Increased oxidative capacity does not protect skeletal muscle fibers from eccentric contraction-induced injury.
Increased oxidative capacity does not protect skeletal muscle fibers from eccentric contraction-induced injury.
复制标题
氧化能力的增加并不能保护骨骼肌纤维免受离心收缩引起的损伤。
DOI：
10.1152/ajpregu.1998.274.5.r1300
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Lieber,RL
中科院分区：
文献类型：
--
作者：
Patel,TJ;Cuizon,D;Mathieu-Costello,O;Fridén,J;Lieber,RL
以10 Hz的频率对家兔背屈肌进行等长电刺激，持续1 s，持续30 min，5 d/wk，持续3 wk，以诱导肌肉氧化能力的增加。刺激训练的肌肉以及未经训练的肌肉，然后进行30分钟的离心运动回合，以测试是否增加氧化能力提供了对肌肉损伤的保护作用。电刺激导致趾长伸肌（EDL）和胫骨前肌（TA）的显著训练，其中EDL柠檬酸合酶（CS）活性平均增加67%（P< 0.0001），TA CS活性平均增加27%（P< 0.05）。对于测量的所有参数，EDL的变化幅度远大于TA肌肉。背屈肌疲劳性在3周训练期间显著下降（P< 0.0001），而训练后的EDL和TA单独显示出强烈的疲劳性下降趋势。组织形态计量学测量的TA和EDL毛细血管密度分别从839 ± 56增加到1，026 ± 71 mm−2（P= 0.07）和从589 ± 37增加到792 ± 66 mm−2（P< 0.05）。TA和EDL的毛细血管/纤维比分别从1.32 ± 0.10增加到1.55 ± 0.16（P> 0.2）和1.08 ± 0.07增加到1.36 ± 0.14（P> 0.1）。刺激训练后，2A型纤维的百分比增加了68%（P< 0.0001）的EDL和32%（P> 0.1）的TA在2D型纤维的损失。尽管对趾长伸肌的训练效果较大，对踝前肌的训练效果适中，但在离心性收缩损伤后，刺激训练组和未训练组的最大背屈扭矩（P> 0.3）或最大强直张力（P> 0.3）没有观察到差异。此外，在离心收缩诱导的损伤后，CS活性与最大强直张力之间没有观察到显著相关性（P> 0.2）。因此，我们得出结论，增加肌肉氧化能力的等长电刺激训练并没有保护肌肉免受离心收缩引起的损伤。
Isometric electrical stimulation was delivered to rabbit dorsiflexor muscles at 10 Hz for 1 s on and 1 s off over 30 min, 5 days/wk for 3 wk to induce an increase in muscle oxidative capacity. Stimulation-trained muscles as well as untrained muscles were then subjected to a 30-min eccentric exercise bout to test whether increased oxidative capacity provided a protective effect against muscle injury. Electrical stimulation resulted in significant training of both the extensor digitorum longus (EDL) and tibialis anterior (TA) muscles, with EDL citrate synthase (CS) activity increasing an average of 67% (P< 0.0001) and TA CS activity increasing by 27% (P< 0.05). For all parameters measured, the magnitude of change was much greater for EDL than for TA muscle. Dorsiflexor fatigability decreased significantly during the 3-wk training period (P< 0.0001), whereas the EDL and TA individually showed strong decreasing trends in fatigability after training. TA and EDL capillary density measured histomorphometrically increased from 839 ± 56 to 1,026 ± 71 mm−2(P= 0.07) and from 589 ± 37 to 792 ± 66 mm−2(P< 0.05), respectively. TA and EDL capillary-to-fiber ratio increased from 1.32 ± 0.10 to 1.55 ± 0.16 (P> 0.2) and 1.08 ± 0.07 to 1.36 ± 0.14 (P> 0.1), respectively. Type 2A fiber type percentage increased after stimulation training by 68% (P< 0.0001) for the EDL and by 32% (P> 0.1) for the TA at the expense of type 2D fibers. Despite the large training effect for the EDL and the modest training effect for the TA, no differences were observed between stimulation-trained and untrained groups for maximum dorsiflexion torque (P> 0.3) or maximum tetanic tension (P> 0.3) after eccentric contraction-induced injury. Additionally, no significant correlation was observed between CS activity and maximum tetanic tension after eccentric contraction-induced injury for either muscle (P> 0.2). Thus we conclude that increasing muscle oxidative capacity by isometric electrical stimulation training did not protect muscle against eccentric contraction-induced injury.