Accumulating　research　has　shown　that　chronic　D-galactose　(D-gal)　exposure　induces　symptoms　similar　to　natural　aging　in　animals.　Therefore,　rodents　chronically　exposed　to　D-gal　are　increasingly　used　as　a　model　for　aging　and　delay-of-aging　pharmacological　research.　Mitochondrial　dysfunction　is　thought　to　play　a　vital　role　in　aging　and　age-related　diseases;　however,　whether　mitochondrial　dysfunction　plays　a　significant　role　in　mice　exposed　to　D-gal　remains　unknown.　In　the　present　study,　we　investigated　cognitive　dysfunction,　locomotor　activity,　and　mitochondrial　dysfunction　involved　in　D-gal　exposure　in　mice.　We　found　that　D-gal　exposure　(125　mg/kg/day,　8　weeks)　resulted　in　a　serious　impairment　in　grip　strength　in　mice,　whereas　spatial　memory　and　locomotor　coordination　remained　intact.　Interestingly,　muscular　mitochondrial　complex　I　deficiency　occurred　in　the　skeletal　muscle　of　mice　exposed　to　D-gal.　Mitochondrial　ultrastructure　abnormality　was　implicated　as　a　contributing　factor　in　D-gal-induced　muscular　impairment.　Moreover,　three　combinations　(A,　B,　and　C)　of　nutrients　applied　in　this　study　effectively　reversed　D-gal-induced　muscular　impairment.　Nutrient　formulas　B　and　C　were　especially　effective　in　reversing　complex　I　dysfunction　in　both　skeletal　muscle　and　heart　muscle.　These　findings　suggest　the　following:　(1)　chronic　exposure　to　D-gal　first　results　in　specific　muscular　impairment　in　mice,　rather　than　causing　general,　premature　aging;　(2)　poor　skeletal　muscle　strength　induced　by　D-gal　might　be　due　to　the　mitochondrial　dysfunction　caused　by　complex　I　deficiency;　and　(3)　the　nutrient　complexes　applied　in　the　study　attenuated　the　skeletal　muscle　impairment,　most　likely　by　improving　mitochondrial　function.