Phenotypic plasticity is thought to be critical in allowing organisms to cope with environmental change, but the factors that limit this plasticity are poorly understood, which hampers predictions of species resilience to anthropogenic climate change. Here, we ask if limited plasticity in key traits constrains performance at high temperatures, using two California hatchery strains of rainbow trout (Oncorhynchus mykiss). Aerobic and anaerobic metabolic performance declined at a high but ecologically relevant acclimation temperature (24°C), suggesting performance cannot be maintained at this temperature, despite acclimation. Similarly, while both whole-organism thermal tolerance and hypoxia tolerance improved with acclimation to moderately elevated temperatures, compensation was limited at the highest acclimation temperature. These limits at the whole-organism level were aligned with limits at lower levels of biological organization. At the organ level, absolute scope to increase heart rate with acute warming (ΔƒHmax) did not increase between the upper two acclimation temperatures, and the safety margin for cardiac performance decreased at the highest acclimation temperature. At the cellular level, at 24°C, there were transcriptomic changes in the heart consistent with a cellular stress response. These limits across multiple levels of biological organization were observed under conditions that are ecologically relevant at the southern end of the species range, which suggests that thermal plasticity is likely insufficient to buffer rainbow trout against even modest anthropogenic warming in these regions.

Heavy crude oil, like bitumen, is used globally for plastics, petrochemicals and road surfacing. Canada's oil sands are the world's third largest crude oil reserve, and diluted bitumen (dilbit) is transported across North America primarily via pipeline and rail. Two environmentally-relevant concentrations of dilbit were used with a suite of toxicological endpoints to determine if a 3 °C increase in ambient temperature (Ta) water modulated the effects of dilbit to coho salmon (Oncorhynchus kisutch) when exposed from fertilization to swim-up. The 10-20 % increase in mortality and 25 % reduction in hypoxia tolerance with dilbit exposure was magnified by 18 % and 40 %, respectively, in warmer water. Consequences of dilbit exposure persisted after 6 weeks of additional rearing in clean Ta water but were greatest in fish exposed to dilbit at elevated temperature: additional 20 % mortality and 30 % decrease in mass relative to controls, and a residual 20 % reduction in hypoxia tolerance not seen with dilbit exposure alone. Relatively lower induction of the Phase I biotransformation enzyme cyp1a and greater tissue PAC content in warm-exposed coho suggests reduced PAC metabolism as a mechanism for the observed potentiation. Thus, seasonal fluctuations and baseline increases in water temperature from climate change can exacerbate the adverse effects of oil spills on developing fish.

The thermal sensitivity of heart rate (fH) in fishes has fascinated comparative physiologists for well over a century. We now know that elevating fH is the primary mechanism through which fishes increase convective oxygen delivery during warming to meet the concomitant rise in tissue oxygen consumption. Thus, limits on fH can constrain whole-animal aerobic metabolism. In this Review, we discuss an increasingly popular methodology to study these limits, the measurement of pharmacologically induced maximum fH (fH,max) during acute warming of an anaesthetized fish. During acute warming, fH,max increases exponentially over moderate temperatures (Q10∼2-3), but this response is blunted with further warming (Q10∼1-2), with fH,max ultimately reaching a peak (Q10≤1) and the heartbeat becoming arrhythmic. Because the temperatures at which these transitions occur commonly align with whole-animal optimum and critical temperatures (e.g. aerobic scope and the critical thermal maximum), they can be valuable indicators of thermal performance. The method can be performed simultaneously on multiple individuals over a few hours and across a broad size range (<1 to >6000 g) with compact equipment. This simplicity and high throughput make it tractable in lab and field settings and enable large experimental designs that would otherwise be impractical. As with all reductionist approaches, the method does have limitations. Namely, it requires anaesthesia and pharmacological removal of extrinsic cardiac regulation. Nonetheless, the method has proven particularly effective in the study of patterns and limits of thermal plasticity and holds promise for helping to predict and mitigate outcomes of environmental change.

This article reviews the anatomy of the fish heart and its coronary circulation in relation to their functions. The shape, size and anatomy of the cardiac chambers vary greatly among species but, in general, the venous blood enters to sinus venosus from ductus Cuvier. The sino-atrial canal connects the sinus venosus to the atrium, which pumps blood to the ventricle. The ventricle is the largest cardiac chamber by mass and the most muscular. Blood is pumped from ventricle into an arterial outflow vessel, either a bulbus arteriosus or a conus arteriosus. The shape and the size of cardiac chambers are mainly influenced by their function and how they fit into the fish's body shape. In most fish species the ventricle is composed solely from spongy myocardium, but some fish species have compact myocardium that receives coronary circulation, which supplies oxygenated blood directly from gills to the heart. A spongy heart receives oxygen only from the venous deoxygenated blood within its chambers, which is a less reliable oxygen source during exercise, stress and hypoxia. Across all the teleost species, a coronary circulation is present mainly in highly athletic and hypoxia-tolerant species. Air-breathing fishes may have evolved a different way to better secure a reliable oxygen supply to its myocardium.

The fish gill has been optimized over millions of years of evolution to provide vital functions in respiratory gas exchange, osmoregulation, acid-base balance, and nitrogenous waste excretion. Despite a fairly consistent basic morphology, clear differences in gill size, thickness, and function reflect the varying physiological requirements of fishes living in diverse and sometimes challenging aquatic habitats. In many cases, the fish gill also shows the ability to adjust to changing environmental conditions in a matter of days to weeks. This article highlights trends in the plasticity of gill morphology and function on both long-term (evolutionary) and short-term (acclimation) time scales.

Natural selection has produced many vertebrate 'solutions' for the cardiac life-support system, especially among the approximately 30,000 species of fishes. For example, across species, fish have the greatest range for central arterial blood pressure and relative ventricular mass of any vertebrate group. This enormous cardiac diversity is excellent ground material for mechanistic explorations. Added to this species diversity is the emerging field of population-specific diversity, which is revealing that cardiac design and function can be tailored to a fish population's local environmental conditions. Such information is important to conservation biologists and ecologists, as well as physiologists. Furthermore, the cardiac structure and function of an individual adult fish are extremely pliable (through phenotypic plasticity), which is typically beneficial to the heart's function when environmental conditions are variable. Consequently, exploring factors that trigger cardiac remodelling with acclimation to new environments represents a marvellous opportunity for performing mechanistic studies that minimize the genetic differences that accompany cross-species comparisons. What makes the heart an especially good system for the investigation of phenotypic plasticity and species diversity is that its function can be readily evaluated at the organ level using established methodologies, unlike most other organ systems. Although the fish heart has many merits as an organ-level model to provide a mechanistic understanding of phenotypic plasticity and species diversity, bringing this potential to fruition will require productive research collaborations among physiologists, geneticists, developmental biologists and ecologists.

Climatic warming elevates mortality for many salmonid populations during their physically challenging up-river spawning migrations, yet, the mechanisms underlying the increased mortality remain elusive. One hypothesis posits that a cardiac oxygen insufficiency impairs the heart’s capacity to pump sufficient oxygen to body tissues to sustain up-river swimming, especially in warm water when oxygen availability declines and cardiac and whole-animal oxygen demand increases. We tested this hypothesis by measuring cardiac and metabolic (cardiorespiratory) performance, and assessing the upper thermal tolerance of coho salmon (Oncorhynchus kisutch) during sustained swimming and acute warming. By surgically ligating the coronary artery, which naturally accumulates arteriosclerotic lesions in migrating salmon, we partially impaired oxygen supply to the heart. Coronary ligation caused drastic cardiac impairment during swimming, even at benign temperatures, and substantially constrained cardiorespiratory performance during swimming and progressive warming compared to sham-operated control fish. Furthermore, upper thermal tolerance during swimming was markedly reduced (by 4.4 °C) following ligation. While the cardiorespiratory capacity of female salmon was generally lower at higher temperatures compared to males, upper thermal tolerance during swimming was similar between sexes within treatment groups. Cardiac oxygen supply is a crucial determinant for the migratory capacity of salmon facing climatic environmental warming.

Fitness of fish is assumed to be influenced by locomotion performance, but empirical evidence linking swimming capacity to survival in nature remains sparse. Poor triploid (3N) fish aerobic swimming performance in conjunction with production of sibling diploid (2N) and 3N populations of genetically identical origin to minimize variability among compared populations make 3N trout an informative system to test hypotheses about fitness consequences of fish locomotion. Here, we ask if reduced survival of 3N relative to 2N trout in natural ecosystems during periods of high temperature relate to a lower aerobic swimming capacity and aerobic scope of 3N compared with 2N conspecifics. Three-yearly cohorts of conspecific 2N and 3N hatchery-reared, yearling rainbow trout were ranked for swimming endurance, externally marked for their endurance quantile, and then stocked into two lakes as yearlings to quantify their survival in the wild over summer as a function of ploidy, temperature and endurance; all while tracking temperature and depth habitat utilization via telemetry. As expected, 3N swimming endurance was lower than that of 2N, but with considerable individual overlap. Aerobic swimming endurance, especially for 3N, was predictive of summer survival in a warm lake where piscivorous birds potentially exerted high predation pressure, resulting in low fish survival. This empirical evidence of a connection between swimming endurance and fitness provides support for long held assumptions of this relationship and could inform future sport fishing stocking industry practices to match fish strains to ideal habitats.

Phenotypic plasticity manifested after acclimatization is a very important source of biological variability among fish species. We hypothesized that hypoxic acclimation, besides potentially generating a temporary hypoxic respiratory phenotype, would also manifest as a continued benefit after reacclimation to normoxia. Hence, we holistically characterized the respiratory phenotype of European sea bass (Dicentrarchus labrax (Linnaeus, 1758)) acclimated to normoxia with or without prior acclimation to hypoxia. Compared with the original normoxic phenotype, prior acclimation to hypoxia and return to normoxia produced a 27% higher absolute aerobic scope (AAS), a 24% higher citrate synthase activity in red muscle, and a 28% lower excess post exercise O2 consumption. Additional testing of hypoxia-acclimated fish under normoxia explored the specific effects of hypoxic acclimation. The hypoxic phenotype, when compared with the original normoxic phenotype, had a lower standard metabolic rate, a better hypoxia performance, and a lower minimum PO2 for supporting 50% AAS. Thus, respiratory plasticity allows sea bass to improve its maximum aerobic capacity after returning to normoxia from hypoxic acclimation, a potential benefit from exploiting a hypoxic habitat. Given this respiratory malleability, general predictions for marine fish exploiting a more hypoxic future should better consider respiratory plasticity and prolonged effects of hypoxic exposures.

The hypoxic constraint on peak oxygen uptake ((M) over dotO(2,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 (R-2 and AIC) and the model's prediction of three anchor points for hypoxic performance: critical P-O2 (P-crit), maximum (M) over dotO(2,peak) and a new metric, the minimum P-O2 that supports 50% of absolute aerobic scope (PAAS-50). The best-fitting model was curvilinear using five strategically selected P-O2 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.

It is widely regarded that we have entered a new epoch distinct from the Holocene which is defined by the dominance of humans-termed the "Anthropocene." Indeed, for centuries humans have altered aquatic ecosystems by degrading habitats, altering ecosystem structure, and impairing ecosystem function. In the Anthropocene, aquatic ecosystems and their constituent fish populations are exposed to persistent and emerging threats as well as their interactions. Physiological concepts, knowledge and tools have the potential to help understand the threats facing fish and inform the development of science-based management strategies. By understanding the various systems that govern the biology of fish (e.g., cardiorespiratory, endocrine, biomechanics) it is possible to reveal the complex ways in which different environmental conditions and anthropogenic stressors influence organisms and scale up to influence population-level processes. Although the fact that we have entered the Anthropocene is ominous for biodiversity and humanity, conservation physiology offers hope given the growing number of scientists and practitioners focused on understanding and solving conservation problems facing fish and other organisms.

[This corrects the article DOI: 10.1093/conphys/coab016.].

Two hypotheses were tested concerning the consequences to adult sockeye salmon (Oncorhynchus nerka) of escape from commonly used fishing gear (gillnet, seine net and tangle net). First, by experimentally exposing 214 fish to three commonly used fishing gear types (gillnets, tangle nets, or seine nets) and releasing to complete migration after PIT-tagging, we tested the hypothesis that migration success and behaviour are differentially impacted according to the type of fishing gear interaction and escape. Also, by fitting salmon with thermal loggers, we tested whether salmon behaviourally selected cooler lake water following an escape encounter. Migration success was unaffected after escape from the simulated gear types compared to control fish. Surviving sockeye salmon that had gillnet or seine net encounter, but not a tangle net encounter, on average took approximately 2 days longer to migrate to the spawning area (averaging 14.7 days and 14.9 days, respectively) compared to control fish (12.6 days). Furthermore, escaped fish migrated at cooler temperatures through a lake system (average of 14.0 degrees C) compared to control fish (15.3 degrees C), which would reduce their absolute cost of transport during this migration by reducing the standard metabolic rate by about 10%. Consequently, in addition to demonstrating that fish escapement from a fishing gear will alter their subsequent migration behaviour, we introduce the possibility that the associated increase in energy expenditure and migration delay can be partially compensated for by behavioural selection of cooler water, if it is available, to lower basic energy turnover in a fish that is entirely reliant on energy stores to fuel its spawning migration.

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 (fHmax) and cardiac thermal performance during an acute increase of temperature. Whereas warm acclimation prolonged especially the diastolic phase of the ventricular contraction, reduced the fHmax and increased the cardiac arrhythmia temperature (TARR), hypoxic acclimation was without effect on these functional indices. We measured the level of two key proteins involved with cellular relaxation of cardiomyocytes, i.e. sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and Na+/Ca2+ exchanger (NCX). Warm acclimation reduced protein level of both NCX and SERCA and hypoxic acclimation reduced SERCA protein levels without affecting NCX. The changes in ventricular NCX level correlated with the observed changes in diastole duration and fHmax as well as TARR. Our results shed new light on mechanisms of cardiac plasticity to environmental stressors and suggest that NCX might be involved with the observed functional changes, yet future studies should also measure its electrophysiological activity.

Blebbistatin potently inhibits actin-myosin interaction, preventing contractile activity of excitable cells including cardiac myocytes, despite electrical excitation of an action potential (AP). We collected intracellular micro -electrode recordings of pacemaker cells located in the sinoatrial region (SAR) of the zebrafish heart at room temperature and during acute warming to investigate whether or not blebbistatin inhibition of contraction significantly alters pacemaker cell electrophysiology. Changes were evaluated based on 16 variables that char-acterized the AP waveform. None of these AP variables nor the spontaneous heart rate were significantly modified with the application of 10 & mu;M blebbistatin when recordings were made at room temperature. Compared with the control group, the blebbistatin-treated group showed minor changes in the rate of spontaneous diastolic depolarization (P = 0.027) and the 50% and 80% repolarization (P = 0.008 and 0.010, respectively) in the 26 degrees C-29 degrees C temperature bin, but not at higher temperatures. These findings suggest that blebbistatin is an effective excitation-contraction uncoupler that does not appreciably affect APs generated in pacemaking cells of the SAR and can, therefore, be used in zebrafish cardiac studies.

ABSTRACT 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.