The aim of this study was to determine whether and how young participants modulate their postural response to compensate for postural muscle fatigue during predictable but externally initiated continuous and oscillatory perturbations. Twelve participants performed ten postural trials before and after an ankle muscle fatigue protocol. Each postural trial was 1 min long and consisted of continuous backward and forward oscillations of the platform. Fatigue was induced by intermittent, bilateral isometric contractions of the ankle plantar- and dorsiflexors until the force production was reduced to 50 % of the pre-fatigue maximal voluntary contraction. Changes in the center of mass (COM) displacement, center of pressure (COP) displacement, and anterior-posterior location of the COP within the base of support were quantified as well as the activity of the tibialis anterior (TA), medial gastrocnemius (MG), quadriceps, and hamstring. All participants demonstrated postural stability post-fatigue by maintaining the displacement of their COM. Everyone also demonstrated a general forward shift in the anterior-posterior location of the COP within the base of support; however, two distinct postural modifications, corresponding to either an immediate fatigue-induced increase or decrease in the COP displacement during the backward platform translation, were recorded immediately post-fatigue. The changes in muscle onset latencies lasted beyond the recovery of the force production of the fatigued postural muscles. By 10 min post-fatigue, the participants showed a decrease in the COP displacement as well as an earlier activation of the postural muscles and an increased TA/MG co-activation relative to pre-fatigue. Although different strategies were used, the participants were able to adjust to and overcome postural muscle fatigue and remain balanced during the postural perturbations regardless of the direction of the platform movement. These adjustments lasted beyond the recovery of the ankle muscle force production indicating that they may be part of a centrally mediated protective response as opposed to a peripherally induced limitation to performance.

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