Effects of mild-exercise training cessation in human skeletal muscle

Abstract

Stoppage of endurance exercise training leads to complete loss of maximal oxygen uptake ($\dot{V}{\text{O}}_{ 2\max }$) gain but not submaximal exercise blood lactate concentrations. However, the detailed mechanisms are still unknown. Thus, we investigated the effects of exercise-training cessation at lactate threshold (LT) intensity on physiological adaptations and global mRNA expressions in human skeletal muscle. The $\dot{V}{\text{O}}_{ 2\max }$, muscle capillaries density and global gene expression were measured after 12 weeks of LT training, and after 12 weeks of detraining. Twelve weeks of detraining reversed the effect of 12 weeks LT training on $\dot{V}{\text{O}}_{ 2\max }$ and $\dot{V}{\text{O}}_{ 2}$ at LT intensity, although the later value was higher than the pre-training level. Moreover, the training cessation did not affect the number of capillaries around type I fiber, which was increased by training. The training modulated 243 characterized transcripts, in which 77% showed a significant reversible effect by detraining. However, the transcripts most-induced by the training were still elevated after the same period of detraining. The pathway and network analysis revealed that these genes were related to oxidative phosphorylation (OxPhos), calcium signalling and tissue development. Therefore, these physiological and transcriptional changes suggest improved oxygen supply and OxPhos in the skeletal muscle, which may contribute to the incomplete loss of absolute $\dot{V}{\text{O}}_{ 2}$ at LT intensity after training cessation. The present study does not only demonstrate, for the first time, sustained effects of training after detraining at the transcriptional level, but also indicates the possible signalling pathways.