University of Groningen
Motivation, reward and stress: individual difference and neural basis
Xin, Yuanyuan
DOI:
10.33612/diss.143843592
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Publication date: 2020
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Xin, Y. (2020). Motivation, reward and stress: individual difference and neural basis. University of Groningen. https://doi.org/10.33612/diss.143843592
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CHAPTER 3
Recent life stress predicts blunted acute stress response and
the role of executive control
Yuanyuan Xin, Zhuxi Yao, Weiwen Wang, Yuejia Luo, Andre Aleman, Jianhua Wu.
Abstract
The present study examined the associations between recent life stress and responses to acute psychological stress, and how these associations varied with executive control. Heart rate (HR), heart rate variability (HRV), salivary cortisol, and affective states were measured before, during and after the Trier Social Stress Test (TSST), an effective laboratory stressor, in 54 healthy participants, and executive control function was tested with a Go/No-Go task in a neutral context on a different day. The hierarchical multiple regression analysis showed that high frequency of life stress during the last twelve months predicted blunted cardiovascular acute stress response, i.e., smaller HR and HRV reactivity. Moreover, the low executive control group showed a significant association between higher recent life stress and blunted acute stress response, which was not apparent in the high executive control group. The results suggested that greater executive control may benefit us with adaptive acute stress response under recent life stress.
1 Introduction
Stress is pervasive in real life. Exposure to an unpredictable, uncontrollable stressor can evoke allostasis physiologically and emotionally (Ulrich-Lai and Herman 2009). A considerable amount of studies from animals and humans have revealed that acute stress could temporally elicit different responses from autonomic neural system (ANS). Firstly, sympathetic-adrenal-medullary (SAM) axis shows the most immediate responses, e.g., heart rate (HR) increases (see a review, Allen et al., 2014), while heart rate variability (HRV) decreases (Tharion et al. 2009; Li et al. 2010; Castaldo et al. 2015). Then, the hypothalamic-pituitary-adrenocortical (HPA) axis, which functions as a relatively slower stress response, would modulate cortisol secretion (Dickerson and Kemeny 2004). Along with these physiological responses, acute stress also induce some emotional response, e.g., increased fear, anxiety and tension (Kelly et al. 2008; Sparrenberger et al. 2009).
Proper acute stress response is considered as an adaptive function (McEwen 1998), but excessive and prolonged stress exposure might cause deleterious consequences including prefrontal cognition dysfunction (e.g., attenuated performance in working memory, cognitive flexibility and cognitive inhibition, for a review, see Shields et al., 2016), physical disease (Lovallo 2012; Dhabhar 2014), and mental disorders like anxiety, depression, eating disorder (De Kloet et al. 2005; Allen et al. 2014) and post-traumatic stress disorder (PTSD) (Davidson et al. 2004).
Individuals vary substantially in their response to acute stress. Recently, studies have showed increasing interest in the factors predicting individual differences in stress response. A meta-analysis study reviewed that age, gender, genetics, personality traits, and social factors (i.e., social support, social status and social culture) modulate individual stress responses to acute stressors (Allen et al., 2014). In addition, cognitive factors including general intelligence (Ginty et al. 2011, 2012), executive function (Hendrawan et al. 2012), cognitive control (Compton et al., 2011, 2008; Plieger et al., 2017), error-awareness (Wu et al., 2017), and attention bias (Fox et al., 2010; Pilgrim et al., 2010), have also been found associated with stress response magnitude.
Recent life stress has been found to be one factor contributing to individual differences in stress responses. However, previous studies have yielded mixed results. For example, while most studies indicated a negative association
between recent life stress and heart rate responses to acute stressors in adults and adolescents (Phillips et al., 2005; Murali and Chen, 2005; Matthews et al., 2001), some studies did not show a statistically significant relationship between life events and heart rate stress responses (Cohen et al., 1986; Jorgensen and Houston, 1989; Lepore et al., 1997).
The mixed results have been found to be due to some modulating variables, such as personality, coping style, and social network (Roy et al. 1998; Phillips et al. 2005; Peng et al. 2012). Among many potential moderators of the relationship between life stress and acute stress responses, executive control function could be an important one. Executive control has strong link with stress regulation. On behavioral level, executive control performance is predictive of dampened responses to acute stress (Hendrawan et al., 2012; Williams et al., 2009). On neural level, prefrontal cortex is crucial both in executive control (Ridderinkhof et al. 2004) and stress regulation (Cerqueira et al. 2007). In addition, previous studies found that executive control can modulate the relationship between life stress and stress response. For instance, greater neural activity during error-monitoring process has been found to predict less stress reactivity to daily stress (Compton et al. 2011). Thus, executive control may be a crucial modulator in the relationship between acute stress response and life stress.
Most studies on the relationship between recent life stress and acute stress response focused on HR or blood pressure stress reactivity. However, studies on other aspects of stress response, i.e., HRV, cortisol level, and subjective affect, are limited. HRV is a measure of the continuous interplay between the influences of SNS and PNS on heart rate, indicating adaptive ability of the heart under variable circumstances (Appelhans and Luecken, 2006; Castaldo et al., 2015). Up to now, one study has reported that accumulation of violence experiences was associated with smaller HRV decline towards acute stressor in adolescent (Murali and Chen 2005). For cortisol response, one study showed that more stressful life events were associated with a reduced cortisol stress response in children (8 - 12 years) (Armbruster et al. 2012); a recent study revealed that participants' exposure to entire life stressors predicts a blunted cortisol response to acute stress in adults (Lam et al. 2019). However, how recent life stress would predict these different aspects of acute stress responses in young adults remains unclear.
This study aimed to examine whether recent life stress would predict acute stress responses and how executive control function would modulate their
associations. We used a standard laboratory stressor to elicit acute stress responses in healthy adults. The stress responses were collected and calculated comprehensively before, during and after the acute stress induction, including HR, HRV, cortisol, positive and negative affect, and control feeling of the cute stressor. Furthermore, executive control function was measured as false alarm rate (FAR) in the Go/No-Go task (Cheung et al. 2004). Based on previous findings, we firstly test the hypothesis that high frequency of recent life stress would be associated with lower stress responses. We also explored the role of executive control in the relationship between recent life stress and acute stress responses.
2 Methods and Materials
2.1 ParticipantsThis study was based on a secondary analysis of data from a project on individual psychophysiological response to acute stress (Xin et al. 2017). fifty-four participants (35 males), aged from 18 to 25 years (mean 22.57±1.67) with 13-18 education years (mean 15.89±1.34) were recruited. Participants were excluded in case of a) psychiatric illnesses, neurological diseases, endocrine disorders or major physical illness; b) severe head trauma or brain damage (e.g., brain surgery, cerebral haemorrhage); and c) major operation in the last 6 months. Also, participants were not to be ill, taking medicines, suffering from certain chronic diseases, be pregnant, live an irregular lifestyle (i.e. prolonged reversed day and night schedule) or staying up during the 3 days prior to the study. Female subjects were not in their ovulation phase of menstrual cycle. All participants were right-handed, not heavy smokers (no more than five cigarettes a day) and not alcoholics (no more than two alcoholic drinks a day), with normal or corrected-to-normal vision. The study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of Human Experimentation in the Institute of Psychology, Chinese Academy of Sciences. The written informed consent was obtained from every subject before participating in the experiment.
2.2 General procedure
To avoid the influence of circadian rhythm of cortisol levels (Dickerson and Kemeny 2004) the study was conducted during afternoon, starting at approximately 13:30. Participants were asked not drinking or eating anything
except water and avoid vigorous exercise within one hour before coming to the laboratory. All participants reported that they did comply with these requirements. Participants came twice in two weeks. On the first afternoon, participants were asked to complete a Go/No-Go task. On the second afternoon, participants were instructed to remain seated for 30 minutes in a quiet room before the acute stress induction. During this resting period, they filled out questionnaires including demographic information (i.e., age, sex, education), personality with the mini-International Personality Item Pool (see details in Xin et al., 2017) and the Adolescent Self-Rating Life Events Check List (Liu et al., 1997) (see details below). Baseline measurements of salivary sample (SS), HR, positive affect (PA) and negative affect (NA) were collected immediately after rest. Then, the stress induction was conducted with the Trier Social Stress Test (TSST, see details below). HR was constantly recorded during the preparation, speech, and arithmetic parts of the TSST. After the TSST task, SS, HR (continuous recording for 5 minutes), PA, NA, and feeling of Control (FoC) on TSST were collected again. Then SS and HR were collected at 20 min, 45 min, and 60 min after the end of TSST. The general procedure is illustrated in Figure 1.
Figure1. The general procedure. Each participant visited our laboratory twice. On the first visit, they performed a Go/No-Go task after a short rest. Then they came for the TSST on the second visit. Heart rate (HR), salivary sample, positive affect (PA), negative affect (NA) and feeling of control (FoC) were collected around the TSST.
2.2.1 Go/No-Go Task
Participants were asked to complete a Go/No-Go task similar to that of previous studies in our project (Wu et al. 2017). The task included one practice block of 10 trials and two experimental blocks of 240 trails in each one. Stimuli were the digits of “1” or “9”. The probability was 20% for No-Go trials and 80% for Go trials. In each trail, one digit was presented in the center of the screen for 150 ms followed by an inter-stimulus interval varied randomly between 1200 and 1500 ms. Participants were asked to respond as quickly as possible to Go trials (either “1” or “9”) by pressing a button on the keyboard and inhibit the response in No-Go trials (“9” or “1”, respectively). The target stimulus for Go trails (“1” or “9”) was counterbalanced across participants.
2.2.2 The laboratory stress task-Trier Social Stress Test
A modified TSST from Kirschbaum and his colleagues (Buchanan et al. 2009) was used to induce acute stress. During the preparation period, participants were asked to prepare a 5-min speech to defend themselves (in an imaginary situation) against a store manager who charged them of shoplifting. They could take notes at preparation but were not allowed to take the notes during speaking. After the preparation, participants completed the speech and mental arithmetic tasks with a microphone and were videotaped (which they were aware of). Throughout the speech and mental arithmetic tasks, three experimenters (two females and one male) with white coats and neutral facial expressions were present. For the mental arithmetic task, participants were asked to subtract 13 consecutively, beginning with 1022. They were asked to respond as quickly and accurately as possible and restart at 1022 if a mistake occurred.
2.2.3 Recent life stress
Recent life stress was assessed using the Adolescent Self-Rating Life Events
Check List (ASLEC) (Liu et al. 1997). This scale has 27 items, including six
dimensions of interpersonal relationship, study pressure, being punished, bereavement, change for adaption, and others, which are all typical negative life event in college student. Subjects were asked whether they had experienced events pertaining to these items in the last 12 months and their perceived severity of the event they experienced. The life events frequency (LEF) was reported as the recent life stress score. The Cronbach’s alpha was 0.85 for perceived severity, but not applied for the frequency (Liu et al. 1997).
2.2.4 The Positive and Negative Affect
The subjective affective was rated using the Positive and Negative Affect Schedule (PANAS) (Watson et al. 1988) with a 5-point Likert scale (1-not at all, to 5-very much). The scale consists of 20 items, with 10 for positive affect (interested, excited, inspired and alert) and 10 for negative affect (distressed, nervous, scared and upset). The PANAS has strong internal consistency for moment-measurement with Cronbach’s alphas of 0.89 for PA and 0.85 for NA (Watson et al. 1988).
2.2.5 Feeling of control
Participants rated their subjective control levels on the speech and arithmetic task of the TSST with a visual analog scale from 0- “out of control” to 10- “a strong sense of control”.
2.2.6 Physiological stress response measurement
HR was recorded with a Biopac Amplifier System (MP150; Biopac, Goleta, CA, USA) with a sample rate of 1,000 Hz. During the recording, three electrocardiograph electrodes were placed on the right side of the neck and the left and right inner ankles. HR was defined as the number of beats per minute (bpm), calculated by the mean of 5-min continuous recording at each collection point using AcqKnowledge software. HRV was analyzed with Kubios Analysis software (Biomedical Signal Analysis Group, University of Kuopio, Finland). Root mean square of successive differences (RMSSD) of inter beat intervals and high frequency (0.15-0.4 HZ) component of HRV (HF-HRV) were used as the indices of HRV, which are mainly mediated by vagal activity (Task Force of the European Society of Cardiology and Task Force of the European Society of Cardiology, 1996). Saliva samples were collected using Salivettes (Sarstedt, Rommelsdorf, Germany). Samples were frozen at −22 ◦C until analysis. Before analysis,
samples were dissolved and centrifuged at 3,000 rpm for 10 min. Then cortisol in saliva was measured using electrochemiluminescence immunoassay (Cobas e 601, Roche Diagnostics, Numbrecht, Germany). The lower sensitivity for cortisol was 0.5 nmol/L. Intra- and inter-assay variations were less than 10%. 2.3 Data analysis
To examine whether the stress elicitation was effective, the repeated measure ANOVA was conducted on HR, RMSSD, HF-HRV and Cortisol across time points, and the paired sample t-test was applied to PA and NA.
Greenhouse-Geisser corrections were applied in the repeated measure ANOVA when the sphericity assumption was violated. Post hoc comparisons between time points were assessed by Bonferroni correction.
Hierarchical multiple regression analyses were applied to examine how recent life stress predicted acute stress responses. Acute stress responses were calculated by the difference values between TSST and baseline. Specifically, HR, RMSSD, and HF-HRV responses to TSST (ΔHR, ΔRMSSD, ΔHF-HRV) were calculated by subtracting their baseline from averaged value during TSST. The salivary cortisol change (ΔCortisol) was defined as the subtraction of baseline from peak cortisol which was the one collected at 20 min after the end of TSST. The affect changes (ΔPA and ΔNA) were subtractions of baseline from values collected immediately after completion of TSST. The feeling of control score was the mean of control feeling on speech and mental arithmetic task. As studies have showed sex difference in acute stress responses (see a meta-analysis, Liu et al., 2017), and neuroticism was found significantly linked with acute stress responses in our previous study ( Xin et al., 2017),, they were entered at step 1 as covariates in the hierarchical regression analysis. The recent life stress was entered at step 2.
Next, we performed a moderation analysis using PROCESS macro for SPSS (Hayes 2017). Firstly, subjects were divided into high and low executive control groups by FAR median (Cerqueira et al. 2007). The FAR was calculated by the proportion of error in all No-Go trials, with higher FAR meaning lower executive control. Then the moderation analysis was conducted with 5,000 bootstrap samples with executive control as moderator, stress responses as dependent variables, recent life stress as independent variable, and sex and neuroticism as covariates.
Extreme values (values larger than three times of the interquartile range) in independent variables were deleted before the hierarchical multiple regression analyses. Two participants were excluded from the HR and HRV analyses. Recent life stress score was transformed to normal distribution with Box-Cox transformation (Box and Cox, 1964) with MedCalc Statistical Software version 15.6.1 (MedCalc Software bvba, Ostend, Belgium; https://www.medcalc.org; 2015). Other statistical analyses were implemented with SPSS 20.0 (IBM Corp. Armonk, NY). All reported p-values were two-tailed with the significance level of .05.
3 Results
3.1 Description of recent life stress and false alarm rate
Subjects had an average of 7.593 (SD = 6.045) stressful life events in the last 12 months, and an average FAR of 13.5% (SD = 9.8%).
3.2 Physiological and psychological stress response
For HR, the repeated measure ANOVA revealed a significant main effect of time, F (3.237,171.542) = 85.483, p < 0.001, partial Eta-square = 0.617. Post hoc analysis indicated that HR during speech and mental arithmetic periods was higher than HR at all other time points, with all p values < 0.05. HR during preparation was higher than HR at baseline and time points after the end of the TSST, p values < 0.01. No other significant differences were found between time points, with all p values > 0.10. The mean (± SD) of ΔHR was 11.728 (±8.209) bpm (see Figure 2a).
For RMSSD, the repeated measure ANOVA revealed a significant main effect of time, F (3.456, 183.165) = 23.601, p < 0.001, partial Eta-square = 0.308. Post hoc analysis indicated that RMSSD during the speech and mental arithmetic periods was significantly lower than measures at other time points, with all p values < 0.001. No other significant differences were found between time points, with all p values > 0.05. The mean (± SD) of ΔRMSSD was -9.601 (± 16.585) (see Figure 2b).
For HF-HRV, the repeated measure ANOVA revealed a significant main effect of time, F (3.936, 208.590) = 17.140, p < 0.001, partial Eta-square = 0.562. Post hoc analysis indicated that HF-HRV during the speech and mental arithmetic periods was significantly lower than measures at other time points, with all p values < 0.05. No other significant differences were found between time points, with all p values > 0.05. The mean (± SD) of ΔHF-HRV was -208.55 (± 880.10) (see Figure 2c)
For cortisol, results of the repeated measure ANOVA using the factor of time revealed a significant main effect, F (2.405, 127.479) = 40.465, p < 0.001, partial Eta-square = 0.433. Cortisol reached its peak at 20 min after the completion of TSST (M = 14.693, SD = 5.550), which was significantly higher than cortisol concentration measured at other time, with all p values < 0.001. Cortisol at 0 min and 45 min after the completion of TSST was higher than that of baseline and 60
min after the completion of the TSST, with all p values < 0.01. However, there was no difference in cortisol between 0 min and 45 min after the completion of TSST, and between baseline and 60 min after the completion of the TSST. The mean (± SD) of ΔCortisol was 5.924 (± 5.855) nmol/l (see Figure 2d).
For PA, the paired sample t-test revealed no significant difference between PA at baseline and end of TSST, t (53) = -1.204, p = 0.234. The mean (± SD) of ΔPA was -0.852 (± 5.199) (see Figure 2e).
For NA, participants experienced more negative affect (NA) at the end of TSST than baseline, t (53) = -4.836, p < 0.001. The mean (± SD) of ΔNA was 3.278 (± 4.981) (see Figure 2f).
C HA P T ER 3 Fi gur e 2. Tr end of (a ) HR, (b ) RMS SD , ( c) HF -HR V, (d) C or tis ol , ( e) P A , a nd (f ) NA a cr oss me asu re tim e. E rr or ba r re pr ese sta nd ar d de via tio n. 0, 20 , 45 , 60 a re 0 mi nu te , 20 m inu te s, 45 m inu te s and 6 0 m inu te s a fte r th e end of the T rie r S oci al S tr es Te st (T SS T) se pa ra te ly . HR: he ar t ra te , RMS SD : ro ot m ea n squ ar e of su cc ess iv e di ffe re nce s, H F-HR V: hi gh fre que ncy co mp on ent o f h ea rt ra te v aria bil ity , P A : p osi tiv e af fe ct , NA : n eg ativ e a ffe ct
3.3 Results of the hierarchical regression analyses
Table 1 shows the hierarchical multiple regression results of recent life stress on stress responses towards TSST.
3.3.1 Regression of recent life stress on HR stress response
The result showed that recent life stress significantly added 7.2% of the explained variance after controlling for covariates (ΔR2 = 0.072, R2 = 0.156, F (3,
48) = 2.955, p = 0.042. And recent life stress could independently predict HR response (beta = -0.274, t = -2.025, p = 0.048), the more stressful life events subjects experienced, the smaller HR acute stress response was, for scatterplot of simple correlation, see Figure 3a.
3.3.2 Regression of recent life stress on RMSSD stress response
The result showed that recent life stress significantly added 12.6% of the explained variance after controlling for covariates (ΔR2 = 0.126, R2 = 0.165, F (3,
48) = 3.151, p = 0.033). And recent life stress could independently predict RMSSD response (beta = 0.362, t = 2.693, p = 0.010), the more stressful life event subjects experienced, the smaller RMSSD decrease was, for scatterplot of simple correlation, see Figure 3b.
3.3.3 Regression of recent life stress on HF-HRV stress response
The result showed that recent life stress added 9.2% of the explained variance (ΔR2 = 0.092, R2 = 0.108, F (3, 48) = 1.942, p = 0.135). And recent life
stress could independently predict the HF-HRV response after controlling for covariates (beta = 0.310, t = 2.227, p = 0.031), the more stressful life event subjects experienced, the smaller HF-HRV decrease was, for scatterplot of simple correlation, see Figure 3c.
3.3.4 Regression of recent life stress on Cortisol stress response
The predictions of recent life stress or covariates on Cortisol change were not significant, see Table 1.
3.3.5 Regression of recent life stress on PA response to TSST
The result showed that recent life stress was not a significant predictor to PA change after controlling for covariates (beta = 0.124, t = 0.978, p = 0.333). In addition, the covariates significantly contributed 21.1% explained variance to the regression model (ΔR2 = 0.211, R2 = 0.226, F (3, 50) = 4.864, p = 0.005).
3.3.6 Regression of recent life stress on NA response to TSST
The predictions of recent life stress or covariates on NA change were not significant, see Table 1.
3.3.7 Regression of recent life stress on FoC of TSST
The result showed that recent life stress was not a significant predictor to FoC of TSST after controlling for covariates (beta = -0.196, t = -1.498, p = 0.141). In addition, the covariates significantly contributed 13.7% explained variance to the regression model (ΔR2 = 0.137, R2 = 0.174, F (3, 50) = 3.512, p = 0.022).
Figure 3. Scatter plots showing associations between LEF and (a) ΔHR, (b) ΔRMSSD, (c) ΔHF-HRV. LEF: life event frequency. ΔHR/ΔRMSSD/ ΔHF-HRV: HR/ RMSSD/ HF-HRV change during TSST to baseline.
3.4 The moderation effect of executive control
Independent samples T-tests showed that there is no difference on recent life stress between high and low executive control group, neither difference on demographic variables, see Supplementary Table S1.
The results of moderation analysis with 5,000 bootstrap samples revealed that executive control significantly moderated the relationship between recent life stress and HRV changes including ΔRMSSD and ΔHF-HRV, after controlling for sex and neuroticism. Specifically, the effect of recent life stress on HRV change is statistically different from zero in the low executive control group, for ΔRMSSD, t = 2.793, p = 0.008, 95% CI = [0.745, 4.591], for ΔHF-HRV, t = 2.743, p = 0.009, 95% CI = [32.277, 210.279]; but not in the high group, for ΔRMSSD, t = 0.815, p = 0.419, 95% CI = [-1.440, 3.400], for ΔHF-HRV, t = -0.137, p = 0.891, 95% CI = [-119.657, 104.361]. For scatterplot of simple correlation in each group, see Figure 4a and Figure 4b.
Figure 4. The relationships between LEF and (a) ΔRMSSD, (b) ΔHF-HRV was significantly moderated by executive control. LEF: life event. ΔRMSSD/ ΔHF-HRV: RMSSD/ HF-HRV change during TSST to baseline. EC: executive control.
C HA P T ER 3 Ta ble 1. R esu lts of hi er ar chi ca l mu ltiple r eg re ss io n on str ess re sp ons es. Respo ns es Th e h ie ra rchi ca l r eg re ss io n analys is pre di ct ors be ta t p R 2 ΔR 2 F si g-F Δ HR ste p 1 se x 0.098 0.736 0.465 0.084 0.084 2.241 0.117 neuro ticis m -0.232 -1.714 0.093 ste p2 LE F -0.274 -2.025 0.048 0.156 0.072 2.955 0.042 pre di ct ors be ta t p R 2 ΔR 2 F si g-F Δ RMS SD ste p 1 se x -0.171 -1.288 0.204 0.038 0.038 0.977 0.384 neuro ticis m 0.066 0.486 0.629 ste p2 LE F 0.362 2.693 0.010 0.165 0.126 3.151 0.033 pre di ct ors be ta t p R 2 ΔR 2 F si g-F Δ HF -HRV ste p 1 se x -0.083 -0.605 0.548 0.016 0.016 0.401 0.672 neuro ticis m 0.054 0.387 0.700 ste p2 LE F 0.310 2.227 0.031 0.108 0.092 1.942 0.135 pre di ct ors be ta t p R 2 ΔR 2 F si g-F Δ C ort is ol ste p 1 se x -0.113 -0.798 0.429 0.013 0.013 0.347 0.709
neuro ticis m -0.029 -0.203 0.840 ste p2 LE F 0.032 0.223 0.825 0.014 0.001 0.243 0.860 pre di ct ors be ta t p R 2 ΔR 2 F si g-F ΔPA ste p 1 se x 0.336 2.687 0.010 0.211 0.211 6.823 0.002 neuro ticis m -0.361 -2.849 0.006 ste p2 LE F 0.124 0.978 0.333 0.226 0.015 4.864 0.005 pre di ct ors be ta t p R 2 ΔR 2 F si g-F Δ NA ste p 1 se x -0.120 -0.859 0.394 0.022 0.022 0.570 0.569 neuro ticis m 0.084 0.595 0.555 ste p2 LE F 0.128 0.908 0.368 0.038 0.016 0.654 0.584 pre di ct ors be ta t p R 2 ΔR 2 F si g-F Fo C ste p 1 se x -0.125 -0.968 0.338 0.137 0.137 4.048 0.023 neuro ticis m -0.301 -2.297 0.026 ste p2 LE F -0.196 -1.498 0.141 0.174 0.037 3.512 0.022 No te . Δ HR/ Δ RMS SD / Δ HF -HR V/ Δ C or tis ol / Δ PA / Δ NA : HR / R MSS D / HF -HR V/ C or tiso l/ PA / NA c hang es to T SS T. F oC : av era ge fe el ing of c ontr ol o n spe ech an d ment al a rit hm etic. b et a: st and ar d c oe ffi cie nt . LE F: re ce nt li fe e ve nt fr eque ncy . E nt er me tho d: e nt er .
4 Discussion
The current study was aimed to examine the relationship between recent life stress and acute stress responses, and how executive control moderated this relationship. The result has showed that the TSST caused an increase in HR, a decrease in HRV, and an increase in cortisol, indicating a successful stress induction. Importantly, recent life stress negatively predicted cardiovascular responses to acute stress (blunted HR increment and HRV decrement), but did not predict cortisol or subjective stress responses. Notably, people with different levels of executive control function manifest different patterns of relationship between recent life stress and HRV stress response, i.e., the group with low executive control showed a negative correlation in line with the overall trend, however, such correlation was not found in the high executive control group.
This study related high frequency of life stress exposure during the last twelve months to a low level of cardiovascular responses to acute stress. The finding is consistent with prior studies on cardiovascular stress responses (see a cohort study, Phillips et al., 2005) and extended earlier reports by finding the relationship between recent life stress and HRV, i.e., a smaller HRV decline to acute stress (representing lower stress response). Our finding is also consistent with the result of a previous study in adolescence which focused on violence-related experiences in life events (Murali and Chen 2005) and extended this study by measuring a broad range of stressful life events in adults, including interpersonal relationship problems, study pressure, and being punished, thus providing new evidence that general stressful life experience was related to heart rate dynamic change under acute stress in adults.
The findings may be interpreted in two different perspectives. Firstly, people experiencing a lot of adverse events over a period may become hypo-sensitive to emergencies (Boyce and Chesterman 1990), thus the laboratory-stressor was evaluated as less stressful, plausibly arouse relatively smaller autonomic acute stress response. Secondly, being exposed to stressful life events frequently over a defined period, the body might be chronically stressed and stay in a high arousal state (Vente et al. 2003), causing psychophysiological resources being occupied and consumed. This allostatic load (Logan and Barksdale 2008; Duan et al. 2015) then makes it hard to mobilize and reallocate resource to deal with emergency, thus showing a dampened acute response.
between recent life stress and HRV stress response in the present study. Subjects were divided into lower group and higher group by the median of executive control score. The group in low executive control showed the negative association found in the whole group, i.e., greater recent life stress exposure, smaller RMSSD/ HF-HRV decline to the TSST. According to our knowledge, no similar study has explored how executive control moderated the relationship between recent life stress and acute stress response. The lack of association between recent life stress and acute stress response in high executive control group might be explained by that higher executive control is linked to more effective prefrontal cortex function. Competitive PFC function in the higher executive control group may provide them with greater capacity to cope with life stressors, i.e., they may appraise some stressful life events in more flexible and adaptive ways (Williams et al. 2009). Thus, accumulated life events may not be experienced much stressful to cause maladaptive reactivity to acute stress. Our finding of the role of executive control on acute stress response under recent life stress may also help to explain the mixed results in literature regarding the relationship between recent life stress and acute stress response.
There are some limitations. Firstly, although the TSST is a standard task for acute stress induction and stress responses can be conveniently measured in the laboratory, the intensity of this laboratory-based acute stressor is in the moderate level, which may not necessarily represent real-world life stressors. Secondly, the present study indicated that one aspect of executive control, inhibitory control, played a role in modulating the relationship between recent life stress and HRV reactivity to stress, roles of other aspects of executive control (e.g. cognitive flexibility, working memory, emotion regulation, decision making and so on), need further consideration. Third, being limited to the relatively small sample size which had a test power (1-β) range of 0.74 ~ 0.92 by post-hoc analyses with G*Power 3.1 (http://www.gpower.hhu.de/en.html), more work is needed to validate this finding in a generalized population.
5 Conclusion
In conclusion, this study suggested that individual’s cardiovascular responses to acute stress was predicted by recent life stress and this relationship was moderated by executive control, i.e., this association was less apparent in individuals with higher executive control. Notwithstanding the relatively limited
sample, these findings suggest that higher frequency of recent life stress could probably influence our adaptive response to acute stress, which may be caused by the allostatic load or by the under-evaluation of stressful event, but greater executive control can possibly prevent such adverse effects.
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Supplementary Materials
Table S1. Comparison of mean values (±SD) for demographic variables between high and low executive control groups.
Low EC (N=27) High EC (N=27) t df sig. LEF 6.93(6.94) 8.26(5.04) -0.81 52 0.42 age 22.44 (1.99) 22.70 (1.30) -0.57 52 0.57 edu 15.70 (1.61) 16.07 (1.00) -1.02 52 0.32
SD: standard deviation; EC: executive control; LEF: life event frequency; edu: education years.
