Neither myonuclear accretion nor a myonuclear domain size ceiling is a feature of the attenuated hypertrophic potential of aged human skeletal muscle.

Neither myonuclear accretion nor a myonuclear domain size ceiling is a feature of the attenuated hypertrophic potential of aged human skeletal muscle.
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肌核增生和肌核域大小上限都不是老年人骨骼肌肥大潜力减弱的特征。

DOI:
10.1007/s11357-022-00651-y
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发表时间:
2023-03
期刊:
影响因子:
5.6
通讯作者:
Atherton, Philip J.
Atherton, Philip J.
中科院分区:
医学1区
文献类型:
--
作者:
Brook, Matthew S.;Wilkinson, Daniel J.;Tarum, Janelle;Mitchell, Kyle W.;Lund, Jonathan L.;Phillips, Bethan E.;Szewczyk, Nathaniel J.;Kadi, Fawzi;Greenhaff, Paul L.;Smith, Ken;Atherton, Philip J.

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衰老限制了骨骼肌的生长能力(例如,对阻力运动的反应),但卫星细胞(SC)功能在驱动这种现象中的作用却定义不清。年轻(Y)(~ 23岁)和老年(O)男性(~ 69岁)(正常体重BMI)接受6周单侧抗阻运动训练(RET)。在基线和3-/6周训练后进行肌肉活检。我们通过纤维CSA(和类型)、SC数量、肌核计数和DNA合成(通过D2 O摄入)确定肌肉大小。在基线时,Y和O之间的纤维面积没有显著差异。RET在第3周和第6周均增加了Y的I型纤维面积(基线:4509 ± 534 µm2,3周; 5497 ± 510 µm2 P < 0.05,6周; 5402 ± 352 µm2 P < 0.05),而O仅在6周时较基线增加(基线5120 ± 403 µm2,3周; 5606 ± 620 µm2,6周; 6017 ± 482 µm2 P < 0.05)。然而,在第3周和第6周时,Y的II型纤维面积均较基线增加(基线:4949 ± 459 µm2,3周; 6145 ± 484 µm2(P < 0.01),6周; 5992 ± 491 µm2(P < 0.01),而O显示无变化(基线5210 ± 410 µm2,3周; 5356 ± 535 µm2(P = 0.9),6周; 5857 ± 478 µm2(P = 0.1)。在基线时,Y和O之间的纤维肌核数量没有差异。RET治疗3周和6周时,Y和O的I型纤维肌核数量均较基线增加(年轻:基线2.47 ± 0.16,3周; 3.19 ± 0.16(P < 0.001),6周; 3.70 ± 0.29(P < 0.0001);老年组:基线2.29 ± 0.09,3周; 3.01 ± 0.09(P < 0.001),6周; 3.65 ± 0.18(P < 0.0001))。同样,在第3周和第6周时,Y和O组II型纤维肌核数量均较基线增加(年轻:基线2.49 ± 0.14,3周; 3.31 ± 0.21(P < 0.001),6周; 3.86 ± 0.29(P < 0.0001);老年组:基线2.43 ± 0.12,3周; 3.37 ± 0.12(P < 0.001),6周; 3.81 ± 0.15(P < 0.0001))。DNA合成率%.d-1表现出训练的主要影响,但没有年龄歧视。在老年人中,肌核增加的下降并不构成肌肉生长能力受损的基础,这支持了我们先前报道的核糖体和蛋白质稳态损伤。
Ageing limits growth capacity of skeletal muscle (e.g. in response to resistance exercise), but the role of satellite cell (SC) function in driving this phenomenon is poorly defined. Younger (Y) (~ 23 years) and older (O) men (~ 69 years) (normal-weight BMI) underwent 6 weeks of unilateral resistance exercise training (RET). Muscle biopsies were taken at baseline and after 3-/6-week training. We determined muscle size by fibre CSA (and type), SC number, myonuclei counts and DNA synthesis (via D2O ingestion). At baseline, there were no significant differences in fibre areas between Y and O. RET increased type I fibre area in Y from baseline at both 3 weeks and 6 weeks (baseline: 4509 ± 534 µm2, 3 weeks; 5497 ± 510 µm2 P < 0.05, 6 weeks; 5402 ± 352 µm2 P < 0.05), whilst O increased from baseline at 6 weeks only (baseline 5120 ± 403 µm2, 3 weeks; 5606 ± 620 µm2, 6 weeks; 6017 ± 482 µm2 P < 0.05). However, type II fibre area increased from baseline in Y at both 3 weeks and 6 weeks (baseline: 4949 ± 459 µm2, 3 weeks; 6145 ± 484 µm2 (P < 0.01), 6 weeks; 5992 ± 491 µm2 (P < 0.01), whilst O showed no change (baseline 5210 ± 410 µm2, 3 weeks; 5356 ± 535 µm2 (P = 0.9), 6 weeks; 5857 ± 478 µm2 (P = 0.1). At baseline, there were no differences in fibre myonuclei number between Y and O. RET increased type I fibre myonuclei number from baseline in both Y and O at 3 weeks and 6 weeks with RET (younger: baseline 2.47 ± 0.16, 3 weeks; 3.19 ± 0.16 (P < 0.001), 6 weeks; 3.70 ± 0.29 (P < 0.0001); older: baseline 2.29 ± 0.09, 3 weeks; 3.01 ± 0.09 (P < 0.001), 6 weeks; 3.65 ± 0.18 (P < 0.0001)). Similarly, type II fibre myonuclei number increased from baseline in both Y and O at 3 weeks and 6 weeks (younger: baseline 2.49 ± 0.14, 3 weeks; 3.31 ± 0.21 (P < 0.001), 6 weeks; 3.86 ± 0.29 (P < 0.0001); older: baseline 2.43 ± 0.12, 3 weeks; 3.37 ± 0.12 (P < 0.001), 6 weeks; 3.81 ± 0.15 (P < 0.0001)). DNA synthesis rates %.d−1 exhibited a main effect of training but no age discrimination. Declines in myonuclei addition do not underlie impaired muscle growth capacity in older humans, supporting ribosomal and proteostasis impairments as we have previously reported.
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影响因子: --
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