Acute change of titin at mid-sarcomere remains despite 8 wk of plyometric training
Acute change of titin at mid-sarcomere remains despite 8 wk of plyometric training
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DOI：
10.1152/japplphysiol.00420.2013
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发表时间：
2014-06-01
影响因子：
3.3
通讯作者：
Myburgh, K. H.
中科院分区：
文献类型：
--
作者：
Macaluso, F.;Isaacs, A. W.;Myburgh, K. H.
本研究的目的是研究在PlyEx训练之前和之后由急性间歇性运动（PlyEx）引起的骨骼肌变化，以了解PlyEx训练后肌联蛋白是否受到不同的影响。健康的未经训练的个体（N = 11）完成1stPlyEx（10 X 10个蹲跳，1分钟休息）。此后，6名受试者完成了8周的PlyEx，而5名对照者放弃了任何跳跃活动。最后一次训练后7天，所有受试者完成第二次PlyEx。在每次PlyEx急性发作之前和之后6小时以及1、2、3和4天收集血液样品，并且在每次PlyEx急性发作之前4天和之后3天收集肌肉活组织检查。1stPlyEx诱导循环肌红蛋白浓度增加。肌肉样本分析显示Z盘流，肌联蛋白（免疫金）的拉伸或片段化，并增加钙蛋白酶-3自溶。训练后，2ndPlyEx没有诱导Z盘流或钙蛋白酶-3激活。先前观察到的1stPlyEx后肌联蛋白COOH末端的位置变化仍然存在于2ndPlyEx前，在所有训练和所有对照受试者中。只有两个对照组在2ndPlyEx后出现Z盘流，而所有对照组中均不存在钙蛋白酶-3激活。离心爆发性运动引起肌联蛋白的拉伸或断裂，表现为COOH末端的位置变化。当肌联蛋白在爆发性跳跃之前已经被拉伸时，钙蛋白酶-3的激活不会发生。酶消化导致肌联蛋白片段化，但由于钙蛋白酶-3自溶的增加仅在1stPlyEx急性发作后可见，片段化不能解释长时间的位置变化。
The purpose of this study was to investigate skeletal muscle changes induced by an acute bout of plyometric exercise (PlyEx) both before and after PlyEx training, to understand if titin is affected differently after PlyEx training. Healthy untrained individuals (N = 11) completed the 1stPlyEx (10 X 10 squat-jumps, 1-min rest). Thereafter, six subjects completed 8 wk of PlyEx, while five controls abstained from any jumping activity. Seven days after the last training session, all subjects completed the 2ndPlyEx. Blood samples were collected before and 6 h and 1, 2, 3, and 4 days after each acute bout of PlyEx, and muscle biopsies 4 days before and 3 days after each acute bout of PlyEx. The 1stPlyEx induced an increase in circulating myoglobin concentration. Muscle sample analysis revealed Z-disk streaming, a stretch or a fragmentation of titin (immunogold), and increased calpain-3 autolysis. After training, 2ndPlyEx did not induce Z-disk streaming or calpain-3 activation. The previously observed post-1stPlyEx positional change of the titin COOH terminus was still present pre-2ndPlyEx, in all trained and all control subjects. Only two controls presented with Z-disk streaming after 2ndPlyEx, while calpain-3 activation was absent in all controls. Eccentric explosive exercise induced a stretch or fragmentation of titin, which presented as a positional change of the COOH terminus. Calpain-3 activation does not occur when titin is already stretched before explosive jumping. Enzymatic digestion results in titin fragmentation, but since an increase in calpain-3 autolysis was visible only after the 1stPlyEx acute bout, fragmentation cannot explain the prolonged positional change.