Ageing is associated with disruption of circadian homeostasis, including reduced entraiment to light-dark cycles, reduced amplitude and desynchronization of circadian physiological rhythms, and shortening or lengthening of the endogenous circadian period length (tau). αMUPA mice carry a transgene encoding the urokinase-type plasminogen activator, an extracellular protease implicated in fibrinolysis, tissue remodeling, and brain plasticity. Female αMUPA mice spontaneously eat ~25% less, live ~20% longer, and show high-amplitude circadian rhythms in food intake, body temperature, and in hepatic clock gene expression levels, compared with WT mice. Herein we examined the tau of locomotor activity of mature (8-month old) and aged (18-month old) female αMUPA and WT mice under total darkness. We show that tau changed in WT mice from a period <24 h at 8 months to a period >24 h at 18 months. However, tau of αMUPA mice was ~24 h at both ages. Deviation of tau from 24 h has shown to be inversely related to life span of rodents and non-human primates. Hence, our results suggest that the sustainable endogenous period of ~24 h in αMUPA mice may contribute to their longevity. These results support the hypothesis that although a non-24-h tau has an adaptive significance in allowing a better response to natural daylight changes, such a lack of resonance between tau and external period length entails a life-shortening metabolic cost.