Behavior
Author (Year) | Cohen's : D1DR | | D1DR | Human | −2.20 | | −2.47 |
| D1DR | Human | −1.02 | | −2.40 |
| D1DR | Primate | −1.64 | | −1.79 |
| D1DR | Rodent | 0.88 | | −1.32 |
| D1DR | Rodent | −3.24 | | −1.10 |
| D1DR | Primate | −1.31 | | −0.99 |
| D1DR | Primate | −0.92 | | −0.97 |
| D1DR | Rodent | −0.55 | | −0.79 |
| D1DR | Rodent | −1.30 | | −0.78 |
| D1DR | Rodent | −1.98 | | −0.77 |
| D1DR | Rodent | −0.02 | | −0.68 |
| D1DR | Rodent | −0.10 | | −0.68 |
| D1DR | Rodent | 0.68 | | −0.64 |
| D1DR | Rodent | −0.04 | | −0.64 |
| D1DR | Rodent | 1.06 | | −0.57 |
| D1DR | Rodent | −0.10 | | −0.57 |
| D1DR | Rodent | 1.34 | | −0.50 |
| D1DR | Rodent | 1.03 | | −0.32 |
| D1DR | Rodent | 0.50 | | −0.11 |
| D1DR | Rodent | −0.17 | | −0.11 |
| D1DR | Rodent | 0.22 | | −0.10 |
| D1DR | Rodent | −1.23 | | 0.00 |
| D1DR | Rodent | −0.97 | | 0.00 |
| D1DR | Rodent | 0.41 | | 0.00 |
| D1DR | Primate | −1.26 | | 0.19 |
| D1DR | Rodent | −1.06 | | 0.32 |
| D1DR | Rodent | −0.63 | | 0.38 |
| D1DR | Rodent | −1.21 | | 0.47 |
| D1DR | Human | −1.13 | | 0.87 |
| D1DR | Rodent | −2.34 | | 0.95 |
| D1DR | Rodent | −0.45 | | 1.09 |
| D1DR | Rodent | −1.23 | | 1.17 |
| D1DR | Rodent | −0.97 | | 1.17 |
| D1DR | Rodent | −1.17 | Areal et al (2015) | 1.47 |
| D1DR | Rodent | −1.89 | | 1.74 |
| D1DR | Rodent | −3.14 | | 1.93 |
| D1DR | Primate | −3.34 | | 2.09 |
Statistical analyses were completed using R software, version 4.1.1. All code and raw data are available at https://narayanan.lab.uiowa.edu . All statistical analyses were performed and verified independently by the Biostatistics, Epidemiology, and Research Design Core within the Institute for Clinical and Translational Science at the University of Iowa.
The primary goal of this meta-analysis was to identify polynomial models (up to order three) that explain changes in working memory performance with changes in prefrontal dopamine and/or D1DRs. We developed models based on the relationship between working memory effect sizes and prefrontal dopamine and D1DR effect sizes. We excluded values greater than or less than a Cohen’s d of +/− 4, as these could have an outsized effect on our models. First, we fit a model based on working memory performance and all prefrontal dopamine and D1DRs. This analysis was followed by stratifying the data set to develop a model fit based on working memory performance and prefrontal dopamine and a model fit based on working memory performance and prefrontal D1DRs. Several publications contributed multiple values to the final data set, and this was accounted for by including a random intercept for each publication. Model fits between different polynomial orders were compared via Akaike Information Criteria (AIC), with lower AICs indicating a better combination of parsimony and goodness of fit.
We used a bootstrap analysis approach to compare R 2 values for prefrontal dopamine and prefrontal D1DRs. This process began by simulating a new dataset for both prefrontal dopamine and prefrontal D1DRs; we resampled the original datasets with replacement to create new datasets the same size as the original. Then, a quadratic model was built on each resampled dataset, and the R 2 value of the dopamine model was subtracted from the R 2 values of the D1DR model. This process was repeated 10,000 times to obtain bootstrap-estimated intervals that reflect 95% confidence for the difference between the two models and that one model’s fit is superior to the other. Here, a positive confidence interval that does not contain zero would indicate that the prefrontal D1DR model provides a superior R 2 value compared to the prefrontal dopamine R 2 value.
Our literature search and screening procedures yielded 75 journal articles that fit our criteria, resulting in 165 data points ( Tables 1 and and2). 2 ). After extreme values (Cohen’s d >+4 and <− 4) were excluded, 156 data points remained. We found that a quadratic function provided the optimal model fit (2 nd order polynomial; p<0.001; AIC = 400.2 vs. linear AIC = 412.7). The R 2 value for the negative quadratic fit was 0.10. A higher order polynomial model did not decrease AIC values (3 rd order AIC = 408.8), suggesting that the 2 nd order model is optimal.
We then stratified our data based on type of prefrontal measure, with a sub-analysis focused on prefrontal dopamine (i.e., dopamine content or turnover, tyrosine hydroxylase, dopamine transporter, etc.). These could include direct manipulations of prefrontal dopamine (e.g., dopamine depletion via 6-hydroxydopamine) or indirect manipulation such as stress or peripheral drug administration. For this analysis, we found 61 studies and 119 data points. A negative quadratic function provided the strongest fit with AIC = 314.4 (p<0.001; vs. linear AIC = 317.2, 3 rd order AIC = 322.7). The R 2 value for our quadratic model was 0.10.
Prefrontal dopamine released from synaptic terminals can powerfully act on prefrontal D1DRs ( Goldman-Rakic et al., 2004 , p.; Seamans and Yang, 2004 ). We examined the role of prefrontal D1DR manipulations on working memory performance in 17 studies with 37 data points. In line with data on prefrontal dopamine, we found that a negative quadratic function again provided the best fit, with AIC = 102.6 (p<0.001; vs. linear AIC = 110.2; 3 rd order AIC = 106.3). The R 2 value for this model was 0.26. Increasing the polynomial order coincided with an increase in the AIC values, suggesting that the negative quadratic model again provided the best combination of parsimony and goodness of fit. Adding an effect for the species being studied did not notably enhance our model’s goodness of fit, possibly due to insufficient sample size to detect this effect. When a variable controlling for species was added to our negative quadratic model, our AIC worsened from 314.4 to 315.5 for the prefrontal dopamine model and from 102.6 to 103.0 for the prefrontal D1DR model.
We then built new quadratic models using the resampling bootstrapped analysis described above for both prefrontal dopamine and prefrontal D1DRs and determined the difference between the two newly-built models. The average difference between R 2 values for the 10,000 iterations was 0.14, where a positive value indicated that the prefrontal D1DR models had a greater R 2 value. The 95% confidence interval for this result was (−0.10, 0.38) and the bootstrapped two-sided p value was 0.31.
Our goal was to quantify the relationship of working memory performance with prefrontal dopamine and D1DRs. We conducted a meta-analysis of 75 studies spanning rodents, non-human primates, and humans. These data suggest that 10% of the variance in working memory behavior was explained by manipulations of prefrontal dopamine, and 26% of the variance was explained by prefrontal D1DR manipulations. These data provide insight into how prefrontal dopamine and D1DRs affects cognitive behaviors.
Our findings are broadly consistent with past work that has proposed an inverted U-shaped relationship between prefrontal dopaminergic dynamics and working memory performance ( Cools and D’Esposito, 2011 ; Floresco, 2013 ). We were able to demonstrate this idea by quantitatively fitting an inverted quadratic function, supporting the idea that there is an optimal regime for dopamine function in the prefrontal cortex that may facilitate a wide range of interacting synaptic and post-synaptic proteins ( Arnsten et al., 2012 ; Arnsten and Li, 2005 ). In establishing this function, we show that prefrontal dopamine has strikingly different signaling principles than striatal dopamine ( Kreitzer, 2009 ; Mohebi et al., 2019 ; Yahr et al., 1969 ), in which striatal dopamine depletion can impair movement ( Burns et al., 1983 ; Schultz et al., 1989 ; Kirik et al., 1998 ) . However, in the striatum there are important differences in that many principal neurons express largely either D1- or D2-type dopamine receptors, and these systems can work in tandem to coordinate a wide range of behaviors. For instance, increasing striatal dopamine or stimulating D1 medium spiny neurons can facilitate or hyperstimulate movement ( Fredriksson et al., 1990 ; Brannan et al., 1998 ; Carta et al., 2006 ; Kravitz et al., 2010). However, both decreasing and increasing striatal dopamine can impair motivation ( Bryce & Floresco, 2019 ; Filla et al., 2018 ; Fry et al., 2021 ; Kamada & Hata, 2020; Salamone et al., 2012 ). Thus, the details of the dopaminergic effects on a behavior depend not just on the complex pharmacodynamics of the dopamine receptor, but how neurons expressing these receptors are precisely integrated into circuits.
While this work supports the hypothesis that working memory performance follows an inverted U-shape function dependent on prefrontal dopamine and D1DRs, our results should be interpreted carefully. For example, the bootstrapped analysis for models of prefrontal D1DRs were not significantly different from models of prefrontal dopamine; however, we note that there were fewer studies for prefrontal D1DRs, which may have affected our statistical power in separating prefrontal D1DRs from prefrontal dopamine manipulations. We also note that there may be important sampling bias; for instance, there are more studies that disrupt prefrontal dopamine/D1DRs than increase dopamine or D1DRs, and very few studies describing increased prefrontal dopamine or D1DRs result in increased working memory function. This insight may suggest that it is challenging to consistently improve working memory with dopaminergic manipulations, at least in intact prefrontal circuits.
Another key constraint is that rodents do not have lateral prefrontal regions that are present in primates ( Laubach et al., 2018 ), although dopamine is strongly released in medial prefrontal regions, and dopamine in these circuits may function according to similar principles ( Floresco, 2013 ; Zahrt et al., 1997 ). It is also important to acknowledge that changes to working memory performance are not only impacted by manipulations of prefrontal dopamine and D1DRs. Other prefrontal dopamine receptors ( Druzin et al., 2000 ; Glickstein et al., 2002 ), neurotransmitter systems ( Monaco et al., 2015 ; Robbins and Arnsten, 2009 ), brain regions ( Bolkan et al., 2017 ; Hart et al., 2018 ), and behaviors (i.e. interval timing, behavioral flexibility – Kim et al., 2017 ; Ragozzino, 2002 ; Zhang et al., 2019 ) are critical for optimal working memory performance. Furthermore, there are other paradigms that can be used to study executive functions, and U-shaped dynamics may be relevant for some behavioral paradigms such as attention, reversal learning, and interval timing ( Floresco, 2013 ; Parker et al., 2015 ; Robbins, 2007 ). However, other behavioral paradigms such as set-shifting or risk-based decision making may have distinct prefrontal dopaminergic dynamics, suggesting that these cognitive paradigms may have distinct relationships between prefrontal dopamine and D1DRs ( Floresco, 2013 ). However, our literature search revealed among manipulations of prefrontal dopamine and cognition that working memory paradigms had the largest number of studies, making it a reasonable starting point for comparisons across metholodogies and species. This work also has limitations that derive from comparing a broad range of studies across several different methodologies and model systems. However, this diversity is also a strength in that we report effects that are consistent across a range of approaches. Finally, publication bias may have affected this analysis, meaning that non-reviewed and unpublished research could have influenced our conclusions. While there are many small effect sizes within our datasets, the wealth of unpublished research possibly reporting nonsignificant prefrontal dopamine, prefrontal D1DR, or working memory changes could alter our interpretation of the inverted U-shape function.
In summary, this study advances the approach of bringing together diverse studies to elucidate patterns in prefrontal dopamine. A key finding here is that, while not statistically significant, the prefrontal D1DRs explained more variance than prefrontal dopamine. Fascinatingly, the initial description of the inverted-U shaped working memory function is based largely on pharmacological activation or inhibition of prefrontal D1DRs. It is possible that working memory performance is more strongly dependent on dopamine receptor activation than specific levels of prefrontal dopamine. This pattern will be useful in designing and interpreting preclinical studies, as well as in designing and optimizing new therapies for diseases such as ADHD, schizophrenia, and PD, which involve profound disruptions in prefrontal dopamine signaling.
We included studies that measured both working memory performance and either prefrontal D1DRs or dopamine levels. We included studies from rodents, non-human primates, and humans, and expressed effect sizes in Cohen’s d . We found that studies that measured prefrontal D1DRs (red), prefrontal dopamine (blue) were best fit by a negative quadratic function. The model aggregating both prefrontal dopamine and D1DR measurements is shown in grey. Data from 75 studies and a total of 156 data points; 119 that measured prefrontal dopamine levels and 37 that measured prefrontal D1DR levels.
Studies that reported comparisons of prefrontal cortex dopamine and working memory between control and experimental subjects.
Author (Year) | Type | Species | Cohen's : Behavior | Author (Year) | Cohen's : Dopamine |
---|
| Dopamine | Rodent | −2.50 | | −3.76 |
| Dopamine | Primate | −3.30 | | −3.68 |
| Dopamine | Rodent | −3.73 | | −3.55 |
| Dopamine | Rodent | −0.37 | | −3.46 |
| Dopamine | Rodent | −1.38 | | −3.31 |
| Dopamine | Rodent | −1.51 | | −3.31 |
| Dopamine | Rodent | −1.49 | | −3.31 |
| Dopamine | Rodent | −1.05 | | −2.71 |
| Dopamine | Rodent | −0.88 | | −2.71 |
| Dopamine | Rodent | −0.96 | | −2.49 |
Gibbs & D'Esposito (2006) | Dopamine | Human | −0.63 | Gibbs & D’Esposito (2006) | −2.43 |
| Dopamine | Rodent | −2.62 | | −2.20 |
| Dopamine | Primate | −0.94 | | −1.84 |
Bertolino et al (2006) | Dopamine | Human | −0.13 | Bertolino et al (2006) | −1.83 |
| Dopamine | Rodent | −1.24 | | −1.79 |
| Dopamine | Rodent | −1.13 | | −1.73 |
| Dopamine | Human | 0.14 | | −1.67 |
| Dopamine | Rodent | −2.34 | | −1.64 |
| Dopamine | Rodent | −1.89 | | −1.57 |
| Dopamine | Rodent | −0.59 | | −1.54 |
| Dopamine | Rodent | −1.17 | Areal et al (2015) | −1.43 |
| Dopamine | Rodent | −2.89 | | −1.43 |
| Dopamine | Rodent | −0.35 | | −1.39 |
| Dopamine | Human | −0.42 | | −1.36 |
Zhang et al (2021) | Dopamine | Rodent | −1.68 | Zhang et al (2021) | −1.33 |
| Dopamine | Human | 0.29 | | −1.30 |
| Dopamine | Human | 0.48 | | −1.25 |
| Dopamine | Rodent | −0.50 | | −1.23 |
| Dopamine | Primate | −0.44 | | −1.23 |
| Dopamine | Human | −1.22 | | −1.16 |
| Dopamine | Rodent | 0.37 | | −1.15 |
| Dopamine | Rodent | 0.00 | | −1.12 |
| Dopamine | Rodent | −0.17 | | −1.09 |
| Dopamine | Rodent | 0.00 | | −1.09 |
| Dopamine | Human | −0.25 | | −0.98 |
| Dopamine | Human | −0.49 | | −0.97 |
| Dopamine | Rodent | −1.36 | | −0.76 |
| Dopamine | Rodent | −0.14 | | −0.75 |
| Dopamine | Rodent | 0.08 | | −0.73 |
| Dopamine | Human | −0.09 | | −0.64 |
| Dopamine | Rodent | 0.16 | | −0.61 |
| Dopamine | Rodent | −0.55 | | −0.60 |
| Dopamine | Primate | −2.24 | | −0.55 |
| Dopamine | Rodent | −3.10 | | −0.51 |
| Dopamine | Rodent | −0.66 | | −0.46 |
Yamada et al (1999) | Dopamine | Rodent | −3.18 | Yamada et al (1999) | −0.45 |
Yamada et al (1999) | Dopamine | Rodent | −2.27 | Yamada et al (1999) | −0.45 |
| Dopamine | Human | −0.38 | | −0.44 |
| Dopamine | Rodent | 1.34 | | −0.42 |
| Dopamine | Rodent | −1.18 | | −0.40 |
| Dopamine | Human | −1.32 | | −0.40 |
| Dopamine | Rodent | −0.62 | | −0.39 |
| Dopamine | Rodent | −1.08 | | −0.36 |
| Dopamine | Rodent | 0.15 | | −0.35 |
Baumgartner et al (2012a) | Dopamine | Rodent | −1.93 | Baumgartner et al (2012a) | −0.33 |
| Dopamine | Rodent | 0.25 | | −0.29 |
| Dopamine | Rodent | 0.58 | | −0.29 |
| Dopamine | Rodent | 0.63 | | −0.29 |
| Dopamine | Rodent | −0.52 | | −0.26 |
| Dopamine | Rodent | −0.35 | | −0.18 |
| Dopamine | Rodent | −2.74 | | −0.11 |
| Dopamine | Rodent | 1.03 | | −0.11 |
| Dopamine | Rodent | 0.88 | | −0.09 |
| Dopamine | Rodent | −1.07 | | −0.08 |
| Dopamine | Rodent | −0.85 | | −0.08 |
| Dopamine | Rodent | −0.08 | | −0.08 |
| Dopamine | Rodent | −1.68 | | −0.04 |
| Dopamine | Rodent | −0.41 | | −0.04 |
| Dopamine | Rodent | −0.66 | | −0.03 |
Baumgartner et al (2012a) | Dopamine | Rodent | −1.96 | Baumgartner et al (2012a) | 0.00 |
Baumgartner et al (2012a) | Dopamine | Rodent | −1.47 | Baumgartner et al (2012a) | 0.00 |
| Dopamine | Rodent | −0.71 | | 0.00 |
| Dopamine | Rodent | −1.27 | | 0.07 |
| Dopamine | Rodent | −1.22 | | 0.10 |
| Dopamine | Rodent | −0.89 | | 0.11 |
| Dopamine | Rodent | −1.23 | | 0.12 |
| Dopamine | Rodent | −0.97 | | 0.12 |
| Dopamine | Rodent | −0.14 | | 0.14 |
| Dopamine | Rodent | −0.46 | | 0.18 |
Baumgartner et al (2012b) | Dopamine | Rodent | −0.61 | Baumgartner et al (2012b) | 0.33 |
| Dopamine | Rodent | −1.35 | | 0.40 |
| Dopamine | Rodent | −0.59 | | 0.44 |
| Dopamine | Rodent | −1.23 | | 0.55 |
| Dopamine | Rodent | −0.97 | | 0.55 |
| Dopamine | Rodent | −0.04 | | 0.55 |
| Dopamine | Rodent | 0.21 | | 0.58 |
| Dopamine | Rodent | −1.05 | | 0.65 |
| Dopamine | Rodent | −0.41 | | 0.67 |
Baumgartner et al (2012b) | Dopamine | Rodent | −1.42 | Baumgartner et al (2012b) | 0.67 |
Baumgartner et al (2012b) | Dopamine | Rodent | −1.03 | Baumgartner et al (2012b) | 0.67 |
Zhang et al (2021) | Dopamine | Rodent | 0.19 | Zhang et al (2021) | 0.76 |
| Dopamine | Rodent | −1.68 | | 0.78 |
| Dopamine | Rodent | −1.79 | | 0.78 |
| Dopamine | Rodent | −1.26 | | 0.79 |
| Dopamine | Rodent | 1.00 | | 0.83 |
| Dopamine | Rodent | −0.29 | | 0.84 |
| Dopamine | Rodent | −0.96 | | 0.89 |
| Dopamine | Rodent | −0.19 | | 0.93 |
| Dopamine | Human | −0.75 | | 0.93 |
| Dopamine | Rodent | −2.32 | | 0.98 |
| Dopamine | Rodent | −0.37 | | 1.01 |
| Dopamine | Rodent | 1.50 | | 1.06 |
| Dopamine | Rodent | −0.54 | | 1.11 |
| Dopamine | Rodent | −1.00 | | 1.11 |
| Dopamine | Rodent | −1.31 | | 1.13 |
| Dopamine | Rodent | −2.43 | | 1.21 |
Baumgartner et al (2012b) | Dopamine | Rodent | −0.67 | Baumgartner et al (2012b) | 1.33 |
| Dopamine | Rodent | −1.54 | | 1.41 |
| Dopamine | Rodent | 0.46 | | 1.43 |
| Dopamine | Rodent | −1.35 | | 1.53 |
| Dopamine | Rodent | −3.36 | | 1.63 |
| Dopamine | Rodent | −1.94 | | 1.74 |
Zhang et al (2021) | Dopamine | Rodent | 0.09 | Zhang et al (2021) | 1.86 |
| Dopamine | Rodent | −1.35 | | 2.04 |
| Dopamine | Rodent | −1.35 | | 2.28 |
| Dopamine | Rodent | −2.44 | | 2.28 |
Zhang et al (2021) | Dopamine | Rodent | −0.13 | Zhang et al (2021) | 2.58 |
| Dopamine | Rodent | −1.80 | | 2.94 |
| Dopamine | Rodent | −1.19 | | 3.44 |
Acknowledgements and Author Note:
MAW and NSN designed the meta-analysis. MAW and MMC independently screened abstracts for appropriateness. MAW collected the data, which was independently checked by NSN and HRS. LW, PTE, and NSN wrote the code and checked the analysis. MAW and NSN wrote the manuscript. HRS, LW, and PTE reviewed the manuscript. All code and raw data are available at https://narayanan.lab.uiowa.edu . This work was funded by NIH R01s MH116043, NS120987 to NN, and UL1TR002537.
This work was funded by NIH R01s MH116043, NS120987 to NSN. This study was partially supported by NIH UL1TR002537 to the Institute for Clinical and Translational Science at the University of Iowa.
Conflict of Interest:
There are no conflicts of interest.
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- DOI: 10.1080/02701367.2003.10609113
- Corpus ID: 7886976
Arousal, Anxiety, and Performance: A Reexamination of the Inverted-U Hypothesis
- S. Arent , D. Landers
- Published in Research Quarterly for… 1 December 2003
176 Citations
Relationship between arousal and choice reaction time, regulatory fit: impact on anxiety, arousal, and performance in college-level soccer players., the influence of cortisol, flow, and anxiety on performance in e-sports: a field study, the relationship between test anxiety and cognitive performance : mediated by state and trait self-control, the relationship between arousal zone, anxiety, stress and sports performance, arousal and activation in choice reaction time task, the effects of caffeine on arousal, response time, accuracy, and performance in division i collegiate fencers, a multidisciplinary investigation of the effects of competitive state anxiety on serve kinematics in table tennis, relationship between athletes' emotional intelligence and precompetitive anxiety, exploring the relationship between exercise-induced arousal and cognition using fractionated response time.
39 References
The relationship between the competitive state anxiety inventory-2 and sport performance: a meta-analysis, a catastrophe model of anxiety and performance., relationship between competitive state anxiety inventory-2 subscale scores and pistol shooting performance, do anxious swimmers swim slower reexamining the elusive anxiety-performance relationship.
Conceptual and Methodological Considerations in Sport Anxiety Research: From the Inverted-U Hypothesis to Catastrophe Theory
Confirmatory factor analysis of the competitive state anxiety inventory-2., reexamining the factorial composition and factor structure of the sport anxiety scale, measurement and correlates of sport-specific cognitive and somatic trait anxiety: the sport anxiety scale, test anxiety and direction of attention., motor performance under stress: a test of the inverted-u hypothesis., related papers.
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D. a and b E. b and c, The inverted-U hypothesis predicts that A. as arousal increases, performance decreases B. arousal can be either too low or too high C. top performance occurs at a moderate level of arousal D. a and c E. b and c, A highly trait-anxious athlete (compared to a less trait-anxious athlete) would perceive competition as A. more ...
The inverted-U curve looks a little different for each person and probably even changes at different points in your life. ... The Yerkes-Dodson law is the theory that there's an optimal level of ...
How the Law Works. The Yerkes-Dodson law describes the empirical relationship between stress and performance. In particular, it posits that performance increases with physiological or mental arousal, but only up to a certain point. This is also known as the inverted U model of arousal. When stress gets too high, performance decreases.
The optima vary between people doing the same task and one person doing different tasks. A basic assumption in the hypothesis is that arousal is unidimensional and that there is, consequently, a very close correlation between indicators of arousal; this is not the case. See also catastrophe theory. inverted-U hypothesis
The Inverted-U Theory helps you to observe and manage these four factors, aiming for a balance that supports engagement, well-being, and peak performance. You can use the model by managing these four influencers, and by being aware of how they can positively or negatively influence your people's performance.
The Inverted U Hypothesis is an appealing explanation for performance flaws. In many ways this explanation fits into the observations from sport performers but in reality is too simplistic. In addition to what the Inverted U hypothesis predicts, it is important to consider that beginners usually need a greater amount of attention to the ...
Abstract. Arousal level is thought to be a key determinant of variability in cognitive performance. In a recent study, Beerendonk, Mejías et al. show that peak performance in decision-making tasks is reached at moderate levels of arousal. They also propose a neurobiologically informed computational model that can explain the inverted-U-shaped ...
The longest-standing approach to the relationship between stress, anxiety and performance in sport is probably the inverted-U hypothesis, derived from the work of Yerkes and Dodson (1908). This hypothesis predicts that performance improves with increases in arousal until a peak is reached, after which further arousal leads to a deterioration in performance. Although arousal and anxiety are not ...
Inverted-U Hypothesis. In the inverted-U hypothesis performance is best at a moderate level of arousal. Both low and high levels of arousal are associated with decrements in performance. The original work done on the inverted-U hypothesis related to the strength of stimulus and habit-formation (learning) in mice (Yerkes & Dodson, 1908). Mice ...
As predicted by the Inverted-U hypothesis, optimal performance on the simple task was seen at 60 and 70% of maximum arousal. Furthermore, for the simple task used in this study, only somatic ...
Stress often has negative effects. But in the right amounts, stress can be good for us. A theory known as the "inverted-U" hypothesis attempts to explain how varying levels of stress influence us ...
The inverted u theory may also be referred to as the Yerkes-Dodson law due to its creation by two researchers - Yerkes and Dodson. In 1908, these researchers were trying to understand the relationship between the strength of a stimulus and forming habits in mice. They found that there was a negative relationship between the two i.e. the ...
These findings lead to the hypothesis that working memory follows an inverted U-shaped function, in which optimal working memory performance is achieved with optimal levels of prefrontal dopamine and D1DR activation. While inverted U-shaped dynamics have substantial supporting evidence, the contours of this function are not clear.
As predicted by the Inverted-U hypothesis, optimal performance on the simple task was seen at 60 and 70% of maximum arousal. Furthermore, for the simple task used in this study, only somatic anxiety as measured by the SAS accounted for significant variance in performance beyond that accounted for by arousal alone. These findings support ...
Findings support predictions of the Inverted-U hypothesis and raise doubts about the utility theories that rely on differentiation of cognitive and somatic anxiety to predict performance on simple tasks that are not cognitively loaded. Abstract Until recently, the traditional Inverted-U hypothesis had been the primary model used by sport psychologists to describe the arousal-performance ...
Study with Quizlet and memorize flashcards containing terms like There is a direct relationship between one's level of, The importance placed on an event and the uncertainty that surrounds the actions of that event are sources of, The inverted-U hypothesis predicts that and more.
Yerkes-Dodson Law (The Inverted-U Hypothesis) - Performance rises as arousal levels rise, up to an optimum point, after which the person becomes over-aroused and their performance level decreases. - Sports requiring fine motor skills such as golf require low arousal for optimum performance, whereas high strength and less skillfull sports such ...
The Multi-dimensional Theory of Anxiety is based on the distinction between somatic and cognitive anxiety. The theory predicts that there is a negative, linear relationship between somatic and cognitive anxiety, that there will be an Inverted-U relationship between somatic anxiety and performance, and that somatic anxiety should decline once performance begins although cognitive anxiety may ...
The inverted-U hypothesis predicts that. False (T/F) The inverted-U hypothesis is the only theory used to explain stress and performance. an optimal level of state anxiety and other emotions.
The Inverted-U Hypothesis predicts that engagement will be highest at a moderate level of challenge, neither too hard nor too easy (Figure 1). In these studies, we operationalized challenge as the ...
A negative emotional state. anxiety. A nondirective, generalized bodily reaction-activation. arousal. Using stress in a constructive manner that benefits performance. eustress. An individual's anxiety at a particular moment. state anxiety. A specific to sports, multidimensional measure of trait anxiety.