BJMB! ! ! ! ! ! ! ! Current Opinion!
Brazilian(Journal(of(Motor(Behavior(
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https://doi.org/10.20338/bjmb.v15i3.241
increases in gait velocity (~9%) are consistently observed during overground walking after
different fatiguing protocols in different populations (healthy young and older adults,
Parkinson’s disease).
3–7
Besides, the mechanisms that explain such increases are still
uncertain. Between the attempts to explain such increase, the literature uses two main
theoretical arguments: a potential compensatory strategy to improve stability during
walking;
4,7
and a response of the motor system in increasing the neural drive,
8
similar to
the effects of warm-up activities.
9
Regarding the first argument (the compensatory strategy), the increase in gait
velocity during overground walking after a fatiguing protocol was associated with a more
stable gait pattern,
4,7
because the faster walking velocity is accompanied by longer
stride/step length and shorter step duration.
4,5
Such gait adaptations are attributed to an
improved balance control
9
by seeking more stability in the anterior-posterior direction. For
instance, the extrapolated center of mass, which is velocity-dependent, is anterior to the
base of support, and the increased forward step (length) is a natural response to enhanced
stability by decreasing the magnitude of the margin of stability during walking.
9
Increasing
the step length and decreasing the duration (to increase gait velocity) may be a safe, fast,
effective compensatory strategy to increase the stability and avoid further consequences of
fatigability on gait.
Considering the second argument (warm-up), fatiguing protocols might result in a
preparatory elevation of muscle temperature, alertness, cardiovascular, and hormonal
functions, invoking an increase in gait velocity. Since the metabolic and mechanical
energy-wise minimal effort required during overground walking is low, gait performance
would hardly be limited by fatiguing protocols. Additionally, typical fatigability-related
increases in neural drive
8
might also be an after-effect of warm-up activities that, in some
tasks, result in increased muscle activation amplitude.
9
Thus, the interpretation that
fatigability causes compensatory increase neural drive to maintain the desired
performance, may also be due to warm-up effects, mainly in submaximal tasks (as gait) in
which the power/strength demands are below the levels of reductions in power/strength
that fatiguing protocols could induce.
Although these two hypothetical explanations are described separately, those
arguments might be complementary to elucidate the unexpected increase in gait velocity
after fatigability. However, to the best of our knowledge, there is no direct evidence that
could support these two hypothetical explanations. Accordingly, future studies aiming to
verify the effects of performance fatigability on walking should measure fatigability in a
broader domain (e.g., physiological and biomechanical) combined with assessments of
neuromuscular control, kinetics, stability, and kinematics of gait. Fatiguing protocols should
consider the specificity of muscles on gait and populations since most studies induced
fatigability on knee extensors despite the fact that in old populations mainly, the
plantarflexors thrust is the putative mechanism driving gait. Additionally, study designs
should consider long-distance walking in a less controlled environment (outside walking) -
most studies assessed short-distance (~10m) lab walking tasks since it may interfere with
movement economy and affect gait velocity. These protocol characteristics may avoid
alternative explanations that the increase in gait velocity induced by performance
fatigability may be a strategy of finishing the task rapidly.
5
Also, protocols comparing
maximum vs. self-selected speed after muscle fatigability would provide information on
whether underlying neuromechanims related to fatigability-induced gait changes support