Myofibre damage in human skeletal muscle:: effects of electrical stimulation versus voluntary contraction
Myofibre damage in human skeletal muscle:: effects of electrical stimulation versus voluntary contraction
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DOI：
10.1113/jphysiol.2007.128827
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发表时间：
2007-08-15
影响因子：
5.5
通讯作者：
Kjaer, M.
中科院分区：
文献类型：
--
作者：
Crameri, R. M.;Aagaard, P.;Kjaer, M.
假设单次不习惯的离心运动后肌纤维内蛋白质的破坏会诱导肌肉酸痛的延迟发作，并与卫星细胞的激活有关。这已经在使用电刺激的动物模型中得到了证实，但在使用自愿运动的人类中却没有。未经训练的男性（n = 8，范围22-27岁）进行2 - 10最大离心收缩，每条腿上的等速测力计，自愿（VOL）与一条腿和电诱导（ES）与另一条腿。在运动前和运动后5、24、96和192 h获得骨骼肌评估。24小时后，VOL和ES的肌肉压痛增加，组间无差异。最大等长收缩强度，速度的力量发展和冲动下降，在VOL腿从4小时后，运动，但没有在ES（除了在24小时）。与此相反，细胞骨架蛋白（结蛋白）的显着破坏和肌生长因子（myogenin）的上升只发生在ES。ES（40%）中细胞内破坏和破坏的Z线明显比VOL（10%）更明显。同样，卫星细胞标志物[神经细胞粘附分子（N-CAM）和配对盒转录因子（Pax-7）]的增加在ES中比在Vol中更明显。最后，肌内结缔组织（腱生蛋白C）的染色在ES和VOL中同样增加运动后。本研究表明，在人体肌肉中，延迟发作的肌肉酸痛是没有显着差异，尽管两种治疗方法之间的肌内组织学标记物，特别是肌纤维蛋白和卫星细胞标记物的显着差异。两条腿骨骼肌中腹中腱生蛋白C表达的增加进一步证明了细胞外基质在肌肉疼痛延迟发作现象中的潜在作用。
Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n = 8, range 22-27 years) performed 2 10 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.