The deterioration of skeletal muscle into old age (sarcopenia) poses a significant risk to human health and well-being. Sarcopenia is not a uniform condition, with large inter-species variability in the intensity and progression of sarcopenia observed. With underlying genetics not able to adequately explain such variability in the condition, it leads one to suggest that environmental encounters, at least in part, regulate the sarcopenic milieu. In this regard, epigenetics, referring to gene expression changes not caused by underlying genetic variation, becomes a plausible candidate for the regulation of skeletal muscle during environmental insult. Indeed, recent work from has begun to characterise the role of epigenetic modifications in mammalian skeletal muscle during periods of both anabolism and catabolism. For example, we have previously shown an important role for promotor associated DNA methylation of atro-genes during periods of acute muscular atrophy and recovery (Fisher et al., 2017) and global methylome changes during both acute and chronic resistance training induced muscular anabolism (Seaborne et al., 2018). Furthermore, classical research has shown the mammalian organism to be susceptible to early life stress encounters inducing adverse life-long phenotypic outcomes, referred to as developmental/foetal programming. Such a model has also been linked to epigenetics, where underlying modifications are maintained over time, leading to long-term regulation of the phenotype (Holland et al., 2016; Sharples, Stewart and Seaborne, 2016). We have recently shown a similar molecular memory mechanism in skeletal muscle (Seaborne et al., 2018). Epigenetic modifications may therefore act as the link between environmental insult and adverse transcriptomic and phenotypic outcome in skeletal muscle. We will therefore detail our current understanding of skeletal muscle epigenetics, the epigenetic aberrations associated with the sarcopenic niche and how exercise may alleviate these adverse outcomes.