Training-Induced Increase in V·O2max and Critical Power, and Acceleration of V·O2 on-Kinetics Result from Attenuated Pi Increase Caused by Elevated OXPHOS Activity.

Abstract

Computer simulations using a dynamic model of the skeletal muscle bioenergetic system, involving the Pi-double-threshold mechanism of muscle fatigue, demonstrate that the training-induced increase in V·O2max, increase in critical power (CP) and acceleration of primary phase II of the V·O2 on kinetics (decrease in t0.63) is caused by elevated OXPHOS activity acting through a decrease in and slowing of the Pi (inorganic phosphate) rise during the rest-to-work transition. This change leads to attenuation of the reaching by Pi of Pipeak, peak Pi at which exercise is terminated because of fatigue. The delayed (in time and in relation to V·O2 increase) Pi rise for a given power output (PO) in trained muscle causes Pi to reach Pipeak (in very heavy exercise) after a longer time and at a higher V·O2; thus, exercise duration is lengthened, and V·O2max is elevated compared to untrained muscle. The diminished Pi increase during exercise with a given PO can cause Pi to stabilize at a steady state less than Pipeak, and exercise can continue potentially ad infinitum (heavy exercise), instead of rising unceasingly and ultimately reaching Pipeak 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 Pi 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, t0.63 is shortened. This effect of elevated OXPHOS activity is possibly somewhat diminished by the training-induced decrease in Pipeak.