Task difficulty effects on cardiac activity MICHAEL RICHTER, a ANTONIA FRIEDRICH, b and GUIDO H. E. GENDOLLA a a Department of Psychology, University of Geneva, Geneva, Switzerland b Department of Psychology, University of Leipzig, Leipzig, Germany Abstract An experiment with 64 participants manipulated task difficulty and assessed cardiac reactivity in active coping over four levels of demand. Participants performed a memory task while preejection period, heart rate, and blood pressure were assessed. In accordance with the theoretical predictions of R. A. Wright’s (1996) integration of motivational intensity theory (J. W. Brehm & E. A. Self, 1989) with Obrist’s active coping approach (P. A. Obrist, 1981), preejection period and systolic blood pressure reactivity increased with task difficulty across the first three difficulty levels. On the fourth difficulty levelFwhere success was impossibleFreactivity of both preejection period and systolic blood pres- sure were low. These findings provide the first clear evidence for the notion of Wright’s integrative model that energy mobilization in active coping is mediated by beta-adrenergic impact on the heart. Descriptors: Task difficulty, Beta-adrenergic response, Cardiovascular reactivity, Active coping According to motivational intensity theory (Brehm & Self, 1989), human behavior is guided by a resource conservation principle. Drawing on this basic assumption, the theory predicts that diffi- culty and success importance are the two major determinants of energy investment in instrumental behavior (i.e., behavior that allows one to attain a certain goal). Energy expenditure should be proportional to a behavior’s difficulty as long as success is pos- sible and justified. If a behavior is either too difficult or the nec- essary amount of energy for its execution exceeds the justified level, energy investment should be low. Wright (1996) integrated these predictions with Obrist’s (1981) active coping approach. According to this perspective, energy mobilization in active copingFwhen individuals have control over performance outcomesFis reflected in cardiovascular reactivity. More spe- cifically, based on Obrist’s demonstration that task engagement is mediated by sympathetic (beta-adrenergic) discharge to the myocardium (Obrist, 1976, 1981; see also Fredrikson, Klein, & Oehman, 1990; Winzer et al., 1999), Wright postulated that effects on cardiovascular reactivity should be mediated by beta- adrenergic activity. Past research supported this integrative perspective by dem- onstrating that standard parameters of cardiovascular activ- ityFheart rate and systolic, diastolic, and mean arterial blood pressure follow the predicted interaction of task difficulty and success importance. Especially, responses of systolic blood pres- sure (SBP) reliably showed the expected pattern (see Gendolla & Wright, 2005; Richter, Gendolla, & Kru¨ sken, 2006; Wright, 1996, 1998; Wright & Kirby, 2001, for reviews). However, these previous findings are only of limited conclusiveness regarding the postulated mediation of energy mobilization by beta-adrenergic activity. Systolic, diastolic, and mean arterial blood pressure de- pend more or less strongly on the force of myocardial contrac- tion, which primarily reflects beta-adrenergic discharge to the heart. However, increases in blood pressure due to changes in myocardial contractility can be counteracted by other effects. For instance, beta-adrenergic impact on the vasculature may decrease peripheral resistance and, thus, negate myocardial beta- adrenergic effects. Furthermore, blood pressure measures are not very diagnostic for changes in beta-adrenergic activity because increases in peripheral resistanceFeither sympathetically or pa- rasympathetically mediatedFmay have the same effect on blood pressure as increases in myocardial beta-adrenergic activity: an increase in blood pressure (e.g., Levick, 2003). The same logic applies to heart rate. Increases in beta-adrenergic activity may increase heart rate. However, these effects may be counter- acted by concurrent increases in parasympathetic activity. Furthermore, increases in heart rate may be due to increases in sympathetic beta-adrenergic activity or due to decreases in parasympathetic activity (e.g., Levick, 2003). Thus, there is only limited evidence for Wright’s (1996) pre- diction that energy mobilization is accompanied by increases in myocardial beta-adrenergic activity. Given the basic role of beta- adrenergic activity in Wright’s adaptation of motivational inten- sity theory to psychophysiology, it is astonishing that research on the integrative perspective has nearly exclusively been limited to cardiovascular measures that are, at best, mediocre indicators of myocardial beta-adrenergic activity. A more valid indicator of beta-adrenergic impact on the myocardium is preejection pe- riodFthe time interval between the onset of ventricular depo- larization and the opening of the aortic valve. Preejection period (PEP) reflects the force of myocardial contraction and is mainly influenced by beta-adrenergic activity (e.g., Benschop et al., We are grateful to Kerstin Brinkmann, Judith Dirk, and Nicolas Silvestrini for helpful comments on an early draft of this article. Address reprint requests to: Michael Richter, University of Geneva, FPSE, Department of Psychology, 40, Bd. du Pont-d’Arve, CH-1211 Geneva 4, Switzerland. E-mail: Michael.Richter@pse.unige.ch Psychophysiology, 45 (2008), 869–875. Wiley Periodicals, Inc. Printed in the USA. Copyright r 2008 Society for Psychophysiological Research DOI: 10.1111/j.1469-8986.2008.00688.x 869