Sleep onset and cardiovascular activity in primary insomnia

• Published in: Journal of sleep research 2011-06, Vol.20 (2), p.318-325
• Main Authors: DE ZAMBOTTI, MASSIMILIANO, COVASSIN, NAIMA, DE MIN TONA, GIULIANO, SARLO, MICHELA, STEGAGNO, LUCIANO
• Format: Article
• Language: English
• Subjects: Adult; Arousal - physiology; Cardiac Output - physiology; Cardiography, Impedance; cardiovascular system; Female; Heart - innervation; Heart Rate - physiology; Hemodynamics - physiology; Humans; hyperarousal; impedance cardiography; Male; Parasympathetic Nervous System - physiopathology; Polysomnography; primary insomnia; Reference Values; Sleep - physiology; Sleep Initiation and Maintenance Disorders - physiopathology; sleep onset; Stroke Volume - physiology; Sympathetic Nervous System - physiopathology; Wakefulness - physiology; Young Adult
• ISSN: 0962-1105; 1365-2869
• DOI: 10.1111/j.1365-2869.2010.00871.x

Summary The transition from wakefulness to sleep is characterized typically by a shift from sympathetic to parasympathetic regulation. Physiological functions, depending on the neurovegetative system, decrease overall. Previous studies have shown cardiovascular and electroencephalographic hyperactivity during wakefulness and sleep in insomniacs compared with normal sleepers, but there is very little evidence of this in the process of sleep onset. The purpose of this study was to compare cardiovascular and autonomic responses before and after falling asleep in eight insomniacs (who met DSM‐IV criteria for primary insomnia) and eight normal sleepers. Non‐invasive measures of heart rate (HR), stroke volume (SV), cardiac output (CO) and pre‐ejection period (PEP) were collected by impedance cardiography during a night of polysomnographic recording. Frequency domain measures [low‐frequency (LF), high‐frequency (HF)] of heart rate variability (HRV) were also estimated. Decrements in HR and CO and increases in SV and HF normalized units (n.u.) were found in both groups after sleep onset compared with wakefulness. Conversely, PEP (related inversely to sympathetic β‐adrenergic activity) showed increases after sleep onset in controls, but remained unchanged in insomniacs. PEP was also significantly lower in insomniacs than in normal sleepers in both conditions. These data suggest that, whereas normal sleepers follow the expected progressive autonomic drop, constant sympathetic hyperactivation is detected in insomniacs. These results support the aetiological hypothesis of physiological hyperarousal underlying primary insomnia.