The sleep apnoea/hypopnoea syndrome depresses waking vagal tone independent of sympathetic activation

The modest daytime hypertension and sympathetic upregulation associated,vith the sleep apnoea/hypopnoea syndrome (SAHS), does not explain the relatively large increased risk of cardiac morbidity and mortality in the SANS patients population. Therefore, efferent vagal and sympathetic activity was evaluated during wakefulness in SANS subjects and matched healthy controls, in order to determine if vagal downregulation may play a role in the aetiology of cardiac disease in the SAHS. The awake autonomic nervous system function of 15 male subjects, with mild-to-moderate SANS was compared to that of 14 healthy controls matched for age, body mass index, gender and blood pressure, All subjects were free from comorbidity, Vagal activity was estimated from measurements of heart rate variability high frequency power (HF) and sympathetic activity was measured from urine catecholamine excretion. The %HF power was significantly (p <0.03) reduced in SAHS patients (10 +/-1.6 (mean +/- SEM) as compared to controls (17 +/- 3), In addition, HF power correlated with the apnoea/hypopnoea index in the SANS subjects (R = -0.592, p = 0.02). There was no statistically significant difference in the daytime excretion of nonadrenaline between control (242 +/- 30 nmol(.)collection(-1)) and SANS (316 +/- 46 nmol(.)collection(-1)) subjects (P = 0(.)38). In these sleep apnoea/hypopnoea syndrome patients there was limited evidence of increased waking levels of urine catecholamines, The principal component altering waking autonomic nervous system function, in the sleep apnoea/hypopnoea syndrome subjects, was a reduced daytime efferent vagal tone.