We conducted a preregistered multilaboratory project ( k = 36; N = 3,531) to assess the size and robustness of ego-depletion effects using a novel replication method, termed the paradigmatic replication approach. Each laboratory implemented one of two procedures that was intended to manipulate self-control and tested performance on a subsequent measure of self-control. Confirmatory tests found a nonsignificant result ( d = 0.06). Confirmatory Bayesian meta-analyses using an informed-prior hypothesis (δ = 0.30, SD = 0.15) found that the data were 4 times more likely under the null than the alternative hypothesis. Hence, preregistered analyses did not find evidence for a depletion effect. Exploratory analyses on the full sample (i.e., ignoring exclusion criteria) found a statistically significant effect ( d = 0.08); Bayesian analyses showed that the data were about equally likely under the null and informed-prior hypotheses. Exploratory moderator tests suggested that the depletion effect was larger for participants who reported more fatigue but was not moderated by trait self-control, willpower beliefs, or action orientation.

Using a high-throughput mitochondrial phenotyping platform to quantify multiple mitochondrial features among molecularly-defined immune cell subtypes, we quantify the natural variation in citrate synthase, mitochondrial DNA copy number (mtDNAcn), and respiratory chain enzymatic activities in human neutrophils, monocytes, B cells, and naïve and memory T lymphocyte subtypes. In mixed peripheral blood mononuclear cells (PBMCs) from the same individuals, we show to what extent mitochondrial measures are confounded by both cell type distributions and contaminating platelets. Cell subtype-specific measures among women and men spanning 4 decades of life indicate potential age- and sex-related differences, including an age-related elevation in mtDNAcn, which are masked or blunted in mixed PBMCs. Finally, a proof-of-concept, repeated-measures study in a single individual validates cell type differences and also reveals week-to-week changes in mitochondrial activities. Larger studies are required to validate and mechanistically extend these findings. These mitochondrial phenotyping data build upon established immunometabolic differences among leukocyte sub-populations, and provide foundational quantitative knowledge to develop interpretable blood-based assays of mitochondrial health.

Self-regulation, or the ability to modulate one's thoughts, actions and emotions, is necessary for achieving one's goals and functioning well. Poor self-regulation can lead to ineffective problem solving, passive coping techniques, difficulties altering one's mood, and difficulties in overriding impulses (Vohs & Baumeister, 2004). Evidence of self-regulatory failure can be seen in many of the problems plaguing society, such as obesity, aggression, and drug and alcohol abuse. The process of self-regulation may be conscious and deliberate or unconscious and automatic. Likewise, the substrates of selfregulation may be accessible or inaccessible to consciousness. Although individuals have some insight into their typical self-regulatory capacity, they are often unaware of phasic decrements in their ability to meet self-regulatory demands (Baumeister, Bratslavsky, Muraven, & Tice, 1998;Vohs & Baumeister, 2004). Therefore, self-regulation is a more expansive concept than self-control, which typically connotes only conscious control over the self. Furthermore, self-regulation can encompass both psychosocial and physiological systems; indeed, one aim of this chapter is to demonstrate how psychological and cardiac regulation are related.

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Objective Misestimation as a consequence of small sample sizes, small effect sizes, and noisy measurement may be particularly problematic in biomarker studies, the cost of which can adversely affect design decisions. This simulation study used real study designs reported in a meta-analysis of psychosocial correlates of the cortisol awakening response to investigate the probability that the results of these designs would yield misestimates in a cross-sectional study. Methods For each of the 212 designs, 100,000 simulated data sets were produced and the percentages of effects that were in the wrong direction and/or that differed by more than 0.10 from the true effect (b = 0.10) were calculated. Results As expected, small samples (n < 100) and noisy measurement contributed to higher probability of errors. The average probability of an effect being in the wrong direction was around 20%, with some designs reaching 40%; misestimation probabilities were around 40%, with some designs reaching 80%. This was true for all studies as well as those reporting statistically significant effects. Conclusion Results call for better study designs, and this article provides suggestions for how to achieve more accurate estimates.