Increase in muscle power is associated with myofibrillar ATPase adaptations during resistance training.

Abstract

What is the central question of this study? The aim of this study was to examine the effects of resistance training on gains in the external mechanical power output developed during climbing and myofibrillar ATPase activity in rats. What is the main finding and its importance? Using rapid flow quench experiments, we show that resistance training increases both the power output and the myofibrillar ATPase activity in the flexor digitorum profundus, biceps and deltoid muscles. Data fitting reveals that these functional ameliorations are explained by an increase in the rate constant of liberation of ATP hydrolysis products and contribute to performance gains. Skeletal muscle shows a remarkable plasticity that permits functional adaptations in response to different stimulations. To date, modifications of the proportions of myosin heavy chain (MHC) isoforms and increases in fibre size are considered to be the main factors providing sarcomeric plasticity in response to exercise training. In this study, we investigated the effects of a resistance training protocol on the myofibrillar ATPase (m-ATPase) cycle, muscle performance (power output) and MHC gene expression. For this purpose, 8-week-old Wistar Han rats were subjected to 4weeks of resistance training, with five sessions per week. Muscle samples of flexor digitorum profundus (FDP), biceps and deltoid were collected and subjected to RT-qPCR analyses and assessment of m-ATPase activity with rapid flow quench apparatus. Training led to a significant increase in muscle mass, except for the biceps, and in total mechanical power output (+135.7%, P<0.001). A shift towards an intermediate fibre type (i.e. MHC2x-to-MHC2a isoform transition) was also observed in biceps and FDP but not in the deltoid muscle. Importantly, rapid flow quench experiments revealed an enhancement of the m-ATPase activity during contraction at maximal velocity (kF ) in the three muscles, with a more marked effect in FDP (+242%, P<0.001). Data fitting revealed that the rate constant of liberation of ATP hydrolysis products (k3 ) appears to be the main factor influencing the increase in m-ATPase activity. In conclusion, the data showed that, in addition to classically observed changes in MHC isoform content and fibre hypertrophy, m-ATPase activity is enhanced during resistance training and might contribute significantly to performance gains.