The Incommensurability Principle in Biological Transport
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arXiv
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| Format: | Preprint |
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2026
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| _version_ | 1866917541772787712 |
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| author | Marchesi, Riccardo |
| author_facet | Marchesi, Riccardo |
| contents | Why does the mammalian vascular tree maintain a conserved branching exponent $α^* \approx 2.72$ across a $10^7$-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 $O(10^2$--$10^3)$ 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 $(G, N, p, α_w)$, independent of all metabolic quantities. A self-consistency condition on the viscous--inertial energy partition yields a dual-threshold framework with $\mathrm{Wo}_c^{\mathrm{fluid}} = \sqrt{3}$ and $\mathrm{Wo}_c^{\mathrm{wave}} = 3/\sqrt{2}$. The symmetric model yields $α^*_{\mathrm{model}} \approx 2.626$, in agreement with mammals near the allometric transition; morphometric heterogeneities shift large-mammal values toward $2.72$. The framework explains developmental stability of cardiovascular networks as a consequence of architecture being decoupled from biochemistry. |
| format | Preprint |
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arxiv_https___arxiv_org_abs_2605_03219 |
| institution | arXiv |
| publishDate | 2026 |
| record_format | arxiv |
| spellingShingle | The Incommensurability Principle in Biological Transport Marchesi, Riccardo Biological Physics Tissues and Organs 92C35, 92C05, 49K30 Why does the mammalian vascular tree maintain a conserved branching exponent $α^* \approx 2.72$ across a $10^7$-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 $O(10^2$--$10^3)$ 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 $(G, N, p, α_w)$, independent of all metabolic quantities. A self-consistency condition on the viscous--inertial energy partition yields a dual-threshold framework with $\mathrm{Wo}_c^{\mathrm{fluid}} = \sqrt{3}$ and $\mathrm{Wo}_c^{\mathrm{wave}} = 3/\sqrt{2}$. The symmetric model yields $α^*_{\mathrm{model}} \approx 2.626$, in agreement with mammals near the allometric transition; morphometric heterogeneities shift large-mammal values toward $2.72$. The framework explains developmental stability of cardiovascular networks as a consequence of architecture being decoupled from biochemistry. |
| title | The Incommensurability Principle in Biological Transport |
| topic | Biological Physics Tissues and Organs 92C35, 92C05, 49K30 |
| url | https://arxiv.org/abs/2605.03219 |