Training-Induced Increase in  [Formula: see text] O(2max) and Critical Power, and Acceleration of  [Formula: see text] O(2) on-Kinetics Result from Attenuated P(i) Increase Caused by Elevated OXPHOS Activity

Computer simulations using a dynamic model of the skeletal muscle bioenergetic system, involving the P(i)-double-threshold mechanism of muscle fatigue, demonstrate that the training-induced increase in [Formula: see text] O(2max), increase in critical power (CP) and acceleration of primary phase II of the [Formula: see text] O(2) on kinetics (decrease in t(0.63)) is caused by elevated OXPHOS activity acting through a decrease in and slowing of the P(i) (inorganic phosphate) rise during the rest-to-work transition. This change leads to attenuation of the reaching by P(i) of Pi(peak), peak P(i) at which exercise is terminated because of fatigue. The delayed (in time and in relation to [Formula: see text] O(2) increase) P(i) rise for a given power output (PO) in trained muscle causes P(i) to reach Pi(peak) (in very heavy exercise) after a longer time and at a higher [Formula: see text] O(2); thus, exercise duration is lengthened, and [Formula: see text] O(2max) is elevated compared to untrained muscle. The diminished P(i) increase during exercise with a given PO can cause P(i) to stabilize at a steady state less than P(ipeak), and exercise can continue potentially ad infinitum (heavy exercise), instead of rising unceasingly and ultimately reaching Pi(peak) and causing exercise termination (very heavy exercise). This outcome means that CP rises, as the given PO is now less than, and not greater than CP. Finally, the diminished P(i) increase (and other metabolite changes) results in, at a given PO (moderate exercise), the steady state of fluxes (including [Formula: see text] O(2)) and metabolites being reached faster; thus, t(0.63) is shortened. This effect of elevated OXPHOS activity is possibly somewhat diminished by the training-induced decrease in Pi(peak).