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Effort deficits and depression: The influence of anhedonic depressive symptoms on cardiac autonomic activity during a mental challenge

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Abstract

Motivational approaches to depression emphasize the role of dysfunctional motivational dynamics, particularly diminished reward and incentive processes associated with anhedonia. A study examined how anhedonic depressive symptoms, measured continuously across a wide range of severity, influenced the physiological mobilization of effort during a cognitive task. Using motivational intensity theory as a guide, we expected that the diminished incentive value associated with anhedonic depressive symptoms would reduce effort during a “do your best” challenge (also known as an unfixed or self-paced challenge), in which effort is a function of the value of achieving the task’s goal. Using impedance cardiography, two cardiac autonomic responses were assessed: pre-ejection period (PEP), a measure of sympathetic activity and our primary measure of interest, and respiratory sinus arrhythmia (RSA), a measure of parasympathetic activity. As expected, PEP slowed from baseline to task as anhedonic depressive symptoms increased (as measured with the Depression Anxiety Stress Scale), indicating diminished effort-related sympathetic activity. No significant effects appeared for RSA. The findings support motivational intensity theory as a translational model of effort processes in depression and clarify some inconsistent effects of depressive symptoms on effort-related physiology found in past work.

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Notes

  1. We also included the Center for Epidemiological Studies—Depression Scale (CES-D; Radloff 1977) as a secondary measure of depressive symptoms. The CES-D covers a broader range of symptoms, not just anhedonic ones, and it is the scale used in all the studies reported by Brinkmann and her colleagues on dysphoria and effort. We thus included it to evaluate the unlikely possibility of scale-specific effects that might explain differences between the present study and their findings. The DASS and CES-D correlated highly (r = .81, p < .001), and the physiological effects were essentially identical: everything that was significant for the DASS was significant for the CES-D, and vice versa. Differences between the present findings and past research thus aren’t due to using different depression scales.

  2. Several researchers have recently suggested using the time difference (in ms) between the R point (the peak of the ECG) and the Z point (the peak of the dZ/dt) as a measure of contractility (e.g., Cybulski 2011; Meijer et al. 2008; van Lien et al. 2013). This index has been called the RZ interval or the initial systolic time interval, and several studies suggest it is an effective measure of left ventricular contractility (e.g., van der Meer et al. 1999; Wilde et al. 1981). To inform this emerging literature, we estimated the same multilevel model using RZ intervals as the outcome. The same effects appeared: RZ intervals decreased from task to baseline overall, reflecting increased sympathetic activity (b = −1.41, SE = .43, p < .001); DASS scores had a main effect on RZ intervals, reflecting less baseline sympathetic impact as depressive symptoms increased (b = 7.62, SE = 2.42, p = .002); and DASS scores moderated the effect of time on RZ intervals, reflecting larger RZ intervals (and hence less sympathetic impact) as depressive symptoms increased (b = 2.45, SE = .55, p < .001). The similar pattern and higher significance levels lend some weight to the use of RZ intervals as a complementary measure of sympathetic influence.

  3. Some research on effort and HRV (e.g., Segerstrom and Nes 2007) has used time-domain measures, such as the root mean square of successive differences (RMSSD) of the interbeat intervals, instead of frequency-domain measures (e.g., RSA). In our data, the results were largely the same for RMSSD, with one notable difference. At the within-person level, there was a marginal main effect of time, b = 3.42, SE = 1.82, p = .061. Unlike RSA, which had a null effect, RMSSD increased from baseline to task, reflecting stronger parasympathetic activity. At the between-person level, depressive symptoms did not predict either the RMSSD intercept (b = 2.03, SE = 6.88, p = .768) or change in RMSSD from baseline to task (b = −1.66, SE = 2.36, p = .483). The main effect of time—an increase in RMSSD from baseline to task—is consistent with Segerstrom’s proposal that HRV can reflect increased self-regulatory control under some circumstances (Segerstrom et al. 2012).

  4. We can appreciate that multilevel models are unfamiliar for many motivation researchers, so we also analyzed the central PEP finding using more common reactivity scores. These analyses are more familiar and illustrate the parallels between multilevel models and traditional difference-score approaches. We created a PEP reactivity score by subtracting PEP scores during the baseline (the average of the 5 periods) from the PEP scores (averaged across the 5 periods) during the parity task. The reactivity scores didn’t correlate with the baseline scores (r = .12, p = .22), so they were not residualized with respect to the baseline (Llabre et al. 1991). For the full sample, DASS scores correlated with baseline scores (r = .23, p = .012), which is akin to the between-person main effect of DASS scores on PEP scores in the multilevel model—PEP slowed as DASS scores increased. DASS scores also correlated with PEP reactivity scores (r = .29, p = .002), which is akin to the significant interaction between DASS scores and time (baseline vs. task) in the multilevel model. People with lower DASS scores had more strongly negative change scores, and vice versa. We then selected the upper and lower 30 % based on DASS scores, akin to the use of extreme groups in past work (e.g., Brinkmann and Gendolla 2007, 2008), which yielded a sample of 72 people. The average reactivity score was M = −.58 (SE = .33), indicating that for the sample as whole, PEP was faster during the parity task. But PEP reactivity was faster in the low DASS group (M = -1.43, SE = .55, 95 % CI = −2.56, −.30) than in the high DASS group (M = .15, SE = .36, 95 % CI = −.59, .88). As the confidence intervals show, the low DASS group had PEP reactivity scores that both differed significantly from zero (reflecting significant change from the baseline) and from the high DASS group (reflecting a significant between-group difference). PEP reactivity in the high DASS group, in contrast, didn’t differ significantly from zero, reflecting a lack of effort mobilization.

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Acknowledgments

We thank Christina Chai Chang, Emily Galloway, Bryonna Jackson, Kimberly Jung, Edna Kabisa, Lance Moore, Joseph Nardello, Rachel Sopko, and Ceaira Walker for their assistance. This research was supported by award number R15MH079374 from the National Institute of Mental Health.

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Silvia, P.J., Nusbaum, E.C., Eddington, K.M. et al. Effort deficits and depression: The influence of anhedonic depressive symptoms on cardiac autonomic activity during a mental challenge. Motiv Emot 38, 779–789 (2014). https://doi.org/10.1007/s11031-014-9443-0

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