Coevolution of body size and metabolic rate in vertebrates: a life-history perspective.

Coevolution of body size and metabolic rate in vertebrates: a life-history perspective.
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DOI:
10.1111/brv.12615
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发表时间:
2020-10
影响因子:
--
通讯作者:
Czarnoleski M
Czarnoleski M
中科院分区:
其他
文献类型:
--
作者:
Kozłowski J;Konarzewski M;Czarnoleski M

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尽管几十年的研究,代谢率(MRs)的异速缩放仍然知之甚少。在这里,我们认为这些异速生长的比例指数本身并不反映一个普遍的自然规律,而是统计上近似MR和体重之间的非线性关系。这种“统计学”观点必须被“允许”生物体进化出具有不同生理特征的无数不同生命策略的生命史观点所取代。我们假设mr的低异速异速(指数小于1的质量缩放)是生态死亡对分配“决策”的选择压力的间接结果,这种选择压力将资源分配给生长、繁殖和反映在标准或基础代谢率(SMR或BMR)中的基本代谢成本进行修复和维持,这通常是异速分析的结果。这些“决定”形成了丰富的生命史变化,这些变化可以根据生态死亡率和能源使用效率控制的轴来定义。我们将这种变化以及低异速缩放与MR的机制决定因素联系起来,例如代谢惰性成分比例,内部器官的相对大小和活性,细胞大小和细胞膜组成,以及肌肉在静息状态和活跃状态之间剧烈代谢变化的贡献。决定磁振共振的多种机制使我们得出结论,对磁振共振的大规模扩展寻求单一原因的解释是徒劳的。我们认为,基于生命史进化理论的解释是最好的方法。
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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