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The unique contribution of the serotonin transporter-linked polymorphic region (5-HTTLPR), intronic region 2 (STin2), and monoamine oxidase A (MAO-A) genes to individual differences in personality traits has been widely explored, and research has shown that certain forms of these polymorphisms relate to impulsivity and impulsivity-related disorders. Humans showing these traits are also described as having an asymmetrical prefrontal cortical activity when compared to others. In this explorative study, we examine the relationship between serotonergic neurotransmission polymorphisms, cortical activity features (prefrontal alpha asymmetry, individual alpha peak frequency [iAPF]), emotion-related and non-emotion-related impulsivity in humans. 5-HTTLPR, MAO-A, and STin2 polymorphisms were assessed in blood taken from 91 participants with high emotion-related impulsivity levels. Sixty-seven participants completed resting electroencephalography and a more comprehensive impulsivity index. In univariate analyses, iAPF correlated with both forms of emotion-related impulsivity. In multiple linear regression models, 5-HTTLPR polymorphism (model 1, adj. R2 = 15.2%) and iAPF were significant interacting predictors of emotion-related impulsivity, explaining a large share of the results' variance (model 2, adj. R2 = 21.2%). Carriers of the low transcriptional activity 5-HTTPLR and MAO-A phenotypes obtained higher emotion-related impulsivity scores than others did. No significant results were detected for non-emotion-related impulsivity or for a form of emotion-related impulsivity involving cognitive/motivational reactivity to emotion. Our findings support an endophenotypic approach to impulsivity, showing that tri-allelic 5-HTTLPR polymorphism, iAPF, and their interaction are relevant predictors of one form of emotion-related impulsivity. [ABSTRACT FROM AUTHOR]

Background: Data on changes in natural killer cell cytolytic activity (NKCA) in response to acute physical exercise are contradictory. Objective: The aim of this systematic review, meta-analysis and meta-regression is to (1) examine the effect of acute physical exercise on NKCA, (2) shed more light on the moderating factors, and (3) test the assumption of NKCA suppression subsequent to performing sports. Methods: Two comparisons of NKCA were performed: (1) pre- versus post-exercise and (2) pre-exercise versus recovery. Data were acquired through a systematic search of MEDLINE (via PubMed), Scopus, and SportDiscus. Studies were eligible for inclusion if the effect of acute physical exercise was assessed including a passive control group and reporting NKCA prior to and immediately after the trial, and during the first 2 h of recovery. To better explain between-study heterogeneity, a moderator analysis was conducted. Results: Pooled estimate from 12 studies reporting 18 effect sizes show that NKCA is largely elevated by acute physical exercise (Hedges' g = 1.02, 95% CI 0.59–1.46, p < 0.01). Meta-regressions reveal that this effect is larger for endurance versus resistance exercise and increases with the intensity of exercise (both p < 0.01), whereas the blood material used in the assay (p = 0.71), and the quantitative change in NK-cell count (R2 = 0%, p = 0.55) do not play a significant role. Physical exercise does not affect the level of NKCA after the recovery period (g = 0.06, 95% CI − 0.37 to 0.50, p < 0.76). Conclusions: This work provides solid evidence for elevated NKCA through performing sports which returns to baseline during the first 1–2 h of recovery, but not below the pre-exercise values providing counterevidence to the assumption of temporarily reduced NKCA. Remarkably, the functional change in NKCA exists independently from the quantitative change in NK-cell count. PROSPERO registration number: CRD42020134257. [ABSTRACT FROM AUTHOR]

The increasing demand of space flights requires a profound knowledge of the chronologic reactions of the human body to extreme conditions. Prior studies already have shown the adverse effects of long-term isolation on psycho-physiological well-being. The chronology of the effects and whether short-term isolation periods already lead to similar effects has not been investigated. Therefore, the aim of the current study was to investigate the effects of short-term isolation (30 days) on mood, cognition, cortisol, neurotrophic factors, and brain activity. 16 participants were isolated in the Human Exploration Research Analog at NASA for 30 days. 17 non-isolated control participants were tested simultaneously. On mission days − 5, 7, 14, 28, and + 5, multiple tests including the Positive and Negative Affect Schedule-X and cognitive tests were conducted, and a 5-min resting electroencephalography was recorded. A fasted morning blood drawing was also done. Increased stress was observed via augmented cortisol levels during the isolation period. Activity within the parietal cortex was reduced over time, probably representing a neural adaptation to less external stimuli. Cognitive performance was not affected, but rather enhanced in both groups. No further significant changes in neurotrophic factors BDNF/IGF-1 and mood could be detected. These results suggest that 30 days of isolation do not have a significant impact on brain activity, neurotrophic factors, cognition, or mood, even though stress levels were significantly increased during isolation. Further studies need to address the question as to what extent increased levels of stress do not affect mental functions during isolation periods. [ABSTRACT FROM AUTHOR]