title: Reinforcement of the adrenergic overdrive in the metabolic syndrome complicated by obstructive sleep apnea.
abstract: BACKGROUND
  Metabolic syndrome is characterized by a marked sympathetic overactivity. It is unknown, however, whether the neuroadrenergic activation can be ascribed to obstructive sleep apnoea (OSA), OSA exerts potentiating effects on the metabolic syndrome-related sympathetic activation and reflex/metabolic variables (insulin resistance) participate at the phenomenon.
  
  
  RESULTS
  We conducted a cross-sectional study of healthy individuals and metabolic syndrome patients recruited in our outpatient clinic. Fifty-five middle-age men classified according to Adult Treatment Panel III criteria and apnea-hypopnea index (overnight polysomnographic evaluation) as healthy controls without OSA and metabolic syndrome patients without and with OSA were studied. Blood pressure (Finapres), heart rate (ECG) and muscle sympathetic nerve activity (MSNA; microneurography) were measured at rest and during baroreflex manipulation. Compared with controls, patients with metabolic syndrome with and without OSA displayed higher waist-hip ratio, blood pressure, triglycerides and homeostasis model assessment index values but lower high-density lipoprotein cholesterol. MSNA was significantly higher in patients with metabolic syndrome without OSA than in controls (61.9 +/- 3.9 vs. 37.7 +/- 4.1 bursts/100 heartbeats, respectively, P < 0.01), a further marked increase being detected in patients with metabolic syndrome with OSA (77.1 +/- 4.3 bursts/100 heart beats, P < 0.01). Compared with controls, baroreflex control of heart rate and MSNA was markedly impaired in patients with metabolic syndrome with OSA, a further impairment in baroreflex-heart rate modulation being detected in metabolic syndrome with OSA. In the metabolic syndrome group as a whole, at the multivariate analysis, MSNA was significantly related to the apnoea-hypopnoea index but not to other variables.
  
  
  CONCLUSIONS
  Thus the sympathetic activation of metabolic syndrome occurs independently on OSA. OSA, however, markedly potentiates this neuroadrenergic abnormality via a hypoxic-dependent chemoreflex activation.
authors.affiliation: Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Monza, Italy. guido.grassi@unimib.it
authors.forename: Guido
authors.initials: G
authors.lastname: Grassi
authors.forename: Gino
authors.initials: G
authors.lastname: Seravalle
authors.forename: Fosca
authors.initials: F
authors.lastname: Quarti-Trevano
authors.forename: Claudia
authors.initials: C
authors.lastname: Mineo
authors.forename: Laura
authors.initials: L
authors.lastname: Lonati
authors.forename: Rita
authors.initials: R
authors.lastname: Facchetti
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D006801:Humans; D024821:Metabolic Syndrome / Q000150:complications / Q000378:metabolism*; D008875:Middle Aged; D011941:Receptors, Adrenergic / Q000378:metabolism*; D012891:Sleep Apnea Syndromes / Q000150:complications / Q000378:metabolism*
chemical_list: D011941:Receptors, Adrenergic