BACKGROUND Successful strategies to halt or reverse sarcopenia require a basic understanding of the factors that cause muscle loss with age. Acute periods of muscle loss in older individuals have an incomplete recovery of muscle mass and strength, thus accelerating sarcopenic progression. The purpose of the current study was to further understand the mechanisms underlying the failure of old animals to completely recover muscle mass and function after a period of hindlimb unloading. METHODS Hindlimb unloading was used to induce muscle atrophy in Fischer 344-Brown Norway (F344BN F1) rats at 24, 28, and 30 months of age. Rats were hindlimb unloaded for 14 days and then reloaded at 24 months (Reloaded 24), 28 months (Reloaded 28), and 24 and 28 months (Reloaded 24/28) of age. Isometric torque was determined at 24 months of age (24 months), at 28 months of age (28 months), immediately after 14 days of reloading, and at 30 months of age (30 months). During control or reloaded conditions, rats were labelled with deuterium oxide (D2 O) to determine rates of muscle protein synthesis and RNA synthesis. RESULTS After 14 days of reloading, in vivo isometric torque returned to baseline in Reloaded 24, but not Reloaded 28 and Reloaded 24/28. Despite the failure of Reloaded 28 and Reloaded 24/28 to regain peak force, all groups were equally depressed in peak force generation at 30 months. Increased age did not decrease muscle protein synthesis rates, and in fact, increased resting rates of protein synthesis were measured in the myofibrillar fraction (Fractional synthesis rate (FSR): %/day) of the plantaris (24 months: 2.53 ± 0.17; 30 months: 3.29 ± 0.17), and in the myofibrillar (24 months: 2.29 ± 0.07; 30 months: 3.34 ± 0.11), collagen (24 months: 1.11 ± 0.07; 30 months: 1.55 ± 0.14), and mitochondrial (24 months: 2.38 ± 0.16; 30 months: 3.20 ± 0.10) fractions of the tibialis anterior (TA). All muscles increased myofibrillar protein synthesis (%/day) in Reloaded 24 (soleus: 3.36 ± 0.11, 5.23 ± 0.19; plantaris: 2.53 ± 0.17, 3.66 ± 0.07; TA: 2.29 ± 0.14, 3.15 ± 0.12); however, in Reloaded 28, only the soleus had myofibrillar protein synthesis rates (%/day) >28 months (28 months: 3.80 ± 0.10; Reloaded 28: 4.86 ± 0.19). Across the muscles, rates of protein synthesis were correlated with RNA synthesis (all muscles combined, R2 = 0.807, P < 0.0001). CONCLUSIONS These data add to the growing body of literature that indicate that changes with age, including following disuse atrophy, differ by muscle. In addition, our findings lead to additional questions of the underlying mechanisms by which some muscles are maintained with age while others are not.

中文翻译：

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废用萎缩后，蛋白质合成中的肌肉特异性变化会随着衰老和重新加载而变化。

背景技术停止或逆转肌肉减少症的成功策略需要对引起年龄增长的肌肉损失的因素有基本的了解。老年个体的急性肌肉丧失期会导致肌肉质量和力量的恢复不完全，从而加速肌肉减少症的发展。本研究的目的是进一步了解在后肢卸载一段时间后，老动物无法完全恢复肌肉质量和功能的潜在机制。方法采用后肢卸载技术在24、28和30个月大的Fischer 344-Brown Norway（F344BN F1）大鼠中诱发肌肉萎缩。将大鼠后肢卸载14天，然后在24个月（重新加载24），28个月（重新加载28）以及24和28个月（重新加载24/28）龄时重新加载。等距扭矩是在24个月大（24个月）时确定的，在重装14天后立即在28个月大（28个月）时以及在30个月大（30个月）时。在对照或重载条件下，用氧化氘（D2 O）标记大鼠以确定肌肉蛋白质合成和RNA合成的速率。结果在重装14天后，体内等距扭矩在“重装24”中恢复到基线，但未在“重装28”和“ 24/28中重载”中恢复到基线。尽管Reloaded 28和Reloaded 24/28无法恢复峰值力，但所有组在30个月时的峰值力产生均受到压抑。年龄的增加并没有降低肌肉蛋白质的合成率，实际上，在plant肌的肌原纤维部分（分数合成率（FSR）：％/天）（24个月：2.53±0.17； 30）中，蛋白质合成的静息率增加了月：3.29±0.17），以及在肌原纤维中（24个月：2.29±0.07；30个月：3.34±0.11），胶原蛋白（24个月：1.11±0.07； 30个月：1.55±0.14）和线粒体（24个月：2.38±0.16； 30个月：3.20±0.10） 。在Reloaded 24（比目鱼眼：3.36±0.11，5.23±0.19; plant肌：2.53±0.17，3.66±0.07; TA：2.29±0.14，3.15±0.12）中，所有肌肉均增加了肌原纤维蛋白合成（％/天）; 然而，在Reloaded 28中，只有比目鱼肌的肌原纤维蛋白合成率（％/天）> 28个月（28个月：3.80±0.10； Reloaded 28：4.86±0.19）。在整个肌肉中，蛋白质的合成速率与RNA合成相关（所有肌肉相加，R2 = 0.807，P <0.0001）。结论这些数据增加了越来越多的文献，这些文献表明，随着年龄的变化（包括废用的萎缩后），肌肉也会有所不同。此外，