  The fractality of human gait, namely, the long-range correlation that
characterizes scale-free fluctuations of gait descriptors, such as the stride
intervals during steady-state walking, depends on the well-tuned organization
of the sensorimotor controller. Gait fractality is apparent in healthy young
adults but tends to disappear in elderly individuals and neurological patients.
Therefore, its partial loss may be indicative of pathological conditions.
Despite its potential to be used as a dynamical biomarker for fall risk
assessment, the mechanistic origin of gait fractality has been investigated by
only a few studies, and even less attention has been devoted to the link
between gait fractality and gait stability. Here, we propose a novel
computational model of gait by addressing the flexibility-stability trade-off
first, and then by showing that gait fractality is a natural consequence of the
developed control mechanisms, including phase resetting and intermittent
control, which supplement instability in a linear feedback controller operated
at stability's edge. The results suggest that pathological gait, characterized
by joint-rigidity and/or loss of fractality, may be caused by dysfunction in
some of these mechanisms.
