Commentary on: an (un)paralleled process?

Abstract

As highlighted in the Viewpoint article by Rossiter (2013), studying the adjustment of the energy pathway to cope with ATP demand at the onset of both acute exercise and following exercise training provides a unique window to understand muscle function. Traditionally, it has been thought that the increase in mitochondrial respiration capacity associated with exercise training leads to faster O2 uptake kinetics and smaller relative changes in the cytosolic modulators of oxidative phosphorylation, implying an increased respiration sensitivity of the mitochondria. In this regard, the study by Zoladz et al. (2013) is particularly intriguing and supports previous suggestions that in the early stage of exercise training the sensitivity of mitochondrial respiration can be increased before a change in mitochondrial capacity or mitochondrial density (Green et al. 1991). A potential mechanism contributing to this improved kinetic control may be related to the compartmentalization of energy exchange and the existence of intracellular energetic units. Indeed, it has been suggested that mitochondria, sarcoplasmic reticulum and myofibrils may all be associated functionally in skeletal muscle, such that the ADP produced during intracellular ATPase reactions (myosin- and calcium-ATPases) can be directly channelled to the mitochondria. Considering the substantial, although not significant, reduction in muscle fibre cross-sectional area reported by Zoladz et al. (2013) and the recent documentation of increased ADP sensitivity with short-term training (Layec et al. 2013), one can speculate that the structural arrangement of mitochondria around myofibrils might occur rapidly, after only a few days of exercise training, improving the channelling and regulation of energy within these functional units and metabolic stability.