Speed at the edge of stability: a recovery-limited model of metabolic flux in the cheetah.

Abstract

The cheetah (Acinonyx jubatus) achieves unmatched terrestrial speed through anatomical and muscular specialization for explosive power. Its type IIX glycolytic muscle phenotype, phosphocreatine (PCr) buffering and rapid glycolysis supply adenosine triphosphate at exceptionally high rates. This design enables acceleration but carries a metabolic cost: PCr is depleted, inorganic phosphate (Pi) and proton balance are disturbed, lactate is redistributed, and glucose and glycogen are used. We propose that feeding ecology may add to this cost. After a successful hunt, a substantial carcass meal imposes a second load through gastric acid secretion, the alkaline tide, pancreatic and biliary bicarbonate flux, bile acid signalling, and amino acid and lipid processing. Recovery starts when the chase ends, but its components resolve at different rates. PCr resynthesis and lactate transport may begin within minutes, whereas acid-base and electrolyte normalization, glycogen replenishment and intermediary-metabolite clearance may take longer. Feeding may therefore begin while slower recovery processes remain active, allowing the two loads to overlap. The model predicts that shorter hunt-to-feed or inter-meal intervals will increase the magnitude, duration or cumulative carry-over of acid-base, electrolyte and metabolomic perturbations. Direct cheetah evidence includes the fast-glycolytic muscle phenotype, high spot urinary creatinine concentrations, abundant urinary organic acids and altered acylcarnitine profiles. The timing and interaction of sprint recovery, digestion and metabolite clearance remain unmeasured. This Perspective integrates the adaptations that permit exceptional speed with their potential metabolic costs and provides a testable framework for evaluating how feeding ecology and managed feeding schedules influence recovery.

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