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1. Muscle fatigue (i.e. the decrease in muscle performance during exercise) has been studied extensively using a variety of experimental paradigms, from mouse to human, from single cell to whole-body exercise. Given the disparity of models used to characterize muscle fatigue, it can be difficult to establish whether the results of basicin vitrostudies are applicable to exercise in humans.2. In the present brief review, our attempt is to relate neuromuscular alterations caused by repeated or sustained isometric contraction in humans to changes in excitation-contraction (E-C) coupling observed in intact single muscle fibres, where force and the free myoplasmic [Ca2+] can be measured.3. Accumulated data indicate that impairment of E-C coupling, most likely located within muscle fibres, accounts for the fatigue-induced decrease in maximal force in humans, whereas central (neural) fatigue is of greater importance for the inability to continue a sustained low-intensity contraction. Based on data from intact single muscle fibres, the fatigue-induced impairment in E-C coupling involves: (i) a reduced number of active cross-bridges owing to a decreased release of Ca2+; (ii) a decreased sensitivity of the myofilaments to Ca2+; and/or (iii) a reduced force produced by each active cross-bridge.4. In conclusion, data from single muscle fibre studies can be used to increase our understanding of fatigue mechanisms in some, but not all, types of human exercise. To further increase the understanding of fatigue mechanisms in humans, we propose future studies usingin vitrostimulation patterns that are closer to thein vivosituation.