Non-technical summary The mechanisms determining exercise intolerance are poorly understood. A reduction in work efficiency in the form of an additional energy cost and oxygen requirement occurs during high-intensity exercise and contributes to exercise limitation. Muscle fatigue and subsequent recruitment of poorly efficient muscle fibres has been proposed to mediate this decline. These data demonstrate in humans, that muscle fatigue, generated in the initial minutes of exercise, is correlated with the increasing energy demands of high-intensity exercise. Surprisingly, however, while muscle fatigue reached a plateau, oxygen uptake continued to increase throughout 8 min of exercise. This suggests that additional recruitment of inefficient muscle fibres may not be the sole mechanism contributing to the decline in work efficiency during high-intensity exercise.Abstract During constant work rate (CWR) exercise above the lactate threshold (LT), the exponential kinetics of oxygen uptake (V O 2 ) are supplemented by aV O 2 slow component (V O 2 sc ) which reduces work efficiency. This has been hypothesised to result from 'fatigue and recruitment' , where muscle fatigue during supra-LT exercise elicits recruitment of additional, but poorly efficient, fibres to maintain power production. To test this hypothesis we characterised changes in the power-velocity relationship during sub-and supra-LT cycle ergometry in concert withV O 2 kinetics. Eight healthy participants completed a randomized series of 18 experiments consisting of: (1) a CWR phase of 3 or 8 min followed immediately by; (2) a 5 s maximal isokinetic effort to characterize peak power at 60, 90 and 120 rpm. CWR bouts were: 20 W (Con); 80% LT (Mod); 20% (H); 60% (VH); where is the difference between the work rate at LT andV O 2 max . TheV O 2 sc was 238 ± 128 and 686 ± 194 ml min −1 during H and VH, with no discernibleV O 2 sc during Mod. Peak power in Con was 1025 ± 400, 1219 ± 167 and 1298 ± 233 W, at 60, 90 and 120 rpm, respectively, and was not different after Mod (P > 0.05). Velocity-specific peak power was significantly reduced (P < 0.05) by 3 min of H (−103 ± 46 W) and VH (−216 ± 60 W), with no further change by 8 min. TheV O 2 sc was correlated with the reduction in peak power (R 2 = 0.49; P < 0.05). These results suggest that muscle fatigue is requisite for theV O 2 sc . However, the maintenance of velocity-specific peak power between 3 and 8 min suggests that progressive muscle recruitment is not obligatory. Rather, a reduction in mechanical efficiency in fatigued fibres is implicated.