For high-intensity muscular exercise, the time-to-exhaustion (t) increases as a predictable and hyperbolic function of decreasing power (P) or velocity (V ). This relationship is highly conserved across diverse species and different modes of exercise and is well described by two parameters: the "critical power" (CP or CV), which is the asymptote for power or velocity, and the curvature constant (W') of the relationship such that t = W'/(P - CP). CP represents the highest rate of energy transduction (oxidative ATP production, V˙O2) that can be sustained without continuously drawing on the energy store W' (composed in part of anaerobic energy sources and expressed in kilojoules). The limit of tolerance (time t) occurs when W' is depleted. The CP concept constitutes a practical framework in which to explore mechanisms of fatigue and help resolve crucial questions regarding the plasticity of exercise performance and muscular systems physiology. This brief review presents the practical and theoretical foundations for the CP concept, explores rigorous alternative mathematical approaches, and highlights exciting new evidence regarding its mechanistic bases and its broad applicability to human athletic performance.

During a 3-min all-out cycling test, power output declined to a stable value in approximately the last 45 s, and this power output was not significantly different from the independently measured critical power.

It is well known that physiological variables such as maximal oxygen uptake (V O 2max ), exercise economy, the lactate threshold, and critical power are highly correlated with endurance exercise performance. In this review, we explore the basis for these relationships by explaining the influence of these ''traditional'' variables on the dynamic profiles of the V O 2 response to exercise of different intensities, and how these differences in V O 2 dynamics are related to exercise tolerance and fatigue. The existence of a ''slow component'' of V O 2 during exercise above the lactate threshold reduces exercise efficiency and mandates a greater consumption of endogenous fuel stores (chiefly muscle glycogen) for muscle respiration. For higher exercise intensities (above critical power), steady states in blood acid Ábase status and pulmonary gas exchange are not attainable and V O 2 will increase with time until V O 2max is reached. Here, we show that it is the interaction of the V O 2 slow component, V O 2max , and the ''anaerobic capacity'' that determines the exercise tolerance. Essentially, we take the view that an appreciation of the various exercise intensity ''domains'' and their characteristic effects on V O 2 dynamics can be helpful in improving our understanding of the determinants of exercise tolerance and the limitations to endurance sports performance. The reciprocal effects of interventions such as training, prior exercise, and manipulations of muscle oxygen availability on aspects of V O 2 kinetics and exercise tolerance are consistent with this view.