![]() The ‘repeated bout effect’ is based on the observation of reduced muscle damage and soreness in trained compared with untrained muscle 8, 9. In addition, it is unclear how the training status affects the molecular response to an acute bout of exercise and how changes in gene expression are ultimately linked to persistent modulation of protein levels, organelle function and tissue plasticity. In particular, the mechanistic framework that links the perturbations evoked by individual exercise bouts to long-term training adaptations are largely unknown 3, 4. In light of the powerful health benefits of exercise 6, 7, it is, however, surprising that the molecular underpinnings of muscle plasticity in exercise are still only rudimentarily understood 4. Morphologically, endurance training adaptations include mitochondrial expansion, vascularization and energy substrate storage 4. Remodelling of skeletal muscle requires interventions that disrupt homeostasis, to which muscle will progressively adapt only if repeated over time 3, 4. Skeletal muscle thus exhibits not only a broad morphological and functional specification, but also a remarkably adaptive plasticity to react to perturbations 4. However, the main task of skeletal muscle is the generation of force for different types of contractile activities, including strength, endurance, fine motor control, posture and breathing. Skeletal muscle exerts pleiotropic functions, from thermoregulation to endocrine signalling by myokines and myometabolites, and detoxification of endogenous compounds, for example, kynurenines or aberrantly high levels of ketone bodies 1, 2, 3, 4, 5. Together, these results provide a molecular framework of the temporal and training status-dependent exercise response that underpins muscle plasticity in training. Finally, transiently activated factors such as the peroxisome proliferator-activated receptor-γ coactivator 1α are indispensable for normal training adaptation. Our results reveal that, even though at baseline an unexpectedly low number of genes define the trained muscle, training status substantially affects the transcriptional response to an acute challenge, both quantitatively and qualitatively, in part associated with epigenetic modifications. ![]() We therefore aimed to elucidate the molecular signature of muscles of trained male mice and unravel the training status-dependent responses to an acute bout of exercise. Although morphological changes in endurance-trained muscles are well described, the molecular underpinnings of training adaptation are poorly understood. Skeletal muscle has an enormous plastic potential to adapt to various external and internal perturbations. ![]()
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