Obstructive sleep apnoea (OSA) is associated with cardiovascular morbidity and recognised as an independent risk factor for hypertension. Sympathetic nervous activity is commonly reported to be increased in OSA patients and animal models exposed to chronic intermittent hypoxia (CIH) and thought to result in increased vasoconstrictor tone. Our previous results indicate that CIH-induced hypertension is not a result of decreased femoral vascular conductance (FVC). We hypothesised that CIH induced systemic hypertension is driven by increased cardiac output and that the lumbar sympathetic chain does not significantly contribute to the hypertensive state. Age-matched adult male Wistar rats (335±4g) were exposed to CIH (n=23) consisting of 90s hypoxia (5% O2 nadir)/210s normoxia cycles, or sham (n=23) treatment (normoxia), for 8h/day for 2 weeks. Under urethane anaesthesia (1.5g/kg, administered via intraperitoneal injection), the cardiac output was determined using transthoracic echocardiography. FVC was determined by placement of a flow probe on the femoral artery. Lumbar sympathetic activity/stimulation was performed using bipolar silver wire electrodes placed at the L3-L4 region. Lumbar sympathetic network density was determined using a glyoxylic acid stain. Data are presented as mean ± S.E.M and were analysed by Student’s t-test or two-way ANOVA. CIH exposure significantly increased mean arterial pressure (81.4 ± 2 vs. 91.6 ± 2 mmHg; p= 0.001 n=23) and hematocrit concentration (42.4 ± 0.4 vs. 45 ± 0.4 %; p <0.0001, n=23). In addition, CIH exposure significantly increased cardiac output (25.8 ± 2.6 vs. 19.3 ± 1.7 ml/min/100g; p=0.027, n=8) without any change in FVC or blood volume. Lumbar sympathetic activity was not significantly different, nor was vascular sensitivity to lumbar sympathetic nerve stimulation. Sympathetic hyperinnervation within hindlimb arteries was increased in CIH animals (p=0.012, n=8), however vascular sensitivity to phenylephrine was significantly blunted (p=0.049, n=7). Our findings show that CIH-induced hypertension is a result of increased cardiac output and that the lumbar sympathetic chain does not significantly contribute to the hypertensive state through its influences on FVC. We conclude that hypertension is a compensatory response to CIH exposure whereby the cardiac output is increased, in combination with increased hematocrit, in an attempt to increase oxygen flow to the hypoxic tissues.