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Background: Allergic rhinitis (AR) is a pervasive condition among competitive athletes, especially in endurance and aquatic disciplines. IgE-mediated Th2-type inflammation causes mucosal edema and increased upper airway resistance, forcing nocturnal mouth-breathing mechanics. This instability triggers frequent micro-arousals and disrupts sleep architecture, leading to documented reductions in restorative slow-wave and rapid eye movement sleep. Aim: To synthesize evidence on how AR-mediated sleep fragmentation degrades neurocognitive function, motor control, and physical output in athletes, while evaluating the safety and efficacy of contemporary pharmacotherapy. Material and methods: Narrative review integrating clinical, immunological, somnological, and sports science research from primary databases, including PubMed and Scopus. Results: Systemic pro-inflammatory cytokines and nocturnal airway obstruction disrupt sleep-wake regulation centers. Resulting fragmentation impairs executive function, spatial working memory, and reaction times. Physiological decrements manifest as reduced aerobic efficiency, decreased explosive power, and diminished agility, often accompanied by an elevated rate of perceived exertion. While sedating first-generation antihistamines further impair performance and sleep architecture, intranasal corticosteroids and second-generation antihistamines provide effective symptom relief without cognitive impairment or World Anti-Doping Agency compliance issues. Conclusions: AR-induced sleep disruption is a significant, underdiagnosed performance-limiting factor. Proactive allergy screening, longitudinal sleep tracking, and the optimization of non-sedating therapeutic regimens are essential for safeguarding athlete health and maintaining the competitive edge.
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Szymański et al. (2026) studied this question.
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