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1994; Krishnan et al. 1996). These observations are not surprising given the fact that blood flow redistribution between the respiratory muscles and the locomotor muscles only occurs at exercise intensities >85�C90% of (Harms et al. 1997) and not at or below 80% of (Wetter et al. 1999). However, when constant-load exercise is performed at intensities greater than 85�C90%, respiratory muscle unloading was found to increase endurance time to exhaustion significantly (Wilson & Welch, 1980; Johnson et al. 1996). For example, during constant-load cycling at 90%, a 60% reduction in Wresp resulted in increased limb vascular conductance Moroxydine and 3�C4% increases in leg O2 transport and uptake, even in the face of a reduced cardiac output (Harms et al. 1997). Time to exhaustion was increased by ?14% when Wresp was reduced find more by ?50%. This significant effect on exercise performance has been confirmed indirectly by increasing Wresp by ?28%, resulting in ?15% reduction in time to exhaustion (Harms et al. 2000b). Even the relatively small reductions in O2 transport associated with exercise-induced haemoglobin desaturation >5% from rest, or the high Wresp, exacerbate the rate of development of peripheral locomotor muscle fatigue during exercise (Amann & Calbet, 2008). For example, during constant-load exercise (>90%), increases in locomotor muscle O2 transport secondary to a ?60% reduction in Wresp (via proportional assist ventilation) alleviated end-exercise quadriceps fatigue by 25�C30% compared with control exercise (Romer et al. 2006b; Fig. 3). Furthermore, when exercise-induced arterial desaturation was prevented during constant-load leg cycling (>90%; via adding supplemental O2 to the inspired air), end-exercise quadriceps fatigue was nearly 50% less compared with control conditions (Romer et al. 2006a). In contrast, no effect of maintaining resting on peripheral fatigue was observed in those Temozolomide datasheet individuals who sustained haemoglobin saturation above 95% during the exercise (Romer et al. 2006a). The effect of O2 delivery on peripheral fatigue development has been shown to be a key determinant of endurance exercise performance (Amann et al. 2006, 2011). We recently proposed that exercise-induced alterations of locomotor muscle fatigue affect, in a dose-dependent manner, the firing rate (and thus the central projection) of group III/IV muscle afferents, which are known to provide inhibitory feedback to the determination of central motor drive during exercise (Amann et al. 2006, 2009; Amann, 2011). In other words, acting via inhibitory feedback to higher motor areas, the highly O2 delivery-sensitive peripheral locomotor muscle fatigue influences central motor drive and therefore exercise performance.