Among local faunas, the maximum body size and taxonomic affiliation of the top terrestrial vertebrate vary greatly. Does this variation reflect how food requirements differ between trophic levels (herbivores vs. carnivores) and with taxonomic affiliation (mammals and birds vs. reptiles)? We gathered data on the body size and food requirements of the top terrestrial herbivores and carnivores, over the past 65,000 years, from oceanic islands and continents. The body mass of the top species was found to increase with increasing land area, with a slope similar to that of the relation between body mass and home range area, suggesting that maximum body size is determined by the number of home ranges that can fit into a given land area. For a given land area, the body size of the top species decreased in the sequence: ectothermic herbivore > endothermic herbivore > ectothermic carnivore > endothermic carnivore. When we converted body mass to food requirements, the food consumption of a top herbivore was about 8 times that of a top carnivore, in accord with the factor expected from the trophic pyramid. Although top ectotherms were heavier than top endotherms at a given trophic level, lower metabolic rates per gram of body mass in ectotherms resulted in endotherms and ectotherms having the same food consumption. These patterns explain the size of the largest-ever extinct mammal, but the size of the largest dinosaurs exceeds that predicted from land areas and remains unexplained.T he size and taxonomic affiliation of the largest locally present species (''top species'') of terrestrial vertebrate vary greatly among faunas, raising many unsolved questions. Why are the top species on continents bigger than those on even the largest islands, bigger in turn than those on small islands? Why are the top mammals marsupials on Australia but placentals on the other continents? Why is the world's largest extant lizard (the Komodo dragon) native to a modest-sized Indonesian island, of all unlikely places? Why is the top herbivore larger than the top carnivore at most sites? Why were the largest dinosaurs bigger than any modern terrestrial species?A useful starting point is the observation of Marquet and Taper (1), based on three data sets (Great Basin mountaintops, Sea of Cortez islands, and the continents), that the size of a landmass's top mammal increases with the landmass's area. To explain this pattern, they noted that populations numbering less than some minimum number of individuals are at high risk of extinction, but larger individuals require more food and hence larger home ranges, thus only large landmasses can support at least the necessary minimum number of individuals of largerbodied species. If this reasoning were correct, one might expect body size of the top species also to depend on other correlates of food requirements and population densities, such as trophic level and metabolic rate. Hence we assembled a data set consisting of the top terrestrial herbivores and carnivores on 25 oceanic islands and the 5 continents...

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Exposure to maternally derived glucocorticoids during embryonic development impacts offspring phenotype. Although many of these effects appear to be transiently 'negative', embryonic exposure to maternally derived stress hormones is hypothesized to induce preparative responses that increase survival prospects for offspring in low-quality environments; however, little is known about how maternal stress influences longer-term survival-related performance traits in free-living individuals. Using an experimental elevation of yolk corticosterone (embryonic signal of low maternal quality), we examined potential impacts of embryonic exposure to maternally derived stress on flight performance, wing loading, muscle morphology and muscle physiology in juvenile European starlings (Sturnus vulgaris). Here we report that fledglings exposed to experimentally increased corticosterone in ovo performed better during flight performance trials than control fledglings. Consistent with differences in performance, individuals exposed to elevated embryonic corticosterone fledged with lower wing loading and had heavier and more functionally mature flight muscles compared with control fledglings. Our results indicate that the positive effects on a survivalrelated trait in response to embryonic exposure to maternally derived stress hormones may balance some of the associated negative developmental costs that have recently been reported. Moreover, if embryonic experience is a good predictor of the quality or risk of future environments, a preparative phenotype associated with exposure to apparently negative stimuli during development may be adaptive.

SUMMARYThere has been recent interest in understanding trade-offs between immune function and other fitness-related traits. At proximate levels, such trade-offs are presumed to result from the differential allocation of limited energy resources. Whether the costs of immunity are sufficient to necessitate such energy reallocation remains unclear. We tested the metabolic and behavioural response of male zebra finches (Taeniopygia guttata) to the combined effects of thermoregulation and generation of an acute phase response (APR). The APR is the first line of defence against pathogens, and is considered energetically costly. We predicted that at cold temperatures zebra finches would exhibit an attenuated APR when compared with individuals at thermoneutrality. We challenged individuals with bacterial lipopolysaccharide (LPS), an immunogenic compound that stimulates an APR. Following LPS injection, we measured changes in food intake, body mass, activity, and resting and total energy expenditure. When challenged with LPS under ad libitum food, individuals at both temperatures decreased food intake and activity, resulting in similar mass loss. In contrast to predicted energetic trade-offs, cold-exposed individuals injected with LPS increased their nocturnal resting energy expenditure more than did individuals held at thermoneutrality, yet paradoxically lost less mass overnight. Although responding to LPS was energetically costly, resulting in a 10% increase in resting expenditure and 16% increase in total expenditure, there were few obvious energetic trade-offs. Our data support recent suggestions that the energetic cost of an immune response may not be the primary mechanism driving trade-offs between immune system function and other fitness-related traits.

Cold-water fishes are becoming increasingly vulnerable as changing thermal conditions threaten their future sustainability. Thermal stress and habitat loss from increasing water temperatures are expected to impact population viability, particularly for inland populations with limited adaptive resources. Although the long-term persistence of cold-adapted species will depend on their ability to cope with and adapt to changing thermal conditions, very little is known about the scope and variation of thermal tolerance within and among conspecific populations and evolutionary lineages. We studied the upper thermal tolerance and capacity for acclimation in three captive populations of brook trout (Salvelinus fontinalis) from different ancestral thermal environments. Populations differed in their upper thermal tolerance and capacity for acclimation, consistent with their ancestry: the northernmost strain (Lake Nipigon) had the lowest thermal tolerance, while the strain with the most southern ancestry (Hill's Lake) had the highest thermal tolerance. Standard metabolic rate increased following acclimation to warm temperatures, but the response to acclimation varied among strains, suggesting that climatic warming may have differential effects across populations. Swimming performance varied among strains and among acclimation temperatures, but strains responded in a similar way to temperature acclimation. To explore potential physiological mechanisms underlying intraspecific differences in thermal tolerance, we quantified inducible and constitutive heat shock proteins (HSP70 and HSC70, respectively). HSPs were associated with variation in thermal tolerance among strains and acclimation temperatures; HSP70 in cardiac and white muscle tissues exhibited similar patterns, whereas expression in hepatic tissue varied among acclimation temperatures but not strains. Taken together, these results suggest that populations of brook trout will vary in their ability to cope with a changing climate.

Empirical studies often reveal deleterious effects of parasites on host survival, but the ecological and environmental processes modulating parasite‐associated host mortality are not well understood. We conducted meta‐analysis of experimental studies assessing parasite‐associated mortality (n = 52) to evaluate broad‐scale patterns in host mortality risk relative to host or parasite taxon, parasite life cycle, or local environmental conditions. Overall, likelihood of host mortality was ∼2.6 times higher among infected individuals when compared with hosts that either lacked parasites or had experimentally‐reduced parasite burdens. Parasites with complex life cycles reliant on predation‐mediated transmission generally were associated with higher mortality risk than those exploiting other transmission strategies. We also detected a negative relationship between parasite‐associated host mortality and latitude; host mortality risk declined by ∼2.6% with each degree increase in latitude. This result indicated the likely importance of abiotic factors in determining parasite effects. Host taxonomy further influenced parasite‐associated mortality risk, with amphibian, fish, and mollusc hosts generally having higher hazard than arthropod, mammal, and bird hosts. Our results suggest patterns that conform to the predicted link between host mortality and parasite transmissibility, and pathogenicity. The relationship between host mortality and latitude in particular may portend marked shifts in host–parasite relationships pursuant to ongoing and projected global climate change.

Detrimental effects of parasitism on host fitness are frequently attributed to parasite-associated perturbations to host energy budgets. It has therefore been widely hypothesized that energetic costs of infection may be manifest as changes in host resting metabolic rate (RMR). Attempts to quantify these effects have yielded contradictory results across host–parasite systems. We used a meta-analysis of the literature to test the effects of parasites on mass-specific (n = 22) and whole-body (n = 15) host RMR. Parasites resulted in a qualitative increase in host RMR in the majority of studies; however, the overall effect of parasites on host RMR was small and statistically nonsignificant. Additionally, substantial among-study variation in host RMR could not be explained by any of the tested covariates. We conclude that the lack of an overall effect of parasites on host metabolism reflects inconsistent directionality and varying magnitudes of parasite-associated effects across studies, rather than an absence of system-specific effects. We contend that a general understanding of parasite effects on host energetics may be best achieved through identifying mechanisms underlying among-system variance in parasite effects on host RMR and relating parasite-associated perturbations of host energy budgets to robust estimates of host fitness.