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.

衰老限制了骨骼肌的生长能力（例如抵抗运动的反应），但卫星细胞 (SC) 功能在驱动这种现象中的作用尚不清楚。年轻 (Y)（~ 23 岁）和老年 (O) 男性（~ 69 岁）（正常体重 BMI）接受了 6 周的单侧阻力运动训练 (RET)。在基线和 3 周/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 D ₂ O 摄取）确定了肌肉大小。在基线时，Y 和 O 之间的纤维面积没有显着差异。RET 在 3 周和 6 周时从基线增加了 Y 中的 I 型纤维面积（基线：4509 ± 534 µm 2，3 周；5497 ± ⁵¹⁰ µm ² P < 0.05，6 周；5402 ± 352 µm ² P  < 0.05），而 O 仅在 6 周时从基线增加（基线 5120 ± 403 µm ²， 3 周；5606 ± 620 µm ²， 6 周；6017 ± 482 µm ² P  < 0.05）。然而，在第 3 周和第 6 周时，Y 中的 II 型纤维面积从基线增加（基线：4949 ± 459 µm ^2，3周；6145 ± 484 µm ²（P  < 0.01），6 周；5992 ± 491 µm ²（P  < 0.01)，而 O 未显示变化（基线 5210 ± 410 µm ^2，3周；5356 ± 535 µm ²（P  = 0.9），6 周；5857 ± 478 µm ²（P  = 0.1）。在基线时，Y 和 O 之间的纤维肌核数量没有差异。RET 在 3 周和 6 周时 Y 和 O 的 I 型纤维肌核数量从基线增加（较年轻：基线 2.47 ± 0.16，3 周；3.19 ± 0.16 ( P  < 0.001)，6 周；3.70 ± 0.29 ( P  < 0.0001)；年龄较大：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 的 II 型纤维肌核数量均从基线增加（较年轻：基线 2.49 ± 0.14，3 周；3.31 ± 0.21（P < 0.001），6 周；3.86 ± 0.29  （P  < 0.0001)；年长者：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。正如我们之前报道的那样，肌核增加的减少并不是老年人肌肉生长能力受损的基础，支持核糖体和蛋白质稳态损伤。