We have observed that chronic exposure to stretch shortening cycles (SSC) exhibits hypertrophy and increased muscular strength in young adult rats but decreased strength and maladaptation in aged rats. This indicates that recovery from SSC is impaired with aging. The objective of this pilot study was to examine if apoptosis is involved in this impaired muscle adaptation during chronic exposure to SSC in aged rats. Left dorsiflexor muscles of 30 mo old Fisher Brown Norway rats (bodyweight 338 ± 32 g, N = 5) were exposed in vivo to SSC under anesthetization 3 days per week over a 4.5 week period. The right dorsiflexor muscle served as an intra-animal control. Each exposure consisted of 8 sets of 10 SSC with two minutes rest between sets. Tibialis anterior muscles of both limbs were then dissected. Protein content of heat shock protein (HSP) 72, apoptosis inducing factor (AIF), and cytoplasmic superoxide dismutase (CuZnSOD) was determined in the extracted cytosolic protein fraction by Western immunoblot. Apoptotic DNA fragmentation and total cytosolic cytochrome c level was assessed by ELISA. Moreover, a spectrofluorometric enzyme assay was used to measure the protease activity of caspase-3 and -9. We did not find difference in the protein content of HSP72, AIF, and CuZnSOD between the SSC and control muscles (P > 0.05). Caspase-9 enzyme activity was similar in the SSC and control samples (P < 0.05). However, the level of apoptotic DNA fragmentation, cytochrome c, and caspases-3 protease activity tended to increase by 11% (P=0.056), 30% (P=0.061), and 39% (P=0.088) in the SSC muscle when compared to contralateral control muscle, respectively. These pilot data are consistent with the hypothesis that apoptosis may be involved in the maladaptation of aged skeletal muscle during chronic SCC stimulation. Nevertheless, our results are limited by the sample size and further investigation is warranted to confirm our findings with inclusion of a larger number of animals.