Psychoneuroendocrinology 74 (2016) 111–120 Contents lists available at ScienceDirect Psychoneuroendocrinology journal homepage: www.elsevier.com/locate/psyneuen Boosting recovery rather than buffering reactivity: Higher stress-induced oxytocin secretion is associated with increased cortisol reactivity and faster vagal recovery after acute psychosocial stress Veronika Engert (PhD) ∗ , Anna M. Koester (MSc), Antje Riepenhausen (BSc), Tania Singer (PhD) Max Planck Institute for Human Cognitive and Brain Sciences, Department of Social Neuroscience, 04103 Leipzig, Germany a r t i c l e i n f o Article history: Received 4 May 2016 Received in revised form 3 August 2016 Accepted 30 August 2016 Keywords: Stress Reactivity Recovery Plasma oxytocin Cortisol Heart rate variability a b s t r a c t Animal models and human studies using paradigms designed to stimulate endogenous oxytocin release suggest a stress-buffering role of oxytocin. We here examined the involvement of stress-induced periph- eral oxytocin secretion in reactivity and recovery phases of the human psychosocial stress response. Healthy male and female participants (N = 114) were subjected to a standardized laboratory stressor, the Trier Social Stress Test. In addition to plasma oxytocin, cortisol was assessed as a marker of hypothalamic- pituitary-adrenal (HPA-) axis activity, alpha-amylase and heart rate as markers of sympathetic activity, high frequency heart rate variability as a marker of vagal tone and self-rated anxiety as an indicator of subjective stress experience. On average, oxytocin levels increased by 51% following psychosocial stress. The stress-induced oxytocin secretion, however, did not reduce stress reactivity. To the contrary, higher oxytocin secretion was associated with greater cortisol reactivity and peak cortisol levels in both sexes. In the second phase of the stress response the opposite pattern was observed, with higher oxy- tocin secretion associated with faster vagal recovery. We suggest that after an early stage of oxytocin and HPA-axis co-activation, the stress-reducing action of oxytocin unfolds. Due to the time lag it man- ifests as a recovery-boosting rather than a reactivity-buffering effect. By reinforcing parasympathetic autonomic activity, specifically during stress recovery, oxytocin may provide an important protective function against the health-compromising effects of sustained stress. © 2016 Elsevier Ltd. All rights reserved. 1. Introduction The neuropeptide oxytocin is best known as a modulator of social behavior (Lee et al., 2009; McCall and Singer, 2012; Meyer- Lindenberg et al., 2011; Neumann and Landgraf, 2012). As such, it plays a critical role in social cognition, affect (McCall and Singer, 2012; Winslow and Insel, 2004), attachment and pair bonding (Insel and Young, 2001). Above and beyond its role as a social hormone, oxytocin is hypothesized to act as a stress buffer in the mam- malian stress response, including humans (Engelmann et al., 2004; Heinrichs et al., 2009; Neumann, 2002). Oxytocin is primarily synthesized in the magnocellular neu- rons of the paraventricular and supraoptic nuclei (PVN, SON) of ∗ Corresponding author at: Max Planck Institute for Human Cognitive and Brain Sciences, Department of Social Neuroscience, Stephanstr. 1a, 04103, Leipzig, Germany. E-mail address: engert@cbs.mpg.de (V. Engert). the hypothalamus (Gimpl and Fahrenholz, 2001). The bulk of the neuropeptide is transported to the posterior pituitary where it is released into the systemic blood stream. Lesser amounts are released into the central nervous system and act as neuromod- ulator via widely distributed pathways (Gimpl and Fahrenholz, 2001). The animal literature describes two approaches to the study of oxytocin-stress interactions. Stimulation studies inform about whether relatively increased central oxytocin release after lacta- tion or central oxytocin administration reduces the magnitude of acute stress responses. Alternatively, investigating the effect of stress induction on oxytocin release can demonstrate whether the organism makes use of this buffering mechanism in naturalistic conditions, i.e., when exposed to acute stress. Both approaches to studying oxytocin-stress interactions are well established in ani- mal research (Engelmann et al., 2004; Neumann, 2002; Neumann and Landgraf, 2012). In humans, the measurement of neuropeptides in the cere- brospinal fluid is highly invasive and not feasible in experimental research. As a result, central oxytocin effects are typically studied http://dx.doi.org/10.1016/j.psyneuen.2016.08.029 0306-4530/© 2016 Elsevier Ltd. All rights reserved.