TRAJECTORY CONTROL IN TARGETED FORCE IMPULSES .3. COMPENSATORY ADJUSTMENTS FOR INITIAL ERRORS
TRAJECTORY CONTROL IN TARGETED FORCE IMPULSES .3. COMPENSATORY ADJUSTMENTS FOR INITIAL ERRORS
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DOI：
10.1007/bf00248547
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发表时间：
1987-01-01
影响因子：
2
通讯作者：
GHEZ, C
中科院分区：
文献类型：
--
作者：
GORDON, J;GHEZ, C
在之前的研究中（Gordon和Ghez 1987），我们表明，由人类受试者产生的精确定向等长力脉冲受脉冲高度控制策略的控制。通过调节力的上升速率来实现不同的峰值力，同时力的上升时间保持接近恒定值并且与峰值力无关。力上升速率的早期测量值（峰值d2 F/dt 2）按比例缩放至所需的力（目标振幅），并高度预测达到的峰值力。在6名受试者中，峰值d2 F/dt 2占峰值力总方差的70%至96%。在本研究中，我们进一步检查了这些目标响应，以确定是否可以通过调整力轨迹来解释峰d2 F/dt 2未预测的残差变异性，该力轨迹补偿了d2 F/dt 2缩放中的初始误差。测试了峰值力决定因素的统计模型。该模型包括两条路径，目标振幅可通过这两条路径独立影响所达到的峰值力。第一条路径是预编程脉冲高度控制。在该路径中，目标振幅确定了力的初始上升速率（峰值d2 F/dt 2），其进而确定了达到的最终峰值力。第二个路径是峰d2 F/dt 2初始缩放误差对峰力的独立影响。在每种条件下，对每名受试者的反应集内的轨迹变量进行多元回归分析，以确定第二条路径是否对解释峰值力的方差有显著贡献。在每个受试者和条件下，d2 F/dt 2的误差对峰值力有显著的独立影响，这种影响的方向是降低峰值力误差的幅度。这些补偿性调整占峰值力总方差的1%至14%。进一步的多元回归分析显示，轨迹的初始阶段的不适当缩放通过缩短或延长力上升时间来补偿。这些轨迹调整又通过调节产生力轨迹的激动剂和拮抗剂肌肉中收缩的时间和幅度来实现。由于这些补偿性调整在睡眠时间太短的EMG模式中很明显，无法通过外周反馈来解释，我们假设它们依赖于对展开的神经命令的内部监测。这些内部反馈过程与编程命令并行作用，两者都确定力的轨迹。
In the preceding study (Gordon and Ghez 1987), we showed that accurately targeted isometric force impulses produced by human subjects are governed by a pulse height control policy. Different peak forces were achieved by modulating the rate of rise of force while force rise time was maintained close to a constant value and independent of peak force. An early measure of the rate of rise of force, peak d2F/dt2, was scaled to the required force (target amplitude) and highly predictive of the peak force achieved. In six subjects examined, peak d2F/dt2 accounted for between 70% and 96% of the total variance in peak force. In the present study, we further examined these targeted responses to determine whether the residual variability not predicted by peak d2F/dt2 could be accounted for by adjustments to the force trajectories which compensated for initial errors in the scaling of the d2F/dt2. A statistical model of the determinants of peak force was tested. This model included two paths by which the target amplitude could independently influence the peak force achieved. The first path was preprogrammed pulse height control. In this path, target amplitude determined the initial rate of rise of force (peak d2F/dt2) which in turn determined the final peak force achieved. The second path was an independent influence of errors in the initial scaling of peak d2F/dt2 on peak force. Multiple regression analysis was performed on trajectory variables within the sets of responses by each subject in each condition to determine whether the second path contributed significantly to explaining the variance in peak force. In each subject and condition, there was a significant independent influence of error in d2F/dt2 on peak force, and the direction of this effect was to decrease the magnitudes of peak force errors. These compensatory adjustments accounted for between 1% and 14% of the total variance in peak force. Further multiple regression analyses revealed that inappropriate scaling of the initial phase of the trajectories was compensated for by shortening or prolonging the force rise time. These trajectory adjustments were in turn implemented by modulation of the timing and magnitude of the contractions in the agonist and antagonist muscles that produced the force trajectories. Because these compensatory adjustments were evident in the EMG pattern at latencies too short to be accounted for by peripheral feedback, we assume that they depend on internal monitoring of the unfolding neural commands. These internal feedback processes act in parallel with the programmed commands, both determining the force trajectory.