Macaluso F, Isaacs A W, Di Felice V, Myburgh K H
Department of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa; and Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Università di Palermo, Palermo, Italy
Department of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa; and.
J Appl Physiol (1985). 2014 Jun 1;116(11):1512-9. doi: 10.1152/japplphysiol.00420.2013. Epub 2014 Jan 23.
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 × 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.
本研究的目的是调查在进行增强式训练（PlyEx）之前和之后，单次急性增强式运动（PlyEx）所引发的骨骼肌变化，以了解在PlyEx训练后肌联蛋白是否受到不同影响。健康的未经训练个体（N = 11）完成了第一次PlyEx（10×10次深蹲跳，休息1分钟）。此后，六名受试者完成了为期8周的PlyEx训练，而五名对照组受试者未进行任何跳跃活动。在最后一次训练 session 后的七天，所有受试者完成了第二次PlyEx。在每次急性PlyEx运动之前、运动后6小时以及运动后1、2、3和4天采集血样，并在每次急性PlyEx运动之前4天和运动之后3天进行肌肉活检。第一次PlyEx导致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）的拉伸或断裂，以及钙蛋白酶-3自溶增加。训练后，第二次PlyEx未引发Z盘流或钙蛋白酶-3激活。在所有训练组和所有对照组受试者中，在第二次PlyEx之前，仍存在第一次PlyEx后观察到的肌联蛋白COOH末端的位置变化。第二次PlyEx后，只有两名对照组受试者出现Z盘流，而所有对照组均未出现钙蛋白酶-3激活。离心爆发性运动导致肌联蛋白拉伸或断裂，表现为COOH末端的位置变化。当肌联蛋白在爆发性跳跃前已经被拉伸时，不会发生钙蛋白酶-3激活。酶消化导致肌联蛋白断裂，但由于仅在第一次PlyEx急性运动后可见钙蛋白酶-3自溶增加，断裂无法解释这种长期的位置变化。
