Relative rDNA copy number is not associated with resistance training-induced skeletal muscle hypertrophy and does not affect myotube anabolism in vitro.

IF 2.2 3区 医学 Q3 PHYSIOLOGY American journal of physiology. Regulatory, integrative and comparative physiology Pub Date : 2024-09-01 Epub Date: 2024-07-15 DOI:10.1152/ajpregu.00131.2024
Joshua S Godwin, J Max Michel, Andrew T Ludlow, Andrew D Frugé, C Brooks Mobley, Gustavo A Nader, Michael D Roberts
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Abstract

Ribosomal DNA (rDNA) copies exist across multiple chromosomes, and interindividual variation in copy number is speculated to influence the hypertrophic response to resistance training. Thus, we examined if rDNA copy number was associated with resistance training-induced skeletal muscle hypertrophy. Participants (n = 53 male, 21 ± 1 yr old; n = 29 female, 21 ± 2 yr old) performed 10-12 wk of full-body resistance training. Hypertrophy outcomes were determined, as was relative rDNA copy number from preintervention vastus lateralis (VL) biopsies. Pre- and postintervention VL biopsy total RNA was assayed in all participants, and mRNA/rRNA markers of ribosome content and biogenesis were also assayed in the 29 female participants before training, 24 h following training bout 1, and in the basal state after 10 wk of training. Across all participants, no significant associations were evident between relative rDNA copy number and training-induced changes in whole body lean mass (r = -0.034, P = 0.764), vastus lateralis thickness (r = 0.093, P = 0.408), mean myofiber cross-sectional area (r = -0.128, P = 0.259), or changes in muscle RNA concentrations (r = 0.026, P = 0.818), and these trends were similar when examining each gender. However, all Pol-I regulon mRNAs as well as 45S pre-rRNA, 28S rRNA, and 18S rRNA increased 24 h following the first training bout in female participants. Follow-up studies using LHCN-M2 myotubes demonstrated that a reduction in relative rDNA copy number induced by bisphenol A did not significantly affect insulin-like-growth factor-induced myotube hypertrophy. These findings suggest that relative rDNA copy number is not associated with myofiber hypertrophy.NEW & NOTEWORTHY We examined ribosomal DNA (rDNA) copy numbers in men and women who resistance trained for 10-12 wk and found no significant associations with skeletal muscle hypertrophy outcomes. These data, along with in vitro data in immortalized human myotubes whereby rDNA copy number was reduced, provide strong evidence that relative rDNA copy number is not associated with anabolism.

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相对 rDNA 拷贝数与阻力训练诱导的骨骼肌肥大无关,也不影响体外肌管合成代谢。
核糖体 DNA(rDNA)拷贝存在于多个染色体上,拷贝数的个体间差异被推测会影响阻力训练的肥大反应。因此,我们研究了 rDNA 拷贝数是否与阻力训练诱导的骨骼肌肥大有关。参与者(53 名男性,21±1 岁;29 名女性,21±2 岁)进行了为期 10-12 周的全身阻力训练。对肥大结果以及干预前阔筋膜(VL)活检的相对 rDNA 拷贝数进行了测定。对所有参与者进行了干预前和干预后的 VL 活检总 RNA 检测,还对 29 名女性进行了核糖体含量和生物生成的 mRNA/rRNA 标记检测,检测时间分别为训练前、第一轮训练后 24 小时以及训练 10 周后的基础状态。在所有参与者中,相对 rDNA 拷贝数与训练引起的全身瘦体重变化(r = -0.034,p=0.764)、侧肌厚度(r = 0.093,p=0.408)、平均肌纤维横截面积(r = -0.128,p=0.259)或肌肉 RNA 浓度变化(r = 0.026,p=0.818)之间没有明显的关联,而且在研究每个性别时,这些趋势相似。不过,女性在第一次训练后 24 小时,所有 Pol-I 调节子 mRNA 以及 45S pre-RRNA、28S rRNA 和 18S rRNA 都有所增加。使用 LHCN-M2 肌管进行的后续研究表明,双酚 A(BPA)诱导的相对 rDNA 拷贝数减少并不会显著影响胰岛素样生长因子诱导的肌管肥大。这些发现表明,相对 rDNA 拷贝数与肌纤维肥大无关。
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来源期刊
CiteScore
5.30
自引率
3.60%
发文量
145
审稿时长
2 months
期刊介绍: The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology publishes original investigations that illuminate normal or abnormal regulation and integration of physiological mechanisms at all levels of biological organization, ranging from molecules to humans, including clinical investigations. Major areas of emphasis include regulation in genetically modified animals; model organisms; development and tissue plasticity; neurohumoral control of circulation and hypertension; local control of circulation; cardiac and renal integration; thirst and volume, electrolyte homeostasis; glucose homeostasis and energy balance; appetite and obesity; inflammation and cytokines; integrative physiology of pregnancy-parturition-lactation; and thermoregulation and adaptations to exercise and environmental stress.
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