Broad interest has evolved in the interaction between sleep apnoea and autonomic function. Much of this interest has resulted from a suspicion that cardiovascular morbidity and mortality1-6 is increased in individuals with untreated apnoea. Further interest has recently been generated by evidence that sleep-disordered breathing is common among asymptomatic middle aged adults6 and that systemic hypertension is far more common in such individuals.5

Soon after the initial description of the sleep apnoea syndrome, polysomnographic recordings coupled with cardiac catheterisation findings during apnoeic events demonstrated cardiovascular instability. For example, transient but striking increases in systemic blood pressure at apnoea termination, along with significant decrements in heart rate during periods of apnoea, were found to be characteristic of apnoeic events associated with arterial hypoxaemia. These alterations in cardiovascular homeostasis, along with the understanding that untreated apnoea is associated with cardiovascular morbidity and mortality, has stimulated investigational activity in the association between sleep apnoea and autonomic nervous system control and this subject has recently been reviewed.7

This paper will describe only two of the important interactions between apnoea and autonomic function. Since bradycardia appears to be a common feature of prolonged apnoeic events associated with hypoxaemia, its mechanism will be discussed. The influence of apnoea on the development of transient and fixed sympathetic nervous system excitation will also be reviewed because of the recent evidence that untreated apnoea, even if mild, may be associated with sustained hypertension.