Sarcopenia, the age-related degenerative loss of muscle mass and function, is considered a muscle disease (i.e., muscle failure) 1) and is central to functional and metabolic alterations in various clinical conditions such as critical illness (e.g., burn injury and cancer), chronic diseases (e.g., heart failure), insulin resistance, obesity, and osteoporosis. 2) Therefore, discovering effective therapeutic means to counteract sarcopenia progression is of utmost importance to improve the quality of life in older adults and is a major target for drug development; however, efforts have not yet led to clinically meaningful success. 3) The etiology of sarcopenia is multifactorial, including alterations in hormones and sex steroids, physical inactivity, and comorbidities. 4) It is, therefore, difficult to understand the underlying mechanism(s) at molecular Sarcopenia, which is the loss of muscle mass and strength that occurs with aging, involves imbalanced muscle protein turnover (i.e., protein breakdown exceeding synthesis), which in turn exacerbates other clinical conditions such as type 2 diabetes mellitus, obesity, osteoporosis, and cancer, thereby worsening the quality of life in older adults. This imbalance is attributed in part to the resistance of aged muscle to anabolic stimuli such as dietary protein/amino acids and resistance exercise known as anabolic resistance. Despite research efforts, no practical therapeutics have been successfully discovered possibly because of a lack of understanding of the dynamic nature of muscle protein, and the use of indirect assessments of muscle mass. Herein, we briefly discuss the regulation of protein turnover in response to the abovementioned anabolic stimuli with respect to anabolic resistance and optimal protein intake, followed by methodological considerations for advancing sarcopenia research, including assessments of muscle mass and dynamics.