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雌激素对抗阻运动后骨骼肌卫星细胞和肌核领域大小的影响。

Influence of oestrogen on satellite cells and myonuclear domain size in skeletal muscles following resistance exercise.

机构信息

Institute of Health and Sports & Medicine, Juntendo University, Chiba, Japan.

Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.

出版信息

J Cachexia Sarcopenia Muscle. 2022 Oct;13(5):2525-2536. doi: 10.1002/jcsm.13031. Epub 2022 Jul 11.

DOI:10.1002/jcsm.13031
PMID:35818664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9530499/
Abstract

BACKGROUND

Oestrogen deficiency reduces skeletal muscle mass and force generation in postmenopausal women. Muscle mass is maintained by satellite cells, which are regulated by oestrogen. Although oestrogen therapy enhances muscle hypertrophy induced by resistance training in postmenopausal women, the molecular mechanism is unclear.

METHODS

Adult female rats (10 weeks old) were divided into six groups: sham sedentary (Sham-Sed), sham climbing training (Sham-CT), ovariectomy sedentary (OVX-Sed), ovariectomy climbing training (OVX-CT), ovariectomy plus oestrogen treatment sedentary (OVX+E-Sed), and ovariectomy plus oestrogen treatment climbing training (OVX+E-CT). At 8 weeks after ovariectomy, rats in the training group were trained (one session every 3 days for 8 weeks) to climb a ladder while bearing a load. Oestrogen treatment involved subcutaneous insertion of a 17β-oestradiol pellet. After 8 weeks, the flexor hallucis longus muscle was collected and analysed.

RESULTS

Following climbing training, the flexor hallucis longus muscle mass and muscle-to-body weight ratios were dramatically increased by training (main effect of training, P < 0.01); the OVX+E-CT group showed the highest values (main effect of group, P < 0.01). The cross-sectional area of all muscle fibre types was increased by training (main effect of training, P < 0.01). Particularly, the cross-sectional area of MHC IIa in the OVX+E-CT group was significantly larger than that in the Sham-CT and OVX-CT groups. Satellite cell numbers were increased in all training groups (main effect of training, P < 0.05), and the myonuclear number was increased by training (main effect of training, P < 0.01), but there was no main group effect. The myonuclear domain size of all muscle fibre types and MHC IIa was increased in all training groups (main effect of training, P < 0.01) and showed a main group effect (P < 0.01). The myonuclear domain sizes of all muscle fibre types and MHC IIa in the OVX+E-CT group were significantly larger than those in the Sham-CT and OVX-CT groups. The total RNA contents revealed main effects of training and the group (P < 0.01); the OVX+E-CT group showed the highest contents (main effect of group, P < 0.01). The mRNA and protein levels of rpS6 were increased in the OVX+E-Sed and CT groups (main effects of group, P < 0.05). Particularly, the 28S ribosomal RNA content in OVX+E-Sed group was significantly higher than that in the OVX-Sed group.

CONCLUSIONS

Oestrogen enhanced the resistance training-induced increase in myonuclear domain size but did not affect satellite cells and ribosome biogenesis.

摘要

背景

雌激素缺乏会减少绝经后女性的骨骼肌质量和产生力量。卫星细胞维持着肌肉质量,而雌激素对卫星细胞进行调节。尽管雌激素治疗可以增强绝经后女性抗阻训练引起的肌肉肥大,但其中的分子机制尚不清楚。

方法

成年雌性大鼠(10 周龄)分为 6 组:假手术安静组(Sham-Sed)、假手术爬梯训练组(Sham-CT)、卵巢切除术安静组(OVX-Sed)、卵巢切除术爬梯训练组(OVX-CT)、卵巢切除术加雌激素治疗安静组(OVX+E-Sed)和卵巢切除术加雌激素治疗爬梯训练组(OVX+E-CT)。卵巢切除 8 周后,训练组(每 3 天训练 1 次,持续 8 周)进行爬梯训练,以承担负荷。雌激素治疗涉及皮下插入 17β-雌二醇微球。8 周后,采集并分析比目鱼肌。

结果

爬梯训练后,比目鱼肌质量和肌肉与体重比显著增加(训练的主要作用,P<0.01);OVX+E-CT 组的数值最高(组的主要作用,P<0.01)。所有肌纤维类型的横截面积均增加(训练的主要作用,P<0.01)。特别是,OVX+E-CT 组的 MHC IIa 肌纤维横截面积明显大于 Sham-CT 和 OVX-CT 组。所有训练组的卫星细胞数量均增加(训练的主要作用,P<0.05),肌核数量增加(训练的主要作用,P<0.01),但没有组的主要作用。所有肌纤维类型和 MHC IIa 的肌核域大小在所有训练组中均增加(训练的主要作用,P<0.01),并具有组的主要作用(P<0.01)。OVX+E-CT 组的所有肌纤维类型和 MHC IIa 的肌核域大小明显大于 Sham-CT 和 OVX-CT 组。总 RNA 含量显示出训练和组的主要作用(P<0.01);OVX+E-CT 组的含量最高(组的主要作用,P<0.01)。rpS6 的 mRNA 和蛋白质水平在 OVX+E-Sed 和 CT 组中增加(组的主要作用,P<0.05)。特别是,OVX+E-Sed 组的 28S 核糖体 RNA 含量明显高于 OVX-Sed 组。

结论

雌激素增强了抗阻训练引起的肌核域大小的增加,但不影响卫星细胞和核糖体生物发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/58ab3d693738/JCSM-13-2525-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/7fb9065cbeb2/JCSM-13-2525-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/b78e404984b5/JCSM-13-2525-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/58ab3d693738/JCSM-13-2525-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/7fb9065cbeb2/JCSM-13-2525-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/3e7e30c685e5/JCSM-13-2525-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/8a1e5001c148/JCSM-13-2525-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/3e25de370a9a/JCSM-13-2525-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d0/9530499/58ab3d693738/JCSM-13-2525-g006.jpg

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