Sensory and motor impairment after spinal cord injury (SCI) is well studied and classified with international standardized assessment tools. Meanwhile, autonomic impairment after SCI, is without a standardized clinical assessment tool/exam, is challenging to treat and causes greater impairment in quality of life than paralysis alone.1,2 One sequela of autonomic injury post SCI is thermal dysregulation. It is well accepted that persons with spinal cord injury have impaired ability to regulate core temperature due to compromised thermoregulatory vasomotor and sudomotor activity.3 In the setting of heat stress, impaired cutaneous vasodilation obviates skin blood flow (SkBF) increases and prevents convective cooling while impaired sweating responses (SR) prevents evaporative cooling. As a result, persons with SCI have difficulty maintaining thermal homeostasis, especially under heat stress. Body cooling intervention trials performed to date have all proven minimally successful likely due to lack of clear mechanistic understanding of autonomic change post-SCI. In non-SCI persons, sympathetic cholinergic mechanisms that mediate efferent control of both SkBF and SR are commonly thought to involve one and the same set of nerves; however, definitive proof is lacking. Indeed, cholinergic vasodilator nerves and cholinergic sudomotor nerves could actually be anatomically separate. Interestingly, it has been reported that during heat stress, persons with complete SCI have skin regions where SkBF increases without concomitant SR increases and other regions where SR increases without concomitant SkBF increases.7,8 These results suggest that efferent cholinergic sympathetic vasomotor nerves and efferent cholinergic sympathetic sudomotor nerves are separate, rather one and the same. Being able to study cholinergic vasodilator nerves and cholinergic sudomotor nerves in isolation in SCI will provide a valuable model for thermoregulatory physiology studies in non-SCI and SCI persons, and guide next steps in development of 1) An effective cooling technique so as to minimize heat related illness during exercise in the SCI population with a high prevalence of cardiometabolic disease and 2) A more quantitative assessement of thermoregulatory and autonomic function post-SCI to determine persons at greatest risk of its sequela. OBJECTIVES - To define and test the neurological control mechanisms of sudomotor and vasomotor activity after SCI to determine if their efferent cholinergic control is through an anatomically separate set of nerves. (1) Map areas of vasomotor and sudomotor activity during heat stress in persons with SCI and compare thermoregulatory level of injury (TLOI) with sensorimotor LOI. (2) Test whether increased noradrenergic vasoconstrictor activity attenuates SkBF increases in regions that show SR increases but no SkBF increases during whole body heat stress. (3) Test the hypothesis that cholinergic presynaptic nerve activity effects vasomotor and/or sudo...