In the present study we analysed by the means of the computer model of oxidative phosphorylation in intact muscle (Korzeniewski & Zoladz, 2001) two potential mechanisms responsible for the endurance training-induced acceleration of the VO2 kinetics at the onset of exercise: (1) increase in the amount of mitochondrial enzymes and (2) increase in the parallel activation of ATP supply and ATP usage during rest ┌ work transition (Korzeniewski, 1998). Within the parallel-activation mechanism it is assumed that, starting from the onset of exercise, some external factor(s) (e.g. Ca2+ ions) stimulate(s) directly all oxidative phosphorylation enzymes, in parallel with ATP usage. The computer simulations were performed under the assumption that oxygen delivery does not limit VO2 by oxidative phosphorylation.
The present theoretical studies show that both mechanisms can markedly shorten the t1/2 (half-transition time) for VO2 from 88 s (extreme case) to 40 and 26 s, respectively (for the assumed increase in the amount of mitochondria and in the degree of parallel activation), for an exercise causing an ~7-fold increase in VO2 in relation to resting state. Therefore, in order to distinguish between these two mechanisms it is necessary to compare their effect on the values of VO2 and ADP during rest ┌ work transition. Figure 1 presents the simulated dependence between VO2 and [ADP] for three cases: (1) untrained muscle without parallel activation, (2) trained muscle with a 2-fold increase in mitochondrial enzymes and (3) trained muscle with an induced parallel activation. It can be seen from Fig. 1 that an increase in mitochondrial enzymes does not increase by itself the relative sensitivity of oxidative phosphorylation to ADP (the ratio of the relative increase in VO2 to the relative increase in ADP) ((VO2(work)/VO2(rest))/([ADP](work)/[ADP](rest))), while an increase in parallel activation causes large relative changes in VO2 that are accompanied by smaller relative changes in ADP.
Comparison of the theoretical results presented in Fig. 1 with experimental data (Constable et al. 1987; Dudley et al. 1987; Clark et al. 1988) suggests that an increase in parallel activation, leading to an increase in the phenomenological ‘sensitivity’ of oxidative phosphorylation to ADP, can be at least partly responsible for the training/conditioning-induced shortening of the transition time in VO2 kinetics.
This work was supported by grant 6P04A07120 from Polish State Committee for Scientific Research.