The V¿O2 slow component, a slowly-developing increase in V¿O2 during constant-work-rate (CWR) exercise performed above the lactate threshold, represents a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the current state of knowledge concerning the mechanistic bases of the V¿O2 slow component and describes practical interventions which can attenuate the slow componentand thus enhance exercise tolerance. There is strong evidence that, during CWR exercise, the development of the V¿O2 slow component is associated with the progressive recruitment of additional (type II) muscle fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting in a 'mirror-image'V¿O2 slow component) during fatiguing, high-intensity exercise in which additional fiber recruitment is unlikely or impossible. Therefore, it appears that muscle fatigue underpins the V¿O2 slow component, although the greater fatigue-sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations.Several interventions can reduce the magnitude of the V¿O2slow component and these are typically associated with an enhanced exercise tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative capacity and thus metabolic stability and/or by enhancing bulk muscle O2 delivery or local QO2-to- V¿O2 matching. Future honing of these interventions to maximize their impact on the V¿O2slow component might improve sports performance in athletes and exercise tolerance in the elderly or in patient populations.