Individual differences in the energy cost of self-maintenance (resting metabolic rate, RMR) are substantial and the focus of an emerging research area. These differences may influence fitness because selfmaintenance is considered as a life-history component along with growth and reproduction. In this review, we ask why do some individuals have two to three times the 'maintenance costs' of conspecifics, and what are the fitness consequences? Using evidence from a range of species, we demonstrate that diverse factors, such as genotypes, maternal effects, early developmental conditions and personality differences contribute to variation in individual RMR. We review evidence that RMR is linked with fitness, showing correlations with traits such as growth and survival. However, these relationships are modulated by environmental conditions (e.g. food supply), suggesting that the fitness consequences of a given RMR may be context-dependent. Then, using empirical examples, we discuss broad-scale reasons why variation in RMR might persist in natural populations, including the role of both spatial and temporal variation in selection pressures and trans-generational effects. To conclude, we discuss experimental approaches that will enable more rigorous examination of the causes and consequences of individual variation in this key physiological trait.Keywords: standard metabolic rate; resting metabolic rate; basal metabolic rate; maternal effects; metabolism; energetics INTRODUCTIONThe energy cost of self-maintenance (when measured as minimal rates of energy metabolism) varies remarkably within species. It effectively forms a central component of life-history theory which concerns how individuals must allocate a finite-energy budget among the competing interests of growth, reproduction and self-maintenance [1]. Compulsory trade-offs among these functions mean that variation in the rate of using energy will probably have implications for life-history traits and hence fitness. Consequently, there is great contemporary interest in amongindividual variation in minimal rates of energy metabolism. In this review, we address two issues: (i) why do some individuals consistently have two or three times the maintenance costs of conspecifics of the same size, age and sex; and (ii) what are the consequences for fitness? For our purposes, the 'baseline' measures of energy metabolism-basal, standard and resting metabolic rate (BMR, SMR and RMR, respectively) are most relevant. When measured on quiescent individuals, at a common temperature and corrected for body mass, these estimate the compulsory energy cost of self-maintenance that is central to life-history theory. The definitions of each vary slightly. SMR is the lowest rate of metabolism, measured at a

The consequences of early developmental conditions for performance in later life are now subjected to convergent interest from many different biological sub-disciplines. However, striking data, largely from the biomedical literature, show that environmental effects experienced even before conception can be transmissible to subsequent generations. Here, we review the growing evidence from natural systems for these cross-generational effects of early life conditions, showing that they can be generated by diverse environmental stressors, affect offspring in many ways and can be transmitted directly or indirectly by both parental lines for several generations. In doing so, we emphasize why early life might be so sensitive to the transmission of environmentally induced effects across generations. We also summarize recent theoretical advancements within the field of developmental plasticity, and discuss how parents might assemble different ‘internal’ and ‘external’ cues, even from the earliest stages of life, to instruct their investment decisions in offspring. In doing so, we provide a preliminary framework within the context of adaptive plasticity for understanding inter-generational phenomena that arise from early life conditions.

Summary1. Social status can vary considerably among individuals and has significant implications for performance. In addition to a genetic component, social status may be influenced by environmental factors including maternal effects such as prenatal hormone exposure. Maternal effects on traits determining social status have previously been examined in species where mothers provide parental care for relatively few offspring and therefore directly influence postnatal development. However, the generality of conclusions arising from these investigations is unclear because species that employ different reproductive strategies have not been studied. 2. We investigated the hypothesis that egg steroid hormone levels influence the social status of juvenile brown trout (Salmo trutta). We manipulated intra-clutch levels of cortisol and testosterone in eggs from 15 mothers using dilute hormone baths at the time of fertilization and examined their effects on traits that correlate with social status in juveniles [including standard body size, aggression, competitive ability and standard metabolic rate (SMR)]. 3. Hormone treatment did not affect whole-animal or mass-corrected SMR at the critical developmental stage when juveniles switch from reliance on a maternally provisioned yolk sac to independent feeding. However, juveniles from cortisol-treated eggs were smaller at this developmental stage. They were also less aggressive than, and subordinate to, fish from untreated eggs in socially competitive conditions, even after correcting for the observed effect of cortisol on body size. Egg testosterone treatment resulted in a likely pharmacological or toxicological dose with subsequent effects on both body size and behaviour in independently feeding juveniles. 4.Results from this study demonstrate that variation in the amount of cortisol deposited in eggs by spawning females influences juvenile social status and performance. The effects of elevated egg cortisol in fish are similar to the actions of embryonic glucocorticoids reported in other vertebrate taxa with very different reproductive strategies, suggesting a widespread mechanism for the effects of maternal stress on offspring. Possible adaptive aspects of this relationship are discussed.

Abstract. Both the environments experienced by a mother as a juvenile and an adult can affect her investment in offspring. However, the implications of these maternal legacies, both juvenile and adult, for offspring fitness in natural populations are unclear. We investigated whether the juvenile growth rate and adult reproductive traits (length, body condition, and reproductive investment at spawning) of female wild Atlantic salmon (Salmo salar) were related to the growth and survival of their offspring. Adult salmon captured on their upstream migration were used to create experimental full-sib clutches of eggs, which were mixed and then placed in artificial nests in a natural stream that lacked salmon due to a migration barrier. Four months later we resampled the stream to obtain family-level estimates of offspring size and survival. Mothers that had grown slowly as juveniles (as determined by scalimetry) but had invested heavily in reproduction (egg production for a given body length) and were in relatively poor body condition (somatic mass for a given body length) at spawning produced the largest eggs. Larger eggs resulted in larger juveniles and higher juvenile survival. However, after controlling for egg size, offspring growth was positively related to maternal juvenile growth rate and reproductive investment. The predictors of offspring survival (i.e., reproductive success) varied with the juvenile growth rate of the mother: If females grew slowly as juveniles, their reproductive success was negatively related to their own body condition. In contrast, the reproductive success of females that grew quickly as juveniles was instead related positively to their own body condition. Our results show that maternal influences on offspring in the wild can be complex, with reproductive success related to the early life performance of the mother, as well as her state at the time of breeding.

An experienced change in environmental temperature may result in a phenotypic trait value to deviate from optimality. This may be caused by an acute phenotypic change (i.e. passive phenotypic plasticity), and/or a shift in the optimal value for that trait. This in turn triggers an acclimation response that may last from days to months, whereby the organisms attempt to regain optimality of phenotype. Their capacity to acclimate will influence their ability to cope with ongoing global changes in thermal regimes (Stillman, 2003). To gain insights into the sources of variation in acclimation capacity Rohr et al. (2018) reanalyzed the data of Seebacher, White, and Franklin (2015). However, we believe that their approach introduces two problems: 1. Data analyzed by Rohr et al. originate from studies that were primarily (322 of 333 cases) conducted by measuring traits (mostly physiological/biochemical) in 2×2 factorial design experiments, with two acclimation temperatures and two measurement temperatures (Figure 1a). Yet, they only use the data obtained when measuring the traits at the temperature that the individuals were acclimated to ("post-acclimation response"), and define a high acclimation capacity as a flat post-acclimation response, independent of changes occurring during acclimation (Figure 1a,b). This may introduce a bias, because it requires more pronounced changes in the quantity and quality of cellular biochemistry and structures to obtain a flat post-acclimation response for traits that show a steep acute response (Figure 1a vs. 1b). Evidence of such a bias is revealed by a strong negative correlation between the index of acclimation capacity used by Rohr et al. and the estimated mean acute response measured in the same studies (i.e. high mean acute responses are associated with low acclimation capacity values, Figure 2, R = −0.55, df = 320, p < 0.001; cases selected as below). Therefore, variation in acclimation capacity as calculated by Rohr et al. is largely driven by variation in the acute response. 2. The approach used by Rohr et al. follows the implicit assumption of Seebacher et al. (2015) that all acclimation responses cause a reduced thermal response in a trait post-acclimation compared to the acute response (Figure 1a,b). We contend that any measure of acclimation capacity should acknowledge that acclimation may also result in organisms showing an increased trait response after acclimation is complete (Figure 1c). This will occur if the optimal value of a trait increases with temperature, and animals need time to produce this altered phenotype. For example, when the zooplankter Daphnia magna is exposed to a high temperature they gradually (over ca. 5 days) increase their hemoglobin concentration to allow for oxygen supply to match demand (Seidl, Pirow, & Paul, 2005). This allows them to maintain fitness across temperatures by increasing the thermal response of a trait through acclimation. To evaluate the prevalence of this type of acclimation, we considered the data subset of Seebacher et al. an...