Cardiovascular reactivity to mental stress is associated with insomnia susceptibility

Trait vulnerability to stress-related sleep disturbance (i.e., sleep reactivity) is associated with incident insomnia. However, the physiological mechanisms underlying stress-related insomnia susceptibility remain unknown. The purpose of the present study was to investigate whether cardiovascular reactivity to mental stress differs between individuals with high (HSR) versus low (LSR) sleep reactivity, an index of trait vulnerability to stress-related sleep disturbance. We hypothesized that cardiovascular reactivity would be elevated in individuals with HSR. A total of 50 participants included 33 LSR (16 male, 17 female; age: 21±4 years; BMI: 23±3 kg/m2) and 17 HSR (7 male, 10 female; age: 21±4 years; BMI: 22±3 kg/m2) adults. Continuous heart rate (HR, electrocardiogram) and beat-to-beat blood pressure (finger plethysmography) were recorded during 10-minutes of rest followed by exposure to the Trier Social Stress Test (TSST). The TSST consisted of a nonverbal speech anticipatory stress phase (5 min) followed by a verbal stress phase consisting of an impromptu speech (5 min) and mental math (5 min) in front of laboratory judges. HR reactivity during nonverbal anticipatory stress was elevated in the HSR group (HSR: Δ10±7 vs. LSR: Δ6±5 bpm; p=0.032). Conversely, mean arterial pressure (MAP) responses to nonverbal anticipatory stress were similar between groups. MAP and HR reactivity to the verbal stress phase (i.e., speech and mental math) did not differ between groups. In conclusion, individuals with HSR exhibit elevated HR reactivity to nonverbal stress, representing a potential physiological mechanism contributing to interindividual susceptibility to stress-related insomnia.