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Fatigue and the associated exercise limitation has wide reaching human performance and health implications, however the mechanisms are poorly understood. Muscle fatigue during exercise originates from a combination of peripheral and central processes, and their interaction, which are influenced by exercise-induced metabolic stress. Developments in non-invasive brain stimulation techniques such as transcranial magnetic stimulation (TMS), have allowed for measurement of central nervous system (CNS) processes alongside measurements of muscle performance and metabolic disturbances, but there are few studies to do so during locomotor exercise. Furthermore, although endurance training is a potent enhancer of exercise tolerance, the effect of training on fatigue mechanisms and the limiting factors to exercise tolerance is poorly understood. The aim of this thesis is to examine the central and peripheral contributions to fatigue in response to the exercise-induced metabolic demand before and after training in order to better understand the integrated physiology of fatigue as well as the mechanisms contributing to fatigue resistance and exercise tolerance. Study 1 examined the within- and between-day reliability of a number of motor nerve stimulation and single- and paired-pulse TMS (ppTMS) techniques that examine aspects of neuromuscular and corticospinal function which have been implicated in fatigue. The results confirmed that measures of neuromuscular and corticospinal function demonstrate good reliability and provide the first evidence that ppTMS can be reliably measured in a functional locomotor muscle of the knee extensors, however the stimulation parameters should be considered in order to optimise reliability and minimise variability. Study 2 investigated the relationships between corticospinal and neuromuscular function with exercise capacity in order to better understand the peripheral and central factors underpinning exercise tolerance. This study revealed a number of neuromuscular and motor cortical properties related to submaximal and maximal exercise capacity which could be indicative of central fatigue resistance. Study 3 examined the central and peripheral contributions to fatigue resulting from non-exhaustive and exhaustive exercise of high and low metabolic stress in order to better understand the integration between peripheral and central mechanisms and how they contribute to exhaustion. This study revealed that high metabolic stress accelerates the development of peripheral and central fatigue, however central fatigue was similar at exhaustion, suggesting this is an important mechanism in exercise termination. Additionally, a number of disturbances in cortical cell function were identified in a manner dependent on the exercise-induced metabolic strain. Study 4 examined the effect of endurance training on high-intensity exercise tolerance and the associated central and peripheral fatigue mechanisms. High-intensity interval training, but not work-matched moderate-intensity continuous endurance training, increased tolerance of exercise that elicited the same metabolic demand as pre-training. Better exercise tolerance was accompanied by a greater tolerance of peripheral fatigue and ischaemic muscle pain, and attenuated central fatigue. These studies provide novel insight to the central and peripheral contributions to fatigue and exercise tolerance, and the associated adaptations to exercise training.