In addition to the established increases in muscle size and strength, low load resistance training with blood flow restriction (BFR) may cause remodelling of the peripheral vasculature, as demonstrated by increases in conduit artery maximal diameter (Hunt et al. 2011) and reactive hyperaemic blood flow (Patterson & Ferguson, 2010). However, due to a lack of longitudinal measures it is unknown if functional changes precede these structural adaptations (Tinken et al. 2008). To gain insight we examined the effects of six weeks low load dynamic plantar flexion training with BFR on conduit artery function and structural capacity. With ethics committee approval six male participants (24 ± 4 yrs, 178.0 ± 3.2 cm, 78.7 ± 9.4 kg) performed 3 sets of unilateral plantar flexion exercise to volitional fatigue (3 days/week), at 30% of 1 repetition maximum, with a pneumatic cuff inflated at 110mmHg on their upper thigh. The contralateral leg (assigned in a counterbalanced manner to the dominant or non-dominant leg) was used as a non-exercised control (CON). The popliteal artery (PA), of both legs, was examined using Doppler ultrasound at 2-week intervals throughout the 6-week intervention. Artery diameter and flow velocity were measured at rest and following 5-mins of ischemia (peak diameter) and ischemic exercise (maximal diameter) to determine flow mediated dilation (FMD) and dilatory capacity (DC). Values are means ± SD, compared by repeated measures ANOVA. A priori sample contrasts with week 0 as the reference was used and cohen’s d effect size stated. There were no changes to resting PA parameters in either leg. In the BFR leg, FMD appeared to increase from baseline (6.1 ± 1.8%) at week 2 (8.0 ± 3.7%; t-test, P=0.068, d=1.14) before decreasing at week 4 & 6 (6.8 ± 2.5%, 6.3 ± 1.9%, respectively) but this was not significant (ANOVA, P=0.101). No change in FMD was observed in the CON leg (5.8 ± 1.4% vs. 5.7 ± 1.0% vs. 5.5 ± 1.0% vs. 5.9 ± 1.1%, week 0, 2, 4 and 6, respectively, ANOVA, P=0.567). Maximal diameter increased in the BFR but not the CON leg (Two-way ANOVA condition x time interaction, P=0.021). However, the increase in maximal diameter from baseline (5.95 ± 0.35mm) at week 2, 4 & 6 (6.04 ± 0.34mm, 6.04 ± 0.33mm, 6.19 ± 0.37mm, respectively) was not significant (ANOVA, P=0.068). There were no changes in peak diameter, shear rate stimulus and DC in either leg. Trends of enhanced FMD and maximal diameter in the BFR leg were masked by a heterogeneous response. Although these trends fit with established models of vascular adaptation (Tinken et al. 2008) a larger sample size is required to verify if dynamic low load resistance training with BFR induces complimentary adaptations in arterial function and structure.