Eccentric exercise (i.e. the lengthening of a muscle under tension) can induce muscle damage, inflammation and oxidative stress. Inflammation and oxidative stress are related to vascular dysfunction. It has previously been shown that 48 hours following bilateral eccentric leg press exercise there is an increase in central pulse wave velocity, indicative of an increase in large artery stiffness [1]. Given that the microvasculature is reportedly more susceptible than the large arteries to the deleterious effects of inflammation [2], we hypothesised that along with unfavourable changes in macrovascular function, eccentric exercise would elicit impairments in microvasculature function. To examine this, twelve healthy, non-weight trained males (age 22±4 years; mean ± SE) were recruited, and participated in either; 1) an eccentric exercise group (n=7) or, 2) a no exercise time control group (n=5). Participants in the exercise condition performed 50 eccentric repetitions of bilateral leg press exercise at 110% of their concentric 1 repetition maximum. The eccentric exercise group were assessed pre-exercise (baseline), 24 and 48 hours post-exercise, and the control group were assessed on 3 separate time-matched days. At each experimental session cutaneous microvasculature responses to iontophoresis of acetylcholine (1%, endothelial-dependent vasodilator) and sodium nitroprusside (1%, endothelial-independent vasodilator) were assessed using laser Doppler flowmetry. Measures of large artery stiffness (augmentation index), heart rate (ECG), blood pressure (brachial artery), arm and leg blood flow (venous occlusion plethysmography) and leg muscle pain (McGill Pain Questionnaire) were also made. Statistical analyses were performed using one-way repeated-measures ANOVA. Post-exercise muscle damage was verified by elevated ratings of leg muscle pain at 24 and 48 hours following eccentric exercise. Arterial stiffness (augmentation index -16.3±4.2, -9.7±4.8, -3.7±3.1% at baseline, 24 hours and 48 hours respectively) was significantly increased 48 hours following eccentric exercise (P<0.05 vs. baseline). Increases in cutaneous perfusion in response to iontophoresis of endothelial-dependent (843±91, 730±100, 733±182 %Δ at baseline, 24 and 48 hours, respectively) and -independent (1176±148, 1066±140, 1219±251 %Δ at baseline, 24 and 48 hours, respectively) vasodilators were not different following eccentric exercise (P>0.05). Similarly, arm and leg blood flow, heart rate and blood pressure were similar before and after eccentric exercise (P>0.05). In the time control group, arterial stiffness, cutaneous microvasculature responsiveness, leg and arm blood flow, heart rate and blood pressure were similar at all time points studied (P>0.05). Our preliminary data suggest that bilateral eccentric leg press exercise elicits increases in large artery stiffness, while cutaneous microvascular function appears unaltered.