Ageing in skeletal muscle results in motor frailty and a reduced capacity for self repair after injury. The contractile characteristics of muscle are determined principally by the myosin heavy chain (MHC) composition of its myofibers. During the restorative process, satellite cells play a central role. The present study compares the levator ani muscle of very old (32 months) and young (4 months) male WI/HicksCar rats in terms of structural integrity, MHC and satellite cell content. Myofiber typing was carried out by indirect immunohistochemistry using a panel of anti-MHC antibodies. Single myofibers for nuclear enumeration were isolated by an enzymatic technique while fiber cross-sectional areas and satellite cell frequencies were determined by computerized planimetry and electron microscopy. In both groups of rats, the myofiber population was homogeneously MHC type IIb-reactive. Cross-sectional data reflected a marked degree of atrophy in the muscle of the senile rats (710.05 +/- 63.6 microm2, compared with 1519.98 +/- 79.0 microm2 in young). The myofiber population was reduced by only about 6.7% with ageing and the representation of satellite cells, as a fraction of total sublaminal nuclei, was relatively stable (1.15 versus 1.91% in young; P > 0.05). The results indicate that ageing had a considerable atrophic effect on the levator ani muscle but induced neither MHC isoform transition nor massive depletion of the satellite cell pool. They suggest that the well-documented impairment of the restorative capacity of senile muscle could be due more to alterations in the nature of microenvironmental cues than to quantitative aspects of its cellular capacity to respond.