An (un)paralleled process?

Abstract

exercise is challenged because classical biochemical models are unable to explain the increased rate of oxidative ATP production on the basis of altered concentrations of respiratory substrates alone. The paper by Zoladz et al. (2013) exploresparallelactivationtheoryinhuman skeletal muscle by applying innovative reasoning,asfollows:(i) adaptationtofaster oxygenuptakekineticsfollowingendurance exercise training, observed in as few as two training sessions, occurs more rapidly than theexpansionofthemitochondrialvolume, suggesting enhancements of allosteric control in mitochondrial energy supply; and (ii) following training, a more tightly controlled, metabolically stable, parallel system would be accompanied by a reduction in the energy demands of exercise. The data show convincing support for these hypotheses, in that moderateintensity exercise training speeded the kinetics aerobic adjustment during exercise by almost 25% and reduced the oxygen cost of the exercise by nearly 5%; these effects were observed in the absence of changes in markers of mitochondrial respiratory capacity or biogenesis. These human data are consistent with features of parallel control recently demonstrated in single Xenopus myocytes (Gandra et al. 2012) andinthegastrocnemius‐superficialdigital flexorcomplexofthedog(W¨ ustetal.2011). Considering the wide interest in the control of oxidative metabolism during exercise, the molecular mechanisms contributing to kinetic control of oxidative phosphorylation in vivo have received relatively little attention. As such, the training-induced reduction in sarcoplasmic