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\"This book describes research on training using cognitive psychology to build a complete empirical and theoretical picture of the training process. It includes a review of relevant cognitive psychological literature, a summary of recent laboratory experiments, a presentation of original theoretical ideas, and a discussion of possible applications to real-world training settings\"--Provided by publisher.

Introduction: The purpose of the present study was to investigate the effects of a winter military field training course consisting of strenuous physical stressors (e.g. physical activity, sleep deprivation and cold weather) on cognitive performance among Finnish soldiers. Methods: Fifty-eight (age 19 ± 1 years, height 182 ± 6 cm, body mass 78.5 ± 7.2 kg) male soldiers took part in a 20-day military field training course in northern Finland. Cognitive performance was assessed before, during, and after the course four times on a tablet computer. Sustained Attention to Response Task (SART) was used to assess soldier's executive and inhibitory function. Baddeley's 3-min reasoning task (BRT) was used to assess grammatical reasoning, and Change Blindness (CB) task was used to assess visual perception. Results: Strenuous winter field training had detrimental effects in all performance tests compared to baseline. SART response rate decreased 27.3% (p < 0.001), and BRT and CB task scores decreased 20.6% (p < 0.01) and 14.1% (p < .05), respectively. Conclusion: The present study showed a decline in soldier's cognitive performance after 20-days of physically demanding winter military field training. To be able to optimise field training, it is important to be aware of how cognitive performance changes during military exercises and missions.

\"With the proliferation of social media, the intense pressure to succeed, and our overreliance on external rewards, metrics, and validation, FOPO is running rampant. Our concern with what other people think about us has become an irrational, unproductive, and unhealthy obsession in the modern world. And its negative effects reach into all aspects of our lives. In The First Rule of Mastery, Michael Gervais shows us the key to leading a high-performance life is to redirect our attention from the world outside us to the world inside us. As one of the world's leading experts on the relationship between the mind and human performance, Gervais takes an in-depth look at the noxious effects of FOPO while laying out the mental skills and practices we need to achieve personal excellence-the same skills he's taught to the top performers in the world including sports MVPs and Fortune 100 leaders and teams. Filled with fascinating stories from the worlds of sports and business, leading-edge science, and insights from the popular Finding Mastery podcast, The First Rule of Mastery is a much-needed wake-up call that when we give more value to other people's opinions than our own, we live life on their terms, not ours\"-- Provided by publisher.

Hypoxia is increasingly recognized as an important physiological driving force. A specific transcriptional program, induced by a decrease in oxygen (O2) availability, for example, inspiratory hypoxia at high altitude, allows cells to adapt to lower O2 and limited energy metabolism. This transcriptional program is partly controlled by and partly independent of hypoxia‐inducible factors. Remarkably, this same transcriptional program is stimulated in the brain by extensive motor‐cognitive exercise, leading to a relative decrease in O2 supply, compared to the acutely augmented O2 requirement. We have coined the term “functional hypoxia” for this important demand‐responsive, relative reduction in O2 availability. Functional hypoxia seems to be critical for enduring adaptation to higher physiological challenge that includes substantial “brain hardware upgrade,” underlying advanced performance. Hypoxia‐induced erythropoietin expression in the brain likely plays a decisive role in these processes, which can be imitated by recombinant human erythropoietin treatment. This article review presents hints of how inspiratory O2 manipulations can potentially contribute to enhanced brain function. It thereby provides the ground for exploiting moderate inspiratory plus functional hypoxia to treat individuals with brain disease. Finally, it sketches a planned multistep pilot study in healthy volunteers and first patients, about to start, aiming at improved performance upon motor‐cognitive training under inspiratory hypoxia. This article review presents hints of how inspiratory O2 manipulations can potentially contribute to enhanced brain function. It thereby provides the ground for exploiting moderate inspiratory plus functional hypoxia to treat individuals with brain disease. Finally, it sketches a planned multistep pilot study in healthy volunteers and first patients, about to start, aiming at improved performance upon motor‐cognitive training under inspiratory hypoxia. Highlights This review focuses on the brain and sketches hypoxia as a physiological driving force, inducing specific transcriptional programs. Moderate inspiratory hypoxia may improve brain function and performance. Our concept of “functional hypoxia” is introduced as a demand‐responsive mediator of “brain hardware upgrade” on extensive motor‐cognitive exercise. Hypoxia‐induced erythropoietin (EPO) expression in the brain plays a decisive role in these processes, constituting what we coined the “brain EPO circle.” The brain EPO circle underlies the adaptation to challenge, that is, enhanced brain function including cognition and accomplishment on demand: “Brain doping.” Recombinant human EPO imitates the effects of brain‐expressed EPO, explaining the strong neuroprotective and procognitive impact of this treatment. A pilot study in healthy volunteers and first patients is outlined, exploiting moderate inspiratory plus functional hypoxia in humans for improving cognition.

Emerging evidence suggests that dietary-derived flavonoids have the potential to improve human memory and neuro-cognitive performance via their ability to protect vulnerable neurons, enhance existing neuronal function and stimulate neuronal regeneration. Long-term potentiation (LTP) is widely considered to be one of the major mechanisms underlying memory acquisition, consolidation and storage in the brain and is known to be controlled at the molecular level by the activation of a number of neuronal signalling pathways. These pathways include the phosphatidylinositol-3 kinase/protein kinase B/Akt (Akt), protein kinase C, protein kinase A, Ca–calmodulin kinase and mitogen-activated protein kinase pathways. Growing evidence suggests that flavonoids exert effects on LTP, and consequently memory and cognitive performance, through their interactions with these signalling pathways. Of particular interest is the ability of flavonoids to activate the extracellular signal-regulated kinase and the Akt signalling pathways leading to the activation of the cAMP-response element-binding protein, a transcription factor responsible for increasing the expression of a number of neurotrophins important in LTP and long-term memory. One such neurotrophin is brain-derived neurotrophic factor, which is known to be crucial in controlling synapse growth, in promoting an increase in dendritic spine density and in enhancing synaptic receptor density. The present review explores the potential of flavonoids and their metabolite forms to promote memory and learning through their interactions with neuronal signalling pathways pivotal in controlling LTP and memory in human subjects.

Electroconvulsive therapy (ECT) is effective in the treatment of treatment-resistant major depression. The fear of cognitive impairment after ECT often deters patients from choosing this treatment option. There is little reliable information regarding the effects of ECT on overall cognitive performance, while short-term memory deficits are well known but not easy to measure within clinical routines. In this pilot study, we examined ECT recipients’ pre- and posttreatment performances on a digital ascending number tapping test. We found that cognitive performance measures exhibited good reproducibility in individual patients and that ECT did not significantly alter cognitive performance up to 2 hours after this therapy was applied. Our results can help patients and physicians make decisions regarding the administration of ECT. Digital measurements are recommended, especially when screening for the most common side effects on cognitive performance and short-term memory.

Environmental noise causes cognitive impairment, particularly in executive function and episodic memory domains, in healthy populations. However, the possible moderating influences on this relationship are less clear. This study assessed 54 healthy participants (24 men) on a cognitive battery (measuring psychomotor speed, attention, executive function, working memory, and verbal learning and memory) under three (quiet, urban, and social) noise conditions. IQ, subjective noise sensitivity, sleep, personality, paranoia, depression, anxiety, stress, and schizotypy were assessed on a single occasion. We found significantly slower psychomotor speed (urban), reduced working memory and episodic memory (urban and social), and more cautious decision-making (executive function, urban) under noise conditions. There was no effect of sex. Variance in urban noise-induced changes in psychomotor speed, attention, Trail Making B-A (executive function), and immediate recall and social noise-induced changes in verbal fluency (executive function) and immediate recall were explained by a combination of baseline cognition and paranoia, noise sensitivity, sleep, or cognitive disorganization. Higher baseline cognition (but not IQ) predicted greater impairment under urban and social noise for most cognitive variables. Paranoia predicted psychomotor speed, attention, and executive function impairment. Subjective noise sensitivity predicted executive function and memory impairment. Poor sleep quality predicted less memory impairment. Finally, lower levels of cognitive disorganization predicted slower psychomotor speed and greater memory impairment. The identified moderators should be considered in studies aiming to reduce the detrimental effects of occupational and residential noise. These results highlight the importance of studying noise effects in clinical populations characterized by high levels of the paranoia, sleep disturbances, noise sensitivity, and cognitive disorganization.

There is growing interest recently in the outdoor environment surrounding schools where students spent time during breaks, in-school activities, and after-school programs. Several reviews have examined the impact of long-term exposures to nearby nature on students’ academic achievement, but none has focused on the effects of short-term contacts with nature on students’ cognitive performance. The aim of this review is to understand the context in which short-term passive exposures to greenness occur, how cognitive performance is measured, and the conditions under which cognitive benefits emerge at various educational levels. We reviewed 14 studies in the extant literature that report investigations involving students at different educational levels, from elementary school to university, in a short exposure to nature lasting from 10 to 90 min during a study day. The review shows that in 12 out of the 14 studies, across educational levels, cognitive benefits emerge in terms of directed attention restoration from mental fatigue due to contact with nature. A no-cost opportunity to sustain students’ cognition is a break in a green environment after mentally demanding activities.

Cognitive dysfunction and brain structural connectivity alterations have been observed in major depressive disorder (MDD). However, little is known about their interrelation. The present study follows a network approach to evaluate alterations in cognition-related brain structural networks. Cognitive performance of = 805 healthy and = 679 acutely depressed or remitted individuals was assessed using 14 cognitive tests aggregated into cognitive factors. The structural connectome was reconstructed from structural and diffusion-weighted magnetic resonance imaging. Associations between global connectivity strength and cognitive factors were established using linear regressions. Network-based statistics were applied to identify subnetworks of connections underlying these global-level associations. In exploratory analyses, effects of depression were assessed by evaluating remission status-related group differences in subnetwork-specific connectivity. Partial correlations were employed to directly test the complete triad of cognitive factors, depressive symptom severity, and subnetwork-specific connectivity strength. All cognitive factors were associated with global connectivity strength. For each cognitive factor, network-based statistics identified a subnetwork of connections, revealing, for example, a subnetwork positively associated with processing speed. Within that subnetwork, acutely depressed patients showed significantly reduced connectivity strength compared to healthy controls. Moreover, connectivity strength in that subnetwork was associated to current depressive symptom severity independent of the previous disease course. Our study is the first to identify cognition-related structural brain networks in MDD patients, thereby revealing associations between cognitive deficits, depressive symptoms, and reduced structural connectivity. This supports the hypothesis that structural connectome alterations may mediate the association of cognitive deficits and depression severity.