Clinical efficacy of skeletal myoblast (skMb) transplantation is controversial whether this treatment produces beneficial outcome in patients with dilated cardiomyopathy (DCM). Based on immunological tolerance between wild-type and DCM hamsters with the deletion of δ-sarcoglycan (SG) gene, skMb engraftment in TO-2 myocardium (3×105 cells in ∼100mg heart) was verified by the donor-specific expression of δ-SG transgene constitutively produced throughout myogenesis. At 5 weeks after the transplantation, the cell rates expressing fast-myosin heavy chain (MHC) exceeded slow-MHC in δ-SG+ cells. Fifteen weeks after (corresponding to ∼12 years in humans), fast MHC+ cells nullified, but the δ-SG+ and slow MHC+ cell number remained unaltered. These skMbs fused with host cardiomyocytes via connexin-43 and intercalated disc, modestly improving the hemodynamics without arrhythmia, when engrafted skMbs were sparsely disseminated in autopsied myocardium. These results provide us evidence that disseminating delivery of slow-MHC+ myoblasts is promising for repairing DCM heart using histocompatible skeletal myoblasts in future.