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To study the effects of exercise on muscle in a preclinical setting, we developed a combined endurance\u2013resistance training stimulus for mice called progressive weighted wheel running (PoWeR). PoWeR improves molecular, biochemical, cellular and functional characteristics of skeletal muscle and promotes aspects of partial epigenetic reprogramming when performed late in life (22\u201324\u00a0months of age). In this investigation, we leveraged pan\u2010mammalian DNA methylome arrays and tandem mass\u2010spectrometry proteomics in skeletal muscle to provide detailed information on late\u2010life PoWeR adaptations in female mice relative to age\u2010matched sedentary controls (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a07\u201310 per group). Differential CpG methylation at conserved promoter sites was related to transcriptional regulation genes as well as\n                      <jats:italic>Nr4a3<\/jats:italic>\n                      ,\n                      <jats:italic>Hes1<\/jats:italic>\n                      and\n                      <jats:italic>Hox<\/jats:italic>\n                      genes after PoWeR. Using a holistic method of \u2010omics integration called binding and expression target analysis (BETA), methylome changes were associated with upregulated proteins related to global and mitochondrial translation after PoWeR (\n                      <jats:italic>P\u00a0=\u00a0<\/jats:italic>\n                      0.03). Specifically, BETA implicated methylation control of ribosomal, mitoribosomal, and mitochondrial complex I protein abundance after training. DNA methylation may also influence LACTB, MIB1 and UBR4 protein induction with exercise \u2013 all are mechanistically linked to muscle health. Computational cistrome analysis predicted several transcription factors including MYC as regulators of the exercise trained methylome\u2013proteome landscape, corroborating prior late\u2010life PoWeR transcriptome data. Correlating the proteome to muscle mass and fatigue resistance revealed positive relationships with VPS13A and NPL levels, respectively. Our findings expose differential epigenetic and proteomic adaptations associated with translational regulation after PoWeR that could influence skeletal muscle mass and function in aged mice.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16220-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            Late\u2010life combined endurance\u2013resistance exercise training from 22\u201324\u00a0months of age in mice is shown to improve molecular, biochemical, cellular and\n                            <jats:italic>in vivo<\/jats:italic>\n                            functional characteristics of skeletal muscle and promote aspects of partial epigenetic reprogramming and epigenetic age mitigation.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Integration of DNA CpG 36k methylation arrays using conserved sites (which also contain methylation ageing clock sites) with exploratory proteomics in skeletal muscle extends our prior work and reveals coordinated and widespread regulation of ribosomal, translation initiation, mitochondrial ribosomal (mitoribosomal) and complex I proteins after combined voluntary exercise training in a sizeable cohort of female mice (\n                            <jats:italic>n<\/jats:italic>\n                            \u00a0=\u00a07\u201310 per group and analysis).\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Multi\u2010omics integration predicted epigenetic regulation of serine \u03b2\u2010lactamase\u2010like protein (LACTB \u2013 linked to tumour resistance in muscle), mind bomb 1 (MIB1 \u2013 linked to satellite cell and type 2 fibre maintenance) and ubiquitin protein ligase E3 component N\u2010recognin 4 (UBR4 \u2013 linked to muscle protein quality control) after training.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Computational cistrome analysis identified MYC as a regulator of the late\u2010life training proteome, in agreement with prior transcriptional analyses.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Vacuolar protein sorting 13\u00a0homolog A (VPS13A) was positively correlated to muscle mass, and the glycoprotein\/glycolipid associated sialylation enzyme\n                            <jats:italic>N<\/jats:italic>\n                            \u2010acetylneuraminate pyruvate lyase (NPL) was associated to\n                            <jats:italic>in vivo<\/jats:italic>\n                            muscle fatigue resistance.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  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