeye tolerated high-load systemic PRV blood infections. ISG transcription was transiently induced at peak PRV loads without associated morbidity, microscopic lesions, or major changes in aerobic or anaerobic respiratory performance, but some individuals with high-load blood infections experienced a transient, minor reduction in hemoglobin concentration and increased duration of excess post-exercise oxygen consumption. Conclusions Contrary to our first hypothesis, effective resistance against life-threatening rhabdovirus infections or tolerance to high-load reovirus infections incurred minimal metabolic costs to salmon. Even robust systemic activation of the interferon system did not levy an allostatic load sufficient to compromise host homeostasis or respiratory performance, rejecting our second hypothesis that this ancient innate vertebrate antiviral defense is itself energetically expensive. Lastly, an acute stress experienced during testing did not weaken host antiviral defenses sufficiently to promote viral replication; however, a possibility for disease intensification contingent upon underlying inflammation was indicated. These data cumulatively demonstrate that fundamental innate vertebrate defense strategies against potentially life-threatening viral exposure impose limited putative costs on concurrent aerobic or energetic demands of the organism.

In recent decades, the relative proportion of female sockeye salmon (Oncorhynchus nerka) on spawning grounds of several British Columbia populations has declined. Coincident with the decline has been large changes to oceanic, estuarine, and river migration environments. Over the past 30 years, numerous telemetry tracking and laboratory studies have examined mortality of adult Fraser River sockeye salmon during ocean and freshwater migrations. We reviewed 19 studies that provided 40 situations where male and female mortality could be directly compared. Female mortality averaged 2.1 times greater than that of males and up to eightfold higher. High female mortality was also evident in migrating coho salmon (Oncorhynchus kisutch) and Chinook salmon (Oncorhynchus tshawytscha) and for sockeye salmon in other systems. Female mortality was highest when migration conditions were challenging (e.g., high or turbulent flows, high temperatures, confinement, or handling) and towards end of river migration. We review mechanisms for differential mortality, including energy exhaustion, cardiac performance, physiological stress, and immune factors. Female-specific mortality will become even more pronounced in coming years as ocean and riverine conditions continue to change.

Millions of liters of diluted bitumen (dilbit), a crude oil product from Canada's oil sands region, is transported through critical Pacific salmon habitat each day. While the toxicity of the water-soluble fraction of dilbit (WSFd) to early life-stages of salmon is known, quantitative data on life-stage differences in sensitivity to WSFd is missing. To fill this knowledge gap, we exposed two juvenile life-stages of coho salmon (O. kisutch) in parallel to very low (parts per billion), environmentally-relevant concentrations of WSFd for acute (48 h) and sub-chronic (4 wk) durations. The relative sensitivities of the two life-stages (fry and parr) were assessed by comparing the timing and magnitude of biological responses using common organismal and molecular endpoints of crude oil exposure. A significant reduction in body condition occurred in both fry and parr after 4 wk exposure to WSFd. Both life-stages also experienced a concentration-dependent decrease in time-to-loss-of-equilibrium during a hypoxia challenge test at both 48 h and 4 wk of exposure. Although organismal responses were similar, molecular responses were distinct between life-stages. In general, unexposed fry had higher baseline values of hepatic phase I biotransformation indicators than unexposed parr, but induction of EROD activity and cyp1a mRNA expression in response to WSFd exposure was greater in parr than in fry. Neither gst nor hsp70 mRNA expression, markers of phase II biotransformation and cell stress, respectively, were reliably altered by WSFd exposure in either life-stage. Taken together, results of this study do not support differential sensitivities of coho fry and parr to WSFd. All the same, the potential for ontogenic differences in the expression and induction of phase I biotransformation need to be considered because age does matter for these endpoints if they are used as bioindicators of exposure in post-spill impact assessments.

The hypoxic constraint on peak oxygen uptake (ṀO2,peak) was characterized in rainbow trout over a range of ambient oxygen tensions with different testing protocols and statistical models. The best-fit model was selected using both statistical criteria (R2 and AIC) and the model's prediction of three anchor points for hypoxic performance: critical PO2 (Pcrit), maximum ṀO2 and a new metric, the minimum PO2 that supports 50% of absolute aerobic scope (PAAS-50). The best-fitting model was curvilinear using five strategically selected PO2 values. This model predicted PAAS-50 as 70 mmHg (coefficient of variation, CV=9%) for rainbow trout. Thus, while a five-point hypoxic performance curve can characterize the limiting effects of hypoxia in fish, as envisaged by Fry over 75 years ago, PAAS-50 is a promising metric to compare hypoxic constraints on performance in a standardized manner both within and across fish species.

This analysis shows good intentions in the selection of valid and precise oxygen uptake ( M˙ O2 ) measurements by retaining only slopes of declining dissolved oxygen level in a respirometer that have very high values of the coefficient of determination, r2 , are not always successful at excluding nonlinear slopes. Much worse, by potentially removing linear slopes that have low r2 only because of a low signal-to-noise ratio, this procedure can overestimate the calculation of standard metabolic rate (SMR) of the fish. To remedy this possibility, a few simple diagnostic tools are demonstrated to assess the appropriateness of a given minimum acceptable r2 , such as calculating the proportion of rejected M˙ O2 determinations, producing a histogram of the r2 values and a plot of r2 as a function of M˙ O2 . The authors offer solutions for cases when many linear slopes have low r2 . The least satisfactory but easiest to implement is lowering the minimum acceptable r2 . More satisfactory solutions involve processing (smoothing) the raw signal of dissolved oxygen as a function of time to improve the signal-to-noise ratio and the r2 s.

Intraspecific variation in key traits such as tolerance of warming can have profound effects on ecological and evolutionary processes, notably responses to climate change. The empirical evidence for three primary elements of intraspecific variation in tolerance of warming in fishes is reviewed. The first is purely mechanistic that tolerance varies across life stages and as fishes become mature. The limited evidence indicates strongly that this is the case, possibly because of universal physiological principles. The second is intraspecific variation that is because of phenotypic plasticity, also a mechanistic phenomenon that buffers individuals' sensitivity to negative impacts of global warming in their lifetime, or to some extent through epigenetic effects over successive generations. Although the evidence for plasticity in tolerance to warming is extensive, more work is required to understand underlying mechanisms and to reveal whether there are general patterns. The third element is intraspecific variation based on heritable genetic differences in tolerance, which underlies local adaptation and may define long-term adaptability of a species in the face of ongoing global change. There is clear evidence of local adaptation and some evidence of heritability of tolerance to warming, but the knowledge base is limited with detailed information for only a few model or emblematic species. There is also strong evidence of structured variation in tolerance of warming within species, which may have ecological and evolutionary significance irrespective of whether it reflects plasticity or adaptation. Although the overwhelming consensus is that having broader intraspecific variation in tolerance should reduce species vulnerability to impacts of global warming, there are no sufficient data on fishes to provide insights into particular mechanisms by which this may occur.

This study hypothesized that oxygen uptake (ṀO2 ) measured with a novel protocol of chasing rainbow trout Oncorhynchus mykiss to exhaustion inside a static respirometer while simultaneously monitoring ṀO2 (ṀO2chase ) would generate the same and repeatable peak value as when peak active ṀO2 (ṀO2active ) is measured in a critical swimming speed protocol. To reliably determine peak ṀO2chase , and compare to the peak during recovery of ṀO2 after a conventional chase protocol outside the respirometer (ṀO2rec ), this study applied an iterative algorithm and a minimum sampling window duration (i.e., 1 min based on an analysis of the variance in background and exercise ṀO2 ) to account for ṀO2 dynamics. In support of this hypothesis, peak ṀO2active (707 ± 33 mg O2 h-1 kg-1 ) and peak ṀO2chase (663 ± 43 mg O2 h-1 kg-1 ) were similar (P = 0.49) and repeatable (Pearson's and Spearman's correlation test; r ≥ 0.77; P < 0.05) when measured in the same fish. Therefore, estimates of ṀO2max can be independent of whether a fish is exhaustively chased inside a respirometer or swum to fatigue in a swim tunnel, provided ṀO2 is analysed with an iterative algorithm and a minimum but reliable sampling window. The importance of using this analytical approach was illustrated by peak ṀO2chase being 23% higher (P < 0.05) when compared with a conventional sequential interval regression analysis, whereas using the conventional chase protocol (1-min window) outside the respirometer increased this difference to 31% (P < 0.01). Moreover, because peak ṀO2chase was 18% higher (P < 0.05) than peak ṀO2rec , chasing a fish inside a static respirometer may be a better protocol for obtaining maximum ṀO2 .

One of the physiological mechanisms that can limit the fish's ability to face hypoxia or elevated temperature, is maximal cardiac performance. Yet, few studies have measured how cardiac electrical activity and associated calcium cycling proteins change with acclimation to those environmental stressors. To examine this, we acclimated European sea bass for 6 weeks to three experimental conditions: a seasonal average temperature in normoxia (16 °C; 100% air sat.), an elevated temperature in normoxia (25 °C; 100% air sat.) and a seasonal average temperature in hypoxia (16 °C; 50% air sat.). Following each acclimation, the electrocardiogram was measured to assess how acclimation affected the different phases of cardiac cycle, the maximal heart rate (fH

Warm acclimation in fish is often characterized by an increase in heat tolerance and a reduction in physiological rates to improve the scope to respond to additional challenges including further warming. The speed of these responses can determine their effectiveness. However, acclimation rates vary across levels of biological organization and are poorly understood in part because most research is conducted after an acclimation period of3 weeks, when acclimation is presumed to be complete. Here we show that when rainbow trout were transferred from 10 to 18 °C, over 50% of the total reduction of maximum heart rate (ƒ

Multiple stressors are commonly encountered by wild animals, but their cumulative effects are poorly understood, especially regarding infection development. We conducted a holding study with repeated gill and blood sampling to characterize the effects of cumulative stressors on infection development in adult coho salmon. Treatments included chronic thermal stress (15°C vs. 10°C) and acute gill net entanglement with an air exposure (simulating fisheries bycatch release). The potential loadings of 35 infectious agents and the expression of 17 host immune genes were quantified using high-throughput quantitative polymerase chain reaction, while host physiology was characterized with chemical analysis of blood. Temporal increases in infectious agent richness and loads were concurrent with decreased expression of immune genes in fish sampled in the river. In the laboratory, mortality was minimal in cool water regardless of fishery treatment ( 1 wk) and enhanced mortality associated with handling and biopsy (∼40% both sexes). Experimental gillnetting at high temperature further enhanced female mortality (73%). Fish held at high temperature demonstrated heavier infectious agent loads, osmoregulatory impairment, suppressed female maturation, and upregulation of inflammatory and extracellular immune genes. At high temperature, heavy Parvicapsula minibicornis loads were associated with premature mortality. Females exhibited physiological impairment from both stressors after 1 wk, and infection burdens correlated poorly with immune gene regulation compared with males. Cumulative effects of multiple stressors on female mortality are likely a function of physiological impairment and enhanced infections at high temperature.

Icefishes characteristically lack the oxygen-binding protein haemoglobin and therefore are especially reliant on cardiovascular regulation to augment oxygen transport when oxygen demand increases, such as during activity and warming. Using both in vivo and in vitro experiments, we evaluated the roles for adrenaline and adenosine, two well-established cardio- and vasoactive molecules, in regulating the cardiovascular system of the blackfin icefish, Chaenocephalus aceratus. Despite increasing cardiac contractility (increasing twitch force and contraction kinetics in isometric myocardial strip preparations) and accelerating heart rate (ƒ H ), adrenaline (5 nmol kg −1 bolus intra-arterial injection) did not significantly increase cardiac output (Q̇) in vivo because it elicited a large decrease in vascular conductance (G sys ). In contrast, and despite preliminary data suggesting a direct negative inotropic effect of adenosine on isolated atria and little effect on isolated ventricle strips, adenosine (500 nmol kg −1 ) generated a large increase in Q̇ by increasing G sys , a change reminiscent of that previously reported during both acute warming and invoked activity. Our data thus illustrate how Q̇ in C. aceratus may be much more dependent on peripheral control of vasomotor tone than direct regulation of the heart.

Thermal acclimation, a compensatory physiological response, is central to species survival especially during the current era of global warming. By providing the most comprehensive assessment to date for the cardiorespiratory phenotype of rainbow trout (Oncorhynchus mykiss) at six acclimation temperatures from 15°C to 25°C, we tested the hypothesis that, compared with other strains of rainbow trout, an Australian H-strain of rainbow trout has been selectively inbred to have an unusually high and broad thermal acclimation potential. Using a field setting at the breeding hatchery in Western Australia, thermal performance curves were generated for a warm-adapted H-strain by measuring growth, feed conversion efficiency, specific dynamic action, whole-animal oxygen uptake (ṀO2) during normoxia and hypoxia, the critical maximum temperature and the electrocardiographic response to acute warming. Appreciable growth and aerobic capacity were possible up to 23°C. However, growth fell off drastically at 25°C in concert with increases in the time required to digest a meal, its total oxygen cost and its peak ṀO2. The upper thermal tipping points for appetite and food conversion efficiency corresponded with a decrease in the ability to increase heart rate during warming and an increase in the cost to digest a meal. Also, comparison of upper thermal tipping points provides compelling evidence that limitations to increasing heart rate during acute warming occurred well below the critical thermal maximum (CTmax) and that the faltering ability of the heart to deliver oxygen at different acclimation temperatures is not reliably predicted by CTmax for the H-strain of rainbow trout. We, therefore, reasoned the remarkably high thermal acclimation potential revealed here for the Australian H-strain of rainbow trout reflected the existing genetic variation within the founder Californian population, which was then subjected to selective inbreeding in association with severe heat challenges. This is an encouraging discovery for those with conservation concerns for rainbow trout and other fish species. Indeed, those trying to predict the impact of global warming should more fully consider the possibility that the standing intra-specific genetic variation within a fish species could provide a high thermal acclimation potential, similar to that shown here for rainbow trout.

Warming in the region of the Western Antarctic Peninsula is occurring at an unprecedented rate, which may threaten the survival of Antarctic notothenioid fishes. Herein, we review studies characterizing thermal tolerance and cardiac performance in notothenioids – a group that includes both red-blooded species and the white-blooded, haemoglobinless icefishes – as well as the relevant biochemistry associated with cardiac failure during an acute temperature ramp. Because icefishes do not feed in captivity, making long-term acclimation studies unfeasible, we focus only on the responses of red-blooded notothenioids to warm acclimation. With acute warming, hearts of the white-blooded icefish Chaenocephalus aceratus display persistent arrhythmia at a lower temperature (8°C) compared with those of the red-blooded Notothenia coriiceps (14°C). When compared with the icefish, the enhanced cardiac performance of N. coriiceps during warming is associated with greater aerobic capacity, higher ATP levels, less oxidative damage and enhanced membrane integrity. Cardiac performance can be improved in N. coriiceps with warm acclimation to 5°C for 6–9 weeks, accompanied by an increase in the temperature at which cardiac failure occurs. Also, both cardiac mitochondrial and microsomal membranes are remodelled in response to warm acclimation in N. coriiceps, displaying homeoviscous adaptation. Overall, cardiac performance in N. coriiceps is malleable and resilient to warming, yet thermal tolerance and plasticity vary among different species of notothenioid fishes; disruptions to the Antarctic ecosystem driven by climate warming and other anthropogenic activities endanger the survival of notothenioids, warranting greater protection afforded by an expansion of marine protected areas.

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We tested in six fish species [Pacific lamprey (Lampetra richardsoni), Pacific spiny dogfish (Squalus suckleyi), Asian swamp eel (Monopterus albus), white sturgeon (Acipenser transmontanus), zebrafish (Danio rerio), and starry flounder (Platichthys stellatus)] the hypothesis that elevated extracellular [HCO3-] protects spontaneous heart rate and cardiac force development from the known impairments that severe hypoxia and hypercapnic acidosis can induce. Hearts were exposed in vitro to either severe hypoxia (~ 3% of air saturation), or severe hypercapnic acidosis (either 7.5% CO2 or 15% CO2), which reduced heart rate (in six test species) and net force development (in three test species). During hypoxia, heart rate was restored by [HCO3-] in a dose-dependent fashion in lamprey, dogfish and eel (EC50 = 5, 25 and 30mM, respectively), but not in sturgeon, zebrafish or flounder. During hypercapnia, elevated [HCO3-] completely restored heart rate in dogfish, eel and sturgeon (EC50 = 5, 25 and 30mM, respectively), had a partial effect in lamprey and zebrafish, and had no effect in flounder. Elevated [HCO3-], however, had no significant effect on net force of electrically paced ventricular strips from dogfish, eel and flounder during hypoxia and hypercapnia. Only in lamprey hearts did a specific soluble adenylyl cyclase (sAC) inhibitor, KH7, block the HCO3--mediated rescue of heart rate during both hypoxia and hypercapnia, and wasthe only species where we conclusively demonstrated sAC activity was involved in the protective effects of HCO3- on cardiac function. Our results suggest a common HCO3--dependent, sAC-dependent transduction pathway for heart rate recovery exists in cyclostomes and a HCO3--dependent, sAC-independent pathway exists in other fish species.

We show that cardiac sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) activity differs considerably among sockeye salmon (Oncorhynchus nerka) populations. Variability in SERCA activity was significantly correlated with elevation gain and temperature during migration, as well as maximum cardiac stroke volume. Furthermore, because SERCA activity was not lowered during the spawning migration, this aspect of the cardiac contraction machinery is apparently spared during the senescence of these semelparous salmon, likely because it is essential for these fish to complete spawning. Only when spawning had been completed was there a significant reduction in SERCA activity, which was detectable in males at a 25 °C and in females at a 15 °C assay temperature. Hence, we propose that migration conditions act as a strong selective force that has resulted in local adaptation of myocardial SERCA activity among sockeye salmon populations.

Both laboratory and field respirometry are rapidly growing techniques to determine animal performance thresholds. However, replicating protocols to estimate maximum metabolic rate (MMR) between species, populations, and individuals can be difficult, especially in the field. We therefore evaluated seven different exercise treatments-four laboratory methods involving a swim tunnel (critical swim speed [Ucrit], Ucrit postswim fatigue, maximum swim speed [Umax], and Umax postswim fatigue) and three field-based chasing methods (3-min chase with 1-min air exposure, 3-min chase with no air exposure, and chase to exhaustion)-in adult coho salmon (Oncorhynchus kisutch) as a case study to determine best general practices for measuring and quantifying MMR in fish. We found that all seven methods were highly comparable and that chase treatments represent a valuable field alternative to swim tunnels. Moreover, we caution that the type of test and duration of measurement windows used to calculate MMR can have significant effects on estimates of MMR and statistical power for each approach.

Fish released after capture, or fish interacting with gear but escaping, sometimes experience fishing-related incidental mortality (FRIM). For adult Pacific salmon migrations, knowing the magnitude of FRIM is important to estimate escapement accurately and to understand the total impact of a specific fishery. To determine how multiple gear types are associated with FRIM at different levels of maturity, we captured sockeye salmon (Oncorhynchus nerka) by both gill net and beach seine at three locations along their migration route (10%, 26%, and 72% of a 500 km freshwater migration) and determined their migratory success using biotelemetry. FRIM was higher for fish captured by gill net except at the location closest to spawning grounds. In addition, salmon captured by gill net at the lower river locations temporarily delayed migration, potentially indicating a requirement for lengthier recovery time compared with beach-seined fish. These results provide the first empirical and parallel comparison of these two common in-river fishing methods for salmon, revealing clear differences in FRIM between the two fishing methods in lower river fisheries and the importance of maturity.

The early life stages of Pacific salmon are at risk of environmental exposure to diluted bitumen (dilbit) as Canada’s oil sands industry continues to expand. The toxicity and latent effects of dilbit exposure were assessed in sockeye salmon (Oncorhynchus nerka) exposed to water-soluble fractions of dilbit (WSFd) from fertilization to the swim-up stage, and then reared in clean water for 8 months. Mortality was significantly higher in WSFd-exposed embryos, with cumulative mortality up to 4.6-fold higher in exposed relative to unexposed embryos. The sublethal effects of WSFd exposure included transcriptional up-regulation of cyp1a, a concentration-dependent delay in the onset and progression of hatching, as well as increased prevalence of developmental deformities at total polycyclic aromatic hydrocarbon (TPAH) concentrations ≥35 μg L−1. Growth and body composition were negatively affected by WSFd exposure, including a concentration-specific decrease in soluble protein concentration and increases in total body lipid and triglyceride concentrations. Mortality continued during the first 2 months after transferring fish to clean water, reaching 53% in fish exposed to 100 μg L−1 TPAH; but there was no latent impact on swimming performance, heart mass, or heart morphology in surviving fish after 8 months. A latent effect of WSFd exposure on brain morphology was observed, with fish exposed to 4 μg L−1 TPAH having significantly larger brains compared to other treatment groups after 8 months in clean water. This study provides comprehensive data on the acute, sub-chronic, and latent impacts of dilbit exposure in early life stage sockeye, information that is critical for a proper risk analysis of the impact of a dilbit spill on this socioeconomically important fish species.

Temperature is a master environmental factor that limits the geographical distribution of species, especially in ectotherms. To address challenges in biodiversity conservation under ongoing climate change, it is essential to characterize relevant functional limitations and adaptive genomic content at population and species levels. Here, we present evidence for adaptive divergence in cardiac function and genomic regions in redband trout (Oncorhynchus mykiss gairdneri) populations from desert and montane streams. Cardiac phenotypes of individual fish were measured in the field with a custom‐built electrocardiogram apparatus. Maximum heart rate and its rate limiting temperature during acute warming were significantly higher in fish that have evolved in the extreme of a desert climate compared to a montane climate. Association mapping with 526,301 single nucleotide polymorphisms (SNPs) across the genome revealed signatures of thermal selection both within and among ecotypes. Among desert and montane populations, 435 SNPs were identified as putative outliers under natural selection and 20 of these loci showed significant association with average summer water temperatures among populations. Phenotypes for cardiac performance were variable within each ecotype, and 207 genomic regions were strongly associated with either maximum heart rate or rate limiting temperatures among individuals. Annotation of significant loci provided candidate genes that underlie thermal adaptation, including pathways associated with cardiac function (IRX5, CASQ1, CAC1D, and TITIN), neuroendocrine system (GPR17 and NOS), and stress response (SERPH). By integrating comparative physiology and population genomics, results here advance our knowledge on evolutionary processes of thermal adaptation in aquatic ectotherms.

The recovery of oxygen uptake to the standard metabolic rate (SMR) following exhaustive chasing exercise in Atlantic salmon Salmo salar parr occurred in three phases (rapid, plateau and slow). The initial recovery phase lasted 0·7 h and contributed 16% to the total excess post-exercise oxygen consumption (EPOC). It was followed by a longer plateau phase that contributed 53% to the total EPOC. The slow recovery phase that completed recovery of SMR, which has not been reported previously, made a 31% contribution to the total EPOC. The plasticity of EPOC was demonstrated in exercise-trained fish. Exercise training increased EPOC by 39% when compared with control fish (mean ± S.E., 877·7 ± 73·1 v. 629·2 ± 53·4 mg O2 kg-1 , d.f. = 9, P

This study compared parr from three strains of rainbow trout Oncorhynchus mykiss to examine intraspecific variation in metabolic traits, hypoxia tolerance and upper thermal tolerance in this species. At the strain level, variation in absolute aerobic scope (AAS), critical oxygen level (O2crit ), incipient lethal oxygen saturation (ILOS) and critical thermal maximum (CTmax ) generally exhibited consistent differences among the strains, suggesting the possibility of functional associations among these traits. This possibility was further supported at the individual level by a positive correlation between ILOS and O2crit and a negative correlation between O2crit and AAS. These results indicate that intraspecific differences in hypoxia tolerance among strains of O. mykiss may be primarily determined by differences in the ability to maintain oxygen uptake in hypoxia and that variation in aerobic scope in normoxia probably plays a role in determining the ability of these fish to sustain metabolism aerobically as water oxygen saturation is reduced.

Heterogeneous and ever-changing thermal environments drive the evolution of populations and species, especially when extreme conditions increase selection pressure for traits influencing fitness. However, projections of biological diversity under scenarios of climate change rarely consider evolutionary adaptive potential of natural species. In this study, we tested for mechanistic evidence of evolutionary thermal adaptation among ecologically divergent redband trout populations (Oncorhynchus mykiss gairdneri) in cardiorespiratory function, cellular response and genomic variation. In a common garden environment, fish from an extreme desert climate had significantly higher critical thermal maximum (p .05) and broader optimum thermal window for aerobic scope (3°C) than fish from cooler montane climate. In addition, the desert population had the highest maximum heart rate during warming (20% greater than montane populations), indicating improved capacity to deliver oxygen to internal tissues. In response to acute heat stress, distinct sets of cardiac genes were induced among ecotypes, which helps to explain the differences in cardiorespiratory function. Candidate genomic markers and genes underlying these physiological adaptations were also pinpointed, such as genes involved in stress response and metabolic activity (hsp40, ldh-b and camkk2). These markers were developed into a multivariate model that not only accurately predicted critical thermal maxima, but also evolutionary limit of thermal adaptation in these specific redband trout populations relative to the expected limit for the species. This study demonstrates mechanisms and limitations of an aquatic species to evolve under changing environments that can be incorporated into advanced models to predict ecological consequences of climate change for natural organisms.

To evaluate whether oxygen-carrying capacity influences thermal tolerance in fishes, we reared four Chinook salmon families in present-day (+0°C) and possible future (+4°C) temperatures and assessed the response of hematocrit (Hct) to acute temperature stress. In the +4°C treatment, Hct increased above control levels when juvenile fish were exposed to their critical thermal maximum (CTmax). Conversely, no effect of temperature stress on Hct was found in the +0°C treatment. Hct was positively associated with CTmax ([Formula: see text]; [Formula: see text]), contributing to the CTmax of the +4°C treatment being significantly higher than that of the +0°C treatment (mean ± SD, [Formula: see text] and [Formula: see text], respectively). The association between CTmax and Hct found here supports the hypothesis that thermal tolerance is affected by oxygen supply to tissue. Moreover, the developmental plasticity of CTmax and Hct could represent an adaptive mechanism for salmon faced with climate change.

When oil spills occur, behavior is the first line of defense for a fish to avoid being contaminated. We determined the avoidance threshold of the European seabass (Dicentrarchus labrax) to the water-soluble fraction (WSF) of oil using a dual-flow choice box. The results showed that a plume of 20%-diluted WSF (total polycyclic aromatic hydrocarbon [PAH] concentration: 8.54 μg L-1 ) triggered a significant avoidance response that was detected within 7.5 min of introducing WSF-contaminated water into the experimental setup. However, the ecological relevance of seabass capacity to detect and avoid WSF remains to be established. In the short term, such a response is indeed liable to reduce seabass contact time with oil-contaminated water and thus preserve their functional integrity. In the long term, however, avoidance may contribute to the displacement of a population into a possibly less auspicious environment, with consequences very similar to those of contaminant exposure, that is, disturbed population dynamics and demography. Environ Toxicol Chem 2018;37:854-859. © 2017 SETAC.

WOS:000411848700011; We tested the hypothesis that the chronic residual effects of an acute exposure of European sea bass C Dicentrarchus labrax') to chemically dispersed crude oil is manifest in indices of hypoxic performance rather than aerobic performance.Sea bass were pre-screened with a hypoxia challenge test to establish their incipient lethal oxygen saturation (ILOS),but on discovering a wide breadth for individual ILOS values (2.6-11.0% O-2 saturation), fish were subsequently subdivided into either hypoxia sensitive (HS) or hypoxia tolerant (HT) phenotypes,traits that were shown to be experimentally repeatable.The HT phenotype had a lower ILOS and critical oxygen saturation (O-2crit) compared with the HS phenotype and switched to glycolytic metabolism at a lower dissolved oxygen, even though both phenotypes accumulated lactate and glucose to the same plasma concentrations at ILOS. As initially hypothesized, and regardless of the phenotype considered, we found no residual effect of oil on any of the indices of aerobic performance. Contrary to our hypothesis, however, oil exposure had no residual effect on any of the indices of hypoxic performance in the HS phenotype. In the HT phenotype, on the other hand, oil exposure had residual effects as illustrated by the impaired repeatability of hypoxia tolerance and also by the 24% increase in O-2crit, the 40% increase in scope for oxygen deficit, the 17% increase in factorial scope for oxygen deficit and the 57% increase in accumulated oxygen deficit. Thus, sea bass with a HT phenotype remained chronically impaired for a minimum of 167 days following an acute 24-h oil exposure while the HS phenotypes did not. We reasoned that impaired oxygen extraction at gill due to oil exposure activates glycolytic metabolism at a higher dissolved oxygen, conferring on the HT phenotype an inferior hypoxia resistance that might eventually compromise their ability to survive hypoxic episodes.

Survival of prolonged anoxia requires a balance between cellular ATP demand and anaerobic ATP supply from glycolysis, especially in critical tissues such as the brain. To add insight into the ATP demand of the brain of the anoxia-tolerant red-eared slider turtle (Trachemys scripta) during prolonged periods of anoxic submergence, we quantified and compared the number of Na+-K+-ATPase units and their molecular activity in brain tissue from turtles acclimated to either 21°C or 5°C and exposed to either normoxia or anoxia (6h 21°C; 14days at 5°C). Na+-K+-ATPase activity and density per g tissue were similar at 21°C and 5°C in normoxic turtles. Likewise, anoxia exposure at 21°C did not induce any change in Na+-K+-ATPase activity or density. In contrast, prolonged anoxia at 5°C significantly reduced Na+-K+-ATPase activity by 55%, which was largely driven by a 50% reduction of the number of Na+-K+-ATPase units without a change in the activity of existing Na+-K+-ATPase pumps or α-subunit composition. These findings are consistent with the "channel arrest" hypothesis to reduce turtle brain Na+-K+-ATPase activity during prolonged, but not short-term anoxia, a change that likely helps them overwinter under low temperature, anoxic conditions.