Abstract
The problems of organismal agency and phenotypic plasticity present significant interest for modern developmental and evolutionary biology, as well as comparative and biosemiotic approaches. At the same time, the question of how behavioural and other proximal phenotypic factors may potentially drive developmental and evolutionary variation remains open, particularly in relation to life-history and allometric theory (where the issue of agency has been seldom explored). To fill these gaps, this chapter revisits the anti-entropic (negentropic) approach to ontogeny developed by I.A. Arshavsky (1903–1996) and his school. Within this tradition, diverse developmental processes and organisms were studied in order to understand how biological agency and phenotypic plasticity can be interrelated and together affect the formation and integration of biological traits – including the remarkable physiological and morphological features distinguishing primarily altricial (immaturely born) from primarily precocial (maturely born) eutherians. This chapter revisits these concepts and results in the light of current research. In particular, that Arshavsky’s non-equilibrium approach may still help to frame new questions and integrative concepts is shown with respect to certain unresolved problems of metabolic scaling, including the apparent biophysical paradox of increased work capacity and bioenergetic reserves in larger/more precocial organisms. Finally, we shall also consider a novel anti-entropic hypothesis regarding possible agential origins of the prolonged gestation and reduced offspring numbers in such animals, which may have a variety of implications for current work in biology and biosemiotics.
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Notes
- 1.
These two terms are used here synonymously, following Arshavsky (1982).
- 2.
The energetic consequences of this allometric principle are discussed in above. It refers to the principle that due to biophysical and geometrical constraints, as an organism grows in size, its volume increases as a function of the third order; while its surfaces, which govern energy absorption, and elimination, can only increase as a function of the second order.
- 3.
The concept of phenotypic plasticity is defined broadly here, as an organism’s ability to (adaptively) alter its phenotype in response to changes in environmental conditions, regardless of whether the expressed changes are more or less reversible or concern physiological, life history, or morphological characteristics (Kelly et al., 2012). When this plasticity is expressed, primarily or solely, in particular age periods, we speak of developmental plasticity.
- 4.
Generally, instead of a primarily one-way causal arrow from genes to the phenotype (i.e., genetic determinism characteristic of neo-Darwinian models) (Reznick et al., 2002), recent approaches increasingly model evolutionary mechanisms in terms of a reciprocal causation between these levels (Noble, 2021). Here, similarly to Arshavsky’s epigenetic interpretation (1985), the role of developmental and phenotypic processes is considered potentially decisive in terms of exposing – or not – certain gene variants to ecological selection (West-Eberhard, 2003; Uller et al., 2020). Furthermore, according to some recent models (Shapiro, 2011), epigenetic processes may be actively involved in constraining the likelihood of particular genetic mutations in DNA base pair sequences, and thus in regulating genomic evolution. Such findings and epigenetic views lend new actuality to the problems analysed in this chapter.
- 5.
The results published by this group include nearly 250 scientific works by Arshavsky (between 1928 and 1995, most cited in full in Arshavsky, 2002) and probably a comparable number of publications by his co-workers, including numerous Ph.D. dissertations (cf. Arshavsky, 1982). Some relevant papers available in English and not cited in the relatively comprehensive bibliography of Arshavsky (2002), include Arshavsky and Demenshtein (1991), Arshavsky et al. (1975), and Arshavsky et al. (1976).
- 6.
For instance, Arshavsky’s approach was influenced significantly by several frameworks outside the Western tradition. They include the theory of biologically stable non-equilibrium states by E. Bauer (1982 [1935]; cf. Igamberdiev, 2018); the evolutionary biological school of A.N. Severtzov (the teacher of I. Schmalhausen) and, most specifically, the physiological school of Arshavsky’s teacher A.A. Ukhtomsky (1875–1942), who with his concept of physiological dominants began to develop non-equilibrium and agential concepts in neurophysiology (including the notions of biological work, and the non-linear, autocatalytic, and synergetic aspects of physiological processes, to use modern terms) (cf. Arshavsky & Demenshtein, 1991; Kazansky, 2015; Kurismaa, 2015; cf. also Kurismaa, 2023). The same processual orientation, focusing on developmental regularities and physiological variability rather than a search for abstract, timeless constants in biology, is evident in the anti-entropic approach. Indeed, a synthesis and development of these traditions enabled Arshavsky to approach classical problems of comparative physiology from new developmental and agential perspectives. Nevertheless, these less-known sources of inspiration and their methodological specifics may also help explain the limited reception and adoption of this work by contemporary authors.
- 7.
Interestingly, while developmental and systemic approaches to comparative and allometric modelling have been proposed also by other early authors, paradoxically, their concepts have largely disappeared from modern frameworks, as noted by several scholars in the field (cf. Hulbert, 2014; Glazier, 2018). Such neglect of early works may have various, often interlinked and mutually reinforcing reasons that are relevant also here. For example, this may be due to the original work’s appearance in less known or foreign-language journals, the general preference for more recent citations in current papers, and a broader conceptual discrepancy with current models (Glazier, 2018). Although not included in Glazier’s reviews, the same factors seem to apply to Arshavsky’s school. Indeed, little attention has been paid to the phenomena of independent (re)discoveries and ‘sleeping beauties’ in science, which are by no means rare; on the contrary, they seem to be characteristic of progress in life sciences, with its frequent detours and discontinuities (Hulbert, 2014; Glazier, 2018; cf. also Agutter, 2019).
- 8.
In line with classical definitions, basal metabolic rate denotes the lowest metabolic rate of an adult endothermic organism that is postabsorptive (‘fasting’), non-reproducing, and at rest in a thermoneutral environment during the quiescent phase of its daily cycle. Often viewed as the minimum energy required for self-maintenance.
The more general concept of resting metabolic rate denotes the lowest metabolic rate of an endotherm resting in a thermoneutral zone but here one or more criteria defining the basal metabolic rate need be not observed. Unlike the basal metabolic rate, resting metabolic rate is applicable in developmental research (involving non-adult organisms).
The term maximal metabolic rate designates maximal sustained metabolic rate estimated as either exercise-induced maximal metabolic rate (by oxygen uptake rate, VO2 max), cold-induced summit metabolic rate (during thermogenesis), or by daily total energy expenditure (rates of CO2 excretion).
Aerobic scope denotes the animal’s ability to increase its aerobic metabolic rate and functional capacity above maintenance level, as expressed by the possible range between resting metabolic rate (or basal metabolic rate) and maximal metabolic rate, either in absolute (maximal minus resting metabolic rate) or factoral terms (maximal metabolic rate divided by resting metabolic rate). In normal environments, the metabolic rate of an organism usually lies in the mid-range between resting and maximal metabolic rate (Careau et al., 2014; Kurismaa, 2021b). As seen in Table 12.2, Arshavsky assessed the aerobic scope in absolute terms.
- 9.
In these experiments, rabbits, who otherwise dwell in burrows, were subjected to an intense daily schedule of locomotor activity (swimming in water, 24–26 °C), whose duration and timing aimed at optimal levels of physiological stress and activity. The workloads were age-specific, started at 4 weeks of age and lasted for 4–6 months (or, in a special series, until the end of the animals’ life).
- 10.
In contrast to hypoxia, which refers to low oxygen content in tissues, hypoxemia refers to low oxygen concentration in the blood.
- 11.
It is assumed here that the effects of acetylcholine are determined by distinct factors that depend on whether it acts as a tissue hormone or a synaptic mediator (e.g., in the neuromuscular synapse). In the latter case, there is a close correspondence between acetylcholine release and its enzymatic degradation rate, whereas in the former case, instead of such parallelism, high acetylcholinesterase activity can reduce the effects of acetylcholine in the blood and tissues, where it plays non-synaptic roles. In this case, higher levels of blood acetylcholinesterase are associated with higher catecholamine concentrations (adrenaline, noradrenaline) and with increased sympathetic-adrenal activity, which condition the adrenergic features of homeostasis. This is characteristic of newborn and more altricial mammals. In contrast, in all mammals the inhibitory central and peripheral mechanisms of parasympathetic innervations and vagal tone are slower to develop, and the same applies to the corresponding cholinergic features of homeostasis which are typical of more precocial species. The latter typically show a reduced level of catecholamines (adrenaline and noradrenaline) and acetylcholinesterase in the blood (Rozanova, 1968).
Although the mechanisms have not yet been entirely explained, Arshavsky suggests that for the excess acetylcholine concentration in tissues to be anabolically effective, as in precocial animals, it must occur in conditions of physiological hypoxemia whose extent is activity dependent (Arshavsky, 1972). For example, while in the postnatal ontogeny of all mammals the decrease in natural respiratory rate significantly precedes the corresponding developmental decrease in the heart rate, the level of this mismatch – and resulting hypoxemia – is activity dependent. According to Arshavsky, such supply mismatches lead to an economisation and downregulation of resting-state O2 consumption only under sufficiently high workload (Arshavsky, 1972, 1982). It would be interesting to compare this hypothesis with current studies on so-called intermittent metabolic switching, which investigate activity-induced temporary stress responses at a molecular level (but generally with less attention to developmental processes and plasticity) (Mattson et al., 2018; cf. also Raichlen & Gordon, 2011).
- 12.
- 13.
It should be noted (Kurismaa, 2021b) that such comparative facts do not in any way contradict general physical principles, including the second law of thermodynamics – according to which an increased energetic potential accumulating in any living system must be compensated by increased entropy production in the environment (Prigogine & Stengers, 2018; Arshavsky, 1983; Michaelian, 2022). In fact, in precocial animals the production of entropy in resting state is minimised (as noted above), among other things by direct thermal insulation (cf. Table 12.2). Related effects can be seen experimentally, as in the artificially precocialised group, increased work capacity emerges on the background of reduced stable body temperature compared to controls (by 1–1.8 °C) (Arshavsky, 1972). Similarly, the surplus anabolic processes of energy restoration and macroerg accumulation in the muscles after work occur in conditions of reduced muscle temperature (by 1–2 °C) as well as other systemic changes (e.g., membrane hyperpolarisation, muscle cell hyper-relaxation to a length exceeding the initial one, etc.) (cf. Arshavsky, 1972). In this regard, the novel contribution of the anti-entropic framework is to point out that the optimisation of energetic functions in cells, tissues, and organs may importantly depend on baseline energy dissipation minimisation via adaptive changes in the internal milieu of the organism as a whole (Arshavsky, 1972; cf. Igamberdiev, 2018; Kurismaa, 2021b).
- 14.
From this perspective, similar qualifications may be relevant also to the ‘supply limitation’ models, which tend to assume primarily (if not exclusively) biophysical constraints on transport rates and energy exchange capacity, for instance due to differences in relative surface area and/or internal resource transport network structures (Fig. 12.2). Nevertheless, nothing should preclude other, organismic types of supply limitations from affecting metabolic allometries, such as the episodically increased local work rates considered above (section on experimental modelling). Such local and activity dependent limitations may be related to natural ecological stressors, which through biological work and motor responses may stimulate growth and development in the organism via both the first and the second type of anabolic processes (Arshavsky, 1972, 1982).
References
Agutter, P. S. (2019). Why is the history of medicine and biology important? In A guide to the scientific career: Virtues, communication, research and academic writing (pp. 331–334). Wiley.
Agutter, P. S., & Wheatley, D. N. (2008). Thinking about life: The history and philosophy of biology and other sciences. Springer.
Alexander, R. M. (2005). Models and the scaling of energy costs for locomotion. Journal of Experimental Biology, 208(9), 1645–1652.
Arshavsky, I. A. (1960). The physiology of blood circulation during the intrauterine period. Medgiz. (In Russian).
Arshavsky, I. A. (1966). The “energy rule of skeletal muscles” and the physiological mechanisms of divergence and evolution in mammals. The Journal of Evolutionary Biochemistry and Physiology, 2(6), 511–518. (In Russian).
Arshavsky, I. A. (1967). Essays on growth physiology. Medizina. (In Russian).
Arshavsky, I. A. (1968). Adaptive and homeostatic mechanisms in the development of physiologically mature and immature organisms. In G. Newton & S. Levine (Eds.), Early experience and behavior (pp. 299–337). Charles C. Thomas.
Arshavsky, I. A. (1970). Some basic regularities of ontogenesis in relation to the problems of aging and longevity. In V. I. Mahinko (Ed.), Molecular and functional foundations of ontogenesis (pp. 203–223). Medizina. (In Russian).
Arshavsky, I. A. (1972). Musculoskeletal activity and rate of entropy in mammals. In G. Newton & A. H. Riesen (Eds.), Advances in psychobiology (Vol. 1, pp. 1–52). Wiley.
Arshavsky, I. A. (1976). The biological and medical aspects of the problems of adaptation and stress in the light of ontogenetic physiological evidence. In Current problems of modern physiology (pp. 144–191). Nauka. (In Russian).
Arshavsky, I. A. (1982). Physiological mechanisms and regularities of individual development (Foundations of the negentropic theory of ontogeny). Nauka. (In Russian).
Arshavsky, I. A. (1983). On specific peculiarities of transition processes in ontogenesis of mammals. In I. Lamprecht & A. I. Zotin (Eds.), Thermodynamics and kinetics of biological processes (pp. 461–472). Walter de Gruyter.
Arshavsky, I. A. (1985). On the basic principles and tasks of evolutionary physiology in light of comparative ontogenetic studies. The Journal of Evolutionary Biochemistry and Physiology, 21(2), 163–170. (In Russian).
Arshavsky, I. A. (2002). We all have equal rights before one-another (Recollections of A.A. Ukhtomsky. The meaning and fate of the ethical dominant). Pedagogical center “Experiment”. (In Russian).
Arshavsky, I. A., & Demenshtein, A. A. (1991). A.A. Ukhtomsky’s principle of dominanta (on the problem of creation of neurocomputers). In A. V. Holden & V. I. Kriukov (Eds.), Neurocomputers and attention: Neurobiology, synchronisation, and chaos (Vol. 1, pp. 11–19). Manchester University Press.
Arshavsky, I. A., & Mezhevikhina, L. M. (1992). Analysing the causes and mechanisms that determine the emergence of individual development in animals beginning from the zygote (on the role of the cytoskeleton). Biophysics, 37(5), 969. (In Russian).
Arshavsky, I. A., & Rabinovich, E. Z. (1979). Thermodynamics of open systems and the problem of individual development. In G. R. Ivanitskij (Ed.), Methodological and theoretical problems of biophysics (pp. 108–120). Nauka. (In Russian).
Arshavsky, I. A., Darinsky, N. V., Li, L. A., & Siryk, L. A. (1975). Comparative ontogenetic features of skeletal muscles in physiologically mature and immature mammals. Developmental Psychobiology, 8(2), 117–128.
Arshavsky, I. A., Arshavskaya, E. I., & Praznikov, V. P. (1976). Motor reactions during the antenatal period correlated with the periodic change in the activity of the cardiovascular system. Developmental Psychobiology, 9(4), 343–352.
Arshavsky, I. A., Rozanova, V. D., & Savkiv, T. G. (1981). The characteristics and regularities of individual development in males and females in the light of the energy rule of skeletal muscles. Journal of General Biology, 42(5), 698–707.
Arshavsky, I. A., Nemetz, M. G., & Rozanova, V. D. (1985). Experimental modeling of the potential mechanisms of morpho-physiological transformation in wild animals during domestication. In L. V. Davletova (Ed.), Morphology and genetics of the wild boar (pp. 73–87). Nauka. (In Russian).
Arshavsky, I. A., Nemetz, M. G., Rabinovich, E. Z., Rozanova, V. D., & Siryk, L. A. (1987). The principle of the dominant in individual development and in determining the transformation of homeostasis and resilience in various age periods. In D. M. Grozdinsky (Ed.), Resilience and homeostasis in biological systems (pp. 112–129). Naukova Dumka. (In Russian).
Arshavsky, I. A., Kalevich, A. E., & Kefeli, V. I. (1992). Analysing the role of the cytoskeleton in the growth and development of the plant embryo. Biophysics, 35(5), 983. (In Russian).
Bauer, E. S. (1982 [1935]). Theoretical Biology. VIEM. (In Russian). Republished in English by Akadémiai Kiadó, Budapest, 1982.
Bergen, Y. V., & Phillips, K. (2005). Size matters. The Journal of Experimental Biology, 208(9), i–iii.
Billman, G. E., Cagnoli, K. L., Csepe, T., Li, N., Wright, P., Mohler, P. J., & Fedorov, V. V. (2015). Exercise training-induced bradycardia: Evidence for enhanced parasympathetic regulation without changes in intrinsic sinoatrial node function. Journal of Applied Physiology, 118(11), 1344–1355.
Brejcha, J., Pecháček, P., & Kleisner, K. (2019). Complementarity of seeing and appearing. In Cognitive architectures (pp. 13–30). Springer.
Careau, V., Killen, S. S., & Metcalfe, N. B. (2014). Adding fuel to the “fire of life”: Energy budgets across levels of variation in ectotherms and endotherms. In Integrative organismal biology (pp. 219–233). Wiley.
Casasa, S., & Moczek, A. P. (2019). Evolution of, and via, developmental plasticity: Insights through the study of scaling relationships. Integrative and Comparative Biology, 59(5), 1346–1355.
Clauss, M., Dittmann, M. T., Müller, D. W., Zerbe, P., & Codron, D. (2014). Low scaling of a life history variable: Analysing eutherian gestation periods with and without phylogeny-informed statistics. Mammalian Biology, 79(1), 9–16.
Cornish-Bowden, A., Cárdenas, M. L., Letelier, J. C., & Soto-Andrade, J. (2007). Beyond reductionism: Metabolic circularity as a guiding vision for a real biology of systems. Proteomics, 7(6), 839–845.
Deacon, T. W. (2011). Incomplete nature: How mind emerged from matter. WW Norton & Company.
Di Paolo, E. A. (2005). Autopoiesis, adaptivity, teleology, agency. Phenomenology and the Cognitive Sciences, 4(4), 429–452.
Di Paolo, E., Buhrmann, T., & Barandiaran, X. (2017). Sensorimotor life: An enactive proposal. Oxford University Press.
Diogo, R. (2017). Evolution driven by organismal behavior. A unifying view of life, function, form, mismatches and trends. Springer.
Dunsworth, H. M., Warrener, A. G., Deacon, T., Ellison, P. T., & Pontzer, H. (2012). Metabolic hypothesis for human altriciality. Proceedings of the National Academy of Sciences, 109(38), 15212–15216.
Ellis, B. J., & Del Giudice, M. (2019). Developmental adaptation to stress: An evolutionary perspective. Annual Review of Psychology, 70, 111–139.
Flatt, T., & Heyland, A. (Eds.). (2011). Mechanisms of life history evolution: The genetics and physiology of life history traits and trade-offs. Oxford University Press.
Genoud, M., Isler, K., & Martin, R. D. (2018). Comparative analyses of basal rate of metabolism in mammals: Data selection does matter. Biological Reviews, 93(1), 404–438.
Glazier, D. S. (2005). Beyond the ‘3/4-power law’: Variation in the intra-and interspecific scaling of metabolic rate in animals. Biological Reviews, 80(4), 611–662.
Glazier, D. S. (2014). Metabolic scaling in complex living systems. Systems, 2(4), 451–540.
Glazier, D. S. (2015a). Is metabolic rate a universal ‘pacemaker’ for biological processes? Biological Reviews, 90(2), 377–407.
Glazier, D. S. (2015b). Body-mass scaling of metabolic rate: What are the relative roles of cellular versus systemic effects? Biology, 4(1), 187–199.
Glazier, D. S. (2018). Rediscovering and reviving old observations and explanations of metabolic scaling in living systems. Systems, 6(1), 4.
Hargreaves, M. (2015). Exercise and gene expression. Progress in Molecular Biology and Translational Science, 135, 457–469.
Harrison, J. F. (2017). Do performance–safety tradeoffs cause hypometric metabolic scaling in animals? Trends in Ecology & Evolution, 32(9), 653–664.
Hoppeler, H., & Weibel, E. R. (2005). Scaling functions to body size: Theories and facts. The Journal of Experimental Biology, 208(9), 1573–1574.
Hostinar, C. E., & Gunnar, M. R. (2013). The developmental effects of early life stress: An overview of current theoretical frameworks. Current Directions in Psychological Science, 22(5), 400–406.
Hulbert, A. J. (2014). A sceptics view: “Kleiber’s Law” or the “3/4 Rule” is neither a law nor a rule but rather an empirical approximation. Systems, 2(2), 186–202.
Igamberdiev, A. U. (2018). Hyper-restorative non-equilibrium state as a driving force of biological morphogenesis. Biosystems, 173, 104–113.
Jackson, G., Mooers, A. Ø., Dubman, E., Hutchen, J., & Collard, M. (2014). Basal metabolic rate and maternal energetic investment durations in mammals. BMC Evolutionary Biology, 14(1), 1–7.
Jaroš, F., & Klouda, J. (2021). Adolf Portmann: A thinker of self-expressive life. Springer.
Kauffman, S. A. (2000). Investigations. Oxford University Press.
Kauffman, S. (2012). From physics to semiotics. In S. Rattasepp & T. Bennett (Eds.), Gatherings in biosemiotics 11 (pp. 30–46). Tartu Semiotics Library.
Kauffman, S., & Clayton, P. (2006). On emergence, agency, and organization. Biology and Philosophy, 21(4), 501–521.
Kazansky, A. B. (2015). Agential anticipation in the central nervous system. In Anticipation: Learning from the past (pp. 101–112). Springer.
Kelly, S. A., Panhuis, T. M., & Stoehr, A. M. (2012). Phenotypic plasticity: Molecular mechanisms and adaptive significance. Comprehensive Physiology, 2(2), 1417–1439.
Kleisner, K. (2022). Semiotic fitting, co-option, and the art of life. Biosemiotics, 15(1), 31–35.
Koch, L. G., & Britton, S. L. (2008). Aerobic metabolism underlies complexity and capacity. The Journal of Physiology, 586(1), 83–95.
Koch, L. G., Kemi, O. J., Qi, N., Leng, S. X., Bijma, P., Gilligan, L. J., ... & Wisløff, U. (2011). Intrinsic aerobic capacity sets a divide for aging and longevity. Circulation research, 109(10), 1162–1172.
Koch, L. G., & Britton, S. L. (2018). Theoretical and biological evaluation of the link between low exercise capacity and disease risk. Cold Spring Harbor Perspectives in Medicine, 8(1), a029868.
Koch, L. G., Britton, S. L., & Wisløff, U. (2012). A rat model system to study complex disease risks, fitness, aging, and longevity. Trends in Cardiovascular Medicine, 22(2), 29–34.
Kull, K. (2016). The biosemiotic concept of the species. Biosemiotics, 9(1), 61–71.
Kurismaa, A. (2015). Perspectives on time and anticipation in the theory of dominance. In Anticipation: Learning from the past (pp. 37–57). Springer.
Kurismaa, A. (2021a). Revisiting basal anthropology: A developmental approach to human evolution and sociality. In F. Jaroš & J. Klouda (Eds.), Adolf Portmann: A thinker of self-expressive life (pp. 89–118). Springer.
Kurismaa, A. (2021b). The negentropic theory of ontogeny: A new model of eutherian life history transitions? Biosemiotics, 14(2), 391–417.
Kurismaa, A. (2023). From integrative biology to the nerve impulse: Rethinking neural information and semiotics in functional systems perspective. Adaptive Behavior, 31(1), 87–101.
Lambert, D. M., & Spencer, H. G. (Eds.). (1995). Speciation and the recognition concept: Theory and application. Johns Hopkins University Press.
Lema, S. C. (2020). Hormones, developmental plasticity, and adaptive evolution: Endocrine flexibility as a catalyst for ‘plasticity-first’ phenotypic divergence. Molecular and Cellular Endocrinology, 502, 110678.
Letelier, J. C., Cárdenas, M. L., & Cornish-Bowden, A. (2011). From L’Homme machine to metabolic closure: Steps towards understanding life. Journal of Theoretical Biology, 286, 100–113.
Levis, N. A., & Pfennig, D. W. (2020). Plasticity-led evolution: A survey of developmental mechanisms and empirical tests. Evolution & Development, 22(1–2), 71–87.
Louwman, J. W. W. (1973). Breeding the tailless tenrec Tenrec ecaudatus at Wassenaar Zoo. International Zoo Yearbook, 13(1), 125–126.
Markoš, A., & Švorcová, J. (2019). Epigenetic processes and the evolution of life. CRC Press.
Martin, R. D. (1976). The bearing of reproductive behavior and ontogeny on strepsirhine phylogeny. In W. P. Luckett & F. Szalay (Eds.), Phylogeny of the primates (pp. 265–297). Springer.
Martin, R. D., & MacLarnon, A. M. (1985). Gestation period, neonatal size and maternal investment in placental mammals. Nature, 313(5999), 220–223.
Mattson, M. P. (2010). The fundamental role of hormesis in evolution. In M. P. Mattson & E. J. Calabrese (Eds.), Hormesis: A revolution in biology, toxicology and medicine (pp. 57–68). Humana Press.
Mattson, M. P., Moehl, K., Ghena, N., Schmaedick, M., & Cheng, A. (2018). Intermittent metabolic switching, neuroplasticity and brain health. Nature Reviews Neuroscience, 19(2), 81–94.
McEwen, B. S., & Gianaros, P. J. (2011). Stress-and allostasis-induced brain plasticity. Annual Review of Medicine, 62, 431–445.
Michaelian, K. (2022). Non-equilibrium thermodynamic foundations of the origin of life. Foundations, 2(1), 308–337.
Montiglio, P. O., Dammhahn, M., Dubuc Messier, G., & Réale, D. (2018). The pace-of-life syndrome revisited: The role of ecological conditions and natural history on the slow-fast continuum. Behavioral Ecology and Sociobiology, 72(7), 1–9.
Nadin, M. (Ed.). (2015). Anticipation: Learning from the past. Springer.
Noble, D. (2021). The illusions of the modern synthesis. Biosemiotics, 14(1), 5–24.
Pattee, H. H., & Rączaszek-Leonardi, J. (2012). Laws, language and life: Howard Pattee’s classic papers on the physics of symbols with contemporary commentary. Springer Science & Business Media.
Perry, B. W., Schield, D. R., & Castoe, T. A. (2018). Evolution: Plasticity versus selection, or plasticity and selection? Current Biology, 28(18), R1104–R1106.
Pfennig, D. W. (Ed.). (2021). Phenotypic plasticity & evolution: Causes, consequences, controversies. Taylor & Francis.
Pontzer, H. (2015). Constrained total energy expenditure and the evolutionary biology of energy balance. Exercise and Sport Sciences Reviews, 43(3), 110–116.
Pontzer, H. (2018). Energy constraint as a novel mechanism linking exercise and health. Physiology, 33(6), 384–393.
Pontzer, H., Durazo-Arvizu, R., Dugas, L. R., Plange-Rhule, J., Bovet, P., Forrester, T. E., et al. (2016). Constrained total energy expenditure and metabolic adaptation to physical activity in adult humans. Current Biology, 26(3), 410–417.
Portmann, A. (1967). Zoologie aus Vier Jahrzehnten: Gesammelte Abhandlungen. Piper.
Portmann, A. (1990). A Zoologist looks at Humankind. Cambridge University Press.
Prigogine, I., & Stengers, I. (2018). Order out of chaos: Man’s new dialogue with nature. Verso Books.
Raichlen, D. A., & Alexander, G. E. (2017). Adaptive capacity: An evolutionary neuroscience model linking exercise, cognition, and brain health. Trends in Neurosciences, 40(7), 408–421.
Raichlen, D. A., & Gordon, A. D. (2011). Relationship between exercise capacity and brain size in mammals. PLoS One, 6(6), e20601.
Reznick, D., Bryant, M. J., & Bashey, F. (2002). r-and K-selection revisited: The role of population regulation in life-history evolution. Ecology, 83(6), 1509–1520.
Rivers, J. R., & Ashton, J. C. (2013). Age matching animal models to humans-theoretical considerations. Current Drug Discovery Technologies, 10(3), 177–181.
Rozanova, V. D. (1968). Essays on experimental developmental pharmacology. Medizina. (In Russian).
Ruiz-Mirazo, K., & Moreno, A. (2012). Autonomy in evolution: From minimal to complex life. Synthese, 185(1), 21–52.
Savage, V. M., Gillooly, J. F., Woodruff, W. H., West, G. B., Allen, A. P., Enquist, B. J., & Brown, J. H. (2004). The predominance of quarter-power scaling in biology. Functional Ecology, 18(2), 257–282.
Schirrmacher, V. (2021). Less can be more: The hormesis theory of stress adaptation in the global biosphere and its implications. Biomedicine, 9(3), 293.
Selye, H. (1956). The stress of life. McGraw-Hill.
Shapiro, J. A. (2011). Evolution: A view from the 21st century. Pearson education.
Sharov, A. A., & Tønnessen, M. (2021). Semiotic agency. Springer.
Shea, B. T. (2007). Start small and live slow: Encephalization, body size, and life history strategies in primate origins and evolution. In M. J. Ravosa & M. Dagosto (Eds.), Primate origins: Adaptations and evolution (pp. 583–623). Springer.
Uller, T., Feiner, N., Radersma, R., Jackson, I. S., & Rago, A. (2020). Developmental plasticity and evolutionary explanations. Evolution & Development, 22(1–2), 47–55.
von Bertalanffy, L. (1951). Metabolic types and growth types. The American Naturalist, 85(821), 111–117.
Walsh, D. M. (2015). Organisms, agency, and evolution. Cambridge University Press.
Werneburg, I., & Spiekman, S. N. F. (2018). Mammalian embryology and organogenesis. In F. E. Zachos & S. N. Asher (Eds.), Handbook of zoology: Mammalia. Mammalian evolution, diversity, and systematics (pp. 59–116). De Gruyter.
West-Eberhard, M. J. (2003). Developmental plasticity and evolution. Oxford University Press.
Workman, A. D., Charvet, C. J., Clancy, B., Darlington, R. B., & Finlay, B. L. (2013). Modeling transformations of neurodevelopmental sequences across mammalian species. Journal of Neuroscience, 33(17), 7368–7383.
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This study received support from the Estonian Science Foundation (ETAg) grant MOBJD1046 and the Czech Science Foundation (GACR) grant 20-16633S.
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Kurismaa, A. (2024). Agential Patterns in Development and Evolution: Towards an Anti-entropic Approach to the Divergence of Altricial and Precocial Mammals. In: Švorcová, J. (eds) Organismal Agency. Biosemiotics, vol 28. Springer, Cham. https://doi.org/10.1007/978-3-031-53626-7_12
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