In previous works it has been shown that the striated fibers of the cremaster muscle undergo a calcium-dependent healing-over reaction after transection and that the fibers of the diaphragm under the same conditions do not recover. In the present work striated fibers of the cremaster and diaphragm are studied, using electrophysiological techniques, light and electron microscopy, 15, 30, 45 and 60 min after transection in an attempt to clarify the process leading to the recovery of the fibers of the cremaster muscle. The recording of membrane potentials at different times after the lesion in the immediate vicinity of the cut end demonstrates that the new diffusion barrier is formed at the damaged surface. Light microscopy of fibers of cremaster transected in vitro indicates the existence of a rapid process preventing the outflow of particulate constituents of the cytoplasm 1 min after the lesion. Electron microscopy shows that this hindrance is due to a compact disposition of filaments derived from altered myofibrils near the cut end. This filamentary plug does not exist in the diaphragm. Cell membrane closing is a slow phenomenon which is completed between 30 and 60 min after the lesion in different fibers. No reconstitution of the cell membrane was found in the fibers of the diaphragm. Rapid and slow responses are interpreted as particular cases of the surface precipitation reaction known in several cell types for more than 40 years.