The Journal of PhysiologyNov 2, 2026, 01:24 GMT

Human muscle model links weak feeding response to combined changes

Computer simulations based on published data suggested that interacting impairments, rather than one mechanism alone, accounted for reduced muscle protein production after feeding.

Paper by Taylor J. McColl, Daniel R. Moore, Eldon G. Emberly, David D. Church, David C. Clarke · Simon Fraser University

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Mechanisms

Studied:: Computational study of human skeletal muscle models, against simulations with single impairments
What changed:: Simulated muscle protein production after feeding fell with combined impairments, but not with single impairments
The catch:: Feasibility and safety of simulated recovery strategies were not measured

Editor of record: Boris Djordjevic · AgingResearch.News

Paper

Using a computer model of human skeletal muscle, researchers explored why muscle protein production responds less strongly to feeding with age. They set model values using published data and simulated amino acid feeding. Amino acids are the building blocks of proteins.

In the simulations, no single impaired mechanism accounted for the age-related reduction in protein production. Instead, the weaker response emerged when multiple impairments in nutrient sensing and signaling operated together. Signals inside muscle cells that controlled protein production had the strongest influence on the balance between protein production and breakdown. Restoring the feeding response under combined impairments required simulated changes to multiple targets.

Why it matters

Sarcopenia is the age-related loss of muscle mass and function. The authors said their model could guide the design of combined interventions to restore muscle protein production and breakdown in older adults.

Caveats

These were computer simulations, not tests of interventions in people. The simulated recovery strategies identified possible targets, not interventions with established feasibility or safety.