Physical inactivity has been proposed as a major contributor to the age-related loss of muscle mass and strength [1, 2]. Alongside these impairments are several metabolic adaptations, such as the development of insulin resistance [3], which may result from an age-related decline in muscle perfusion [4]. This study investigated the impact of forearm immobilisation on brachial artery blood flow and glucose uptake. We hypothesised that if inactivity induced decrements in muscle blood flow are responsible for blunting forearm glucose uptake, this would be ameliorated by the vasodilatory action of glyceryl trinitrate (GTN). Sixteen healthy men (20.4 ± 0.4yrs, BMI 22.9 ± 0.6kg.m-2) participated and were randomly assigned to placebo or GTN group. Measurements were made before and after 5wks immobilisation of the non-dominant forearm. Subjects underwent an oral glucose tolerance test (OGTT) and received either 400μg sublingual GTN or placebo mouth spray at t=0 and t=30. Brachial artery blood flow (BF) was measured during the OGTT using Doppler ultrasound, forearm glucose uptake (FGU) was calculated from the arterialised-venous and venous difference in blood glucose concentration, and total FGU over the 3hr OGTT was calculated from the incremental AUC. Forearm muscle volume was quantified with MRI and isometric strength was measured using handgrip dynamometry. The study was approved by the University of Nottingham Ethics Committee. Values represent mean ± SEM. Single measures were compared between groups using Student’s t-test. Postprandial responses were analysed using two-way ANOVA with repeated measures. Statistical significance was set at P<0.05. Before immobilisation, GTN did not affect FGU AUC during the OGTT (GTN 99.9 ± 25.7mmol/l/mm2 vs. Placebo 74.8 ± 13.6 mmol/l/mm2, P=0.42). Immobilisation reduced hand grip strength by 27.1 ± 7.3% and 21.0 ± 5.7% from baseline in the placebo and GTN group respectively (P<0.01), but had no effect on muscle volume in either group (placebo change 0.05 ± 1.83% vs. GTN change -0.7 ± 1.33%, P>0.05). Immobilisation reduced FGU AUC by 42.4 ± 14.2% (P<0.05) in the placebo group. GTN increased brachial artery diameter by 15.2 ± 0.7% (P<0.01) throughout the OGTT and increased BF by 17.3 ± 2.9% during the first hour of the OGTT (P<0.05). However the immobilisation induced decrement in FGU AUC was no different from the placebo response (55.9 ± 21.2%, P=0.64). Immobilisation reduced FGU in response to an OGTT. The administration of GTN increased brachial artery diameter and blood flow during the OGTT, but did not improve the immobilisation induced deficit in FGU. This suggests that an immobilisation induced deficit in muscle blood flow is not responsible for the decline in glucose disposal, but instead is a muscle centric phenomenon.