Acute hypobaric or normobaric hypoxic exposure (i.e. inspired oxygen pressure <149 mmHg) accelerates neuromuscular fatigability. Single-joint exercises and whole-body repeated-sprint efforts offer complementary insights: the former enables detailed exploration of fatigue-related mechanisms, while the latter serves as a functional performance-relevant model. Training with repeated sprints in hypoxia (RSH) has also emerged as a promising ergogenic strategy. This review discusses the aetiology of neuromuscular fatigability during both single-joint exercise and repeated-sprint efforts with mild, moderate and severe hypoxia, and explores how RSH may enhance fatigue resistance. Despite differences in exercise intensity and muscle mass, both paradigms share common features. Regardless of hypoxia severity, maximal force and power during isolated efforts remain largely unaffected, while velocity may improve at terrestrial altitude due to lower air resistance. In contrast, repeated efforts in hypoxia accelerate performance declines, increasing peripheral and cerebral deoxygenation in a hypoxia severity-dependent manner. Above ∼3800 m (severe hypoxia), the contribution of central (supraspinal) mechanisms to fatigability increases in single-joint exercise. Differently, the aetiology of fatigability in RSH seems unaffected by hypoxia severity, despite indirect evidence of central limitations. Lastly, we outline the muscular, vascular and molecular mechanisms that may enhance neuromuscular fatigability through RSH training and consider its practical applications. Connecting findings between single-joint and repeated whole-body maximal-intensity exercise is key to translating basic physiology into effective training approaches to improve sport performance.
Ruggiero et al. (Wed,) studied this question.