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Complex I is bypassed during high intensity exercise.

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Human muscles balance endurance and power through ATP synthesis. A metabolic bypass of mitochondrial complex I enhances ATP production per protein gram during high-intensity exercise.

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Area of Science:

  • Exercise Physiology
  • Metabolic Biochemistry
  • Proteomics

Background:

  • Muscles prioritize ATP synthesis for energy.
  • High-intensity exercise shifts glucose metabolism to less efficient lactate production, creating an endurance-power trade-off.
  • Enzyme catalytic capacity limits ATP synthesis rates.

Purpose of the Study:

  • To integrate enzyme-constrained metabolic models with muscle proteomics data.
  • To investigate how proteome allocation influences muscle metabolism during high-intensity exercise.
  • To explore metabolic strategies that enhance ATP synthesis efficiency.

Main Methods:

  • Developed an enzyme-constrained metabolic model.
  • Integrated the model with proteomics data from human muscle fibers.
  • Conducted high-resolution incremental exercise tests on human subjects.
  • Utilized a whole-body metabolic model to analyze gas exchange data.

Main Results:

  • Identified several enzymes that constrain ATP synthesis in muscles.
  • Discovered that bypassing mitochondrial complex I can increase ATP synthesis rate per gram of protein compared to full respiration.
  • Validated the occurrence of this metabolic bypass in vivo during exercise.
  • Accurately reproduced subject gas exchange data using a model incorporating the complex I bypass.

Conclusions:

  • Proteome allocation significantly impacts muscle metabolism during high-intensity exercise.
  • Metabolic strategies like bypassing mitochondrial complex I can optimize ATP synthesis efficiency.
  • This study provides insights into the physiological trade-offs between muscle power and endurance.