Increased skeletal muscle nuclear apoptosis has been suggested to be involved with age-related pathological remodeling that contributes to sarcopenic states. PURPOSE: The purpose of this study was to determine if apoptosis plays a role in age-dependent adaptation and maladaptation in young and old skeletal muscle of rats, respectively, following chronic high-intensity mechanical loading via stretch-shortening contractions (SSCs). METHODS: Left dorsiflexor muscles of young (3 mo, N=6) and old (30 mo, N=6) Fischer 344 x BN rats, were loaded 3 times/week for 4.5-weeks using a protocol of 80 maximal SSCs per exposure in vivo. Twenty-four hours after the last training session, tibialis anterior (TA) muscles were harvested and individual muscle regions were allocated for biochemical or histological analyses. TA muscle was homogenized and prepared for cell death enzyme-linked immunosorbent assay (ELISA), while histomorphology was conducted on transverse sections of the TA muscle mid-belly prepared for terminal dUTP nick-end labeling (TUNEL) and laminin duel immunofluorescence and quantified via standard stereology. RESULTS: Cell death was increased in both old control (-50%) and old SSC-loaded (-105%) skeletal muscle versus young muscle, as quantified by ELISA (p < 0.05). Moreover, ELISA data revealed chronic SSC-loading increased cell death -95% in young rats' skeletal muscle, while old rats' cell death significantly increased -105% (p < 0.05), compared with control muscle. Additionally, aging increased the volume density of TUNEL-positive myonuclei in both control (-125%) and SSC-loaded (-200%) TA muscles compared with young rats (p < 0.05). Interestingly, no increase in TUNEL -positive myonuclei was observed following chronic SSC loading in young or old rats. CONCLUSION: Our data suggest that adaptation and maladaptation following chronic SSC loading is significantly impacted by apoptosis; however apparent differences exist with the individual cell types undergoing apoptosis; specifically, nuclei distinct from skeletal muscle may contribute to these findings. Collectively, these results indicate that apoptotic-related events contribute significantly to age-dependent adaptive and maladaptive remodeling in young and old soft tissue, respectively, following chronic mechanical loading.