Paradoxical muscle movement in human standing
Paradoxical muscle movement in human standing
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DOI：
10.1113/jphysiol.2004.062398
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发表时间：
2004-05-01
影响因子：
5.5
通讯作者：
Lakie, M
中科院分区：
文献类型：
--
作者：
Loram, ID;Maganaris, CN;Lakie, M
当人站立时，重力会导致踝关节前倾，这是通过比目鱼肌和腓肠肌的活动来防止的。长期以来，人们一直认为，当人们向前摇摆时，小腿肌肉会伸展，相反，当人们向后摇摆时，小腿肌肉会缩短。因此，多年来，两种解释站立稳定盛行。首先，强直性肌肉活动本身可能产生足够的踝关节固有僵硬。其次，如果踝关节固有的刚度不足，小腿肌肉对拉伸的抵抗力可以通过拉伸反射或中央控制来增强。这些解释要求传递小腿肌肉张力的被动组织（跟腱，足）是僵硬的。然而，我们最近的测量表明，这种被动组织在站立时并不僵硬。因此，我们预测了一种反直觉的控制模式，即肌肉和身体必须在平均情况下向相反的方向运动（矛盾运动）。在这里，我们使用动态超声成像在体内与新颖的自动跟踪肌肉长度来测试我们的假设。我们发现比目鱼肌和腓肠肌的运动确实是矛盾的，当身体向前摆动时，它们会变短，当身体向后摆动时，它们会变长。这证实了踝关节固有的僵硬度太低，无法稳定人的站立。此外，它还表明主动张力的增加与肌肉缩短有关。这种模式不能由肌肉拉伸反射产生，只能由平衡所必需的肌肉长度的预期神经控制产生。
In human standing, gravity causes forward toppling about the ankle joint which is prevented by activity in the soleus and gastrocnemius muscles. It has long been assumed that when people sway forwards the calf muscles are stretched and conversely that they shorten with backward sway. Consequently, for many years, two explanations for standing stabilization have flourished. First, tonic muscle activity itself may generate adequate intrinsic ankle stiffness. Second, if intrinsic ankle stiffness is inadequate, the resistance to stretch of the calf muscles may be augmented by stretch reflexes or by central control. These explanations require that the passive tissue (Achilles' tendon, foot) transmitting the calf muscle tension is stiff. However, our recent measurements have indicated that this passive tissue is not stiff during standing. Accordingly, we predicted a counterintuitive mode of control where the muscles and body must, on average, move in opposite directions (paradoxical movements). Here we use dynamic ultrasound imaging in vivo with novel automated tracking of muscle length to test our hypothesis. We show that soleus and gastrocnemius do indeed move paradoxically, shortening when the body sways forward and lengthening when the body returns. This confirms that intrinsic ankle stiffness is too low to stabilize human standing. Moreover, it shows that the increase in active tension is associated with muscle shortening. This pattern cannot be produced by muscle stretch reflexes and can only arise from the anticipatory neural control of muscle length that is necessary for balance.