Jeffrey Messer helps develop teaching tool to demonstrate a cellular process.
The article, “A Simple Hydraulic Analog Model of Oxidative Phosphorylation,” describes how mammals metabolize at the cellular level to sustain life and the new model the authors developed to simplify the teaching of the phenomenon.
“Oxidative phosphorylation is what keeps us alive at night, it is non-volitional; we don’t have to think about it,” said Messer. “It took a number of years to develop a model to help demonstrate the cellular process and make it more easily understood. Our model is a relatively simple and effective teaching tool that may provide a novel framework to both plan and interpret studies of mitochondrial bioenergetics.”
In brief, mitochondria, an organelle found in most cells, combust carbohydrate and fat through a series of chemical reactions that involve oxygen and convert the energy released to ATP (adenosine 5’-triphosphate) free energy. This process is called oxidative phosphorylation or aerobic metabolism.
The new hydraulic model uses water tanks, water pressures, and flows to simulate thermodynamic forces and the metabolic fluxes our cells experience. The benefit of using a hydraulic analog system is the laws governing water flow are structurally similar to the major steps of oxidative phosphorylation. As a result, the model closely simulates the thermodynamic forces and metabolic flows that are routinely observed in different muscle cell types in response to environmental forces.
The authors use an analogy of ATP as a biological “energy currency,” noting the currency should include both units of exchange (“bills” = ATP molecules) and denominations (“bill value” = free energy of ATP). Just as devalued currency has less purchasing power, mitochondria in an untrained or fuel-depleted muscle generate ATP that delivers a diminished driving force to a metabolic process. This simple hydraulic model clearly demonstrates the falling “bill value.”
Messer attributes the idea of developing an experimental and teaching model to the article’s lead author, Dr. Wayne T. Willis, from the Center for Metabolic and Vascular Biology, Arizona State University, at Mayo Clinic, Scottsdale.
The authors Messer and Willis along with Matthew Jackman, Division of Endocrinology, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado; Sarah Kuzmiak-Glancy, Department of Biomedical Engineering, The George Washington University, Washington, District of Columbia; and Brian Glancy, Laboratory of Cardiac Energetics, National Heart Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, thank Jeremy Oxley and Leonard Eidson for constructing the first physical prototype of the hydraulic model.
This work was supported by the National Science Foundation (grant No. IBN-0116997). The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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