Our goal was to provide some insights into how the CNS controls and maintains an upright standing posture, which is an integral part of activities of daily living. Although researchers have used simple performance measures of maintenance of this posture quite effectively in clinical decision making, the mechanisms and control principles involved have not been clear. We propose a relatively simple control scheme for regulation of upright posture that provides almost instantaneous corrective response and reduces the operating demands on the CNS. The analytic model is derived and experimentally validated. A stiffness model was developed for quiet standing. The model assumes that muscles act as springs to cause the center-of-pressure (COP) to move in phase with the center-of-mass (COM) as the body sways about some desired position. In the sagittal plane this stiffness control exists at the ankle plantarflexors, in the frontal plane by the hip abductors/adductors. On the basis of observations that the COP-COM error signal continuously oscillates, it is evident that the inverted pendulum model is severely underdamped, approaching the undamped condition. The spectrum of this error signal is seen to match that of a tuned mass, spring, damper system, and a curve fit of this "tuned circuit" yields omega n the undamped natural frequency of the system. The effective stiffness of the system, Ke, is then estimated from Ke = I omega n2, and the damping B is estimated from B = BW X I, where BW is the bandwidth of the tuned response (in rad/s), and I is the moment of inertia of the body about the ankle joint. Ten adult subjects were assessed while standing quietly at three stance widths: 50% hip-to-hip distance, 100 and 150%. Subjects stood for 2 min in each position with eyes open; the 100% stance width was repeated with eyes closed. In all trials and in both planes, the COP oscillated virtually in phase (within 6 ms) with COM, which was predicted by a simple 0th order spring model. Sway amplitude decreased as stance width increased, and Ke increased with stance width. A stiffness model would predict sway to vary as Ke-0.5. The experimental results were close to this prediction: sway was proportional to Ke(-0.55). Reactive control of balance was not evident for several reasons. The visual system does not appear to contribute because no significant difference between eyes open and eyes closed results was found at 100% stance width. Vestibular (otolith) and joint proprioceptive reactive control were discounted because the necessary head accelerations, joint displacements, and velocities were well below reported thresholds. Besides, any reactive control would predict that COP would considerably lag (150-250 ms) behind the COM. Because the average COP was only 4 ms delayed behind the COM, reactive control was not evident; this small delay was accounted for by the damping in the tuned mechanical system.

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This research presents new data and reanalyzed information to refute the criticisms of our model of stiffness control during quiet standing. A re-review of their references to biomechanical research on muscle ankle stiffness confirmed muscle stiffness estimates of the ankle series elastic elements that agreed closely with our estimates. A new technique is presented that directly estimates the muscle stiffness from the ankle moment (N. m) and sway angle (deg). The linear regression of 10 subjects standing quietly for 10 s estimated the stiffness (N x m/deg) to be safely above the gravitational spring. The R(2) scores for this linear regression averaged 0.92, confirming how closely the model approached a perfect spring that would have an R(2) = 1. These results confirm our model of a simple muscle stiffness control and refutes the criticisms.

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