Abstract According to a recent article published in this journal, hypometric scaling of the rate of metabolism in animals (where the log–log scaling slope <1) results from the hypometric scaling of muscle resource demand that is proportional to muscle contraction velocity/frequency. According to this “muscle contraction model” (MCM), larger animals have a relatively low mass‐specific metabolic rate because they expend less energy on slower, less frequent muscular contractions compared with smaller animals. My article offers a different perspective that makes two major points. First, no evidence unequivocally supports, and several lines of evidence contradict the MCM, thus calling into question its tenability and general applicability. Second, no single mechanism can fully explain the diversity of metabolic scaling observed in the living world. Therefore, I advocate a multi‐mechanistic view that includes effects of both resource supply and demand and their regulated interaction, and that distinguishes mechanisms operating in ectotherms versus endotherms and intra‐ versus interspecific metabolic scaling, and via external versus internal and proximate (functional) versus ultimate (evolutionary) causes/constraints. Important proximate mechanisms include various age/size‐dependent resource‐demanding biological processes (e.g., growth, reproduction, thermogenesis, and locomotion) and age/size‐dependent changes in the relative masses of tissues with high versus low metabolic activity that interact with age/size‐dependent resource supply, mediated by cellular and organismal surface areas and internal transport networks that deliver resources to metabolizing cells and expel their wastes (including heat). Mortality rate and associated adaptive life‐history responses appear to be important ultimate causes that drive the “pace of life” and supporting metabolic energy expenditure (“fire of life”) and their scaling with body mass by means of various proximate mechanisms.
D.S. Glazier (2026) studied this question.