Gordon J, Ghez C
Exp Brain Res. 1987;67(2):253-69. doi: 10.1007/BF00248547.
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.
在之前的研究中（戈登和格兹，1987年），我们表明人类受试者产生的精确靶向等长力脉冲受脉冲高度控制策略支配。通过调节力的上升速率实现了不同的峰值力，而力的上升时间保持接近恒定值且与峰值力无关。力上升速率的一个早期测量指标，即峰值d2F/dt2，按所需力（目标幅度）进行缩放，并且对所达到的峰值力具有高度预测性。在接受检查的6名受试者中，峰值d2F/dt2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靶向反应，以确定峰值d2F/dt2未预测到的残余变异性是否可以通过对力轨迹的调整来解释，这些调整补偿了d2F/dt2缩放中的初始误差。测试了一个峰值力决定因素的统计模型。该模型包括目标幅度可以独立影响所达到的峰值力的两条路径。第一条路径是预编程的脉冲高度控制。在这条路径中，目标幅度决定了力的初始上升速率（峰值d2F/dt2），而这又反过来决定了最终达到的峰值力。第二条路径是峰值d2F/dt2初始缩放中的误差对峰值力的独立影响。对每个受试者在每种条件下的反应集中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。在每个受试者和每种条件下，d2F/dt2中的误差对峰值力有显著的独立影响，并且这种影响的方向是减小峰值力误差的大小。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表明，轨迹初始阶段的不适当缩放通过缩短或延长力的上升时间得到补偿。这些轨迹调整反过来通过调节产生力轨迹的主动肌和拮抗肌收缩的时间和幅度来实现。由于这些补偿性调整在肌电图模式中出现在潜伏期过短而无法由外周反馈解释的情况下，我们假设它们依赖于对展开的神经指令的内部监测。这些内部反馈过程与编程指令并行起作用，两者都决定着力轨迹。
