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 R-wave of the electrocardiogram (ECG) and the peak of the correspondi ng sympathetic burst; however, the effects of other forms of sleep disrupti on (i.e. spontaneous arousals and apnoea-induced arousals) on this temporal relationship are unknown. 2. We simultaneously recorded muscle sympathetic nerve activity in the pero neal nerve (intraneural electrodes) and the ECG (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 K complexes (1.297 +/- 0.024 s, mean +/- S.E.M.) and spontaneous arousa ls (1.268 +/- 0.044 s) compared with latencies during periods of stable NRE M sleep (1.369 +/- 0.023 s). In six subjects who demonstrated spontaneous a pnoeas during sleep, apnoea per se did not alter burst latency relative to sleep with stable electroencephalogram (EEG) and breathing (1.313 +/- 0.038 vs. 1.342 +/- 0.026 s); however, following apnoea-induced EEG perturbation s, 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 augmen ted by arousal.