The main aim of this thesis is to characterise sympathetic neural activity and autonomic regulation of BP at high altitude, in Lowlanders during acclimatisation, and in highland native populations, who have adapted to high altitude hypoxia over generations. To address this aim, resting sympathetic neural activity to the skeletal muscle vasculature (MSNA) was assessed, via microneurography, and baroreflex control of MSNA (vascular sympathetic baroreflex) and baroreflex control of the heart (cardiovagal baroreflex) was assessed using the modified Oxford test. Experimental study 1 examines sympathetic neural activity and arterial baroreflex function in Lowlanders following 10–20 days at 5050 m and compares them to Nepalese Sherpa. Experimental study 2 examines sympathetic neural activity and arterial baroreflex function in Andean Quechua who have developed the maladaptation syndrome chronic mountain sickness (CMS), and compares them to healthy Andean Quechua. Experimental study 1 and 2 also examine the mechanistic contribution of the peripheral chemoreflex to sympathetic neural activity and arterial baroreflex function in both Lowlanders and highland native populations. Experimental study 3 aims to extend these findings by investigating the previously unexplored mechanistic role of pressure-sensitive receptors in the pulmonary arteries in Lowlanders at high altitude. The major findings of this thesis are 1) heightened sympathetic neural activity is a feature of high altitude exposure in both acclimatising Lowlanders and highland natives, compared to Lowlanders at low altitude. Nepalese Sherpa, however, appear to have adapted to favour lower basal sympathetic neural activity, compared to Lowlanders and Andean Quechua at high altitude. Thus, divergent pathways of physiological adaptation between highland populations extend to autonomic regulation of resting arterial pressure. Despite heightened sympathetic neural activity, the responsiveness of the sympathetic nervous system to acute fluctuations in BP (i.e. vascular sympathetic baroreflex gain) is well preserved at high altitude. The vascular sympathetic baroreflex is reset to a higher MSNA set-point in all populations, compared to Lowlanders at low altitude. Such resetting permits elevated basal sympathetic vasomotor activity that allows normal resting arterial pressure to be maintained in the face of hypoxic local vasodilation, and potentially altered vascular sensitivity. Despite maintained vascular sympathetic baroreflex gain, the responsiveness of the cardiovagal baroreflex is depressed in both Lowlanders and healthy highlanders at high altitude. This thesis also demonstrates that the peripheral chemoreflex does not play a major role in sympathoexcitation and vascular sympathetic baroreflex resetting at high altitude in either acclimatising Lowlanders or highland natives. Moreover, this thesis demonstrates, for the first time, that hypoxia induced elevations in pulmonary arterial pressure contribute to the sympathoexcitation and baroreflex resetting during acclimatisation to high altitude in Lowlanders