MUSCLE DAMAGE IS NOT A FUNCTION OF MUSCLE FORCE BUT ACTIVE MUSCLE STRAIN
MUSCLE DAMAGE IS NOT A FUNCTION OF MUSCLE FORCE BUT ACTIVE MUSCLE STRAIN
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DOI：
10.1152/jappl.1993.74.2.520
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发表时间：
1993-02-01
影响因子：
3.3
通讯作者：
FRIDEN, J
中科院分区：
文献类型：
--
作者：
LIEBER, RL;FRIDEN, J
为探讨兔胫骨前肌损伤的机制，采用离心收缩法测定了胫骨前肌的收缩特性。在第一个实验中，两组肌肉以相同的速率拉伸25%的肌纤维长度。然而，由于相对于肌肉激活的施加长度变化的时间不同，各组经历了显着不同的肌肉力量。由于在两种应变计时模式下进行30分钟循环活动后测量的肌肉最大强直张力和其他收缩参数相同（P > 0.4），因此我们得出结论，尽管施加的力非常不同，但肌肉损伤是等效的。这一结果得到了第二个实验的支持，在第二个实验中，以一半的应变（12.5%的肌纤维长度）进行相同的方案。同样，在两种应变时间循环12.5%应变后，最大强直张力无差异。两个实验的数据通过双向方差分析进行分析，其揭示了应变幅度的高度显著影响（P < 0.001），但拉伸时间没有显著影响（P > 0.7）。我们将这些数据解释为表明，在离心收缩后引起肌肉损伤的不是高的力本身，而是主动应变的大小（即，主动延长期间的应变）。这一结论得到了形态测定分析的支持，形态测定分析显示在整个肌肉横截面上观察到的受损肌纤维的面积分数相等。主动应变假说是根据肌原纤维细胞骨架、肌节和肌膜之间的相互作用来描述的。
Contractile properties of rabbit tibialis anterior muscles were measured after eccentric contraction to investigate the mechanism of muscle injury. In the first experiment, two groups of muscles were strained 25% of the muscle fiber length at identical rates. However, because the timing of the imposed length change relative to muscle activation was different, the groups experienced dramatically different muscle forces. Because muscle maximum tetanic tension and other contractile parameters measured after 30 min of cyclic activity with either strain timing pattern were identical (P > 0.4), we concluded that muscle damage was equivalent despite very different imposed forces. This result was supported by a second experiment in which the same protocol was performed at one-half the strain (12.5% muscle fiber length). Again, there was no difference in maximum tetanic tension after cyclic 12.5% strain with either strain timing. Data from both experiments were analyzed by two-way analysis of variance, which revealed a highly significant effect of strain magnitude (P < 0.001) but no significant effect of stretch timing (P > 0.7). We interpret these data to signify that it is not high force per se that causes muscle damage after eccentric contraction but the magnitude of the active strain (i.e., strain during active lengthening). This conclusion was supported by morphometric analysis showing equivalent area fractions of damaged muscle fibers that were observed throughout the muscle cross section. The active strain hypothesis is described in terms of the interaction between the myofibrillar cytoskeleton, the sarcomere, and the sarcolemma.