English

The Incommensurability Principle in Biological Transport

Biological Physics 2026-05-29 v2 Tissues and Organs

Abstract

Why does the mammalian vascular tree maintain a conserved branching exponent α2.72\alpha^* \approx 2.72 across a 10710^7-fold range in body mass, despite a fundamental shift from viscous to wave-dominated transport? We prove this universality cannot emerge from local optimization: any junction-level coupling of incommensurable costs requires scale-dependent fine-tuning varying by O(102O(10^2--103)10^3) across the hierarchy. Real networks resolve this through structural heterogeneity, and vascular geometry emerges as a scale-free attractor of a network-level minimax principle. Grounding the fitness penalty in ATP stoichiometry, we prove a Topological Rigidity theorem: the optimal branching exponent depends only on dimensionless structural parameters (G,N,p,αw)(G, N, p, \alpha_w), independent of all metabolic quantities. A self-consistency condition on the viscous--inertial energy partition yields a dual-threshold framework with Wocfluid=3\mathrm{Wo}_c^{\mathrm{fluid}} = \sqrt{3} and Wocwave=3/2\mathrm{Wo}_c^{\mathrm{wave}} = 3/\sqrt{2}. The symmetric model yields αmodel2.626\alpha^*_{\mathrm{model}} \approx 2.626, in agreement with mammals near the allometric transition; morphometric heterogeneities shift large-mammal values toward 2.722.72. The framework explains developmental stability of cardiovascular networks as a consequence of architecture being decoupled from biochemistry.

Keywords

Cite

@article{arxiv.2605.03219,
  title  = {The Incommensurability Principle in Biological Transport},
  author = {Riccardo Marchesi},
  journal= {arXiv preprint arXiv:2605.03219},
  year   = {2026}
}

Comments

46 pages, 2 figures. Paper IV in a series on branching transport networks, Supplemental Material available; see also arXiv:2603.13687 (Paper I), arXiv:2603.14691 (Paper II), and arXiv:2604.10476 (Paper III). Zenodo: https://doi.org/10.5281/zenodo.20030962