Abstract：
Skeletal muscle contractile function is impaired in menopause and exercise may mitigate this decline. We used the 4-vinylcyclohexene diepoxide (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-mo process), the VCD-training group underwent 8 wk of uphill HIIT. Mice were euthanized 8 wk after ovarian failure, representing late menopause. Single fibers from the soleus (SOL) and extensor digitorum longus (EDL) muscles were dissected, chemically permeabilized, and mechanically tested. Single muscle fibers were maximally activated (pCa 4.5), then isotonic load clamps were performed to evaluate force-velocity-power relationships. Absolute force and peak power were 31.0% and 32.2% lower in VCD-sedentary fibers compared with control fibers, respectively, in both SOL and EDL muscles. Despite reductions in absolute force, there were no concomitant increases in contractile velocity to preserve power production. HIIT attenuated force loss in the VCD-training group such that peak force was not different from the control group across muscles and was partially effective at mitigating power loss (21.7% higher peak power in VCD-training compared with VCD-sedentary) but only in fast-type SOL fibers. 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 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. Our 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.
摘要：
绝经期骨骼肌收缩功能受损，运动可以减轻这种下降。我们使用更年期的VCD模型来研究逐渐卵巢衰竭对骨骼肌收缩功能的影响以及高强度间歇训练（HIIT）是否可以减轻损伤。将性成熟的雌性CD-1小鼠分配到三组中的一组：久坐的对照（n=5），VCD-久坐（n=5），或VCD训练(n=5)。卵巢衰竭（4个月的过程）后，VCD训练组接受了8周的上坡HIIT。卵巢衰竭后8周处死小鼠，代表更年期晚期。解剖了比目鱼肌（SOL）和指长伸肌（EDL）的单根纤维，化学渗透，机械测试。最大程度地激活单个肌肉纤维（pCa4.5），然后进行等渗负载钳，以评估力-速度-功率关系。与对照纤维相比，VCD久坐纤维的绝对力和峰值功率分别降低了31％和32％，分别,在SOL和EDL肌肉中。尽管绝对力量减少，收缩速度没有伴随增加以保持功率产生。HIIT减弱了VCD训练组的力损失，因此峰值力与对照组的肌肉没有差异，并且在减轻功率损失方面部分有效（VCD训练中的峰值功率比VCD久坐高22％），但仅限于快速型SOL纤维。这些发现表明，卵巢衰竭损害动态收缩功能-可能是通过较低的力产生能力和较慢的缩短速度的组合，并且HIIT可能不足以在细胞水平上完全抵消更年期的有害影响。
