## 4 Discussion
Consequently, higher impact loads may be transferred to the knee joint for primary regulation. Post-fatigue, the second peak of vertical ground reaction forces significantly increased compared to pre-fatigue, while the first vGRF peak and forces in other directions remained unchanged. These results align with findings by [PERSON] and [PERSON] [23; 24]. The significant increase in vGRF and loading rates during the landing phase following fatigue suggests insufficient mechanical adjustments by the knee joint. This could impair the ability of knee extensors to buffer ground impact effectively, thereby imposing substantial mechanical stress on the musculoskeletal system and increasing the risk and incidence of lower-limb overuse injuries. The discrepancy in vGRF responses to fatigue suggests that running experience, fatigue onset timing, and biomechanical adaptations might play crucial roles in modulating impact forces. The sEMG findings highlighted distinct neuromuscular adaptations in response to fatigue. Increased activation levels of the rectus femoris and biceps femoris during the pre-activation phase underscore the critical role of pre-activation in joint stabilization. This heightened activation aligns with previous studies [25] emphasizing the importance of pre-activation in mitigating joint instability. During the early and late landing phases, a reduction in the coactivation ratio of the biceps femoris, acting as an antagonist during knee extension, was observed. This adjustment may reflect a compensatory strategy by the central nervous system (CNS) to offset diminished quadriceps strength and maintain net torque output. This observation aligns with findings from [PERSON] et al., who reported increased biceps femoris activity during knee flexion post-fatigue, suggesting an adaptive response to maintain joint stability and function [26]. Additionally, [PERSON] and [PERSON] found that older adults exhibited enhanced antagonist muscle coactivation following a fatiguing protocol, indicating an age-related compensatory mechanism to preserve knee extension torque [27]. For the ankle joint, fatigue induced the increased activation of both the tibialis anterior and gastrocnemius. The tibialis anterior's strong pre-activation and early-phase activation highlight its role in maintaining dorsiflexion and preparing the foot for controlled ground contact. Concurrently, the gastrocnemius' enhanced activation during the push-off phase likely compensates for reduced knee extensor strength and aids in recruiting additional muscle fibers to sustain plantar flexion. Notably, the reduced coactivation ratio of the tibialis anterior as an antagonist suggests a CNS-driven adaptation to optimize force output while preserving stability. These findings are consistent with previous research [28; 29] that demonstrated reduced antagonist coactivation as a neuromuscular strategy to address task-specific demands under fatigue. The coordination of agonist and antagonist muscles is a complex process involving the motor cortex, cerebellum, and spinal motor neurons. This coordination is essential for smooth and efficient movement and is modulated by mechanisms such as reciprocal inhibition and coactivation. Reciprocal inhibition allows for the relaxation of antagonist muscles when agonists contract, facilitating movement, while coactivation involves the simultaneous activation of both muscle groups to stabilize joints during certain tasks [30]. Under fatigue conditions, neuromuscular regulation adapts to maintain performance [31]. Initially, the central nervous system (CNS) may increase the activation of both agonist and antagonist muscles, a strategy known as the \"common drive\", to preserve joint stability and force output. However, as fatigue progresses, this strategy may shift. Recent studies suggest that the CNS adopts differentiated control strategies for agonist and antagonist muscles during fatigue progression. Initially, a coordinated \"common drive\" mechanism enhances the activity of both muscle groups.