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Sleep is a crucial bioregulatory process with broad consequences for physical health, cognitive performance, and socioemotional adjustment (Shochat et al., 2014). Research has demonstrated that adolescents do not obtain enough sleep (Roberts et al., 2009), possibly due to shifting circadian rhythms and increases in stress (Byrne et al., 2007; Carskadon, 2011; Spear, 2002). The autonomic nervous system (ANS) is a key component of the stress response system that controls visceral organs and metabolic resources via the parasympathetic and sympathetic nervous system (PNS and SNS, respectively). To our knowledge, no studies have examined associations between PNS or SNS responsivity and sleep among adolescents. However, associations between physiological reactivity to stress and sleep may be particularly consequential during adolescence, given developmental increases in stress and decreases in sleep.
The purpose of the present study was to investigate relations between ANS reactivity across the PNS and SNS branches and multiple sleep parameters in adolescence. Sex was considered as an exploratory moderator of associations because of possible differences in sleep (Gillis & El-Sheikh, 2019) and responses to stress (Stroud et al., 2002) between boys and girls.
Participants were 244 adolescents (M = 15.79 years, SD = 9.56 months; 67.2% White/European-American, 32.8% Black/African-American). Parasympathetic activity was indexed by respiratory sinus arrhythmia (RSA) withdrawal, and sympathetic activity was indexed by skin conductance level reactivity (SCL-r), which were examined in response to a lab-based stressor (star-tracing task). Sleep was assessed with actigraphs (Ambulatory Monitoring, Ardsley, NY) in adolescents’ homes for seven consecutive nights. Two sleep parameters were examined: sleep duration indexed by actual sleep minutes and sleep quality indexed by sleep efficiency from sleep onset to wake time.
To account for possible confounds, age, race, sex, socioeconomic status, body mass index, and baseline RSA or SCL were entered as controls. Path models were fit separately for RSA and SCL and for each sleep parameter. Regression analyses showed that more RSA withdrawal (lower RSA during task than baseline) was associated with shorter sleep, and more SCL-r (higher SCL during task than baseline) was associated with poorer sleep efficiency. Moderation analyses showed that associations linking RSA withdrawal with fewer sleep minutes and poorer sleep efficiency and SCL-r with fewer sleep minutes were significant only for boys (see Figures 1 and 2).
Results show that higher daytime physiological reactivity (increased RSA withdrawal and SCL-r) is negatively associated with sleep duration and efficiency for adolescents, especially boys. Given that adolescents face multiple stressors through shifting biology as well as school, peer, and family experiences, strong responses to repeated moderate stressors (such as the lab-based stress task) may tax the bioregulatory systems that support sleep. Future research should attempt to explain the observed sex differences (e.g., differences in the experience or perception of stressors) and evaluate whether interventions designed to reduce stress reactivity can help preserve adequate sleep in adolescence.