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机械过载和高强度间歇训练对雄性小鼠骨骼肌肥大的联合作用。

Combined effects of mechanical overload and high-intensity interval training on skeletal muscle hypertrophy in male mice.

作者信息

Shinkai Hayato, Shirai Takanaga, Uemichi Kazuki, Iwai Ryoto, Iwata Tomohiro, Tanimura Riku, Sugiyama Shunsuke, Takemasa Tohru

机构信息

Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.

Department of Human Sciences, Kanagawa University, Yokohama-shi, Kanagawa, Japan.

出版信息

Physiol Rep. 2025 Sep;13(17):e70542. doi: 10.14814/phy2.70542.

DOI:10.14814/phy2.70542
PMID:40939109
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12431583/
Abstract

Athletes often perform concurrent training that combines different exercise modalities. It is believed that muscle hypertrophic adaptation is inhibited by endurance exercise; however, the molecular mechanisms underlying the effects of high-intensity, short-duration exercise on muscle hypertrophic responses remain unclear. In this study, we determined the effects of high-intensity interval training (HIIT) on mechanical overload-induced muscle hypertrophy in mice. Eight-week-old male mice were divided into the following three groups (n = 6-8): Sham surgery (Sham), myotenectomy-induced mechanical overload (OL), and OL with HIIT by forced swimming (OL + HIIT). After 4 weeks of intervention, the OL + HIIT group exhibited an increase in plantaris muscle weight and muscle fiber cross-sectional area as well as the OL group. The OL + HIIT group showed a similar increase in mTOR downstream proteins rpS6, S6K1, and 4E-BP1 phosphorylation compared with the OL group. AMPK was activated by HIIE and may play an inhibitory role by attenuating mTOR. To clarify its involvement, acute phase experiments were conducted to evaluate mTOR signaling immediately after a single round of HIIE. The increase of rpS6 and S6K1 phosphorylation was unchanged after a single HIIE exposure, despite AMPK upregulation. Our results suggest that interference effects induced by HIIE may not occur in mechanically overloaded mouse skeletal muscle.

摘要

运动员经常进行结合不同运动方式的联合训练。人们认为耐力运动会抑制肌肉肥大适应;然而,高强度、短时间运动对肌肉肥大反应影响的分子机制仍不清楚。在本研究中,我们确定了高强度间歇训练(HIIT)对小鼠机械负荷诱导的肌肉肥大的影响。将8周龄雄性小鼠分为以下三组(n = 6 - 8):假手术组(Sham)、肌腱切断诱导的机械负荷组(OL)和通过强迫游泳进行HIIT的OL组(OL + HIIT)。干预4周后,OL + HIIT组与OL组一样,比目鱼肌重量和肌纤维横截面积增加。与OL组相比,OL + HIIT组mTOR下游蛋白rpS6、S6K1和4E - BP1磷酸化水平有类似增加。AMPK被高强度间歇运动(HIIE)激活,可能通过减弱mTOR发挥抑制作用。为阐明其作用,进行急性期实验以在一轮HIIE后立即评估mTOR信号传导。尽管AMPK上调,但单次HIIE暴露后rpS6和S6K1磷酸化的增加未改变。我们的结果表明,HIIE诱导的干扰效应可能不会在机械负荷过重的小鼠骨骼肌中发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/3b2047f654bb/PHY2-13-e70542-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/a9d55ac50034/PHY2-13-e70542-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/942c233e68f8/PHY2-13-e70542-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/f696cb08c50e/PHY2-13-e70542-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/0c4a5c490d78/PHY2-13-e70542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/0ba79d84345f/PHY2-13-e70542-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/3b2047f654bb/PHY2-13-e70542-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/a9d55ac50034/PHY2-13-e70542-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/942c233e68f8/PHY2-13-e70542-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/f696cb08c50e/PHY2-13-e70542-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/0c4a5c490d78/PHY2-13-e70542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/0ba79d84345f/PHY2-13-e70542-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b0b/12431583/3b2047f654bb/PHY2-13-e70542-g001.jpg

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