Emotion suppression and acute physiological responses to stress in healthy populations: a quantitative review of experimental and correlational investigations

Abstract

Emotion suppression may be linked to poor health outcomes through elevated stress-related physiology. The current meta-analyses investigate the magnitude of the association between suppression and physiological responses to active psychological stress tasks administered in the laboratory. Relevant articles were identified through Medline, PsychINFO, PubMed, and ProQuest. Studies were eligible if they (a) used a sample of healthy, human subjects; (b) assessed physiology during a resting baseline and active psychological stress task; and (c) measured self-report or experimentally manipulated suppression. Twenty-four studies were identified and grouped within two separate random effects meta-analyses based on study methodology, namely, manipulated suppression (k = 12) and/or self-report (k = 14). Experimentally manipulated suppression was associated with greater physiological stress reactivity compared to controls (H_g = 0.20, 95% CI [0.08, 0.33]), primarily driven by cardiac, hemodynamic, and neuroendocrine parameters. Self-report trait suppression was not associated with overall physiological stress reactivity but was associated with greater neuroendocrine reactivity (r ₌ 0.08, 95% CI [0.01, 0.14]). Significant moderator variables were identified (i.e., type/duration of stress task, nature of control instructions, type of physiology, and gender). This review suggests that suppression may exacerbate stress-induced physiological arousal; however, this may differ based upon the chosen methodological assessment of suppression.

Keywords: Emotion regulation; meta-analysis; physiological stress reactivity; psychological stress; suppression.

Figure 1.

Suppression in Relation to The Process Model of Emotion Regulation. Note. Adapted from ‘Gross, J. J. (2014). Emotion regulation: Conceptual and empirical foundations. In J. J. Gross (Ed.), Handbook of emotion regulation (2nd ed., pp. 3–20). New York, NY: Guilford Press.’

Figure 2.

Prisma Flow Diagram. Note. Adapted from:Moher, D., Liberati, A., Tetzlaff, J., Altman, D. G., & The PRISMA Group (2009). Preferred reporting items for systematic reviews and meta-analyses: The PRISMA statement. PLoS Medicine, 6, e1000097. https://doi.org/10.1371/journal.pmed1000097. For more information, visit www.prisma-statement.org.

Figure 3.

Manipulated Suppression Versus Control on Physiological Stress Reactivity Outcomes. Note. *denotes that the effect sizes of these physiological parameters were reverse coded to maintain consistency of interpretation; RSA = respiratory sinus arrhythmia; PEP = pre-ejection period; SCR = skin conductance response; pNN50 = proportion of NN50 divided by total number of NN (R-R) intervals; RMSSD = root mean square of successive differences; HR = heart rate; CO = cardiac output; IBI = interbeat interval; SV = stroke volume; SBP = systolic blood pressure; DBP = diastolic blood pressure; TPR = total peripheral resistance; MAP = mean arterial pressure.

Figure 4.

Self-Report Trait Suppression on Physiological Stress Reactivity Outcomes. Note. *denotes that the effect sizes of these physiological parameters were reverse coded to maintain consistency of interpretation; RSA = respiratory sinus arrhythmia; HF-HRV = high frequency heart rate variability; sAA = salivary alpha-amylase; pNN50 = proportion of NN50 divided by total number of NN (R-R) intervals; RMSSD = root mean square of successive differences; RSA = respiratory sinus arrythmia; HR = heart rate; IBI = interbeat interval; SBP = systolic blood pressure; DBP = diastolic blood pressure.