## 1 Introduction  
Injuries to the lateral ankle complex upon performing physical activity are notably frequent and pervasive [1]. In epidemiological studies, it has been indicated that up to 76% of individuals suffering an acute lateral ankle sprain (LAS) are at risk of developing chronic ankle instability (CAI) [2; 3]. Such instability is characterized by ankle joint instability, repetitive giving-way episodes, and functional disability [4; 5]. In CAI patients, persistent impairments in proprioception [6], muscle strength [7], neural reflexes [8], and neuroplasticity [9] are common, which can take a long time to recover from and involve a substantial decrease in quality of life [10]. Postural control involves complex neural processes, regulating sensory information from the visual, vestibular, and somatosensory systems to produce adequate motor output to maintain a controlled, upright posture [11]. Studies have revealed associations between CAI and deficits in postural control, which have been attributed to there being less time available for postural corrections when adopting a single-limb stance [12; 13; 14; 15]. Sensorimotor impairments in CAI patients can be attributed to the structural damage to the ligaments and alterations in the mechanoreceptors within the ankle joint, which disrupt the transmission of the proprioceptive signals responsible for the provision of accurate information about joint position and movement [16]. CAI patients often adapt their postural control strategies to compensate for changes in the sensory information being received from the injured joint. In previous studies, such compensatory mechanisms employed by CAI patients were investigated by examining the interaction between visual reliance and balance control under two conditions: with and without vision [17; 18]. CAI patients often exhibit reduced reliance on the somatosensory system and increased dependence on visual information when adopting a single-limb stance, compared with those without an ankle sprain [19]. This increased visual reliance is considered to be an adaptive mechanism for coping with the sensorimotor deficits that such patients commonly suffer [15; 20]. Neuromuscular fatigue is considered to negatively affect performance and impair neuromuscular control of the ankle [21]. This may occur via raising of the threshold for muscle spindle discharge, which can disrupt afferent feedback and subsequently impact conscious sensing of the joint's position [22]. Fatigue-induced changes in somatosensory input can thus potentially lead to deficits in neuromuscular control, which could manifest as deficiencies in postural control [23]. The impact of fatigue in specific muscles of the hip, knee, and ankle on lower-extremity function and postural control deficits was previously investigated [22; 24; 25] and it was postulated that injuries affecting joint integrity, such as CAI, may disrupt afferent-efferent pathways that are essential for maintaining proprioception, kinesthesia, and ultimately neuromuscular control [26]. Fatigue in sports-specific conditions bears certain resemblances to general muscle fatigue. However, the majority of studies on muscle fatigue have primarily involved open kinetic chain movements, emphasizing isolated joint motions and specific muscle groups [27]. This raises concerns about whether the obtained findings can be extrapolated to broader contexts such as overall physical conditioning and actual athletic competitions. It is thus possible that recommendations for prophylactic measures and rehabilitation based on these outcomes are not universally applicable or appropriate. In studies on sports-specific fatigue, closed kinetic chain exercises and their impact are specifically considered. However, it remains unclear whether sports-specific functional fatigue influences the capacity to perform postural control and sensory organization strategies in CAI patients. Moreover, few studies have investigated the cumulative effects of neuromuscular fatigue on reliance on visual input in such patients.