A human skeletal muscle aging atlas was developed by profiling 90,902 single cells and 92,259 single nuclei from 17 donors to map the aging process in adult human intercostal muscle. The study identified cellular changes in each muscle compartment, revealing that distinct subsets of muscle stem cells (MuSCs) exhibit decreased ribosome biogenesis genes and increased CCL2 expression, leading to different aging phenotypes. The atlas also highlights an expansion of nuclei associated with the neuromuscular junction, which may reflect re-innervation, and outlines how the loss of fast-twitch myofibers is mitigated through regeneration and upregulation of fast-type markers in slow-twitch myofibers with age. Additionally, the study documents the function of the aging muscle microenvironment in immune cell attraction. The atlas provides a comprehensive resource for studying muscle aging across species, including an in-house mouse muscle atlas. Skeletal muscle, which makes up 40% of body mass, is essential for movement and has pivotal roles in metabolism and immune regulation. The major components of skeletal muscle, multinucleated myofibers (MFs), are classified into slow-twitch (type I) and fast-twitch (type II, type IIX and intermediate hybrid fibers) based on contraction speed, structural protein composition, and metabolic characteristics. MFs are surrounded by mononuclear muscle stem cells (MuSCs), which can generate new MFs after damage. The muscle microenvironment consists of supporting fibroblasts, vasculature, immune cells, Schwann cells, and neuronal axons, which transmit action potentials to the MFs. Skeletal muscle aging is characterized by the loss of both muscle mass and strength, often leading to sarcopenia. This is a major contributory factor to falls and fractures in older adults, the second-leading cause of injury and deaths. During aging, there is a selective decrease in both the number and size of fast-twitch MFs. Furthermore, the number of MuSCs and their activation and proliferation in response to stimuli decrease with age. However, it is not known whether this increased atrophy is due to MF-intrinsic changes in gene expression, the impact of the cellular microenvironment, or a combination of both. Most previous studies focused on one particular mechanism or cell type, leaving a gap in our understanding of muscle aging as a whole. To address this, recent mouse and human skeletal muscle studies pioneered the use of single-cell RNA sequencing (scRNA-seq) or single-nucleus RNA sequencing (snRNA-seq) to understand muscle cell type heterogeneity and their changes in aging. However, both approaches have limitations when individually applied to muscle: droplet single-cell sequencing approaches cannot capture MFs due to their large size, and single-nucleus sequencing often lacks resolution for the less-abundant MuSCs and other mononuclear cell types in theA human skeletal muscle aging atlas was developed by profiling 90,902 single cells and 92,259 single nuclei from 17 donors to map the aging process in adult human intercostal muscle. The study identified cellular changes in each muscle compartment, revealing that distinct subsets of muscle stem cells (MuSCs) exhibit decreased ribosome biogenesis genes and increased CCL2 expression, leading to different aging phenotypes. The atlas also highlights an expansion of nuclei associated with the neuromuscular junction, which may reflect re-innervation, and outlines how the loss of fast-twitch myofibers is mitigated through regeneration and upregulation of fast-type markers in slow-twitch myofibers with age. Additionally, the study documents the function of the aging muscle microenvironment in immune cell attraction. The atlas provides a comprehensive resource for studying muscle aging across species, including an in-house mouse muscle atlas. Skeletal muscle, which makes up 40% of body mass, is essential for movement and has pivotal roles in metabolism and immune regulation. The major components of skeletal muscle, multinucleated myofibers (MFs), are classified into slow-twitch (type I) and fast-twitch (type II, type IIX and intermediate hybrid fibers) based on contraction speed, structural protein composition, and metabolic characteristics. MFs are surrounded by mononuclear muscle stem cells (MuSCs), which can generate new MFs after damage. The muscle microenvironment consists of supporting fibroblasts, vasculature, immune cells, Schwann cells, and neuronal axons, which transmit action potentials to the MFs. Skeletal muscle aging is characterized by the loss of both muscle mass and strength, often leading to sarcopenia. This is a major contributory factor to falls and fractures in older adults, the second-leading cause of injury and deaths. During aging, there is a selective decrease in both the number and size of fast-twitch MFs. Furthermore, the number of MuSCs and their activation and proliferation in response to stimuli decrease with age. However, it is not known whether this increased atrophy is due to MF-intrinsic changes in gene expression, the impact of the cellular microenvironment, or a combination of both. Most previous studies focused on one particular mechanism or cell type, leaving a gap in our understanding of muscle aging as a whole. To address this, recent mouse and human skeletal muscle studies pioneered the use of single-cell RNA sequencing (scRNA-seq) or single-nucleus RNA sequencing (snRNA-seq) to understand muscle cell type heterogeneity and their changes in aging. However, both approaches have limitations when individually applied to muscle: droplet single-cell sequencing approaches cannot capture MFs due to their large size, and single-nucleus sequencing often lacks resolution for the less-abundant MuSCs and other mononuclear cell types in the