Skeletal muscle is a target of contraction-induced loading (CiL), leading to protein unfolding or cellular perturbations, respectively. While cytoskeletal desmin is responsible for ongoing structural stabilization, in the immediate response to CiL, alpha-crystallin B (CRYAB) is phosphorylated at serine 59 (_pCRYAB^S59) by P38, acutely protecting the cytoskeleton. To reveal adaptation and deadaptation of these myofibrillar subsystems to CiL, we examined CRYAB, P38, and desmin regulation following resistance exercise at diverse time points of a chronic training period. Mechanosensitive JNK phosphorylation (_pJNK^T183/Y185) was determined to indicate the presence of mechanical components in CiL. Within 6 wk, subjects performed 13 resistance exercise bouts at the 8–12 repetition maximum, followed by 10 days detraining and a final 14th bout. Biopsies were taken at baseline and after the 1st, 3rd, 7th, 10th, 13th, and 14th bout. To assess whether potential desensitization to CiL can be mitigated, one group trained with progressive and a second with constant loading. As no group differences were found, all subjects were combined for statistics. Total and phosphorylated P38 was not regulated over the time course. _pCRYAB^S59 and _pJNK^T183/Y185 strongly increased following the unaccustomed first bout. This exercise-induced _pCRYAB^S59/_pJNK^T183/Y185 increase disappeared with the 10th until 13th bout. As response to the detraining period, the 14th bout led to a renewed increase in _pCRYAB^S59. Desmin content followed _pCRYAB^S59 inversely, i.e., was up- when _pCRYAB^S59 was downregulated and vice versa. In conclusion, the _pCRYAB^S59 response indicates increase and decrease in resistance to CiL, in which a reinforced desmin network could play an essential role by structurally stabilizing the cells.

中文翻译：

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协调的α-晶状体蛋白B磷酸化和结蛋白表达表明对人骨骼肌抵抗运动诱导的负荷的适应和适应。

骨骼肌是收缩诱导负荷（CiL）的靶标，分别导致蛋白质解折叠或细胞扰动。尽管细胞骨架的结蛋白负责持续的结构稳定，但在对CiL的即时反应中，α-晶体蛋白B（CRYAB）在丝氨酸59（_p CRYAB ^S59）处被P38磷酸化，从而急性保护了细胞骨架。为了揭示这些肌原纤维子系统对CiL的适应性和适应性，我们在慢性训练期的不同时间点进行了阻力锻炼后，研究了CRYAB，P38和结蛋白调节。机械敏感的JNK磷酸化（_p JNK ^{T183 / Y185}确定（）以指示CiL中存在机械组件。在6周内，受试者以8-12次重复的最大值进行了13次抵抗运动训练，然后进行了10天的训练和最后的第14次训练。在基线，第一次，第三次，第七次，第十次，第十三次和第十四次回合后进行活检。为了评估是否可以缓解对CiL的脱敏，对一组进行渐进式训练，另一组进行恒定负荷训练。由于未发现组差异，因此将所有受试者合并以进行统计。随着时间的推移，总的和磷酸化的P38没有得到调节。在不习惯的第一次回合之后，_p CRYAB ^S59和_p JNK ^{T183 / Y185}大大增加。这种运动引起的_p CRYAB^S59 / _p JNK ^{T183 / Y185的}增加在第10至13次回合中消失。作为对减员期的响应，第14次回合导致_p CRYAB ^S59重新增加。蛋白质含量反比于_p CRYAB ^S59，即，当_p CRYAB ^S59下调时，其升高。反之亦然。总之，_p CRYAB ^S59反应表明_对CiL的抗性增加和减少，其中增强的结蛋白网络可通过结构稳定细胞发挥重要作用。