LAUSR

PURPOSE The consequences of the assumption that the additional ATP usage, underlying the slow component of oxygen consumption ([Formula: see text]) and metabolite on-kinetics, starts when cytosolic inorganic phosphate (Pi) exceeds a certain "critical" Pi concentration, and muscle work terminates because of fatigue when Pi exceeds a certain, higher, "peak" Pi concentration are investigated. METHODS A previously developed computer model of the myocyte bioenergetic system is used. RESULTS Simulated time courses of muscle [Formula: see text], cytosolic ADP, pH, PCr and Pi 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 [Formula: see text] on-kinetics was accelerated, by progressive increase in oxygen tension (hyperoxia). CONCLUSIONS Pi is a major factor responsible for the slow component of the [Formula: see text] 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 Pi exceeds a "critical" Pi concentration, and muscle work terminates when Pi exceeds a "peak" Pi 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 Pi increase and additional ATP usage when "critical" Pi is exceeded.