Compensatory growth and oxidative stress in a damselfly

Physiological costs of compensatory growth are poorly understood, yet may be the key components in explaining why growth rates are typically submaximal. Here we tested the hypothesized direct costs of compensatory growth in terms of oxidative stress. We assessed oxidative stress in a study where we generated compensatory growth in body mass by exposing larvae of the damselfly Lestes viridis to a transient starvation period followed by ad libitum food. Compensatory growth in the larval stage was associated with higher oxidative stress (as measured by induction of superoxide dismutase and catalase) in the adult stage. Our results challenge two traditional views of life-history theory. First, they indicate that age and mass at metamorphosis not necessarily completely translate larval stress into adult fitness and that the observed physiological cost may explain hidden carry-over effects. Second, they support the notion that costs of compensatory growth may be associated with free-radical-mediated trade-offs and not necessarily with resource-mediated trade-offs.     

Short‐term larval food stress and associated compensatory growth reduce adult immune function in a damselfly

Abstract 1. In animals with a complex life cycle, larval stressors may carry over to the adult stage. Carry‐over effects not mediated through age and size at metamorphosis have rarely been studied. The present study focuses on the poorly documented immune costs of short‐term food stress both in the larval stage and after metamorphosis in the adult stage. 2. The present study quantified immune function [number of haemocytes, activity of prophenoloxidase (proPO) and phenoloxidase (PO)] in an experiment where larvae of the damselfly Lestes viridis were exposed to a transient starvation period. 3. Directly after starvation, immune variables were reduced in starved larvae. Levels of proPO and PO remained low after starvation, even after metamorphosis. In contrast, haemocyte numbers were fully compensated by the end of the larval stage, yet were lower in previously starved animals after metamorphosis. This can be explained as a cost of the observed compensatory growth after starvation. Focusing only on potential costs of larval stressors within the larval stage may therefore be misleading. 4. The here‐identified immunological cost in the adult stage of larval short‐term food stress and associated compensatory growth strongly indicates that physiological costs may explain hidden carry‐over effects bridging metamorphosis. This adds to the increasing awareness that the larval and adult stages in animals with a complex life cycle should be jointly studied, as trade‐offs may span metamorphosis.     

Stronger compensatory growth in a permanent-pond Lestes damselfly relative to temporary-pond Lestes

Compensatory growth where animals compensate for time stress or transient nutritional or thermal stress by accelerating their growth rate is widespread. We know, however, relatively little about the evolution and ecological correlates of compensatory growth. For this we need studies on congeneric species with known phylogenetic relationships that also focus on the associated largely understudied costs. Here we tested for compensatory growth and associated costs in response to time stress (manipulated by photoperiod) and a transient period of starvation or cooling in larvae of the permanent-pond damselfly Lestes eurinus , and compare the results with former studies on temporary-pond Lestes . Larvae showed full compensation in body mass at emergence for all combinations of time stress and starvation or cooling. Unexpectedly, compensatory growth to starvation or cooling was not stronger under time stress. Instead, males under time stress delayed emergence after these transient stressors. In line with a stronger compensatory growth response to time stress than to the other stressors, physiological costs in terms of a reduced investment in immune response (measured as phenoloxidase activity) and energy storage (measured as fat content) were detected only under time stress. Compared to temporary-pond Lestes , L. eurinus showed stronger compensatory growth to time stress. We hypothesize that the stronger compensatory (growth) response in permanent-pond Lestes co-evolved with their derived slower lifestyle when they invaded permanent ponds.     

Sublethal metal stress response of larvae of Aedes aegypti

Aedes aegypti (Diptera: Culicidae) has adapted to urban environments. The urbanization process provides suitable habitats for this disease vector, subsequently increasing the probability of the transmission of pathogens in high‐density environments. Urban environments provide metal‐stressed larval habitats. However, little is known about the physiological cost of metal stress or how this might affect the performance of this mosquito species. The present study aims to characterize the sublethal physiological consequences of metal stress in Aedes aegypti. Various parameters of mosquito physiology under larval metal stress are assessed, including larval metallothionein expression and the effects of larval metal stress on adult performance and their progeny. The results show that environmentally relevant larval metal stress compromises larval and adult development and performance, and also results in larval metal tolerance along with an increase in lipid consumption. These performance costs are coupled with a dramatic increase in metallothionein expression in the midgut. Metal stress results in a lowered adult body mass and neutral storage lipids at emergence, starvation tolerance, fecundity and starvation tolerance of offspring compared with non‐metal‐stressed individuals. Ironically, larval metal stress results in increased adult longevity. Taken together, these findings indicate that even low levels of environmentally relevant larval metal stress have considerable physiological consequences for this important disease vector.     

Exposure to a heat wave under food limitation makes an agricultural insecticide lethal: a mechanistic laboratory experiment

Extreme temperatures and exposure to agricultural pesticides are becoming more frequent and intense under global change. Their combination may be especially problematic when animals suffer food limitation. We exposed Coenagrion puella damselfly larvae to a simulated heat wave combined with food limitation and subsequently to a widespread agricultural pesticide (chlorpyrifos) in an indoor laboratory experiment designed to obtain mechanistic insights in the direct effects of these stressors in isolation and when combined. The heat wave reduced immune function (activity of phenoloxidase, PO) and metabolic rate (activity of the electron transport system, ETS). Starvation had both immediate and delayed negative sublethal effects on growth rate and physiology (reductions in Hsp70 levels, total fat content, and activity levels of PO and ETS). Exposure to chlorpyrifos negatively affected all response variables. While the immediate effects of the heat wave were subtle, our results indicate the importance of delayed effects in shaping the total fitness impact of a heat wave when followed by pesticide exposure. Firstly, the combination of delayed negative effects of the heat wave and starvation, and the immediate negative effect of chlorpyrifos considerably (71%) reduced larval growth rate. Secondly and more strikingly, chlorpyrifos only caused considerable (ca. 48%) mortality in larvae that were previously exposed to the combination of the heat wave and starvation. This strong delayed synergism for mortality could be explained by the cumulative metabolic depression caused by each of these stressors. Further studies with increased realism are needed to evaluate the consequences of the here‐identified delayed synergisms at the level of populations and communities. This is especially important as this synergism provides a novel explanation for the poorly understood potential of heat waves and of sublethal pesticide concentrations to cause mass mortality.     

Immune deployment increases larval vulnerability to predators and inhibits adult life‐history traits in a dragonfly

While deploying immune defences early in ontogeny can trade‐off with the production and maintenance of other important traits across the entire life cycle, it remains largely unexplored how features of the environment shape the magnitude or presence of these lifetime costs. Greater predation risk during the juvenile stage may particularly influence such costs by (1) magnifying the survival costs that arise from any handicap of juvenile avoidance traits and/or (2) intensifying allocation trade‐offs with important adult traits. Here, we tested for predator‐dependent costs of immune deployment within and across life stages using the dragonfly, Pachydiplax longipennis. We first examined how larval immune deployment affected two traits associated with larval vulnerability to predators: escape distance and foraging under predation risk. Larvae that were induced to mount an immune response had shorter escape distances but lower foraging activity in the presence of predator cues. We also induced immune responses in larvae and reared them through emergence in mesocosms that differed in the presence of large predatory dragonfly larvae (Aeshnidae spp.). Immune‐challenged larvae had later emergence overall and lower survival in pools with predators. Immune‐challenged males were also smaller at emergence and developed less sexually selected melanin wing coloration, but these effects were independent of predator treatment. Overall, these results highlight how mounting an immune defence early in ontogeny can have substantial ecological and physiological costs that manifest both within and across life stages.     

Life-history evolution when Lestes damselflies invaded vernal ponds

We know little about the macroevolution of life-history traits along environmental gradients, especially with regard to the directionality compared to the ancestral states and the associated costs to other functions. Here we examine how age and size at maturity evolved when Lestes damselflies shifted from their ancestral temporary pond habitat (i.e., ponds that may dry once every decade or so) to extremely ephemeral vernal ponds (ponds that routinely dry completely each year). Larvae of three species were reared from eggs until emergence under different levels of photoperiod and transient starvation stress. Compared to the two temporary-pond Lestes, the phylogenetically derived vernal-pond Lestes dryas developed more rapidly across photoperiod treatments until the final instar, and only expressed plasticity in development time in the final instar under photoperiod levels that simulated a later hatching date. The documented change in development rate can be considered adaptive and underlies the success of the derived species in vernal ponds. Results suggest associated costs of faster development are lower mass at maturity and lower immune function after transient starvation stress. These costs may not only have impeded further evolution of the routine development rate to what is physiologically maximal, but also maintained some degree of plasticity to time constraints when the habitat shift occurred.     

High larval density does not induce a prophylactic immune response in a butterfly

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Effects of larval density and food stress on life‐history traits of Cnaphalocrocis medinalis (Lepidoptera: Pyralidae)

High population density and nutrition restriction can lead to phase variation in morphology and development, and subsequently induce changes in the reaction norms of adult flight in migrant insects. However, response of migratory propensity to such stress in Endopterygote insects, especially in several species of Lepidoptera, remains unclear. In this study, larval and adult developmental responses to crowding and food stress were investigated in the migratory moth, Cnaphalocrocis medinalis (Guenée). A high larval rearing density significantly reduced pupal mass, survival rate and female fecundity. Larvae developed rapidly under crowding conditions, and time to pupation was 2 days earlier than individuals reared alone. By contrast, short‐term starvation and associated compensatory growth prolonged larval duration by 3–4 days and pupal duration by 1–2 days. It also reduced the pupal mass, but showed no detectable effects on female reproductive performance. Both sexes had similar development strategies; however, females seemed to be more sensitive to crowding and food shortage than males. A positive effect was expected if such stress factors acted as cues that triggering a behavioural or physiological shift to a distinct migratory phase. To the contrary, we found no proof that crowding and starvation caused maturation delay in female reproductive development. All treatments did not significantly increase female pre‐oviposition period. Therefore, we concluded that life developmental responses to crowding and food shortage in this species were different. Adult migration propensity was not enhanced under such stress conditions during the larval phase.     

Food level and sex shape predator-induced physiological stress: immune defence and antioxidant defence

Despite the potential impact on prey fitness and predator–prey interactions, most studies of predation risk ignore physiological responses and their dependence upon food level and sex. Therefore, we reared male and female larvae of the damselfly Lestes viridis under predator stress (dragonfly larvae) at high and low food levels, and subsequently scored for important variables of insect immune defence (i.e. phenoloxidase) and antioxidant defence [i.e. superoxide dismutase, and catalase (CAT)]. Under predation risk, larvae did not decrease growth rate or immune defence, and only slightly reduced food intake in the high food treatment, probably because of time stress, i.e. little time available to complete the larval development. However, larvae facing predator stress did show an upregulation of antioxidant enzymes. This upregulation was dependent upon food level for CAT and both food level and sex for SOD, consistent with energetic constraints and sex differences in the link between longevity and adult fitness. Our results illustrate that predator stress can influence life history, behavioural and physiological responses differentially and in a context-dependent way. This implies that non-consumptive physiological effects of predators on their prey show independent yet similar complexities in behavioural and life history response variables. In general, our results advocate that mechanistic studies on predator–prey interactions may benefit from including physiological variables.     

Phenotypic links in complex life cycles: conclusions from studies with decapod crustaceans

I review studies on decapod crustaceans to draw conclusionsabout the importance of effects of past environmental conditionson development, phenotype, performance, and survival in animals.I consider 3 critical points of the life cycle: the allocationof reserves into eggs, the hatching of larvae, and metamorphosisfrom the larval to the juvenile phase. Biomass allocated toeggs varies among females as a response to changes in environmentalconditions. These variations are propagated to the larval stages,influencing the biomass at hatching, subsequent larval developmentalpathways, and survival during periods of limited starvation.Suboptimal conditions experienced by embryos increase the lossof mass during embryogenesis; size or biomass of the juvenileis either positively or negatively correlated with initial biomass.Positive correlations may be the normal pattern; negative correlationsoccur when individuals hatched with low initial biomass followdevelopmental pathways that lead to increased biomass at metamorphosis.In estuarine crabs, salinity experienced by embryos leads tosalinity acclimation in early larval stages. Phenotypic linksoriginate as transgenerational effects that propagate to thejuvenile stages. There are least 3 types of effects: disruptionof physiological processes; direct adaptive responses; and indirectconsequences of adaptive mechanisms. All types appear withina species; they are produced as a response to a single environmentalfactor. Variability in phenotype remains latent and is expressedin terms of survival according to the environmental conditionsexperienced by a particular stage. The fate of individuals isthus affected by interactions between their immediate developmentalprocesses and their environmental history.     

Resource limitation,predation risk and compensatory growth in a damselfly

Periods of poor nutrition during early development may have negative fitness consequences in subsequent periods of ontogeny. In insects, suppression of growth and developmental rate during the larval stage are likely to affect size and timing of maturity, which in turn may lead to reduced reproductive success or survivorship. In light of these costs, individuals may achieve compensatory growth via behavioural or physiological mechanisms following food limitation. In this study, we examined the effects of a temporary period of food restriction on subsequent growth and age and size at maturity in the larval damselfly Ischnura verticalis (Odonata: Coenagrionidae). We also asked whether this temporary period of reduced nutrition affected subsequent foraging behaviour under predation risk. I. verticalis larvae exposed to a temporary food shortage suffered from a reduced growth rate during this period relative to a control group that was fed ad libitum. However, increased growth rates later in development ensured that adult body size measurements (head and pronotum widths) did not differ between the treatments upon emergence. In contrast, adult dry mass did not catch up to that of the controls, indicating that the increased growth rates for size dimensions occur at the cost of similar gains in mass. Predators reduced foraging effort of larvae, but this reduction did not differ between control larvae and those previously exposed to poor nutrition.     

Delayed effects of cold stress on immune response in laboratory mice

This study was undertaken to examine the trade-off between the cost of thermoregulation and immune function in laboratory mice. Mice were maintained either at 23 degrees C or cold exposed at 5 degrees C for 10 days. Then, they were immunized with sheep red blood cells. Thus, the cold-exposed mice had either experienced or not experienced cold stress prior to immunization. Cold stress elicited a substantial increase in food intake, accompanied by a significant reduction in food digestibility. An increase in mass of metabolically active internal organs (small intestines, heart and kidney) was observed in cold-exposed mice. These findings reassured us that costs of increased thermoregulation caused by cold stress were substantial. The immune response of mice exposed to long-lasting cold stress was significantly lower, but immune response was not affected in short-exposed mice. Differences in immune response between experimental groups accompanied changes in mass of immunocompetent organs (thymus and spleen). Our findings indicate that studies of trade-offs should account for the fact that resource reallocation in response to an environmental challenge may not be immediate. In fact, resource reallocation may be postponed until the new environmental state becomes permanent or until an organism attains physiological adaptation to the current conditions.     

Sex-dependent effects of larval food stress on adult performance under semi-natural conditions: only a matter of size?

Organisms with complex life-cycles acquire essential nutrients as juveniles, and hence even a short-term food stress during development can impose serious fitness costs apparent in adults. We used the Glanville fritillary butterfly to investigate the effects of larval food stress on adult performance under semi-natural conditions in a population enclosure. We were specifically interested in whether the negative effects observed were due to body mass reduction only or whether additional effects unrelated to pupal mass were evident. The two sexes responded differently to the larval food stress. In females, larval food stress reduced pupal mass and reproductive performance. The reduced reproductive performance was partially mediated by pupal mass reduction. Food stressed females also had reduced within-patch mobility, and this effect was not dependent on pupal mass. Conversely, food stress had no effect on male pupal mass, suggesting a full compensation via prolonged development time. Nonetheless, food stressed males were less likely to sire any eggs, potentially due to changes in their territorial behavior, as indicated by food stress also increasing male within-patch mobility (i.e., patrolling behavior). When males did sire eggs, the offspring number and viability were unaffected by male food stress treatment. Viability was in general higher for offspring sired by lighter males. Our study highlights how compensatory mechanisms after larval food stress can act in a sex-specific manner and that the alteration in body mass is only partially responsible for the reduced adult performance observed.     

Integrating life history and physiology to understand latitudinal size variation in a damselfly

Our understanding of latitudinal life history patterns may benefit by jointly considering age and mass at maturity and growth rate. Additional insight may be gained by exploring potential constraints through pushing growth rates to their maximum and scoring physiological cost‐related variables. Therefore, we reared animals of a univoltine Spanish and Belgian population and of a semivoltine Swedish population of the damselfly Enallagma cyathigerum (spanning a latitude gradient of ca 2350 km) in a common environment from the eggs until adult emergence and exposed them to a transient starvation period to induce compensatory growth. Besides age and mass at maturity and growth rate we also scored investment in energy storage (i.e. triglycerides) and immune function (i.e. total activity of phenoloxidase). At emergence, body mass was greater in Spain and Sweden and lower in Belgium, suggesting a genetic component for the U‐shaped latitudinal pattern that was found also in a previous study based on field‐collected adults. The mass difference between univoltine populations can be explained by the shorter development time in the Belgian population, and this despite a higher growth rate, a pattern consistent with undercompensating countergradient variation. In line with the assumed shorter growth seasons, Belgian and Swedish animals showed higher routine growth rates and compensatory growth after transient starvation. Despite a strong link with metabolic rates (as measured by oxygen consumption) populations with higher routine growth rates had no lower fat content and had higher immune function (i.e. immune function decreased from Sweden to Spain), which was unexpected. Rapid compensatory growth did, however, result in a lowered immune function. This may contribute to the absence of perfect compensating countergradient variation in the Belgian population and the lowest routine growth rates in the Spanish population. Our results underscore the importance of integrating key life historical with physiological traits for understanding latitudinal population differentiation.     

The Genomic Architecture of Adaptation to Larval Malnutrition Points to a Trade-off with Adult Starvation Resistance in Drosophila

Periods of nutrient shortage impose strong selection on animal populations. Experimental studies of genetic adaptation to nutrient shortage largely focus on resistance to acute starvation at adult stage; it is not clear how conclusions drawn from these studies extrapolate to other forms of nutritional stress. We studied the genomic signature of adaptation to chronic juvenile malnutrition in six populations of Drosophila melanogaster evolved for 150 generations on an extremely nutrient-poor larval diet. Comparison with control populations evolved on standard food revealed repeatable genomic differentiation between the two set of population, involving >3,000 candidate SNPs forming >100 independently evolving clusters. The candidate genomic regions were enriched in genes implicated in hormone, carbohydrate, and lipid metabolism, including some with known effects on fitness-related life-history traits. Rather than being close to fixation, a substantial fraction of candidate SNPs segregated at intermediate allele frequencies in all malnutrition-adapted populations. This, together with patterns of among-population variation in allele frequencies and estimates of Tajima’s D, suggests that the poor diet results in balancing selection on some genomic regions. Our candidate genes for tolerance to larval malnutrition showed a high overlap with genes previously implicated in acute starvation resistance. However, adaptation to larval malnutrition in our study was associated with reduced tolerance to acute adult starvation. Thus, rather than reflecting synergy, the shared genomic architecture appears to mediate an evolutionary trade-off between tolerances to these two forms of nutritional stress.     

COMPLEX TRADE-OFFS AND THE EVOLUTION OF STARVATION RESISTANCE IN DROSOPHILA MELANOGASTER

The measurement of trade-offs may be complicated when selection exploits multiple avenues of adaptation or multiple life-cycle stages. We surveyed 10 populations of Drosophila melanogaster selected for increased resistance to starvation for 60 generations, their paired controls, and their mutual ancestors (a total of 30 outbred populations) for evidence of physiological and life-history trade-offs that span life-cycle stages. The directly selected lines showed an impressive response to starvation selection, with mature adult females resisting starvation death 4–6 times longer than unselected controls or ancestors—up to a maximum of almost 20 days. Starvation-selected flies are already 80% more resistant to starvation death than their controls immediately upon eclosion, suggesting that a significant portion of their selection response was owing to preadult growth and acquisition of metabolites relevant to the stress. These same lines exhibited significantly longer development and lower viability in the larval and pupal stages. Weight and lipid measurements on one of the starvation-selected treatments (SB_1–5), its control populations (CB_1–5), and their ancestor populations (B_1–5) revealed three important findings. First, starvation resistance and lipid content were linearly correlated; second, larval lipid acquisition played a major role in the evolution of adult starvation resistance; finally, increased larval growth rate and lipid acquisition had a fitness cost exacted in reduced viability and slower development. This study implicates multiple life-cycle stages in the response to selection for the stress resistance of only one stage. Our starvation-selected populations illustrate a case that may be common in nature. Patterns of genetic correlation may prove misleading unless multiple pleiotropic interconnections are resolved.     

Temperature extremes and butterfly fitness: conflicting evidence from life history and immune function

Global warming and its associated increase in temperature extremes pose a substantial challenge on natural systems. Tropical ectotherms, living close to their (upper) critical thermal limits, may be particularly vulnerable to global warming, yet they are as a group understudied. Most studies assessing fitness effects under global warming focused on life‐history correlates such as body size and largely neglected immune function. Furthermore they did not consider to what extent temperature effects may be modulated under resource‐based trade‐offs. Against this background we here investigate effects of temperature extremes on fitness‐related adult traits (viz. body mass, fat content, and two key parameters of arthropod immune function: phenoloxidase (PO) activity and haemocyte numbers) at different levels of larval and adult food stress in the tropical butterfly Bicyclus anynana. Body mass and PO activity decreased after short‐term larval food stress, but not fat content and haemocyte numbers (probably owing to compensatory mechanisms during further development). Longer‐term food deprivation in the adult stage, in contrast, diminished performance throughout, confirming that the feeding treatments chosen imposed stress. Temperature manipulations yielded contrary responses between life‐history correlates and immune function: while body mass and fat content increased by increasing temperatures, PO activity and haemocyte numbers decreased. The latter was particularly pronounced under adult food stress, suggesting a resource‐allocation trade‐off. Our data suggest that global warming will not only reduce performance through direct effects of thermal stress, but also through secondary effects on adult immune function, which may be missed when exclusively focussing on other life‐history correlates.     

A hassle a day may keep the pathogens away: The fight-or-flight stress response and the augmentation of immune function

Stress is known to suppress or dysregulate immune function and increase susceptibility to disease. Paradoxically, the short-term fight-or-flight stress response is one of nature's fundamental defense mechanisms that galvanizes the neuroendocrine, cardiovascular, and musculoskeletal systems into action to enable survival. Therefore, it is unlikely that short-term stress would suppress immune function at a time when it may be critically required for survival (e.g., in response to wounding and infection by a predator or aggressor). In fact, studies have shown that stress can enhance immune function under certain conditions. Several factors influence the direction (enhancing versus suppressive) of the effects of stress on immune function: (1) Duration: acute or short-term stress experienced at the time of activation of an immune response enhances innate and adaptive immune responses. Chronic or long-term stress can suppress or dysregulate immune function. (2) Leukocyte distribution: compartments (e.g., skin), that are enriched with immune cells during acute stress show immuno-enhancement, while those that are depleted of leukocytes (e.g., blood), show immuno-suppression. (3) The differential effects of physiologic versus pharmacologic stress hormones: Endogenous hormones in physiological concentrations can have immuno-enhancing effects. Endogenous hormones at pharmacologic concentrations, and synthetic hormones, are immuno-suppressive. (4) Timing: immuno-enhancement is observed when acute stress is experienced during the early stages of an immune response while immuno-suppression may be observed at late stages. The type of immune response (protective, regulatory/inhibitory, or pathological) that is affected determines whether the effects of stress are ultimately beneficial or harmful for the organism. Arguments based on conservation of energy have been invoked to explain potential adaptive benefits of stress-induced immuno-suppression, but generally do not hold true because most mechanisms for immuno-suppression expend, rather than conserve, energy. We propose that it is important to study, and if possible, to clinically harness, the immuno-enhancing effects of the acute stress response that evolution has finely sculpted as a survival mechanism, just as we study its maladaptive ramifications (chronic stress) that evolution has yet to resolve.     

The physiological costs of reproduction in small mammals

Life-history trade-offs between components of fitness arise because reproduction entails both gains and costs. Costs of reproduction can be divided into ecological and physiological costs. The latter have been rarely studied yet are probably a dominant component of the effect. A deeper understanding of life-history evolution will only come about once these physiological costs are better understood. Physiological costs may be direct or indirect. Direct costs include the energy and nutrient demands of the reproductive event, and the morphological changes that are necessary to facilitate achieving these demands. Indirect costs may be optional 'compensatory costs' whereby the animal chooses to reduce investment in some other aspect of its physiology to maximize the input of resource to reproduction. Such costs may be distinguished from consequential costs that are an inescapable consequence of the reproductive event. In small mammals, the direct costs of reproduction involve increased energy, protein and calcium demands during pregnancy, but most particularly during lactation. Organ remodelling is necessary to achieve the high demands of lactation and involves growth of the alimentary tract and associated organs such as the liver and pancreas. Compensatory indirect costs include reductions in thermogenesis, immune function and physical activity. Obligatory consequential costs include hyperthermia, bone loss, disruption of sleep patterns and oxidative stress. This is unlikely to be a complete list. Our knowledge of these physiological costs is currently at best described as rudimentary. For some, we do not even know whether they are compensatory or obligatory. For almost all of them, we have no idea of exact mechanisms or how these costs translate into fitness trade-offs.