PURPOSE: The objective was to examine the impact of non-postural muscle fatigue on anticipatory postural control, during postural perturbations induced by platform translations. The experimental setup investigated the central changes caused by fatigue without the potential confounding influence of peripheral fatigue within the postural muscles. METHODS: Fatigue induced in forearm muscles by a maximal handgrip contraction has been previously shown to influence forearm force production for 10 min, reduce ankle plantarflexion force for 1 min and create measureable central fatigue for 30 s. The peak-to-peak anterior/posterior displacement of the center of mass and center of pressure (COP) and muscle activity were measured during the postural perturbation tasks performed before the fatigue protocol and for 10 min post-fatigue. RESULTS: The fatigue protocol decreased the peak-to-peak COP displacement from 128.0 ± 12.3 mm pre-fatigue to 81.9 ± 7.8 mm post-fatigue during the forwards platform translation (p < 0.05) and from 133.8 ± 12.0 to 89.2 ± 7.9 mm during the backwards translation (p < 0.05). The fatigue protocol also caused the tibialis anterior (TA pre-fatigue = -0.25 ± 0.04 s, TA post-fatigue = -0.41 ± 0.02 s, p = 0.001) and medial gastrocnemius muscles (MG pre-fatigue = -0.39 ± 0.03 s, MG post-fatigue = -0.48 ± 0.02 s, p = 0.028) to be recruited significantly earlier relative to the pre-fatigue condition. CONCLUSION: This experimental setup ensured that peripheral fatigue did not develop in the postural muscles; therefore, a general fatigued-induced modification of the postural strategy is proposed as the origin of the postural changes and delayed recovery.
PURPOSE: The objective was to examine the impact of non-postural muscle fatigue on anticipatory postural control, during postural perturbations induced by platform translations. The experimental setup investigated the central changes caused by fatigue without the potential confounding influence of peripheral fatigue within the postural muscles. METHODS: Fatigue induced in forearm muscles by a maximal handgrip contraction has been previously shown to influence forearm force production for 10 min, reduce ankle plantarflexion force for 1 min and create measureable central fatigue for 30 s. The peak-to-peak anterior/posterior displacement of the center of mass and center of pressure (COP) and muscle activity were measured during the postural perturbation tasks performed before the fatigue protocol and for 10 min post-fatigue. RESULTS: The fatigue protocol decreased the peak-to-peak COP displacement from 128.0 ± 12.3 mm pre-fatigue to 81.9 ± 7.8 mm post-fatigue during the forwards platform translation (p < 0.05) and from 133.8 ± 12.0 to 89.2 ± 7.9 mm during the backwards translation (p < 0.05). The fatigue protocol also caused the tibialis anterior (TA pre-fatigue = -0.25 ± 0.04 s, TA post-fatigue = -0.41 ± 0.02 s, p = 0.001) and medial gastrocnemius muscles (MG pre-fatigue = -0.39 ± 0.03 s, MG post-fatigue = -0.48 ± 0.02 s, p = 0.028) to be recruited significantly earlier relative to the pre-fatigue condition. CONCLUSION: This experimental setup ensured that peripheral fatigue did not develop in the postural muscles; therefore, a general fatigued-induced modification of the postural strategy is proposed as the origin of the postural changes and delayed recovery.