Obstructive sleep apnoea (OSA), the most common sleep-related breathing disorder, is characterised by repetitive airway collapse during sleep. OSA is associated with cardiovascular morbidity and recognised as an independent risk factor for daytime hypertension. Sympathetic activity is commonly increased in OSA patients and animal models exposed to chronic intermittent hypoxia (CIH). Studies of the relationship between CIH, hypertension and sympathetic activity focus on renal sympathetic activity primarily and report sympathetic hyperactivity; however the lumbar sympathetic chain (LSC) has been relatively neglected. We hypothesised that CIH would induce systemic hypertension and sectioning of the LSC would cause a greater drop in mean arterial blood pressure (MAP) and a greater increase in femoral vascular conductance (FVC) compared to sham controls. We also hypothesised that CIH exposure would alter the LSC contribution to haemodynamic responses during brief tracheal occlusions. Age matched adult male Wistar rats (317±6g) were exposed to CIH (n=8) consisting of 90s hypoxia (5% O2 nadir)/210s normoxia cycles, or sham (n=8) treatment (normoxia), for 8h/day for 2 weeks. Under urethane anaesthesia (1.5g/kg, administered via intraperitoneal injection), rats were tracheotomised and vascular cannulations inserted. Both LSC and were prepared for transection at the L2-L3 ganglia to removal central drive to the lower lumbar sympathetic nervous system. Hindlimb flow was measured at the femoral artery with an ultrasonic flow probe. Data is presented as Mean ± S.E.M and analysed by two-way ANOVA. CIH exposure significantly increased MAP (93.5±2.8 vs 81±1.4 mmHg; p= 0.0006) and sectioning of the LSC caused a drop in MAP which was not different in CIH and sham animals (p=0.1463). Sectioning of the LSC resulted in a large increase in FVC (p<0.0001) which was again not found to be different between groups (p=0.0689). In response to tracheal occlusion, CIH exposure significantly affected the MAP (p<0.001) and FVC (p<0.001) response with the LSC intact. After sectioning of the LSC, MAP and FVC responses to occlusion in CIH treated and sham animals were not significantly different (p>0.05). Heart rate response to occlusion, despite a CIH induced tachycardia (p=0.0013), was not different in sham and CIH treated animals, with the chain intact or cut (p>0.05). Haemodynamic responses to apnoeic events are altered after CIH exposure with the LSC intact. In response to obstructive apnoea, CIH treated animals exhibit a smaller drop in MAP and FVC does not increase as much compared to the sham response. We conclude that whilst CIH treatment alters the lumbar sympathetic response during hypoxic events facilitating maintenance of a steady blood pressure and perfusion to the hindlimb, the lumbar sympathetic outflow does not contribute significantly to CIH induced hypertension.