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.

We examined cell size correlations between tissues, and cell size to body mass relationships in passerine birds, amphibians and mammals. The size correlated highly between all cell types in birds and amphibians; mammalian tissues clustered by size correlation in three tissue groups. Erythrocyte size correlated well with the volume of other cell types in birds and amphibians, but poorly in mammals. In birds, body mass correlated positively with the size of all cell types including erythrocytes, and in mammals only with the sizes of some cell types. Size of mammalian erythrocytes correlated with body mass only within the most taxonomically uniform group of species (rodents and lagomorphs). Cell volume increased with body mass of birds and mammals to less than 0.3 power, indicating that body size evolved mostly by changes in cell number. Our evidence suggests that epigenetic mechanisms determining cell size relationships in tissues are conservative in birds and amphibians, but less stringent in mammals. The patterns of cell size to body mass relationships we obtained challenge some key assumptions of fractal and cellular models used by allometric theory to explain mass-scaling of metabolism. We suggest that the assumptions in both models are not universal, and that such models need reformulation.

Though many are convinced otherwise, variability of the size-scaling of metabolism is widespread in nature, and the factors driving that remain unknown. Here we test a hypothesis that the increased expenditure associated with faster growth increases metabolic scaling. We compare metabolic scaling in the fast- and slow-growth phases of ontogeny of Helix aspersa snails artificially selected or not selected for increased adult size. The selected line evolved larger egg and adult sizes and a faster size-specific growth rate, without a change in the developmental rate. Both lines had comparable food consumption but the selected snails grew more efficiently and had lower metabolism early in ontogeny. Attainment of lower metabolism was accompanied by decreased shell production, indicating that the increased growth was fuelled partly at the expense of shell production. As predicted, the scaling of oxygen consumption with body mass was isometric or nearly isometric in the fast-growing (early) ontogenetic stage, and it became negatively allometric in the slow-growing (late) stage; metabolic scaling tended to be steeper in selected (fast-growing) than in control (slow-growing) snails; this difference disappeared later in ontogeny. Differences in metabolic scaling were not related to shifts in the scaling of metabolically inert shell. Our results support the view that changes in metabolic scaling through ontogeny and the variability of metabolic scaling between organisms can be affected by differential growth rates. We stress that future approaches to this phenomenon should consider the metabolic effects of cell size changes which underlie shifts in the growth pattern.

SUMMARY Although plasma membranes benefit cells by regulating the flux of materials to and from the environment, these membranes cost energy to maintain. Because smaller cells provide relatively more membrane area for transport, ectotherms that develop in warm environments should consist of small cells despite the energetic cost. Effects of constant temperatures on cell size qualitatively match this prediction, but effects of thermal fluctuations on cell size are unknown. Thermal fluctuations could favour either small or large cells; small cells facilitate transport during peaks in metabolic demand whereas large cells minimize the resources needed for homeoviscous adaptation. To explore this problem, we examined effects of thermal fluctuations during development on the size of epidermal cells in the wings of Drosophila melanogaster. Flies derived from a temperate population were raised at two mean temperatures (18 and 25°C), with either no variation or a daily variation of ±4°C. Flies developed faster at a mean temperature of 25°C. Thermal fluctuations sped development, but only at 18°C. An increase in the mean and variance of temperature caused flies to develop smaller cells and wings. Thermal fluctuations reduced the size of males at 18°C and the size of females at 25°C. The thorax, the wings and the cells decreased with an increase in the mean and in the variance of temperature, but the response of cells was the strongest. Based on this pattern, we hypothesize that development of the greater area of membranes under thermal fluctuations provides a metabolic advantage that outweighs the greater energetic cost of remodelling membranes.