The loss of muscle mass during aging has been termed sarcopenia. Sarcopenia results in a decrease in physical strength during aging that results in important consequences for more severely affected individuals in terms of function and as a marker for disability and increased mortality. Despite the clinical importance of this condition, the pathophysiology leading to the development of sarcopenia is not well understood, and few treatments exist to prevent or reverse the condition. Recently, sarcopenia has been found to occur during aging in the nematode Caenorhabditis elegans, which is an organism increasingly used to study genetic and biochemical events involved in aging. Like in humans, sarcopenia in C. elegans leads to declines in mobility and serves as a marker for increased mortality. Interestingly, mutations affecting the age-1 gene, which slows aging of the animal, result in significant delays in the development of sarcopenia, suggesting a direct causal relationship between organismal aging and sarcopenia. These findings suggest that, in humans and worms, sarcopenia may represent a biomarker for the biological age, as opposed to chronological age, of the individual. These findings also suggest that C. elegans will develop into an important model system in which to study the biochemical and genetics events responsible for sarcopenia and to test therapeutics designed to prevent or reverse sarcopenia.