Multi-Systemic Evaluation of Biological and Emotional Responses to the Trier Social Stress Test: A Meta-Analysis and Systematic Review

It is widely acknowledged that stress responses entail multi-faceted biological and psychological processes which interact in intricate ways [e.g., 1-3]. On one hand, multiple neuroendocrinological, immunological and cardiovascular systems interact among each other and collectively determine the stress allostatic load (Juster et al., 2010). Therefore, stress outcomes are results of the confluence of changes accumulated across multiple biological systems (Seeman et al., 2001). On the other hand, biology and emotion are inseparable realms in stress responses. According to the classic James-Lange theory, emotions emerge from physiological changes and are closely related to visceral functions (Fehr and Stern, 1970). Overlapping brain centers such as the prefrontal-limbic circuitries orchestrate both biological and emotional responses to stress, providing the neural bases for their tight interactions (Kern et al., 2008, Fanselow and Dong, 2010, Flandreau et al., 2012, Lee et al., 2012). Thus, to understand the global profile of acute stress reactivity and recovery, it is crucial to adopt a multi-systemic approach, through simultaneously and comprehensively examine both biological and emotional responses, as well as the biology-emotion interrelations.

Stress responses are primarily mediated via activating the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic-adreno-medullar (SAM) system (See (Schneiderman et al., 2005) for detailed review). On one hand, the hypothalamus in the HPA axis produces corticotropin releasing factors, which induce the release of adrenocorticotropic hormone (ACTH), and further stimulate the production and secretion of cortisol. Hormonal responses are relatively slower and can last longer. For example, cortisol responses are typically delayed relative to stress onset by around 15 minutes. Cortisol reaction corresponding to the time immediately before or shortly after stressor onset is generally considered as anticipatory stress, whereas cortisol response corresponding to later parts of the stressor is considered to reflect reactive stress (Mikolajczak et al., 2008). On the other hand, the SAM axis secretes adrenaline and noradrenaline to provide rapid physiological adaptation to stress, including the elevation of heart rate (HR), breathing rate and blood pressure (BP). Given the swift changes of these markers, the cardiovascular responses are often monitored during the stress process to capture the immediate stress reaction profile. Other well-documented physiological and hormonal responses to acute stress include the secretion of salivary alpha-amylase (sAA), an enzyme that facilitates digestion in the oral cavity (Petrakova et al., 2015); elevated level of dehydroepiandrosterone (DHEA), an androgen precursor secreted by the adrenal gland (Lennartsson et al., 2012); and changes in BP, skin conductance level (SCL) and heart-rate variability (HRV) (Wemm and Wulfert, 2017, Berntson and Cacioppo, 2004). In addition, the immune systems are also sensitive to stress. Exposure to stressors have been linked with prolonged proinflammatory cytokine releases and increased levels of circulating cytokines, including interleukin-6 (IL-6) and C-reactive protein (CRP) (see (Steptoe et al., 2007) for systematic review).

Besides the biological changes to acute stress, mood states are often self-reported pre- and post-stressor to record the emotional changes. Individuals exposed to stress generally report a subjectively negative experience with increased perceived stress and anxiety [e.g., 16-17]. However, to our best knowledge, there has been no systematic review or meta-analysis on the mood state changes in response to acute stress.

Although a number of previous reviews examined biological responses to acute stress, only one narrative review examined multiple biological and psychological markers (Allen et al., 2014). Also, most existing meta-analyses on biomarkers of acute stress examined only one specific type of marker, such as cortisol (Helminen et al., 2019, Liu et al., 2017 Aug), DHEA (Dutheil et al., 2021), salivary inflammatory markers (Steptoe et al., 2007, Szabo et al., 2020), and blood pressure (Gasperin et al., 2009). Moreover, few reviews have examined the recovery patterns of acute stress responses, or the association of biological and psychological response changes during acute stress response and recovery (Dickerson and Kemeny, 2004, Dickerson, 2008).

Therefore, in this systematic review and meta-analysis, we aimed to comprehensively summarize existing empirical evidence on biological, endocrinological/hormonal and emotional responses to the most commonly adopted acute stress paradigm, the Trier Social Stress Test (TSST) (Kirschbaum et al., 1993), encompassing both stress reactivity and recovery. Importantly, we also reviewed the interrelations between changes in all common biomarkers and both positive and negative emotions across the TSST, in order to provide an updated account on the biology-emotion association in acute stress outcome.

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