## 1 Introduction  
Fatigue is a common complaint among both healthy individuals and patients suffering from acute or chronic medical conditions. Muscle fatigue is generally divided into two components: central and peripheral [1]. Central fatigue originates in the central nervous system (CNS) and is believed to impair central neural drive to lower motor neurons,affecting their excitability [2]. Peripheral fatigue can be objectively assessed by measuring force production after stimulation following strenuous exercise. Motor units typically fire at a frequency of 50-60 Hz to maintain force. When motor unit firing declines, maximal force is reduced and fatigue occurs. Firing rate declines either as a result of repetitive activation that exhausts intercellular calcium stocks or due to presynaptic inhibition as a result of decreased muscle spindle firing [1].  
Fatigue is highly prevalent across a wide range of neurological and non-neurological disorders [3]. Central fatigue may occur in many neurological disorders that affect the CNS, e.g., multiple sclerosis, neurodegenerative disorders, and cerebrovascular diseases, among others [4]. Peripheral fatigue, on the other hand, is typical in neuromuscular disorders and more prominent in neuromuscular junction (NMJ) disorders and in certain myopathies.  
In healthy individuals, low-frequency (3-5 Hz) repetitive nerve stimulation (RNS) applied to a motor nerve depletes presynaptic acetylcholine (Ach) quanta. This depletion reduces the end-plate potential (EPP), which is proportional to the amount of ACh binding to acetylcholine receptors (AChRs), but it remains above the threshold, ensuring the generation of a muscle fiber action potential (MFAP) after each stimulation. The recorded compound muscle action potential (CMAP), representing the summation of MFAPs, remains stable. In patients with NMJ disorders, the safety factor, namely the threshold value needed to generate an MFAP, is reduced. Simple stimulation of a motor nerve produces normal motor responses. But when low frequency RNS is applied, the progressive depletion of ACh quanta leads the EPP below the threshold, resulting in the absence of an MFAP and subsequent progressive decrement of CMAP amplitude. Clinically, these patients do not complain of muscle weakness but of fatigability [5,6].  
Although decremental response in RNS is characteristic and pathognomonic to NMJ disorders, it is also observed in certain myopathies, more specifically in myotonias without dystrophic changes such as myotonia congenita and paramyotonia congenita. In these diseases, muscle weakness is not a general feature but occurs periodically when provoked, often by exercise (paramyotonia), while in some cases, muscle weakness is alleviated by exercise (myotonia congenita) [5]. Lastly, RNS may show decremental responses in certain metabolic myopathies like [PERSON]'s disease, which is dominated by exercise intolerance resulting in prominent fatigue and muscle weakness that is reversible by rest [6].  
Fatigue is an inevitable consequence of physical exertion in sporting activities and can potentially impede an athlete's performance. This raises an important clinical question: can patients with neuromuscular disorders characterized by abnormal RNS responses safely participate in sports activities? The objective of this narrative review was to summarize existing case reports of individuals with these conditions who engage in sports, to evaluate the potential benefits and risks of their participation, and to contribute a novel case to the current literature.