Skeletal muscle contractile function is impaired in menopause and exercise may mitigate this decline. I used the VCD model of menopause to investigate the effects of gradual ovarian failure on skeletal muscle contractile function and whether high intensity interval training (HIIT) can mitigate impairments. Sexually mature female CD-1 mice were assigned to one of three groups: control sedentary (n=5), VCD-sedentary (n=5), or VCD-training (n=5). Following ovarian failure (a 4-month process), the VCD-training group underwent 8 weeks of uphill HIIT. Mice were sacrificed 8 weeks after ovarian failure, representing late menopause. Single fibres from the soleus (SOL) and extensor digitorum longus (EDL) muscles were dissected, chemically permeabilized, and mechanically tested. Single muscle fibres were maximally activated (pCa 4.5), then isotonic load clamps were performed to evaluate force-velocity-power relationships. Absolute force and peak power were 31% & 32% lower in VCD-sedentary fibres compared to control fibres, respectively, in both SOL and EDL muscles. Despite reductions in absolute force and therefore lighter relative loads imposed during the isotonic contractions in VCD-sedentary fibres, there were no concomitant increases in contractile velocity to preserve power production. HIIT attenuated force loss in the VCD-training group such that it was not different from the control group across muscles, and was partially effective at mitigating power loss (22% higher peak power in VCD-training compared to VCD-sedentary), but only in fast-type SOL fibres. These findings indicate that ovarian failure impairs dynamic contractile function – likely through a combination of lower force-generating capacity and slower shortening velocity – and that HIIT may be insufficient to completely counteract the deleterious effects of menopause at the cellular level.