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Accumulation of noncoding DNA and therefore genome size (Cvalue) may be under strong selection toward increase of body size accompanied by low metabolic costs. C-value directly affects cell size and specific metabolic rate indirectly. Body size can enlarge through increase of cell size and͞or cell number, with small cells having higher metabolic rates. We argue that scaling exponents of interspecific allometries of metabolic rates are by-products of evolutionary diversification of C-values within narrow taxonomic groups, which underlines the participation of cell size and cell number in body size optimization. This optimization leads to an inverse relation between slopes of interspecific allometries of metabolic rates and C-value. To test this prediction we extracted literature data on basal metabolic rate (BMR), body mass, and C-value of mammals and birds representing six and eight orders, respectively. Analysis of covariance revealed significant heterogeneity of the allometric slopes of BMR and C-value in both mammals and birds. As we predicted, the correlation between allometric exponents of BMR and C-value was negative and statistically significant among mammalian and avian orders.allometry ͉ genome size ͉ body size optimization ͉ cell number

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Basically all organisms can be classified as determinate growers if their growth stops or almost stops at maturation, or indeterminate growers if growth is still intense after maturation. Adult size for determinate growers is relatively well defined, whereas in indeterminate growers usually two measures are used: size at maturation and asymptotic size. The latter term is in fact not a direct measure but a parameter of a specific growth equation, most often Bertalanffy's growth curve. At a given food level, the growth rate in determinate growers depends under given food level on physiological constraints as well as on investments in repair and other mechanisms that improve future survival. The growth rate in indeterminate growers consists of two phases: juvenile and adult. The mechanisms determining the juvenile growth rate are similar to those in determinate growers, whereas allocation to reproduction (dependent on external mortality rate) seems to be the main factor limiting adult growth. Optimal resource allocation models can explain the temperature-size rule (stating that usually ectotherms grow slower in cold but attain larger size) if the exponents of functions describing the size-dependence of the resource acquisition and metabolic rates change with temperature or mortality increases with temperature. Emerging data support both assumptions. The results obtained with the aid of optimization models represent just a rule and not a law: it is possible to find the ranges of production parameters and mortality rates for which the temperature-size rule does not hold.

Summary1. Species' body size distributions are right-skewed, symmetric or left-skewed, but right-skewness strongly prevails. 2. Skewness changes with taxonomic level, with a tendency to high right-skewness in classes and diverse skewness in orders within a class. Where the number of lower taxa allows for analysis, skewness coefficients have normal distributions, with the majority of taxa being right-skewed. 3. Skewness changes with geographical scale. For a broad range, distributions in a class are usually right-skewed. For a narrower scale, distributions remain right-skewed or become symmetric or even close to uniform. 4. The prevailing right-skewness of species' body size distributions is explained with macroevolutionary models, the fractal character of the environment, or body size optimization. 5. Macroevolutionary models assume either size-biased speciation and extinction, or the existence of a constraint on small size. Macroevolutionary mechanisms seem insufficient to explain the pattern of species' body size distributions, but they may operate together with other mechanisms. 6. Optimization models assume that directional and then stabilizing selection works after speciation events. There are two kinds of optimization approaches to study species' body size distributions. Under the first approach, it is assumed that a single energetic optimum exists for an entire taxon, and that species are distributed around this optimum. Under the second approach, each species has a separate optimum, and the species' body size distribution reflects the distribution of optimal values. 7. Because not only energetic properties but also mortality are important in determining optimal sizes, only the second approach, that is, seeking the distribution of optimal values, seems appropriate in the context of life-history evolution. This approach predicts diverse shapes of body size distributions, with right-skewness prevailing.

Despite many decades of research, the allometric scaling of metabolic rates (MRs) remains poorly understood. Here, we argue that scaling exponents of these allometries do not themselves mirror one universal law of nature but instead statistically approximate the non‐linearity of the relationship between MR and body mass. This ‘statistical’ view must be replaced with the life‐history perspective that ‘allows’ organisms to evolve myriad different life strategies with distinct physiological features. We posit that the hypoallometric allometry of MRs (mass scaling with an exponent smaller than 1) is an indirect outcome of the selective pressure of ecological mortality on allocation ‘decisions’ that divide resources among growth, reproduction, and the basic metabolic costs of repair and maintenance reflected in the standard or basal metabolic rate (SMR or BMR), which are customarily subjected to allometric analyses. Those ‘decisions’ form a wealth of life‐history variation that can be defined based on the axis dictated by ecological mortality and the axis governed by the efficiency of energy use. We link this variation as well as hypoallometric scaling to the mechanistic determinants of MR, such as metabolically inert component proportions, internal organ relative size and activity, cell size and cell membrane composition, and muscle contributions to dramatic metabolic shifts between the resting and active states. The multitude of mechanisms determining MR leads us to conclude that the quest for a single‐cause explanation of the mass scaling of MRs is futile. We argue that an explanation based on the theory of life‐history evolution is the best way forward.

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The metabolic theory of ecology (MTE) predicts the ubiquity of the of 3/4 scaling exponent relating metabolic rate (MR) to body mass, as well as cell-size invariance coupled with body-size dependence of cellular MR in quickly dividing cells. An alternative prediction is that MR scales interspecifically with a coefficient that is between 2/3 and 1, depending on the cell size and cell MR, which is mostly driven by the cell surface-to-volume ratio. We tested (1) the contribution of cell size to interspecific differences in MR and (2) whether the cell size-MR relationship is mediated by genome size (GS), which usually correlates positively with cell size. We tested (1) and (2) using erythrocyte area as a proxy for cell size in 14 eyelid geckos, which belong to a monophyletic group exhibiting large body-size variation. The scaling of standard MR (SMR) was significantly lower than 3/4, whereas mass-specific SMR correlated with erythrocyte area in both phylogenetically adjusted and conventional analyses. This points to cell-size variation as the factor governing metabolic rate scaling, which questions predictions of the MTE. However, the nonsignificance of the correlation between mass-specific SMR and GS undermines the strength of the relation between GS and cell size, at least in these species.