Arousal from sleep shortens sympathetic burst latency in humans

1. Bursts of sympathetic activity in muscle nerves are phase-locked to the cardiac cycle by the sinoaortic baroreflexes. Acoustic arousal from non-rap id eye movement (NREM) sleep reduces the normally invariant interval betwee n the It-wave of the electrocardiogram (ECG) and the peak of the correspond ing sympathetic burst; however, the effects of other forms of sleep disrupt ion (i.e. spontaneous arousals and apnoea-induced arousals) on this tempora l relationship are unknown. 2. We simultaneously recorded muscle sympathetic nerve activity in the pero neal nerve (intraneural electrodes) and the EGG (surface electrodes) in sev en healthy humans and three patients with sleep apnoea syndrome during NREM sleep. 3. In seven subjects, burst latencies were shortened subsequent to spontane ous It complexes (1.297 +/- 0.024 s, mean +/- S.E.M.) and spontaneous arous als (1.268 +/- 0.044 s) compared with latencies during periods of stable NR EM sleep (1.369 +/- 0.023 s). In six subjects who demonstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst latency relative to sleep with stable electroencephalogram (EEG) and breathing (1.313 +/- 0.03 8 vs. 1.342 +/- 0.026 s); however, following apnoea-induced EEG perturbatio ns, burst latencies were reduced (1.214 +/- 0.034 s). 4. Arousal-induced reduction in sympathetic burst latency may reflect a tem porary diminution of baroreflex buffering of sympathetic outflow. If so, th e magnitude of arterial pressure perturbations during sleep (e.g. those cau sed by sleep, disordered breathing and periodic leg movements) may be augme nted by arousal.