The Effect of Gradual Ovarian Failure on Dynamic Muscle Function and the Role of High Intensity Interval Training on Mitigating Impairments

Skeletal muscle function is impaired in menopause and exercise may mitigate tshis decline. We 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 (n=5), VCD-sedentary (n=5), or VCD-training (n=5). Following ovarian failure, the VCD-training group underwent 8 weeks of uphill HIIT. Mice were sacrificed 8 weeks after ovarian failure, representing late menopause. Single muscle 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 calculate force-velocity-power curves. Absolute force and peak power were 31% and 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. HIIT 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. New & Noteworthy Reductions in circulating ovarian hormones impair static muscle contractile performance, but less is known about dynamic properties like power. Typically, rodent models of menopause completely remove the ovaries and fail to mimic the prolonged and complex hormonal transition that includes a retention in ovarian androgen production. Using an ovary intact VCD model of ovarian failure, we found that single fibre power was impaired compared with controls in both SOL and EDL fibres. Our uphill high intensity interval training program was partially sufficient to reverse power loss, but only in fast-type SOL fibres. Impairments in muscle power following ovarian failure are likely driven by a combination of decreased muscle size and force-generating capacity.