Idiosyncratic Characteristics of Postural Sway in Normal and Perturbed Standing.

OBJECTIVE: Are people with a characteristically large physiological sway rendered particularly unstable when standing on a moving surface? Is postural sway in standing individuals idiosyncratic? In this study, we examine postural sway in individuals standing normally, and when subtle continuous sinusoidal disturbances are applied to their support platform. We calculate consistency between conditions to verify if sway can be considered characteristic of each individual. We also correlate two different aspects of participants' responses to disturbance; their sway velocity and their regulation of body orientation. METHODS: Nineteen healthy adults (age 29.2 ± 3.2 years) stood freely on footplates coaxially aligned with their ankles and attached to a motorized platform. They had their eyes closed, and hips and knees locked with a light wooden board attached to their body. Participants either stood quietly on a fixed platform or on a slowly tilting platform (0.1 Hz sinusoid; 0.2 and 0.4 deg). Postural sway size was separated into two entities: (1) the spontaneous sway velocity component (natural random relatively rapid postural adjustments, RMS body angular velocity) and (2) the evoked tilt gain component (much slower 0.1 Hz synchronous tilt induced by the movement of the platform, measured as peak-to-peak (p-p) gain, ratio of body angle to applied footplate rotation). RESULTS: There was no correlation between the velocity of an individual's sway and their evoked tilt gain (r = 0.34, p = 0.15 and r = 0.30, p = 0.22). However, when considered separately, each of the two measurements showed fair to good absolute agreement within conditions. Spontaneous sway velocity consistently increased as participants were subjected to increasing disturbance. Participants who swayed more (or less) did so across all conditions [ICC(3,k) = 0.95]. Evoked tilt gain also showed consistency between conditions [ICC(3,k) = 0.79], but decreased from least to most disturbed conditions. CONCLUSION: The two measurements remain consistent between conditions. Consistency between conditions of two very distinct unrelated measurements reflects the idiosyncratic nature of postural sway. However, sway velocity and tilt gain are not related, which supports the idea that the short-term regulation of stability and the longer-term regulation of orientation are controlled by different processes.

Individual differences in intrinsic ankle stiffness and their relationship to body sway and ankle torque.

When standing, intrinsic ankle stiffness is smaller when measured using large perturbations, when sway size is large, and when background torque is low. However, there is a large variation in individual intrinsic ankle stiffness. Here we determine if individual variation has consequences for postural control. We examined the relationship between ankle stiffness, ankle torque and body sway across different individuals. Ankle stiffness was estimated in 19 standing participants by measuring torque responses to small, brief perturbations. Perturbation sizes of 0.2 & 0.9 degrees (both lasting 140 ms) measured short- and long-range stiffness respectively, while participants either stood quietly on a fixed platform or were imperceptibly tilted to reduce stability (0.1 Hz sinusoid; 0.2 & 0.4 deg). The spontaneous body sway component (natural random relatively rapid postural adjustments) and background ankle torque were averaged from sections immediately before perturbations. The results show that, first, intrinsic ankle stiffness is positively associated with ankle torque, and that this relationship is stronger for long-range stiffness. Second, intrinsic ankle stiffness is negatively associated with body sway, but, in contrast to the relationship with torque, this relationship is stronger for short-range stiffness. We conclude that high short-range intrinsic ankle stiffness is associated with reduced spontaneous sway, although the causal relationship between these two parameters is unknown. These results suggest that, in normal quiet standing where sway is very small, the most important determinant of intrinsic ankle stiffness may be stillness. In less stable conditions, intrinsic ankle stiffness may be more dependent on ankle torque.

Intrinsic ankle stiffness during standing increases with ankle torque and passive stretch of the Achilles tendon.

Individuals may stand with a range of ankle angles. Furthermore, shoes or floor surfaces may elevate or depress their heels. Here we ask how these situations impact ankle stiffness and balance. We performed two studies (each with 10 participants) in which the triceps surae, Achilles tendon and aponeurosis were stretched either passively, by rotating the support surface, or actively by leaning forward. Participants stood freely on footplates which could rotate around the ankle joint axis. Brief, small stiffness-measuring perturbations (<0.7 deg; 140 ms) were applied at intervals of 4-5 s. In study 1, participants stood at selected angles of forward lean. In study 2, normal standing was compared with passive dorsiflexion induced by 15 deg toes-up tilt of the support surface. Smaller perturbations produced higher stiffness estimates, but for all perturbation sizes stiffness increased with active torque or passive stretch. Sway was minimally affected by stretch or lean, suggesting that this did not underlie the alterations in stiffness. In quiet stance, maximum ankle stiffness is limited by the tendon. As tendon strain increases, it becomes stiffer, causing an increase in overall ankle stiffness, which would explain the effects of leaning. However, stiffness also increased considerably with passive stretch, despite a modest torque increase. We discuss possible explanations for this increase.

Sway-dependent changes in standing ankle stiffness caused by muscle thixotropy.

KEY POINTS: The passive stiffness of the calf muscles contributes to standing balance, although the properties of muscle tissue are highly labile. We investigated the effect of sway history upon intrinsic ankle stiffness and demonstrated reductions in stiffness of up to 43% during conditions of increased baseline sway. This sway dependence was most apparent when using low amplitude stiffness-measuring perturbations, and the short-range stiffness component was smaller during periods of high sway. These characteristics are consistent with the thixotropic properties of the calf muscles causing the observed changes in ankle stiffness. Periods of increased sway impair the passive stabilization of standing, demanding more active neural control of balance. Quiet standing is achieved through a combination of active and passive mechanisms, consisting of neural control and intrinsic mechanical stiffness of the ankle joint, respectively. The mechanical stiffness is partly determined by the calf muscles. However, the viscoelastic properties of muscle are highly labile, exhibiting a strong dependence on movement history. By measuring the effect of sway history upon ankle stiffness, the present study determines whether this lability has consequences for the passive stabilization of human standing. Ten subjects stood quietly on a rotating platform whose axis was collinear with the ankle joint. Ankle sway was increased by slowly tilting this platform in a random fashion, or decreased by fixing the body to a board. Ankle stiffness was measured by using the same platform to simultaneously apply small, brief perturbations (<0.6 deg; 140 ms) at the same time as the resulting torque response was recorded. The results show that increasing sway reduces ankle stiffness by up to 43% compared to the body-fixed condition. Normal quiet stance was associated with intermediate values. The effect was most apparent when using smaller perturbation amplitudes to measure stiffness (0.1 vs. 0.6 deg). Furthermore, torque responses exhibited a biphasic pattern, consisting of an initial steep rise followed by a shallower increase. This transition occurred earlier during increased levels of ankle sway. These results are consistent with a movement-dependent change in passive ankle stiffness caused by thixotropic properties of the calf muscle. The consequence is to place increased reliance upon active neural control during times when increased sway renders ankle stiffness low.