In the present work we test the hypothesis that sustained transgenic overexpression of insulin like growth factor - 1 (IGF-1) in skeletal muscle prevents age-related decreases in myoplasmic Ca²⁺ concentration and consequently in specific force in single intact fibres from the flexor digitorum brevis (FDB) muscle from the mouse. Measurements of IGF-1 concentration in FDB muscle showed higher levels in transgenic than in wild type mice at all ages. The specific tetanic force decreased significantly in single muscle fibres from old (286 ± 22 kPa) compared to young wild type (455 ± 28), young transgenic 423 ± 43, and old transgenic mice (386 ± 15) (P < 0.05). These results are consistent with measurements in whole FDB muscles. The peak Ca²⁺ concentration values in response to prolonged stimulation were: 1.47 ± 0.15, 1.70 ± 0.29, 0.97 ± 0.13 and 1.7 ± 0.22 µM, in fibres from young wild type, young transgenic, old wild type and old transgenic mice, respectively. The effects of caffeine on FDB fibres support the conclusion that the age-related decline in peak myoplasmic Ca²⁺ and specific force is not explained by sarcoplasmic reticulum Ca²⁺ depletion. Immunocytochemistry in muscle cross sections was performed to determine whether age and/or IGF-1 overexpression induce changes in fibre type composition. The relative percentage of type IIa, IIx and I MHC isoforms did not change significantly with age or genotype. Therefore, IGF-1 prevents age-related decline in peak intracellular Ca²⁺ and specific force in a muscle that does not exhibit changes in fibre type composition with senescence.