Sarcopenia is a multifactorial disease with complex characteristics. Clinical approaches to managing sarcopenia typically involve exercise, nutrition, and drug interventions. However, the effectiveness of existing drug treatments is limited, and there is a lack of direct evidence regarding their safety. Current studies indicate that NAD+ precursors have the potential to delay muscle aging and combat sarcopenia. The mechanisms of action include enhancing mitochondrial function, suppressing inflammation, and reducing oxidative stress. Furthermore, the combined use of NAD+ precursors with exercise and other medications presents new ideas for delaying skeletal muscle aging and managing sarcopenia. Muscular dystrophies are a group of inherited diseases typically resulting from mutations in crucial genes responsible for muscle protein synthesis. The treatment of muscular dystrophy poses significant challenges, with current treatment options primarily focusing on drug therapy, gene therapy, and stem cell therapy. Studies indicate that muscular dystrophy is associated with NAD+ depletion and disrupted coenzyme homeostasis. Replenishing NAD+ levels could potentially benefit individuals with muscular dystrophy, although further research is required to ascertain its specific effectiveness. Improving mitochondrial function, reducing inflammatory responses, and anti-fibrosis may be potential mechanisms. Mitochondrial myopathies are a group of multi-system diseases caused by genetic defects that result in structural and functional abnormalities in mitochondria, leading to disruptions in cellular respiratory chain and energy metabolism. Currently, effective treatment options are lacking, with existing approaches such as drug therapy, exercise therapy, and dietary therapy focusing on symptomatic relief to enhance quality of life for patients. Gene therapy, cell transplantation, and genetic therapy, which have recently emerged, are still in the exploratory phase. Some studies have suggested that NR and NA may delay the onset and progression of mitochondrial myopathy, but further investigation is needed to determine their specific efficacy, safety, and underlying mechanisms.