Вы находитесь на странице: 1из 14

Emotion 2016 American Psychological Association

2017, Vol. 17, No. 4, 602 615 1528-3542/17/$12.00 http://dx.doi.org/10.1037/emo0000254

Autonomic Reactivity and Vulnerability to Depression:

A Multi-Wave Study

Jonathan P. Stange Jessica L. Hamilton and Thomas M. Olino

Temple University and University of Illinois at Chicago Temple University

David M. Fresco Lauren B. Alloy

Kent State University Temple University
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
This document is copyrighted by the American Psychological Association or one of its allied publishers.

The ability of the autonomic nervous system to flexibly adapt to environmental changes is thought to
indicate efficient use of self-regulatory resources. Deficits in autonomic reactivity appear to characterize
current depression; however, whether autonomic reactivity confers vulnerability to future depression
when individuals encounter environmental stressors is unknown. Fluctuations in respiratory sinus
arrhythmia (RSA) and heart rate (HR) were evaluated in response to emotion-eliciting films among 134
undergraduates. Negative events and depressive symptoms were assessed 5 times across 12 weeks.
Multilevel modeling demonstrated that smaller decreases in RSA in response to sadness, greater increases
in HR following sadness, and smaller increases in HR to amusement were prospectively associated with
greater depressive symptoms when individuals encountered high levels of idiographically assessed
negative events. These results demonstrate that the lack of contextually appropriate autonomic reactivity
may confer vulnerability to depression under conditions of environmental stress, perhaps due to
attenuated capacity for effective self-regulation.

Keywords: depression, respiratory sinus arrhythmia, vulnerability, autonomic nervous system, stress

Supplemental materials: http://dx.doi.org/10.1037/emo0000254.supp

Major depressive disorder (MDD) is the most common mental events, but there are considerable individual differences in suscepti-
disorder, with an estimated lifetime prevalence of 16.6% (Kessler, bility to depression following stressors (Kendler, Karkowski, &
Chiu, Demler, Merikangas, & Walters, 2005). It is associated with Prescott, 1999). Thus, recent work has sought to identify behavioral
tremendous impairment and considerable comorbidity with other and biological factors that serve as indicators of vulnerability to or
psychiatric conditions, resulting in major personal, economic, and protection against depression following negative life events (e.g.,
societal costs (Kessler et al., 2006; Kessler & Wang, 2009). The Abramson et al., 2002). In the present study, we used a multiwave
onset of depression often occurs following exposure to stressful life design to evaluate whether patterns of reactivity of the autonomic
nervous system in response to different emotional contexts would
confer vulnerability to depression in the face of negative life
This article was published Online First December 19, 2016. events.
Jonathan P. Stange, Department of Psychology, Temple University, and The autonomic nervous system, which contains sympathetic and
Center on Depression and Resilience, Department of Psychiatry, Univer- parasympathetic branches, can facilitate adaptive behavioral and
sity of Illinois at Chicago; Jessica L. Hamilton and Thomas M. Olino, emotional responses to meet contextual demands (Beauchaine,
Department of Psychology, Temple University; David M. Fresco, Depart- 2001; Kashdan & Rottenberg, 2010; Kreibig, 2010; Thayer &
ment of Psychology, Kent State University; Lauren B. Alloy, Department Lane, 2009). Autonomic nervous system reactivity can be mea-
of Psychology, Temple University.
sured as the extent to which individuals show patterns of change in
This work was supported by grants to Jonathan P. Stange from the
National Institute of Mental Health (NIMH; F31MH099761), the Associ- activity across different environmental or emotional contexts. One
ation for Psychological Science, the American Psychological Foundation, index of parasympathetic activity is respiratory sinus arrhythmia
and the American Psychological Association. Jessica L. Hamilton was (RSA), a measure of variability in heart rate that occurs over the
supported by National Research Service Award MH106184 from the respiration cycle. During periods of rest, the medial prefrontal
NIMH. Lauren B. Alloy was supported by NIMH Grant MH101168. David cortex exerts inhibitory control over the amygdala, indirectly en-
M. Fresco was supported by National Heart, Lung, and Blood Institute hancing cardiac control via the vagus nerve, and resulting in
Grant R01HL119977 and National Institute of Nursing Research Grant
elevated resting RSA (Thayer, hs, Fredrikson, Sollers, & Wager,
Correspondence concerning this article should be addressed to Jonathan
2012; Thayer, Hansen, Saus-Rose, & Johnsen, 2009). However,
P. Stange, Center on Depression and Resilience, Department of Psychiatry, during periods of emotional or environmental challenge (e.g.,
University of Illinois at Chicago, 1601 West Taylor Street, Chicago, IL stressors, attention to salient stimuli, or during emotion regula-
60608. E-mail: jstange@psych.uic.edu tion), the parasympathetic nervous system typically withdraws its

inhibitory control over heart rate, which results in reductions in With respect to HR, the majority of studies using sad films have
RSA, allowing the body to mobilize resources needed to flexibly reported a deactivating response to sadness in which sympathetic
respond to the challenge (Beauchaine, 2001). When the challenge withdrawal occurs (Kreibig, 2010; Overbeek et al., 2012), which
remits, inhibitory vagal control typically is augmented, resulting in may represent concerned attention or sympathy (Eisenberg et al.,
a return of RSA to resting levels (Rottenberg, 2007). Given the 1989). It is important to note, however, that sadness, including
presence of shared neural pathways, RSA has been proposed as a crying, sometimes is characterized by an increase in HR (Kreibig,
biological index of capacity for effective emotion regulation 2010; Rottenberg, Bylsma, & Vingerhoets, 2008; Vingerhoets &
(Beauchaine & Thayer, 2015; Thayer et al., 2012). Bylsma, 2016). Others have suggested that sympathetic activation
Although RSA reactivity is a common method of assessing is characteristic of impending loss, whereas deactivating responses
vagal control, fluctuations in heart rate (HR) in response to emo- (e.g., decreases in HR) are more common after loss has occurred
tional stimuli also can be used as an indicator of both vagal and (such as in response to commonly used film clips such as The
sympathetic activity (Cacioppo, Uchino, & Berntson, 1994; Champ in which a boys father has died; Gross & Levenson,
Kreibig, 2010). Increases in HR are thought to represent emotional 1997; Kreibig, 2010; Overbeek et al., 2012; Rottenberg, 2007).
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

arousal or regulatory effort, whereas decreases in HR may repre- Thus, although decreases in HR are expected overall, there is
This document is copyrighted by the American Psychological Association or one of its allied publishers.

sent decreased arousal, shifting attention toward salient stimuli, or likely to be variability in affective and sympathetic responses to
regulatory success (Allen, Kuppens, & Sheeber, 2012; Somers, sadness films, and it may not be clear what constitutes a psycho-
Borelli, Smiley, West, & Hilt, 2015). Alterations of typical pat- logically healthy HR response to sad stimuli as the associated
terns of responding to emotional stimuli may represent the inabil- psychological processes may be complex (Kreibig, Wilhelm, Roth,
ity of the autonomic nervous system to respond flexibly to changes & Gross, 2007; Kreibig, 2010). Although initially it might seem
in the environmental context (Kashdan & Rottenberg, 2010). contradictory to anticipate decreases in both RSA and HR to sad
These patterns may be attenuated in MDD, consistent with the films given that in general RSA and HR are inversely related, these
theory that depression is characterized by insensitivity to emo- measures actually do not index completely overlapping processes
tional context (Rottenberg, Salomon, Gross, & Gotlib, 2005; Rot- (Berntson et al., 1997). For example, decreases in HR to sad films
tenberg & Hindash, 2015). could represent concerned attention or an appropriate deactivating
Evaluating fluctuations in the autonomic nervous system (e.g., response following loss (Kreibig, 2010; Eisenberg et al., 1989),
using RSA and HR) in response to emotional stimuli such as whereas simultaneous decreases in RSA could represent the body
sadness, one of the core features of depression, may provide useful attempting to adapt to the emotional demands of the situation or
information about the capacity for flexible adaptation (e.g., preparation for a regulatory response. In line with these hypothe-
Gentzler, Santucci, Kovacs, & Fox, 2009; Porges, 2007; Rotten- ses, previous work has documented decreases in both RSA and HR
berg, 2007). One common method of studying physiological re- to sad films (Overbeek et al., 2012).
sponses to varying emotional contexts is the presentation of films Few studies in the literature have evaluated normative auto-
that are designed to elicit specific emotions, such as sadness and nomic responses during recovery periods following sad films,
amusement (e.g., Gross & Levenson, 1997; Rottenberg, Ray, & when a variety of regulatory processes may occur. On the one
Gross, 2007). On the basis of the existing literature, it can be hand, following a sad film, a return to baseline (an increase in HR)
difficult to articulate normative patterns of autonomic responses might be expected given that concerned attention no longer is
to specific stimuli (Kreibig, 2010). In part, this is because studies directed toward the film (Eisenberg et al., 1989). At the same time,
have used a variety of types of stimuli (e.g., various films, pictures, regulatory efforts to reduce sadness would be expected during
autobiographical recall tasks) and a variety of indices of autonomic recovery, which also should increase HR (Frazier, Strauss, &
functioning, which seem to be imperfect measures of psycholog- Steinhauer, 2004; Obrist, 1981; Overbeek et al., 2012) and main-
ical processes. For example, RSA and HR each are influenced to tain RSA withdrawal (LeMoult, Yoon, & Joormann, 2016). How-
some degree by both parasympathetic and sympathetic systems, ever, once regulation is complete, conservation of autonomic re-
vary based on interactions among autonomic branches and respi- sources and energy should take place by increasing parasympathetic
ration, and each may be related to emotional experience as well as activation (augmentation of RSA) and decreasing sympathetic acti-
effortful emotion regulation (Berntson et al., 1997; Kreibig, 2010; vation (decrease in HR from regulatory levels toward resting levels;
Overbeek, van Boxtel, & Westerink, 2012). Thus, the field has not Rottenberg, 2007). Although it is difficult to interpret these dy-
come to a consensus on exactly what patterns of response to namic and opponent processes by averaging autonomic responses
emotional stimuli are likely to be adaptive, and results across across a recovery period (Rottenberg, Clift, Bolden, & Salomon,
studies have been quite mixed (Kreibig, 2010). Nevertheless, sev- 2007), it might be expected that across recovery, excessive in-
eral studies that have used films to elicit sadness have demon- creases in HR and attenuated RSA augmentation could map onto
strated reductions in RSA to sad films relative to neutral films, psychological processes such as a relatively greater time spent
likely representing vagal withdrawal, which allows the body to regulating, excessive perceived need for continued regulation (Fra-
respond to the emotional challenge (El-Sheikh, Hinnant, & Erath, zier et al., 2004; Obrist, 1981; Overbeek et al., 2012), unsuccessful
2015; Overbeek et al., 2012; Porges, 2007; Rottenberg et al., regulation, or greater use of maladaptive regulatory strategies such
2005). That attenuated vagal withdrawal to sadness is associated as expressive suppression or rumination that inhibit autonomic
with depression concurrently and prospectively is consistent with recovery (Gross & Levenson, 1997; LeMoult et al., 2016). Rela-
the hypothesis that RSA withdrawal during sad films is normative tively few studies have examined normative patterns of autonomic
and may be adaptive for the regulation of sadness (Rottenberg, response to positive affective stimuli such as amusement, but the
2007). available literature suggests that RSA may decrease (Overbeek et

al., 2012) or stay the same (Kreibig, 2010), whereas HR may To date, three prospective studies have suggested that atypical
increase or show no change (Kreibig, 2010). autonomic reactivity could serve as a vulnerability to depression
Given that RSA and HR likely index a variety of physiological that is apparent only in the presence of contextual factors such as
and psychological processes (Berntson et al., 1997, Berntson, marital conflict (El-Sheikh & Whitson, 2006), lack of social sup-
Cacioppo, & Grossman, 2007; El-Sheikh et al., 2015; Kreibig et port (Hopp et al., 2013), and social withdrawal (Morgan, Shaw, &
al., 2007; Kreibig, 2010), it is difficult to completely disentangle Forbes, 2013). In addition, one study did not find evidence that
emotional experience from emotion regulation by measuring au- resting RSA protected against the impact of stressors on depressive
tonomic responses to films. Nevertheless, it is possible that eval- symptoms (Bosch, Riese, Ormel, Verhulst, & Oldehinkel, 2009).
uating individual differences in patterns of response to emotional However, no prospective studies have evaluated whether exposure
stimuli would be useful in identifying individuals who may be to negative life events is particularly likely to lead to depression
vulnerable to depression. However, the depression literature on among individuals with atypical reactivity or recovery of RSA and
autonomic reactivity and recovery in response to emotional stimuli HR. Thus, prior work has provided an incomplete test of whether
is relatively sparse. A few studies have found that RSA withdrawal atypical autonomic reactivity confers vulnerability to future de-
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

to sadness and RSA recovery from sadness or other stressors is pression.

This document is copyrighted by the American Psychological Association or one of its allied publishers.

attenuated among individuals with current MDD (Bylsma, Salo- In the present study, we completed the first multiwave study
mon, Taylor-Clift, Morris, & Rottenberg, 2014; Rottenberg, Wil- of atypical autonomic reactivity as a vulnerability to depres-
helm, Gross, & Gotlib, 2003; Rottenberg et al., 2005; Rottenberg, sion. Importantly, we sought to address many of the limitations
Clift, et al., 2007). Similarly, depressed individuals show blunted of past studies by (a) evaluating fluctuations in both RSA and
HR responses to stressful stimuli (Bylsma, Morris, & Rottenberg, HR in response to emotional contexts (sadness and amusement,
2008; Salomon, Bylsma, White, Panaite, & Rottenberg, 2013; emotions relevant to the core features of depression) relative to
Taylor, 2010). However, although case-controlled studies suggest neutral baselines; (b) examining the effects of controlling for
that impairments in autonomic reactivity are associated with de- respiration, to rule out this important potential confound (Over-
pression, they provide limited information about whether atypical beek et al., 2012); (c) evaluating interactions between naturally
autonomic reactivity could serve as a vulnerability factor for future occurring negative life events and indices of autonomic reac-
tivity when predicting prospective fluctuations in depressive
depression. These studies use a logically backward design, select-
symptoms; and (d) using a multiwave design, which allowed us
ing participants based on the outcome (depression or no depres-
to evaluate fluctuations in negative life events using an idio-
sion) and then comparing on the potential vulnerability factor; they
graphic (person-centered) approach, providing a stronger test of
ignore the possible activating role of stressful events (or shifts in
vulnerability than is possible with the nomothetic (sample
environmental or emotional context) that are particularly relevant
mean-centered) approach that is commonly used with two time-
to depression; and the use of postmorbid participants to test causal
point study designs (Abela & Hankin, 2008). Thus, the present
hypotheses precludes the ability to test whether atypical autonomic
study represents the first to conduct a complete test of whether
activity is a vulnerability to future depression, versus a scar of past
atypical autonomic reactivity confers vulnerability to future
depression or simply a correlate of current depressive symptoms
symptoms of depression, with a number of methodological
(e.g., Just, Abramson, & Alloy, 2001).
improvements on the existing literature.
A modest number of prospective studies have improved upon Given that vagal withdrawal is expected in response to emo-
these methodological limitations. These studies found evidence tionally salient stimuli, and that vagal augmentation is expected
that attenuated RSA reactivity to sadness (but not to amusement) during recovery from negative affective states (Frazier et al., 2004;
predicted a poorer course of current depressive episodes among Rottenberg, 2007; Overbeek et al., 2012), we hypothesized that
adults (Fraguas et al., 2007; Panaite et al., 2016; Rottenberg et al., individuals with smaller reductions in RSA to sadness and amuse-
2005) and that combinations of RSA reactivity were associated ment and smaller augmentations in RSA recovery from sadness
with depressive symptom trajectories among children and adoles- would be more vulnerable to symptoms of depression, particularly
cents (Yaroslavsky, Rottenberg, & Kovacs, 2014). With respect to when exposed to stressful events. Because HR often decreases in
HR reactivity, smaller decreases in HR to sadness were associated response to sad films (Gross & Levenson, 1997; Overbeek et al.,
with prospective increases in depressive symptoms among chil- 2012), we hypothesized that individuals with smaller reductions in
dren (Somers et al., 2015), and a lack of HR increase to amusement HR to sadness would be vulnerable to symptoms of depression
predicted a lower likelihood of recovery from a major depressive (e.g., Somers et al., 2015) following stressful events. During
episode among adults (Rottenberg, Kasch, Gross, & Gotlib, 2002). recovery from sadness, HR is expected to increase to resting
Vulnerability factors may be particularly likely to manifest in levels, representing attentional disengagement from the sad film
psychopathology following context shifts (such as negative life and/or active coping processes (Frazier et al., 2004; Obrist, 1981;
events) that require flexible adaptation. This consideration is par- Overbeek et al., 2012); however, excessive HR increases during
ticularly important given that autonomic reactivity may be helpful recovery also could represent ineffective regulation or excessive
for adapting to difficult experiences brought about by recent stres- perceived need for coping with sadness, and no studies to our
sors. Knowing whether atypical autonomic reactivity is a vulner- knowledge have evaluated HR recovery from sadness in relation to
ability factor, as opposed to a correlate of depression, is a critical depression. Thus, our analyses with respect to HR recovery were
gap in the literature that could inform efforts for early intervention exploratory. Given that the existing literature is mixed on the
to attenuate vulnerability. Indeed, researchers have called for pro- degree to which RSA withdrawal to amusement is normative
spective studies that evaluate autonomic reactivity in the context of (Kreibig, 2010; Overbeek et al., 2012) and is associated with
naturally occurring stressors (e.g., Panaite et al., 2016). depression (Fraguas et al., 2007; Panaite et al., 2016; Rottenberg et

al., 2005), we hypothesized that RSA reactivity to amusement Measures

would not predict symptoms of depression following stressors.
Finally, we expected relative increases in HR during amusement, Autonomic reactivity and recovery. At the Time 1 assess-
as amusement is a relatively high-arousal emotion (Kreibig, 2010; ment, participants were seated comfortably in a small assessment
room and the experimenter attached cardiovascular sensors. After
Rottenberg, Ray, et al., 2007). Given that depression often is
a 5-min rest period to become acclimated to the room and sensors,
characterized by anhedonia and a lack of responsivity to positive
participants watched a series of video clips, which were presented
stimuli (Pizzagalli, 2014; Rottenberg et al., 2005) and that lack of
on a desktop computer approximately 24 in. in front of them. Film
HR reactivity to amusement was associated with a longer course of
selection was based on criteria recommended by Rottenberg, Ray,
current MDD (Rottenberg et al., 2002), we hypothesized that
et al. (2007). To establish physiological parameters during a neu-
individuals exhibiting smaller increases in HR during an amusing
tral baseline film, participants first viewed a 2-min nature film clip
film would be vulnerable to depression, particularly in the context
(a documentary on Denali National Park), followed by a film
of negative life events.
depicting a boy who is distraught at the death of his father (the
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

movie The Champ), which has been demonstrated to elicit sadness

This document is copyrighted by the American Psychological Association or one of its allied publishers.

Method (Rottenberg, Ray, et al., 2007). Previous work indicates that vagal
recovery is most likely to occur during an unchallenged period
immediately following emotional challenges (e.g., 60 to 120 s
Participants and Procedure following the challenge; Mezzacappa, Kelsey, Katkin, & Sloan,
2001; Rottenberg et al., 2003; Rottenberg, Clift, et al., 2007).
Participants were undergraduate students at Temple University
Thus, participants then completed a 2-min recovery period of rest
and could range in age from 18 to 65. For inclusion, participants
in which they were asked to sit quietly. For a second resting
were fluent in English and had normal or corrected-to-normal baseline, participants then viewed another 2-min nature film clip
vision. Participants were recruited from undergraduate psychology (another clip from Denali), followed by an improvisational com-
classes using the departments online listing of studies, and from edy film clip (Whose Line is it Anyway?) that has been demon-
the diverse student body via flyers posted around campus. Students strated to elicit amusement (Rottenberg, Ray, et al., 2007). Partic-
either received psychology course credit or were compensated in ipants completed a brief self-report measure of affect between film
cash for participation. All participants completed informed consent and recovery periods.
approved by the universitys institutional review board. Electrocardiogram (ECG) and respiration signals were assessed
The sample included 178 participants (Mage 21.94, SD with a three-lead electrocardiogram and BioPac BioHarness, and
5.71). The sample was 57.9% female, 9.0% Hispanic or Latino, were continuously recorded on a PC with AcqKnowledge 4.3
20.2% African American/Black, 64.0% Caucasian/White, 12.4% software (equipment and software from Biopac Instruments Inc.,
Asian, 0.6% Pacific Islander, 1.1% Native American, and 6.2% Goleta, CA), sampled at 1000Hz. Cloth base disposable Ag/AgCl
other race. electrodes were placed in a modified Lead-II configuration on the
At Time 1, participants completed a laboratory assessment that chest. ECG signals were amplified with a Biopac MP150 with an
involved completing questionnaires in an online survey and watch- ECG100 amplifier. We measured respiration rate (RR) with an
ing videos while heart rate and respiration were assessed. Every RSP100C amplifier with a TSD100C respiratory transducer, which
three weeks after Time 1, participants completed follow-up assess- was placed around the chest, crossing under the armpits and on top
ments remotely that included measures of current symptoms of of the breastbone. Respiration data were high-pass filtered and
depression and life events experienced in the prior three weeks visually inspected for artifacts and corrected when needed, follow-
(Times 2 through 5). At the Time 5 assessment, participants also ing well-established procedures outlined elsewhere (Grossman,
completed an interview to confirm that life events reported at van Beek, & Wientjes, 1990; Rottenberg, Ray, et al., 2007). HR
Times 1 through 5 fell in the relevant 3-week intervals and that data were manually visually inspected for artifacts with the aid of
events reported met a priori definitional criteria for each event. a channel that computed momentary interbeat interval; artifacts
Follow-up responses at Times 2 through 5 were required to be were manually adjusted as necessary (1% of heartbeats required
completed within a 5-day window surrounding each participants adjustment). RSA was calculated using the well-validated peak-
follow-up target date (i.e., two days on either side of the target valley method (Grossman et al., 1990). The maximum heart rate
date). This approach allowed some flexibility in case participants during the expiration window of respiration was subtracted from
were unable to complete the survey on a given day, but not so the minimum heart rate during the inspiration window of respira-
much time that it would bias the time period over which life events tion. RSA was computed in milliseconds such that higher values
and symptoms were assessed. reflected greater vagal tone (or parasympathetic activity).
To qualify for inclusion in the present multiwave analyses (see Average RSA, HR, and RR were computed separately for each
Data Analysis), participants were required to have completed at experimental period (neutral film #1, sad film, recovery period,
least two of the four possible follow-up assessments, as using at neutral film #2, and amusement film). Given that RR typically is
least three observations is recommended when for the idiographic correlated with RSA and HR (e.g., Overbeek et al., 2012), to
assessment of life events that are centered on each participants examine the possible influence of respiration as a confound, anal-
mean (Abela & Hankin, 2008). This yielded a final sample size of yses were conducted with and without inclusion of RR during the
134. Participants included in the present analyses did not differ relevant periods as a covariate.
from participants excluded from analyses (n 44) on any study Life Events Scale (LES) and Interview (LEI). The LES
variables or demographic characteristics (ps .08). (Alloy & Clements, 1992; Safford, Alloy, Abramson, & Cross-

field, 2007) includes 134 major and minor life events in a variety multilevel modeling (MLM) was used (Raudenbush & Bryk,
of domains relevant to college students (e.g., school, finances, 2002). This design allowed for an idiographic (person-centered)
family, social and romantic relationships). Individuals indicate approach to the measurement of stress, which provides a more
which events have occurred for them over a given time period. The accurate test of vulnerability-stress models of depression than is
validity of these reports is then evaluated objectively by an inter- possible with a nomothetic (sample mean-centered) approach
viewer with the LEI to reduce any problems related to subjective (Abela & Hankin, 2008). Additionally, MLM is advantageous in
report biases. Explicit criteria for event definition and a priori terms of maximizing data usage because it can flexibly handle
probes are provided to the interviewer to help him/her determine cases with missing data, so participants with missing data (e.g.,
whether reported events on the LES meet the criteria of these participants who miss a follow-up visit) are not eliminated from
provided definitions. Any events that do not meet the stringent the data analyses. However, using at least three observations
event definition criteria or that did not occur within the relevant typically is recommended for idiographic assessment of life events
interval(s) are disqualified. For example, one LES item is did that are centered on each participants mean (Abela & Hankin,
poorly on or failed an exam or major project in an important class
2008). Thus, as noted earlier, participants were included only if
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

(i.e., grade less than C). The LEI a priori probes require that the
they had completed at least two follow-up assessments (a total of
This document is copyrighted by the American Psychological Association or one of its allied publishers.

exam or project be worth at least 20% of the final grade to be

three assessments of life events and depressive symptoms when
classified as major. In the event that the exam or project was not
including the baseline assessment). Analyses were conducted with
worth at least 20% of the final grade, or the grade was not less than
the Mplus 6.12 statistical software package (Muthn & Muthn,
a C, the event would be disqualified, thus reducing the subjectivity
of the event (as poorly and major might be interpreted differ- 2011), which allowed for use of full information maximum like-
ently across participants). Interviewers verify the timing of events lihood (FIML) estimation of data (Enders & Bandalos, 2001),
using a variety of strategies to anchor events to days of the week, using maximum likelihood estimation with robust standard errors.
time of year, time during the semester or school break, and in To test the study hypotheses, fluctuations in person-centered life
relation to the timing of other major events. Interviews were events at each wave were evaluated as the focal predictor of
completed by phone or in person by an advanced graduate student, depressive symptoms (BDI) at each wave, with Level 2 observa-
who was blind to individuals autonomic reactivity scores, follow- tions of the six indices of autonomic reactivity at Time 1 serving
ing extensive training and supervision on interview procedures. as moderators (in separate analyses) of this relationship, account-
The LES and LEI have shown excellent reliability and predictive ing for lagged BDI at the previous wave (e.g., controlling for Time
validity (Alloy & Clements, 1992; Boland et al., 2016; Francis- 1 BDI when predicting Time 2 BDI). To compute the measures of
Raniere, Alloy, & Abramson, 2006; Safford et al., 2007; Stange, autonomic reactivity and recovery that were of primary interest in
Hamilton, Abramson, & Alloy, 2014; Weiss et al., 2015). the present study, rather than computing difference scores repre-
Beck Depression Inventory (BDIII; Beck, Steer, Ball, & senting change in RSA and HR across periods, we entered RSA or
Ranieri, 1996). The BDI-II assesses the severity of cognitive, HR as predictors during the current period as well as the previous
affective, and somatic symptoms of depression during the previous period. For example, to assess RSA reactivity to the sad film, RSA
two weeks. It is the most commonly used self-report measure of during the first neutral film and RSA during the sad film were
depressive symptoms and has demonstrated excellent internal con- entered simultaneously as predictors; thus, the value of RSA
sistency and validity in undergraduate samples (Dozois, Dobson, during the sad film represents residual change in RSA after ac-
& Ahnberg, 1998; Storch, Roberti, & Roth, 2004). In the present counting for RSA during the neutral film. To explore the effects of
study, s .87.90 at Times 1 through 5. accounting for respiration rate, we conducted each analysis with
Positive and Negative Affect Scale (PANAS), Brief Version and without RR during the relevant periods as covariates. An
(Mackinnon et al., 1999). The PANASBrief version is a brief, example MLM equation for the analysis of RSA reactivity to
10-item version of the original self-report measure (Watson, Clark, sadness is provided in the Appendix. Significant interactions be-
& Tellegen, 1988) that assesses current emotions and affective
tween indices of autonomic reactivity and negative life events
experiences. Participants indicate the extent to which a number of
were probed by testing the simple slopes of life events on depres-
different affective words describe their current state. It contains
sive symptoms at 1 standard deviation from the mean of the
two subscales, each with five items: positive affect (inspired, alert,
given index of autonomic reactivity (Aiken & West, 1991). Final
excited, enthusiastic, determined) and negative affect (afraid, up-
models included a random intercept and a random slope for the
set, nervous, scared, distressed). The PANAS is a commonly used
measure of affect in experimental studies, and it has excellent relationship between negative life events and symptoms of depres-
validity and reliability (Crawford & Henry, 2004; Watson et al., sion. All measures of autonomic reactivity were standardized.
1988). It was administered as a manipulation check before and Power analyses were conducted a priori following Raudenbush
after each of the film and rest periods in the study to evaluate shifts and Xiao-Feng (2001) using Optimal Design software (Spybrook,
in affect. In the present study, the PANAS had excellent internal Raudenbush, Liu, Congdon, & Martnez, 2006) for multiwave,
consistency across the experimental periods (positive affect repeated-measure longitudinal research designs. We assumed a
.84 .91, negative affect .90 .97). medium effect size given the lack of prior literature evaluating
interactions between autonomic reactivity and life events predict-
ing symptoms of depression. Power analyses suggested that to
Data Analysis
detect significant interactions of moderate effect size with
Given the nested structure of the data (multiple observations of Power .80 and .05, using a 5-time point study a sample size
negative life events and depressive symptoms within each person), of 139 would be required.

Table 1
Descriptive Statistics for Respiratory Sinus Arrhythmia (RSA), Heart Rate (HR), Positive Affect
(PA), and Negative Affect (NA) Across Each Period

Period M SD M SD M SD M SD

Neutral film 1 102.68 58.69 69.16 10.79 13.48 5.24 6.52 3.70
Sad film 92.28 48.24 67.90 10.82 10.76 4.92 8.87 4.32
Recovery period 96.44 49.16 71.92 10.72 11.67 5.41 7.25 4.21
Neutral film 2 95.94 49.95 70.11 10.62 12.08 5.51 6.40 4.00
Amusement film 95.92 46.20 69.46 10.71 13.93 4.90 6.39 4.19
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

Results Prospective Analyses

This document is copyrighted by the American Psychological Association or one of its allied publishers.

Including the baseline assessment, a total of 619 observations were

Preliminary Analyses completed by the 134 participants who completed at least two of the
First, we conducted manipulation checks to evaluate the extent to four follow-up assessments (M 3.62, SD 0.71). Number of
which the emotionally salient films induced the intended emotions. As assessments completed was not related to any study variables. The
expected, compared to the first neutral baseline film, there was an intraclass correlation for an empty model predicting BDI was .651,
increase in negative affect following the sad film (t 9.87, p indicating that 65.1% of the variance in depressive symptoms oc-
.001, d .59), as well as a decrease in positive affect (t 10.36, p curred at the between-subjects level (Level 2), whereas 34.9% of the
.001, d .53). Compared to the sad film, following the recovery variance occurred at the within-subjects level (Level 1).
period there was a significant decrease in negative affect (t 8.57, Results of MLM analyses are presented in Table 3.2 In all models,
p .001, d .38) and an increase in positive affect (t 4.55, p negative life events significantly predicted more symptoms of depres-
.001, d .18). Following the amusement film relative to the second sion. In a model containing only negative life events and lagged BDI
neutral baseline film, there was an increase in positive affect as predictors, negative life events predicted significantly greater levels
(t 7.74, p .001, d .35) and no change in negative affect (t of depressive symptoms (B 0.56, SE 0.05, t 10.61, p .001,
0.42, p .67, d .002). R2 .92, 95% CI for R2 .89 .94).
As expected, participants showed decreases in RSA (t 4.52, p As hypothesized, when controlling for RR, there was a significant
.001, d .19) and HR (t 6.06, p .001, d .12) from the first interaction between RSA reactivity and negative life events (Figure
neutral film to the sad film. From the sad film to the recovery period, 1a), such that negative life events predicted symptoms of depression
there was a marginally significant increase in RSA (t 1.87, p more strongly among individuals with less RSA withdrawal (B
.06, d .08) and a significant increase in HR (t 16.76, p .001, 1.02, SE 0.28, t 3.63, p .001, R2 .40, 95% CI for R2
d .37). From the recovery period to the second neutral film, there .27.52) than among individuals with greater (more contextually
was no significant change in RSA (t 0.27, p .79, d .01), but appropriate) RSA withdrawal (B 0.13, SE 0.30, t 0.42,
there was a significant decrease in HR (t 6.21, p .001, d .17). p .67, R2 .02, 95% CI for R2 .02-.04) to the sad film.3
From the second neutral film to the amusement film, there was no
significant change in RSA (t 0.23, p .82, d .01), but there 1
BDI was positively skewed, as is common in studies of nonclinical
was a small but significant decrease in HR (t 1.98, p .05, d samples. However, values for skewness were within the recommended range
.06). Finally, a comparison of the first neutral film to the second (George & Mallery, 2010) for BDI (1.54) and the residual BDI change score
neutral film revealed that RSA remained significantly lower (t 3.10, (1.17). Sensitivity analyses indicated that removing the most extreme outliers
p .005, d .13) and HR remained significantly higher (t 2.86, (cases in which BDI observations were 3 standard deviations from the mean)
did not alter any of the results meaningfully. For interpretability and consis-
p .005, d .09) during the second neutral film, suggesting that tency with the prior literature, we report results using nontransformed BDI
autonomic recovery from the sad film may not have been complete scores.
following the recovery period (a limitation to which we return in the Although not the primary focus of the manuscript, we also evaluated the
Discussion). As we were more interested in how individual differ- incremental utility of autonomic variables in predicting fluctuations in depres-
sive symptoms beyond self-reported shifts in affect. None of the PANAS
ences in autonomic reactivity predicted vulnerability to depression change variables predicted symptoms of depression as main effects or in
than we were in absolute changes across individuals, we proceeded to interaction with negative life events. Furthermore, controlling for the corre-
test our main hypotheses. sponding PANAS change variables in analyses of autonomic flexibility did not
Overall, participants had relatively low symptoms of depression substantively change the results (all statistically significant results remained
(BDI M 6.90, SD 7.28, range 0 46), but displayed moderate significant). In addition, results were consistent when controlling for other
factors that may influence cardiovascular activity, including body mass index,
levels of negative life events (M 8.64, SD 6.94, range 0 37).1 antidepressant use, any psychiatric medication use, and age (Kemp et al.,
Descriptive statistics for RSA and HR across each period are dis- 2010). Sex did not moderate any of the relationships between autonomic
played in Table 1. Correlations between autonomic variables, BDI, activity and fluctuations in depressive symptoms.
and negative life events at Time 1 are displayed in Table 2. In general, At the suggestion of a reviewer, we also tested for interactions between
baseline RSA (first neutral film) and RSA to the sad film predicting symptoms
increases in RSA were associated with decreases in HR. BDI and of depression. This two-way interaction was not significant, nor was the
negative life events were positively correlated, but were not associated corresponding three-way interaction with life events, with or without control-
with RSA and HR reactivity at Time 1. ling for RR.

Table 2
Correlations Between Depression Symptoms and Negative Life Events at Time 1 and Residual
Change Scores for Respiratory Sinus Arrhythmia (RSA) and Heart Rate (HR) Across
Each Period

Variable 1 2 3 4 5 6 7 8

1. BDI
2. Negative life events .43
3. RSA (sad film) .11 .10
4. RSA (recovery) .01 .10 .37
5. RSA (amusement film) .04 .04 .21 .004
6. HR (sad film) .16 .05 .19 .02 .10
7. HR (recovery) .08 .02 .02 .10 .04 .41
8. HR (amusement film) .11 .02 .02 .06 .14 .21 .32
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

Note. Residual change scores represent RSA or HR for the stated period, controlling for RSA or HR during the
This document is copyrighted by the American Psychological Association or one of its allied publishers.

prior period. BDI Beck Depression Inventory.

p .05. p .01.

However, this interaction was attenuated to nonsignificance when not during recovery from the sad film. When controlling for RR, this
accounting for RR. In contrast, HR reactivity did not predict symp- interaction was reduced to nonsignificance.
toms of depression as a main effect or in interaction with negative life RSA reactivity to the amusement film did not predict symptoms of
events, regardless of whether RR served as a covariate. depression as a main effect or in interaction with negative life events.
RSA recovery did not predict symptoms of depression as a main In contrast, consistent with hypotheses, HR reactivity to the amuse-
effect or in interaction with negative life events, regardless of ment film interacted with negative life events (Figure 1c), such that
whether RR served as a covariate. In contrast, HR recovery from life events predicted symptoms of depression more strongly among
the sad film did interact with life events (Figure 1b), such that life individuals who showed smaller increases in HR (B 0.86, SE
events predicted symptoms of depression among individuals who 0.30, t 2.88, p .01, R2 .34, 95% CI for R2 .21.47), than
showed larger increases in HR (B 1.34, SE 0.40, t 3.36, among individuals who showed larger (more contextually appropri-
p .001, R2 .41, 95% CI for R2 .29 .54), but not among ate) increases in HR (B 0.23, SE 0.14, t 1.12, p .26, R2
individuals who showed smaller increases in HR (B 0.42, SE .07, 95% CI for R2 .01.16) during the amusement film. This
0.36, t 1.16, p .25, R2 .08, 95% CI for R2 .01.16) interaction maintained significance when controlling for RR.

Table 3
Results of Hierarchical Linear Regression Models Assessing Main Effects and Interactions With Negative Life Events for Fluctuations
in Respiratory Sinus Arrhythmia (RSA) and Heart Rate (HR) to Sadness, Recovery From Sadness, and Amusement, Predicting
Symptoms of Depression Across Five Waves of Observation Over 12 Weeks

Main effect Interaction with negative life events

2 2
Model Predictor B SE p R 95% CI for R B SE p R2 95% CI for R2

Reactivity to sad film

1 RSA 1.14 1.28 .43 .07 .01.16 .21 .26 .43 .06 .02.14
2 RSA (controlling RR) 2.69 1.54 .08 .18 .06.30 .57 .27 .04 .24 .11.36
3 HR 4.68 2.70 .08 .16 .05.27 .35 .19 .07 .17 .06.29
4 HR (controlling RR) 4.71 2.67 .08 .13 .03.24 .29 .17 .08 .13 .03.23

Recovery from sad film

5 RSA 1.72 1.09 .12 .13 .03.24 .05 .13 .99 0 00
6 RSA (controlling RR) 1.06 .61 .77 .004 .02.03 .04 .15 .78 .06 .02.14
7 HR 1.07 1.85 .56 .02 .03.07 .88 .37 .02 .26 .14.39
8 HR (controlling RR) 1.12 1.84 .54 .02 .03.06 .59 .38 .12 .11 .01.20

Reactivity to amusement film

9 RSA .79 .82 .34 .03 .02.09 .01 .08 .95 0 00
10 RSA (controlling RR) .41 1.21 .74 .01 .02.03 .01 .11 .95 .001 .01.01
11 HR 1.79 1.01 .08 .16 .05.27 .23 .09 .01 .28 .15.40
12 HR (controlling RR) 1.82 1.08 .09 .12 .02.23 .24 .10 .01 .24 .11.36
Note. R2 partial R2 of focal predictor (proportion of variance in depression symptoms predicted) after accounting for covariates. In all models, RSA
or HR represents the value during the specified period, while controlling for the relevant value during the prior period (e.g., in Model 1, controlling RSA
during neutral film when RSA to sad film is focal predictor).

a Sad Film

Prospective Depression Sx
Smaller Decrease in RSA
6 Larger Decrease in RSA
Fewer Neg. Events More Neg. Events
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

b Recovery Period
This document is copyrighted by the American Psychological Association or one of its allied publishers.

Prospective Depression Sx

Larger Increase in HR
6 Smaller Increase in HR
Fewer Neg. Events More Neg. Events

c Amusement Film
Prospective Depression Sx

Smaller Increase in HR
6 Larger Increase in HR
Fewer Neg. Events More Neg. Events

Figure 1. Interactions between negative life events and (a) respiratory sinus arrhythmia (RSA) reactivity to a
sad film, (b) heart rate (HR) recovery from a sad film, and (c) HR reactivity to an amusing film, predicting
symptoms of depression across five waves of observation. Error bars represent standard errors of the simple
slopes of the relationship between negative life events and prospective symptoms of depression, at high and low
levels of the moderator. See the online article for the color version of this figure.

Discussion stressful events. Consistent with hypotheses, RSA withdrawal to

the amusing film was not associated with future symptoms of
The present study represented the first complete test of compo-
depression. Finally, consistent with hypotheses, attenuated heart
nents of atypical autonomic reactivity to loss and amusement as
rate reactivity to amusement was associated with vulnerability to
vulnerability factors for depression in the context of negative life
depression in the context of stressful events. These results provide
events, using a multiwave prospective study design. Consistent
initial evidence that differential patterns of autonomic reactivity
with hypotheses, we found that less contextually appropriate vagal
withdrawal to sadness was associated with greater levels of de- may not only characterize current depression (Rottenberg, 2007),
pressive symptoms when individuals were exposed to recent life but may actually constitute vulnerability to future symptoms of
stressors, but only when accounting for effects of respiration. depression, above and beyond current depressive symptoms.
Inconsistent with hypotheses, neither smaller reductions in HR to Results with RSA reactivity to the sad film suggest that the lack
the sad film nor attenuated RSA augmentation during recovery of ability to engage with sad stimuli may be an important indicator
from the sad film predicted future symptoms of depression. Our of vulnerability. The rapid withdrawal of the vagal brake is thought
exploratory analyses with HR recovery from the sad film showed to help individuals to meet changing environmental demands, such
that individuals with greater increases in HR during recovery from as responding to physical activity, increasing attention and infor-
sadness had greater vulnerability to depression in the context of mation processing (Suess, Porges, & Plude, 1994), and coping

with negative emotion (Beauchaine, 2001). Indeed, prior empirical depression. This contrasts with a recent study of children (Somers
work suggests that RSA reactivity to sadness is positively associ- et al., 2015), but is consistent with a null finding in a study of
ated with the ability to engage with sad stimuli and adaptively adults receiving treatment for current MDD (Rottenberg et al.,
regulate emotions (Gentzler et al., 2009; LeMoult et al., 2016; 2002). Given that HR decreases to sad films likely are influenced
Yaroslavsky, Bylsma, Rottenberg, & Kovacs, 2013). It is possible by many sources, including parasympathetic and sympathetic ac-
that RSA reactivity to sadness reflects emotional and behavioral tivity, sadness following loss, and concerned attention (Berntson et
adaptability which facilitates goal-directed behavior (e.g., attend- al., 1997; Eisenberg et al., 1989; Gross & Levenson, 1997;
ing to sad stimuli when relevant, or preparing the body for a Kreibig, 2010; Overbeek et al., 2012; Rottenberg, 2007), it may be
regulatory response), a capacity that likely is useful when encoun- difficult to detect relationships between HR reactivity and vulner-
tering negative life events throughout life (Kashdan & Rottenberg, ability to depression in this context. It is possible that using a more
2010; Thayer & Lane, 2009). Thus, RSA reactivity may be an pure measure of sympathetic activity (Berntson et al., 1997;
important substrate for flexible behavior in response to environ- Kreibig, 2010; Mezzacappa et al., 2001) would help to elucidate
mental and emotional changes. Given that in some prior work patterns of sympathetic reactivity that confer vulnerability to de-
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

(e.g., Bylsma et al., 2014; Salomon et al., 2013) attenuated RSA pression. In addition, future work could evaluate autonomic re-
This document is copyrighted by the American Psychological Association or one of its allied publishers.

reactivity to sadness was associated more with current MDD than sponses to anticipated losses (when activating responses are
with remitted MDD, it is possible that attenuated RSA reactivity expected; Kreibig, 2010) rather than after loss has occurred as a
represents a short-term, state-like vulnerability similar to a depres- predictor of vulnerability.
sive prodrome, which may be particularly likely to lead to the In contrast, individuals with greater increases in HR during
onset of depression following exposure to stressful environmental recovery from the sad film were more likely to experience pro-
contexts. Future studies are needed to establish the temporal sta- spective symptoms of depression under conditions of stress than
bility of RSA reactivity to sadness, and to track how it may change were individuals with smaller increases in HR. To our knowledge,
within individuals across different mood states. Interestingly, at- our study is the first to evaluate this question. Although some
tenuated RSA withdrawal to the sad film only appeared to confer increase in HR during the recovery period was expected to be
vulnerability to depression in analyses that controlled for respira- adaptive as attention no longer was drawn to the film, exaggerated
tion. Prior researchers have argued that it is important to account
HR increases could represent increased regulatory effort (Frazier
for respiration when evaluating effects of autonomic constructs, as
et al., 2004; Obrist, 1981; Overbeek et al., 2012) or greater use of
respiration rate impacts RSA (Overbeek et al., 2012) and could
maladaptive regulatory strategies such as expressive suppression
represent regulatory effort that is independent of true vagal with-
or rumination which inhibit autonomic recovery (Gross & Leven-
drawal. The present results suggest that respiration rate could
son, 1997; LeMoult et al., 2016). However, it is important to
suppress the relationship between RSA and depression vulnerabil-
reiterate that HR likely is influenced by multiple autonomic and
ity, as the relationship between attenuated RSA withdrawal and
psychological processes, so these interpretations of the effects of
vulnerability only was apparent after removing variance associated
HR recovery in the present study are admittedly speculative.
with respiration.
Nevertheless, these results could suggest that individuals who lack
RSA recovery from the sad film was not associated with vul-
the ability to efficiently and effectively regulate physiological
nerability to depression across follow-up. This contrasts with prior
cross-sectional work that found that individuals with MDD responses to sadness may be more prone to experiencing pro-
showed attenuated recovery of RSA during crying (Rottenberg et longed periods of distress such as depression, particularly follow-
al., 2003) and during a stressor task (Rottenberg, Clift, et al., ing difficult experiences (e.g., negative events) that elicit sadness.
2007), relative to controls. However, to our knowledge, no other Consistent with hypotheses, blunted HR reactivity to amuse-
prospective studies to date have evaluated RSA recovery from ment conferred vulnerability to depression in the context of neg-
sadness as a predictor of depression course. It is possible that ative life events. This result extends prior work in individuals with
attenuated RSA recovery is a marker of a current depressive state current MDD that found that attenuated HR reactivity to amuse-
rather than a vulnerability to later depression. In addition, RSA ment predicted a lower likelihood of recovery from depression
reactivity to the amusement film also did not predict symptoms of (Rottenberg et al., 2002). These findings are consistent with per-
depression across follow-up, suggesting specificity of RSA reac- spectives suggesting that a lack of HR reactivity reflects blunted
tivity as a vulnerability factor in the context of sadness. Although activity in the behavioral approach system (Fowles, Fisher, &
vagal withdrawal is expected in amusement contexts, sadness Tranel, 1982; Kasch, Rottenberg, Arnow, & Gotlib, 2002). In
typically elicits greater withdrawal (Overbeek et al., 2012); thus, contexts during which amusement is expected, the approach sys-
atypical RSA fluctuations in response to sad films may be more tem may be sensitive to signals of impending reward and to actual
detectable and more relevant to depression vulnerability. Indeed, reward (Fowles et al., 1982). Given that blunted hedonic capacity
prior prospective studies in current MDD have demonstrated that is common in MDD (Pizzagalli, 2013), the present results could
RSA reactivity to amusement was not associated with illness suggest that similar processes are reflected in attenuated HR reac-
course (Fraguas et al., 2007; Panaite et al., 2016; Rottenberg et al., tivity to amusement, which also may characterize vulnerability to
2005). The present study represents the first to evaluate individual future depression. Thus, autonomic reactivity is relevant to eval-
differences in RSA reactivity to amusement as a vulnerability uating components of the positive valence system (e.g., approach
factor for future depressive symptoms in the context of negative motivation, responsiveness to reward), in addition to the negative
life events, finding no evidence of such a relationship. valence system (e.g., loss) and the arousal and modulatory systems
With respect to HR reactivity to the sad film, we did not find that are proposed by NIMHs Research Domain Criteria (RDoC)
evidence that attenuated withdrawal conferred vulnerability to initiative (Sanislow et al., 2010; Beauchaine & Thayer, 2015).

The results of the present study suggest that evaluating auto- the dimensional structure of depression (e.g., Liu, 2016), the
nomic reactivity may be useful for identifying individuals who are immediate clinical significance of the present results is not clear
vulnerable to experiencing symptoms of depression following (although findings in clinical samples have paralleled those in the
stressors, and who may benefit from interventions to attenuate risk. present study; e.g., Fraguas et al., 2007; Panaite et al., 2016;
Biofeedback is one intervention that has promise for helping Rottenberg et al., 2002, 2005). In addition, although our primary
individuals to directly improve their autonomic activity in re- findings remained after accounting for potential confounds of
sponse to emotional stimuli (Karavidas et al., 2007; Nolan et al., autonomic activity such as respiration, antidepressant use, BMI,
2005; Siepmann, Aykac, Unterdrfer, Petrowski, & Mueck- and age, we cannot rule out other possible confounds such as
Weymann, 2008). Future work also should explore the extent to physical activity and smoking. Finally, although the present study
which existing psychosocial treatments can improve autonomic evaluated vulnerability for depression, atypical autonomic reactiv-
reactivity indirectly, perhaps by improving mindfulness (e.g., ity also holds promise as a potential transdiagnostic factor that may
present-moment awareness of emotional states) or the ability to be implicated in other types of psychopathology, including anxiety
engage temporarily with sad stimuli. It is possible that the use of disorders (Beauchaine & Thayer, 2015).
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

strategies to reduce extended engagement following sadness (e.g., Despite these limitations, the present study had numerous
This document is copyrighted by the American Psychological Association or one of its allied publishers.

training reappraisal or distraction rather than rumination) would strengths. We evaluated fluctuations in both RSA and HR in
help to attenuate maladaptive HR recovery following sadness, response to different types of emotional contexts relevant to the
thereby reducing risk. Neurocognitive approaches also hold prom- core features of depression relative to neutral baseline periods, and
ise for improving autonomic activity. For example, repetitive controlled for respiration, self-reported affect shifts, and other
transcranial magnetic stimulation may be able to directly improve potential confounds. We also used a multiwave design to evaluate
autonomic reactivity to stress (e.g., Remue et al., 2016), and interactions between naturally occurring negative life events and
attentional control training (e.g., Siegle et al., 2014; Wells, 2011) autonomic reactivity when predicting prospective fluctuations in
could help people to learn to disengage from repetitive negative depression, using a person-centered approach to assessing fluctu-
thinking. ations in negative events, which allowed for strong tests of the
The current study has a number of limitations. Video clip order vulnerability-stress model that have not been tested in the literature
was not counterbalanced, given that we wanted participants to end to date.
the study on a positive note (the amusement film) for ethical The present study provides the most complete test to date of
reasons; nevertheless, there appeared to be autonomic carry-over atypical autonomic reactivity as a vulnerability to future depres-
effects from the sad film that were not resolved before the amuse- sion, with a number of methodological improvements on the
ment film, so the autonomic responses to the amusement film must existing literature. Our results suggest that components of auto-
be interpreted with this important caveat in mind. In addition, as nomic reactivity may serve as protective factors against depression
we were more interested in recovery from sadness given its theo- when individuals encounter stressful life events. Alternatively,
retical relevance to depression, and in part due to time constraints individuals with deficits in autonomic reactivity may be vulnerable
of the study session, we did not assess autonomic and affective to experiencing symptoms of depression following recent stres-
responses during a similar recovery period following the amuse- sors. However, the precise psychological mechanisms of these
ment film. This limits the ability to determine whether autonomic autonomic constructs require further study. These results also lend
responses during recovery from the sad film are specific to sadness support to theories of self-regulation that suggest the importance of
versus applicable to other emotions. It also is important to note that context in determining when regulatory strategies are likely to lead
video clips that are experimentally intended to be neutral in to adaptive versus maladaptive outcomes (e.g., Aldao, 2013; Al-
valence may in fact elicit other emotions (e.g., awe or interest; dao, Sheppes, & Gross, 2015; Bonanno & Burton, 2013). In
Rottenberg, Ray, et al., 2007; Shiota, Neufeld, Yeung, Moser, & conclusion, the present study suggests that evaluating psychophys-
Perea, 2011); thus, the ecological validity of these indices of iological components of flexibility in response to shifts in envi-
autonomic reactivity and recovery to real-world responses to loss ronmental and emotional context holds promise for improving our
and amusement is not entirely clear. We also did not evaluate understanding of the pathophysiology of depression and for tar-
behavioral responses to the films, such as crying or laughing; this geting these mechanisms to reduce the personal and societal im-
would have provided useful contextual information, given that pact of this illness.
crying is associated with increases in sympathetic activation dur-
ing sadness (Kreibig, 2010; Rottenberg et al., 2008; Vingerhoets &
Bylsma, 2016) as well as improved vagal augmentation during
periods of recovery from sadness in healthy individuals, but not in Abela, J. R. Z., & Hankin, B. L. (2008). Cognitive vulnerability to
depressed individuals (Rottenberg et al., 2003). depression in children and adolescents: A developmental psychopathol-
In addition, the study sample was composed of university stu- ogy perspective. In J. R. Z. Abela & B. L. Hankin (Eds.), Handbook of
dents; although there are high rates of depression in college stu- depression in children and adolescents (pp. 3578). New York, NY:
dents and substantial variability in stressors between individuals as Guilford Press.
Abramson, L. Y., Alloy, L. B., Hankin, B. L., Haeffel, G. J., MacCoon,
well as within individuals across the course of semesters, the
D. G., & Gibb, B. E. (2002). Cognitive vulnerability-stress models of
results cannot necessarily be extended to the general public. We depression in a self-regulatory and psychobiological context. In I. H.
also examined fluctuations in symptoms of depression rather than Gotlib & C. L. Hammen (Eds.), Handbook of depression (pp. 268 294).
clinically significant depressive episodes; although evaluating de- New York, NY: Guilford Press.
pression on a continuum resulted in greater potential power to Aiken, L. S., & West, S. G. (1991). Multiple regression: Testing and
detect nuanced effects and is consistent with evidence supporting interpreting interactions. Newbury Park, CA: SAGE.

Aldao, A. (2013). The future of emotion regulation research: Capturing Dozois, D. J., Dobson, K. S., & Ahnberg, J. L. (1998). A psychometric
context. Perspectives on Psychological Science, 8, 155172. http://dx evaluation of the Beck Depression InventoryII. Psychological Assess-
.doi.org/10.1177/1745691612459518 ment, 10, 83 89. http://dx.doi.org/10.1037/1040-3590.10.2.83
Aldao, A., Sheppes, G., & Gross, J. J. (2015). Emotion regulation flexi- Eisenberg, N., Fabes, R. A., Miller, P. A., Fultz, J., Shell, R., Mathy, R. M.,
bility. Cognitive Therapy and Research, 39, 263278. http://dx.doi.org/ & Reno, R. R. (1989). Relation of sympathy and personal distress to
10.1007/s10608-014-9662-4 prosocial behavior: A multimethod study. Journal of Personality and
Allen, N. B., Kuppens, P., & Sheeber, L. B. (2012). Heart rate responses Social Psychology, 57, 55 66. http://dx.doi.org/10.1037/0022-3514.57
to parental behavior in depressed adolescents. Biological Psychology, .1.55
90, 80 87. http://dx.doi.org/10.1016/j.biopsycho.2012.02.013 El-Sheikh, M., Hinnant, J. B., & Erath, S. A. (2015). Vi. Marital conflict,
Alloy, L. B., & Clements, C. M. (1992). Illusion of control: Invulnerability vagal regulation, and childrens sleep: A longitudinal investigation.
to negative affect and depressive symptoms after laboratory and natural Monographs of the Society for Research in Child Development, 80,
stressors. Journal of Abnormal Psychology, 101, 234 245. http://dx.doi 89 106. http://dx.doi.org/10.1111/mono.12146
.org/10.1037/0021-843X.101.2.234 El-Sheikh, M., & Whitson, S. A. (2006). Longitudinal relations between
Beauchaine, T. (2001). Vagal tone, development, and Grays motivational marital conflict and child adjustment: Vagal regulation as a protective
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

theory: Toward an integrated model of autonomic nervous system func- factor. Journal of Family Psychology, 20, 30 39. http://dx.doi.org/10
This document is copyrighted by the American Psychological Association or one of its allied publishers.

tioning in psychopathology. Development and Psychopathology, 13, .1037/0893-3200.20.1.30

183214. http://dx.doi.org/10.1017/S0954579401002012 Enders, C. K., & Bandalos, D. L. (2001). The relative performance of full
Beauchaine, T. P., & Thayer, J. F. (2015). Heart rate variability as a information maximum likelihood estimation for missing data in struc-
transdiagnostic biomarker of psychopathology. International Journal of tural equation models. Structural Equation Modeling, 8, 430 457.
Psychophysiology, 98, 338 350. http://dx.doi.org/10.1016/j.ijpsycho Fowles, D. C., Fisher, A. E., & Tranel, D. T. (1982). The heart beats to reward: The
.2015.08.004 effect of monetary incentive on heart rate. Psychophysiology, 19, 506513.
Beck, A. T., Steer, R. A., Ball, R., & Ranieri, W. (1996). Comparison of http://dx.doi.org/10.1111/j.1469-8986.1982.tb02577.x
Beck Depression InventoriesIA and II in psychiatric outpatients. Jour- Fraguas, R., Jr., Marci, C., Fava, M., Iosifescu, D. V., Bankier, B., Loh, R.,
nal of Personality Assessment, 67, 588 597. http://dx.doi.org/10.1207/ & Dougherty, D. D. (2007). Autonomic reactivity to induced emotion as
s15327752jpa6703_13 potential predictor of response to antidepressant treatment. Psychiatry
Berntson, G. G., Bigger, J. T., Jr., Eckberg, D. L., Grossman, P., Kauf- Research, 151, 169 172. http://dx.doi.org/10.1016/j.psychres.2006.08
mann, P. G., Malik, M., . . . van der Molen, M. W. (1997). Heart rate .008
variability: Origins, methods, and interpretive caveats. Psychophysiol- Francis-Raniere, E. L., Alloy, L. B., & Abramson, L. Y. (2006). Depressive
ogy, 34, 623 648. http://dx.doi.org/10.1111/j.1469-8986.1997 personality styles and bipolar spectrum disorders: Prospective tests of
.tb02140.x the event congruency hypothesis. Bipolar Disorders, 8, 382399. http://
Berntson, G. G., Cacioppo, J. T., & Grossman, P. (2007). Whither vagal dx.doi.org/10.1111/j.1399-5618.2006.00337.x
tone. Biological Psychology, 74, 295300. Frazier, T. W., Strauss, M. E., & Steinhauer, S. R. (2004). Respiratory
Boland, E. M., Stange, J. P., Labelle, D. R., Shapero, B. G., Weiss, R. B., sinus arrhythmia as an index of emotional response in young adults.
Abramson, L. Y., & Alloy, L. B. (2016). Affective disruption from Psychophysiology, 41, 75 83. http://dx.doi.org/10.1046/j.1469-8986
social rhythm and behavioral approach system (BAS) sensitivities: A .2003.00131.x
test of the integration of the social zeitgeber and BAS theories of bipolar Gentzler, A. L., Santucci, A. K., Kovacs, M., & Fox, N. A. (2009).
disorder. Clinical Psychological Science, 4, 418 432. http://dx.doi.org/ Respiratory sinus arrhythmia reactivity predicts emotion regulation and
10.1177/2167702615603368 depressive symptoms in at-risk and control children. Biological Psychol-
Bonanno, G. A., & Burton, C. L. (2013). Regulatory flexibility: An ogy, 82, 156 163. http://dx.doi.org/10.1016/j.biopsycho.2009.07.002
individual differences perspective on coping and emotion regulation. George, D., & Mallery, M. (2010). SPSS for Windows step by step: A
Perspectives on Psychological Science, 8, 591 612. http://dx.doi.org/10 simple guide and reference, 17.0 update (10th ed.). Boston, MA: Pear-
.1177/1745691613504116 son.
Bosch, N. M., Riese, H., Ormel, J., Verhulst, F., & Oldehinkel, A. J. Gross, J. J., & Levenson, R. W. (1997). Hiding feelings: The acute effects
(2009). Stressful life events and depressive symptoms in young adoles- of inhibiting negative and positive emotion. Journal of Abnormal Psy-
cents: Modulation by respiratory sinus arrhythmia? The TRAILS study. chology, 106, 95103. http://dx.doi.org/10.1037/0021-843X.106.1.95
Biological Psychology, 81, 40 47. http://dx.doi.org/10.1016/j Grossman, P., van Beek, J., & Wientjes, C. (1990). A comparison of three
.biopsycho.2009.01.005 quantification methods for estimation of respiratory sinus arrhythmia.
Bylsma, L. M., Morris, B. H., & Rottenberg, J. (2008). A meta-analysis of Psychophysiology, 27, 702714. http://dx.doi.org/10.1111/j.1469-8986
emotional reactivity in major depressive disorder. Clinical Psychology .1990.tb03198.x
Review, 28, 676 691. http://dx.doi.org/10.1016/j.cpr.2007.10.001 Hopp, H., Shallcross, A. J., Ford, B. Q., Troy, A. S., Wilhelm, F. H., &
Bylsma, L. M., Salomon, K., Taylor-Clift, A., Morris, B. H., & Rottenberg, Mauss, I. B. (2013). High cardiac vagal control protects against future
J. (2014). Respiratory sinus arrhythmia reactivity in current and remitted depressive symptoms under conditions of high social support. Biological
major depressive disorder. Psychosomatic Medicine, 76, 66 73. http:// Psychology, 93, 143149. http://dx.doi.org/10.1016/j.biopsycho.2013.01
dx.doi.org/10.1097/PSY.0000000000000019 .004
Cacioppo, J. T., Uchino, B. N., & Berntson, G. G. (1994). Individual Just, N., Abramson, L. Y., & Alloy, L. B. (2001). Remitted depression
differences in the autonomic origins of heart rate reactivity: The psy- studies as tests of the cognitive vulnerability hypotheses of depression
chometrics of respiratory sinus arrhythmia and preejection period. Psy- onset: A critique and conceptual analysis. Clinical Psychology Review,
chophysiology, 31, 412 419. http://dx.doi.org/10.1111/j.1469-8986 21, 63 83. http://dx.doi.org/10.1016/S0272-7358(99)00035-5
.1994.tb02449.x Karavidas, M. K., Lehrer, P. M., Vaschillo, E., Vaschillo, B., Marin, H.,
Crawford, J. R., & Henry, J. D. (2004). The positive and negative affect Buyske, S., . . . Hassett, A. (2007). Preliminary results of an open label
schedule (PANAS): Construct validity, measurement properties and study of heart rate variability biofeedback for the treatment of major
normative data in a large non-clinical sample. British Journal of Clinical depression. Applied Psychophysiology and Biofeedback, 32, 19 30.
Psychology, 43, 245265. http://dx.doi.org/10.1348/0144665031752934 http://dx.doi.org/10.1007/s10484-006-9029-z

Kasch, K. L., Rottenberg, J., Arnow, B. A., & Gotlib, I. H. (2002). Obrist, P. (1981). Cardiovascular psychophysiology. New York, NY: Ple-
Behavioral activation and inhibition systems and the severity and course num Press. http://dx.doi.org/10.1007/978-1-4684-8491-5
of depression. Journal of Abnormal Psychology, 111, 589 597. http:// Overbeek, T. J., van Boxtel, A., & Westerink, J. H. (2012). Respiratory
dx.doi.org/10.1037/0021-843X.111.4.589 sinus arrhythmia responses to induced emotional states: Effects of RSA
Kashdan, T. B., & Rottenberg, J. (2010). Psychological flexibility as a indices, emotion induction method, age, and sex. Biological Psychology,
fundamental aspect of health. Clinical Psychology Review, 30, 865 878. 91, 128 141. http://dx.doi.org/10.1016/j.biopsycho.2012.05.011
http://dx.doi.org/10.1016/j.cpr.2010.03.001 Panaite, V., Hindash, A. C., Bylsma, L. M., Small, B. J., Salomon, K., &
Kemp, A. H., Quintana, D. S., Gray, M. A., Felmingham, K. L., Brown, K., Rottenberg, J. (2016). Respiratory sinus arrhythmia reactivity to a sad
& Gatt, J. M. (2010). Impact of depression and antidepressant treatment film predicts depression symptom improvement and symptomatic tra-
on heart rate variability: A review and meta-analysis. Biological Psy- jectory. International Journal of Psychophysiology, 99, 108 113. http://
chiatry, 67, 10671074. http://dx.doi.org/10.1016/j.biopsych.2009.12 dx.doi.org/10.1016/j.ijpsycho.2015.12.002
.012 Pizzagalli, D. A. (2014). Depression, stress, and anhedonia: Toward a
Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Causal synthesis and integrated model. Annual Review of Clinical Psychology,
relationship between stressful life events and the onset of major depres- 10, 393 423. http://dx.doi.org/10.1146/annurev-clinpsy-050212-185606
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

sion. The American Journal of Psychiatry, 156, 837 841. http://dx.doi Porges, S. W. (2007). The polyvagal perspective. Biological Psychology,
This document is copyrighted by the American Psychological Association or one of its allied publishers.

.org/10.1176/ajp.156.6.837 74, 116 143. http://dx.doi.org/10.1016/j.biopsycho.2006.06.009

Kessler, R. C., Akiskal, H. S., Ames, M., Birnbaum, H., Greenberg, P., Raudenbush, S. W., & Bryk, A. S. (2002). Hierarchical linear models:
Hirschfeld, R. M., . . . Wang, P. S. (2006). Prevalence and effects of Applications and data analysis methods (2nd ed.). Thousand Oaks, CA:
mood disorders on work performance in a nationally representative SAGE.
sample of U.S. workers. The American Journal of Psychiatry, 163, Raudenbush, S. W., & Xiao-Feng, L. (2001). Effects of study duration,
15611568. http://dx.doi.org/10.1176/ajp.2006.163.9.1561 frequency of observation, and sample size on power in studies of group
Kessler, R. C., Chiu, W. T., Demler, O., Merikangas, K. R., & Walters, differences in polynomial change. Psychological Methods, 6, 387 401.
E. E. (2005). Prevalence, severity, and comorbidity of 12-month http://dx.doi.org/10.1037/1082-989X.6.4.387
DSMIV disorders in the National Comorbidity Survey Replication. Remue, J., Vanderhasselt, M. A., Baeken, C., Rossi, V., Tullo, J., & De
Archives of General Psychiatry, 62, 617 627. http://dx.doi.org/10.1001/ Raedt, R. (2016). The effect of a single HF-rTMS session over the left
archpsyc.62.6.617 DLPFC on the physiological stress response as measured by heart rate
Kessler, R. C., & Wang, P. S. (2009). Epidemiology of depression. In I. H. variability. Neuropsychology, 30, 756 766. http://dx.doi.org/10.1037/
Gotlib & C. L. Hammen (Eds.), Handbook of depression (2nd ed., pp. neu0000255
522). New York, NY: Guilford Press. Rottenberg, J. (2007). Cardiac vagal control in depression: A critical
Kreibig, S. D. (2010). Autonomic nervous system activity in emotion: A analysis. Biological Psychology, 74, 200 211. http://dx.doi.org/10
review. Biological Psychology, 84, 394 421. http://dx.doi.org/10.1016/ .1016/j.biopsycho.2005.08.010
j.biopsycho.2010.03.010 Rottenberg, J., Bylsma, L. M., & Vingerhoets, A. J. (2008). Is crying
Kreibig, S. D., Wilhelm, F. H., Roth, W. T., & Gross, J. J. (2007). beneficial? Current Directions in Psychological Science, 17, 400 404.
Cardiovascular, electrodermal, and respiratory response patterns to fear- http://dx.doi.org/10.1111/j.1467-8721.2008.00614.x
and sadness-inducing films. Psychophysiology, 44, 787 806. Rottenberg, J., Clift, A., Bolden, S., & Salomon, K. (2007). RSA fluctu-
LeMoult, J., Yoon, K. L., & Joormann, J. (2016). Rumination and cogni- ation in major depressive disorder. Psychophysiology, 44, 450 458.
tive distraction in major depressive disorder: An examination of respi- http://dx.doi.org/10.1111/j.1469-8986.2007.00509.x
ratory sinus arrhythmia. Journal of Psychopathology and Behavioral Rottenberg, J., & Hindash, A. C. (2015). Emerging evidence for emotion
Assessment, 38, 20 29. context insensitivity in depression. Current Opinion in Psychology, 4,
Liu, R. T. (2016). Taxometric evidence of a dimensional latent structure for 15. http://dx.doi.org/10.1016/j.copsyc.2014.12.025
depression in an epidemiological sample of children and adolescents. Rottenberg, J., Kasch, K. L., Gross, J. J., & Gotlib, I. H. (2002). Sadness
Psychological Medicine, 46, 12651275. http://dx.doi.org/10.1017/ and amusement reactivity differentially predict concurrent and prospec-
S0033291715002792 tive functioning in major depressive disorder. Emotion, 2, 135146.
Mackinnon, A., Jorm, A. F., Christensen, H., Korten, A. E., Jacomb, P. A., & http://dx.doi.org/10.1037/1528-3542.2.2.135
Rodgers, B. (1999). A short form of the Positive and Negative Affect Schedule: Rottenberg, J., Ray, R. D., & Gross, J. J. (2007). Emotion elicitation using
Evaluation of factorial validity and invariance across demographic variables in films. In J. A. Coan & J. J. B. Allen (Eds.), Handbook of emotion
a community sample. Personality and Individual Differences, 27, 405416. elicitation and assessment. New York, NY: Oxford University Press.
http://dx.doi.org/10.1016/S0191-8869(98)00251-7 Rottenberg, J., Salomon, K., Gross, J. J., & Gotlib, I. H. (2005). Vagal
Mezzacappa, E. S., Kelsey, R. M., Katkin, E. S., & Sloan, R. P. (2001). withdrawal to a sad film predicts subsequent recovery from depression.
Vagal rebound and recovery from psychological stress. Psychoso- Psychophysiology, 42, 277281. http://dx.doi.org/10.1111/j.1469-8986
matic Medicine, 63, 650 657. http://dx.doi.org/10.1097/00006842- .2005.00289.x
200107000-00018 Rottenberg, J., Wilhelm, F. H., Gross, J. J., & Gotlib, I. H. (2003). Vagal
Morgan, J. K., Shaw, D. S., & Forbes, E. E. (2013). Physiological and rebound during resolution of tearful crying among depressed and non-
behavioral engagement in social contexts as predictors of adolescent depressed individuals. Psychophysiology, 40, 1 6. http://dx.doi.org/10
depressive symptoms. Journal of Youth and Adolescence, 42, 1117 .1111/1469-8986.00001
1127. http://dx.doi.org/10.1007/s10964-012-9815-2 Safford, S. M., Alloy, L. B., Abramson, L. Y., & Crossfield, A. G. (2007).
Muthn, L. K., & Muthn, B. O. (1998 2011). Mplus users guide (6th Negative cognitive style as a predictor of negative life events in
ed.). Los Angeles, CA: Author. depression-prone individuals: A test of the stress generation hypothesis.
Nolan, R. P., Kamath, M. V., Floras, J. S., Stanley, J., Pang, C., Picton, P., Journal of Affective Disorders, 99(13), 147154. http://dx.doi.org/10
& Young, Q. R. (2005). Heart rate variability biofeedback as a behav- .1016/j.jad.2006.09.003
ioral neurocardiac intervention to enhance vagal heart rate control. Salomon, K., Bylsma, L. M., White, K. E., Panaite, V., & Rottenberg, J.
American Heart Journal, 149, 1137. http://dx.doi.org/10.1016/j.ahj.2005 (2013). Is blunted cardiovascular reactivity in depression mood-state
.03.015 dependent? A comparison of major depressive disorder remitted depres-

sion and healthy controls. International Journal of Psychophysiology, Suess, P. E., Porges, S. W., & Plude, D. J. (1994). Cardiac vagal tone and
90, 50 57. http://dx.doi.org/10.1016/j.ijpsycho.2013.05.018 sustained attention in school-age children. Psychophysiology, 31, 1722.
Sanislow, C. A., Pine, D. S., Quinn, K. J., Kozak, M. J., Garvey, M. A., Taylor, C. B. (2010). Depression, heart rate related variables and cardio-
Heinssen, R. K., . . . Cuthbert, B. N. (2010). Developing constructs for vascular disease. International Journal of Psychophysiology, 78, 80 88.
psychopathology research: Research domain criteria. Journal of Abnor- http://dx.doi.org/10.1016/j.ijpsycho.2010.04.006
mal Psychology, 119, 631 639. http://dx.doi.org/10.1037/a0020909 Thayer, J. F., hs, F., Fredrikson, M., Sollers, J. J., III, & Wager, T. D.
Shiota, M. N., Neufeld, S. L., Yeung, W. H., Moser, S. E., & Perea, E. F. (2012). A meta-analysis of heart rate variability and neuroimaging
(2011). Feeling good: Autonomic nervous system responding in five studies: Implications for heart rate variability as a marker of stress and
positive emotions. Emotion, 11, 1368 1378. http://dx.doi.org/10.1037/ health. Neuroscience and Biobehavioral Reviews, 36, 747756. http://
a0024278 dx.doi.org/10.1016/j.neubiorev.2011.11.009
Siegle, G. J., Price, R. B., Jones, N. P., Ghinassi, F., Painter, T., & Thase, Thayer, J. F., Hansen, A. L., Saus-Rose, E., & Johnsen, B. H. (2009). Heart
M. E. (2014). You gotta work at it pupillary indices of task focus are rate variability, prefrontal neural function, and cognitive performance:
prognostic for response to a neurocognitive intervention for rumination The neurovisceral integration perspective on self-regulation, adaptation,
in depression. Clinical Psychological Science, 2, 455 471. http://dx.doi and health. Annals of Behavioral Medicine, 37, 141153. http://dx.doi
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

.org/10.1177/2167702614536160 .org/10.1007/s12160-009-9101-z
Thayer, J. F., & Lane, R. D. (2009). Claude Bernard and the heart-brain
This document is copyrighted by the American Psychological Association or one of its allied publishers.

Siepmann, M., Aykac, V., Unterdrfer, J., Petrowski, K., & Mueck-
connection: Further elaboration of a model of neurovisceral integration.
Weymann, M. (2008). A pilot study on the effects of heart rate vari-
Neuroscience and Biobehavioral Reviews, 33, 81 88. http://dx.doi.org/
ability biofeedback in patients with depression and in healthy subjects.
Applied Psychophysiology and Biofeedback, 33, 195201. http://dx.doi
Vingerhoets, A. J., & Bylsma, L. M. (2016). The riddle of human emo-
tional crying: A challenge for emotion researchers. Emotion Review, 8,
Somers, J. A., Borelli, J. L., Smiley, P. A., West, J. L., & Hilt, L. M.
201217. http://dx.doi.org/10.1177/1754073915586226
(2015). Concurrent and prospective associations between emotion reac-
Watson, D., Clark, L. A., & Tellegen, A. (1988). Development and vali-
tivity and depressive symptoms in middle childhood. Journal of Psy-
dation of brief measures of positive and negative affect: The PANAS
chopathology and Behavioral Assessment, 37, 692704. http://dx.doi scales. Journal of Personality and Social Psychology, 54, 10631070.
.org/10.1007/s10862-015-9491-0 http://dx.doi.org/10.1037/0022-3514.54.6.1063
Spybrook, J., Raudenbush, S. W., Liu, X. F., Congdon, R., & Martnez, A. Weiss, R. B., Stange, J. P., Boland, E. M., Black, S. K., LaBelle, D. R., Abramson,
(2006). Optimal design for longitudinal and multilevel research: Doc- L. Y., & Alloy, L. B. (2015). Kindling of life stress in bipolar disorder:
umentation for the Optimal Design software. Lansing, MI: Survey Comparison of sensitization and autonomy models. Journal of Abnormal Psy-
Research Center of the Institute of Social Research at University of chology, 124, 416. http://dx.doi.org/10.1037/abn0000014
Michigan. Wells, A. (2011). Metacognitive therapy for anxiety and depression. New
Stange, J. P., Hamilton, J. L., Abramson, L. Y., & Alloy, L. B. (2014). A York, NY: Guilford Press.
vulnerability-stress examination of response styles theory in adoles- Yaroslavsky, I., Bylsma, L. M., Rottenberg, J., & Kovacs, M. (2013).
cence: Stressors, sex differences, and symptom specificity. Journal of Combinations of resting RSA and RSA reactivity impact maladaptive
Clinical Child and Adolescent Psychology, 43, 813 827. http://dx.doi mood repair and depression symptoms. Biological Psychology, 94, 272
.org/10.1080/15374416.2013.812037 281. http://dx.doi.org/10.1016/j.biopsycho.2013.06.008
Storch, E. A., Roberti, J. W., & Roth, D. A. (2004). Factor structure, Yaroslavsky, I., Rottenberg, J., & Kovacs, M. (2014). Atypical patterns of
concurrent validity, and internal consistency of the Beck Depression respiratory sinus arrhythmia index an endophenotype for depression.
InventoryII in a sample of college students. Depression and Anxiety, Development and Psychopathology, 26, 13371352. http://dx.doi.org/10
19, 187189. http://dx.doi.org/10.1002/da.20002 .1017/S0954579414001060

Structure of Hierarchical Linear Models Predicting Symptoms of Depression, Using
Model 1 (Table 3) as an Example

Level 1 (Within-Subjects) Model: eti Level 1 error term

BDIti(t) 0i 1i * (BDIti(t1)) 2i * (LifeEventsti(t)) eti 00 Level 2 intercept of BDI at time t

Level 2 (Between-Subjects) Model: 01 Regression coefficient of RSA during first neutral film
predicting BDI
0i 00 01 * (RSAneutral1i) 02 * (RSAsadi) r0i
1i 10 02 Regression coefficient of RSA during sad film pre-
2i 20 21 * (RSAneutral1i) 22 * (RSAsadi) r2i dicting BDI
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
This document is copyrighted by the American Psychological Association or one of its allied publishers.

10 Intercept for BDI at time t 1
BDIti(t) Beck Depression Inventory score at time t
20 Intercept for negative life events at time t
BDIti(t 1) Beck Depression Inventory score at time t 1 21 Regression coefficient of RSA during first neutral film
predicting the slope of negative life events at time t
LifeEventsti(t) Number of negative life events at time t
22 Regression coefficient of RSA during sad film pre-
RSAneutral1i RSA during first neutral film
dicting the slope of negative life events at time t
RSAsadi RSA during sad film
r0i Level 2 residual for intercept of BDI at time t
0i Regression coefficient for Level 2 predictors of BDI at
r2i Level 2 residual for negative life events
time t

1i Slope for BDI at time t 1 Received March 17, 2016

Revision received August 2, 2016
2i Slope for negative life events at time t Accepted October 24, 2016