Steady-state metabolite (ADP, ATP, P_i, PCr, NADH) concentrations usually differ little between different workloads with significantly different oxygen consumption rates in heart. However, during transitions between steady-states metabolite concentrations may in some cases change transiently, exhibiting a significant overshoot or undershoot, while in other cases they approach near-exponentially new steady-state values. Oxygen consumption rate usually reaches the new steady-state value very quickly (within a few seconds). The present in silico studies, performed using a computer model of oxidative phosphorylation in heart developed previously, demonstrate that such a behavior of the oxidative phosphorylation system can be reproduced only under the assumption that ATP usage, substrate dehydrogenation and (particular steps of) oxidative phosphorylation are directly activated to a similar extend by some cytosolic factor/mechanism during transition from low work to high work (the so-called parallel-activation mechanism). Computer simulations show that some differences observed between different experimental systems can be explained by a slightly different balance of the activation of particular components of the system and/or by a delay in time of the activation/inactivation of substrate dehydrogenation and oxidative phosphorylation during low-to-high and high-to-low work transitions. Thus, the presented theoretical approach offers a general idea that is able to unify, at least semi-quantitatively, different experimental data available in the literature.