Training-Induced Increase in V·O_2max and Critical Power, and Acceleration of V·O₂ on-Kinetics Result from Attenuated...

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 V·O_2max, increase in critical power (CP) and acceleration of primary phase II of the V·O₂ 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 V·O₂ 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 V·O₂; thus, exercise duration is lengthened, and V·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 V·O₂) 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.