Abstract
Intense exercise leads to muscle fatigue, a contractile and metabolic failure of contracting muscle to sustain desired work. It is widely accepted that the close relationship between intense exercise and the accumulation of metabolic by-products is the major cause of skeletal muscle fatigue. High-intensity exercise activates ATPase activity and strongly promotes ATP production, leading to an alteration of metabolic by-products. However, the complex mechanisms underlying the development of muscle fatigue are not fully understood. In this study, we developed a novel mathematical model for whole-body mechanisms that can reproduce the key biological processes of metabolic fatigue during high-intensity exercise. Five vital compartments are represented: skeletal muscle, liver, lungs, blood vessels and other organs. These compartments capture the key mechanisms involved, including the buffering role of creatine kinase, the bicarbonate buffer system in the regulation of blood pH, and the accumulation of metabolic by-products. The simulation results provide the essential evidence for a better understanding of muscle fatigue such as increases in blood lactate and muscle inorganic phosphate, and drop in blood pH level. Moreover, we revised our previous contraction model by introducing the inhibitory effect of metabolic by-products based on structural and experimental data. The accumulation of metabolic by-products reduces the number of strongly bound cross-bridges, leading to a reduction in maximal contraction. In conclusion, our simplified model reliably reflects metabolic fluxes and concentrations that are in good agreement with experimental findings, yielding a better understanding of metabolic fatigue during high-intensity exercise. • Whole-body mathematical model quantitatively estimates the key metabolic fluxes and concentrations during intense exercise. • The constant workload expressed as percentage of maximum oxygen uptake is used as an input parameter for this novel model. • The model has several parameters that can be modified to analyze the effect of individual differences.
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