Prolonged exposure to cold and often cold/wet conditions can cause non-freezing cold injury (NFCI) in the hands and/or feet. The chronic symptoms of NFCI may last years, reducing the quality of life and limiting employability in certain occupations. The pathophysiology of NFCI is poorly understood, but may involve a combination of neural and vascular impairments. We hypothesised that the vascular responses to deep inspiration (DI), local heating (LH) and post-occlusive reactive hyperaemia (PORH) would be impaired in the Great toe and thumb of NFCI patients compared with matched Controls. Following ethical (MODREC) approval and written informed consent, 14 NFCI patients (age [SD]: 29 [4] years; mass: 76 [7] kg; height: 1.76 [0.07] m; predicted VO2max: 68 [8] mL.kg-1.min-1) and 14 matched cold-exposed Controls (29 [6] years; 78 [11] kg; 1.77 [0.08] m; 70 [11] mL.kg-1.min-1) undertook DI, PORH followed by LH in 24 °C ambient air. Cutaneous vascular conductance (CVC; flux/mean arterial pressure) was measured at the Great toe and thumb pad with local skin temperature clamped at 33 °C. DI protocol: participants took a rapid, deep breath to maximum inspiratory capacity and held it for 10 s followed by normal breathing, repeated three times with a 3 minute interval. The minimum blood flow during inspiration (BFmin) and preceding resting skin blood flow (BF0) were used to calculate DI index: 100*(BF0-BFmin)/BF0. PORH protocol: following a 5 minute baseline, Great toe and thumb blood flow was occluded (220 mmHg) for 3 minutes and then rapidly released. PORH index was calculated as the area under the curve during the first minute after pressure release divided by that during the last minute before cuff inflation. LH protocol: skin temperature was clamped at 33 °C for 10 minutes followed by 42 °C for 20 minutes. Between-group comparisons were conducted using independent samples t-tests for DI and PORH. LH was analysed using a 2-way ANOVA. Vascular responses of the thumb and Great toe pad were similar in NFCI patients and cold-exposed Controls for each protocol (Table 1, P>0.05), thus the hypothesis is rejected. Therefore, either NFCI is not associated with vascular dysfunction, or it is possible that significant cold exposure alone alters vascular function, causing a sub-clinical condition. To investigate this, the same tests are currently being compared in a non-cold exposed Control group.