Exceeding a “critical” muscle P_i: implications for $\dot{\text{V}}\text{O}_{2}$ and metabolite slow components, muscle fatigue and the power–duration relationship

Abstract

Purpose

The consequences of the assumption that the additional ATP usage, underlying the slow component of oxygen consumption ($\dot{\text{V}}\text{O}_{2}$) and metabolite on-kinetics, starts when cytosolic inorganic phosphate (P_i) exceeds a certain “critical” P_i concentration, and muscle work terminates because of fatigue when P_i exceeds a certain, higher, “peak” P_i concentration are investigated.

Methods

A previously developed computer model of the myocyte bioenergetic system is used.

Results

Simulated time courses of muscle $\dot{\text{V}}\text{O}_{2}$, cytosolic ADP, pH, PCr and P_i at various ATP usage activities agreed well with experimental data. Computer simulations resulted in a hyperbolic power–duration relationship, with critical power (CP) as an asymptote. CP was increased, and phase II $\dot{\text{V}}\text{O}_{2}$ on-kinetics was accelerated, by progressive increase in oxygen tension (hyperoxia).

Conclusions

P_i is a major factor responsible for the slow component of the $\dot{\text{V}}\text{O}_{2}$ and metabolite on-kinetics, fatigue-related muscle work termination and hyperbolic power–duration relationship. The successful generation of experimental system properties suggests that the additional ATP usage, underlying the slow component, indeed starts when cytosolic P_i exceeds a “critical” P_i concentration, and muscle work terminates when P_i exceeds a “peak” P_i concentration. The contribution of other factors, such as cytosolic acidification, or glycogen depletion and central fatigue should not be excluded. Thus, a detailed quantitative unifying mechanism underlying various phenomena related to skeletal muscle fatigue and exercise tolerance is offered that was absent in the literature. This mechanism is driven by reciprocal stimulation of P_i increase and additional ATP usage when “critical” P_i is exceeded.