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We utilized a data-driven, unsupervised machine learning approach to examine patterns of peripheral physiological responses during a motivated performance context across two large, independent data sets, each with multiple peripheral physiological measures. Results revealed that patterns of cardiovascular response commonly associated with ‘challenge’ and ‘threat’ states emerged as two of the predominant patterns of peripheral physiological responding within both samples, with these two patterns best differentiated by reactivity in cardiac output (CO), pre-ejection period (PEP), interbeat interval (IBI), and total peripheral resistance (TPR). However, we also identified a third, relatively large group of apparent physiological “non-responders” who exhibited minimal reactivity across all physiological measures in the motivated performance context. This group of “non-responders” was best differentiated from the others by minimal increases in electrodermal activity. We discuss implications for identifying and characterizing this third group of individuals in future research on physiological patterns of challenge and threat.

Mental stress can trigger myocardial infarction, with poor vascular responses to stress implicated as a pathway. Vascular stress reactivity can be assessed by different methods, such as total peripheral resistance (TPR) and forearm blood flow (FBF). Little is known about how these vascular assessments are linked. This was examined in two separate studies. Healthy men (Study 1: N = 29, Study 2: N = 23) completed rest and mental arithmetic (Study 1: 8 min, Study 2: 16 min). In both studies, heart rate, mean arterial pressure, and FBF increased in response to stress. In Study 1, no changes in TPR were seen, but Study 2 found stress-induced increases in TPR. FBF was not linked to TPR at any time (all ps > .05). It appears that limb vasculature and TPR responses to stress do not give the same information about impairments of the vasculature. These findings are relevant to the interpretation of prior research findings and the design of future studies on stress and vascular responses.

This study examined how the outcomes of joint decision making relate to cardiovascular reactions when group members disagree about the decision to be taken. A conflict was experimentally induced during a joint decision-making task, while cardiovascular markers of challenge/threat motivational states were assessed following the biopsychosocial model of challenge and threat (BPSM; J. Blascovich, 2008). Results show that individuals were less likely to adjust their initially preferred decision alternative the more they exhibited a cardiovascular pattern indicative of threat (i.e., relatively high total peripheral resistance and low cardiac output) compared to challenge. This finding extends the BPSM by showing a link between threat and rigidity, and emphasizes the importance of psychophysiological processes for studying intragroup conflict and decision making.

A quantitative, theory-driven model of hemodynamics was developed, relating reactivity in blood pressure to orthogonal dimensions of hemodynamic profile and compensation deficit, which were derived from the (multiplicative) interaction of cardiac output and total peripheral resistance. A Finapres 2300e was used to estimate blood pressure, cardiac output, and total peripheral resistance in 100 healthy men and women during mental arithmetic and cold pressor tasks on two occasions. Results were consistent with model predictions. As predicted, cardiac output and peripheral resistance reactions were curvilinearly related, and blood pressure reactivity was strongly related to compensation deficit (r = .76-.89). Conversely, the orthogonally defined hemodynamic profile remained independent of blood pressure reactivity (r = .11 or less). The data show that the present model overcomes several difficulties and inconsistencies in previous attempts to obtain an independent measure of hemodynamic profile. The new model could help to elucidate sources of cardiovascular pathogenesis not suggested from the study of blood pressure reactivity alone.