Obstructive sleep apnea (OSA) constitutes a common pathological process consisting in sleep-related repetitive obstructions of upper airways with consequent episodes of recurrent or intermittent hypoxia (IH). Oxygen desaturation in each episode of IH is the obvious element of altered respiration and, as a consequence, experimental models of OSA are based on the exposure of animals to atmospheres which composition oscillates from room air to oxygen-poor gas mixtures; frequency of oscillations and of levels of oxygen can be adjusted to mimic different severities of IH encountered in patients suffering OSA. As time progresses, OSA commonly generates a pathologies affecting the cardiovascular system, in the form of hypertension and increased frequency of heart and brain strokes, and the glucose and lipid metabolism in the form of type II diabetes. Altogether define the obstructive sleep apnea syndrome (OSAS). Clinical and experimental evidence supports the notion that the pathogenesis of OSA-associated pathologies is linked to the oxidative status generated by the repetitive hypoxic episodes and to sympathetic hyperactivity mediated by carotid body overdrive of brainstem cardioregulatory center. Obese subjects commonly develop cardiovascular and metabolic pathologies which define the metabolic syndrome (MS) and are analogous to those encountered in OSAS. This fact has lead to propose a bidirectional interrelationship between both processes, with obesity generating or aggravating OSA and OSA aggravating obesity and the associated pathologies. From this perspective, we have aimed: a) to define the effects of IH and obesity on redox status and sympathetic activity assessed as plasma and renal artery catecholamine levels; b) to define the effects of IH and obesity on glycemic metabolism and arterial pressure, and; c) to define the effects of experimentally associating obesity and IH on all those parameters. To achieve those aims we have used male rats which at the age of 12 weeks continued to be fed with standard rodent chow (3.8 kcal/g with 10% Kcal as fat; control, C) or started to be feed with fat-rich diet (5.2 kcal/g with 60% kcal as fat, obese, O) for an additional 12 weeks period. These two groups were further divided: half C rats were exposed to IH (40s, 5% O2/80s, air; 8h/day; for 2 weeks; CIH) and half O rats were equally exposed to IH (OIH). Experiments were performed when the rats reached 24 weeks of age. Breathing parameters were monitored by plethysmography in freely moving animals. Arterial blood pressure (AP) was recorded in ketamine (100 mg/Kg, i.p) and, blood and tissue samples were removed from pentobarbital anaesthetised rats (60 mg/Kg; i.p) and conveniently prepared for analysis. Major findings include: a) IH and O cause an oxidative status (increased liver lipid peroxides and diminished activities of mitochondrial and cytoplasmic superoxide dismutase), an inflammatory status (augmented C-reactive protein and nuclear factor kappa-B activation) and sympathetic hyperactivity (augmented plasma and renal artery catecholamine levels and rate of synthesis); combined treatments in OIH rats worsened those alterations. b) Both IH and O augmented lipid content in liver, plasma cholesterol, triglycerides, and leptin levels, also augmenting glycaemia, insulin levels and HOMA index; IH and O animals were hypertensive and most of the parameters aggravated when IH and O were combined in OIH rats. c) CIH rats had a diminished ventilatory response to hypoxia and hypercapnia and O animals, while maintaining minute ventilation, exhibited a restrictive ventilatory pattern; combination of treatments maintained the restrictive pattern and hypoventilation. As a whole, data indicate that IH and O cause metabolic and cardiovascular pathologies associated to a misregulation of the redox status and sympathetic activity. In our experimental paradigm, which intended to mimic the clinical situation, i.e., the appearance of OSA in O patients, the deviations from normality were more intense in O than in CIH, and the exposure of O animals to IH as in OIH rats worsened the greatest part of the parameters measured. Mechanisms generating the oxidative status and the sympathetic augmented tone and their participation in the genesis of hypertension and metabolic alterations will be discussed.