Background: Aging naturally triggers a decline in cognition as result of deterioration in cerebral circuits, thus the executive functions (EFs) suffer changes that progress from mild to severe states of impairment. Exercise instead, works as a strategy for cognitive enhancement by modulating neuronal plasticity through the regulation of BDNF. However, whether the exercise-dependent BDNF may improve higher complexity processes such as the EFs is still in a studying process.Results: Current data on exercise-dependent BDNF changes for aging individuals in a course of cognitive impairment was summarized to investigate whether the exercise regulation of BDNF is effective to pronounce long term changes on executive controls. While the exercise-dependent regulation of BDNF is currently undeniable, the role of exercise dependent BDNF as a tool for the improvement of EFs in individuals with dementia is still less clear and seldom discussed. The summary of findings indicate a limited number of studies addressing exercise in order to discuss parameters related to either BDNF or executive functioning in such population conditions (n = 215), further narrowing to a total of 5 studies presenting analysis of both parameters. Nonetheless, positive outcomes from BDNF and EF variables were displayed by all the populations exposed to exercise across studies. Aerobic exercise was shown to be a major source for the enhancement of the BDNF-dependent executive functioning, when compared to cognitive stimulation. Moreover, the effect of exercise-dependent BDNF on domains of executive functioning appears to occur in a dose-dependent manner for the aging individuals, independently of cognitive condition.

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This study examined the effects of a nine-week intervention of four different high-intensity training modalities [high-intensity functional training (HIFT), high-intensity interval training (HIIT), high-intensity power training (HIPT), and high-intensity endurance training (HIET)] on the resting concentration of brain-derived neurotropic factor (BDNF). In addition, we evaluated the BDNF responses to Graded Exercise Test (GXT) and Wingate Anaerobic Test (WAnT) in men. Thirty-five healthy individuals with body mass index 25.55 ± 2.35 kg/m2 voluntarily participated in this study and were randomly assigned into four training groups. During nine-weeks they completed three exercise sessions per week for one-hour. BDNF was analyzed before and after a GXT and WAnT in two stages: (stage 0—before training and stage 9—after nine weeks of training). At stage 0, an increase in BDNF concentration was observed in HIFT (33%; p < 0.05), HIPT (36%; p < 0.05) and HIIT (38%; p < 0.05) after GXT. Even though HIET showed an increase in BDNF (10%) this was not statistically significant (p > 0.05). At stage 9, higher BDNF levels after GXT were seen only for the HIFT (30%; p < 0.05) and HIIT (18%; p < 0.05) groups. Reduction in BDNF levels were noted after the WAnT in stage 0 for HIFT (− 47%; p < 0.01), HIPT (− 49%; p < 0.001), HIET (− 18%; p < 0.05)], with no changes in the HIIT group (− 2%). At stage 9, BDNF was also reduced after WAnT, although these changes were lower compared to stage 0. The reduced level of BDNF was noted in the HIFT (− 28%; p < 0.05), and HIPT (− 19%;p < 0.05) groups. Additionally, all groups saw an improvement in VO2max (8%; p < 0.001), while BDNF was also correlated with lactate and minute ventilation and selected WAnT parameters. Our research has shown that resting values of BDNF after nine weeks of different forms of high-intensity training (HIT) have not changed or were reduced. Resting BDNF measured at 3th (before GXT at stage 9) and 6th day after long lasting HITs (before WAnT at stage 9) did not differed (before GXT), but in comparison to the resting value before WAnT at the baseline state, was lower in three groups. It appears that BDNF levels after one bout of exercise is depended on duration time, intensity and type of test/exercise.

Depression is the most common and devastating psychiatric disorder in the world. Its symptoms, especially during the pandemic, are observed in all age groups. Exercise training (ET) is well known as a non-pharmacological strategy to alleviate clinical depression. The brain-derived neurotrophic factor (BDNF) is one of the biological factors whose expression and secretion are intensified in response to ET. BDNF is also secreted by contracted skeletal muscle that likely exerts para-, auto- and endocrine effects, supporting the crosstalk between skeletal muscle and other distant organs/tissues, such as the nervous system. This finding suggests that they communicate and work together to induce improvements on mood, cognition, and learning processes as BDNF is the main player in the neurogenesis, growth, and survival of neurons. Therefore, BDNF has been recognized as a therapeutic factor in clinical depression, especially in response to ET. The underlying mechanisms through which ET impacts depression are varied. The aim of this review was to provide information of the biological markers of depression such as monoamines, tryptophan, endocannabinoids, markers of inflammatory processes (oxidative stress and cytokines) stress and sex hormones and their relationship to BDNF. In addition, we reviewed the effects of ET on BNDF expression and how it impacts depression as well as the potential mechanisms mediating this process, providing a better understanding of underlying ET-related mechanisms in depression.

Background The biological maturation (BM) analyzed by peak height velocity (PHV) and bone age (BA), and lean body mass has been associated with the strength and muscle power of young athletes. However, the ability of BM (PHV and BA) and LM markers to predict muscle strength and power in young athletes remains uncertain. Objective The Aim was determine the predicting power of BM markers (PHV and BA) and LM in relation to muscle power of upper and lower limbs and muscle strength of upper limbs in adolescent athletes at puberty. Methods Ninety-two adolescent athletes (both sexes; age 12.4 ± 1.02 years) were assessed for body composition by dual-energy X-ray absorptiometry (DXA). Power of upper limbs (ULP), force handgrip (HG), vertical jump (VJ) and countermovement jump (CMJ) were recorded. BM was predicted by mathematical models to estimate PHV and BA. Multilayer artificial neural network analyses (MLP’s) were used to determine the power of prediction of LM, PHV and BA on muscle power and strength of upper- and lower-limbs of the athletes. Results LM, BA and PHV were associated with HG (r>0.74, p<0.05) and ULS (r>0.60, p<0.05) in both sexes. In both sexes BA was associated with VJ (r>0.55, p<0.05) and CMJ (r>0.53, p<0.05). LM indicated associations (r>0.60, p<0.05) with BA and with PHV (r<0.83, p<0.05) in both sexes. MLP’s analysis revealed that the LM provides > 72% of probability to predict the muscle power of upper- and lower-limbs, and the strength of the upper limbs; whereas PHV provides > 43% and bone age >64% in both female and male adolescent athletes. Conclusion We identified that, like PHV and BA, LM is a strong predictor of low cost of both upper limbs muscle strength and upper and lower limbs power in adolescent athletes.

Brain-derived neurotrophic factor (BDNF) plays an essential role in nervous system formation and functioning, including metabolism. Present only in humans, the “Val66Met” polymorphism of the BDNF gene (BDNF) is suggested to have a negative influence on the etiology of neurological diseases. However, this polymorphism has only been addressed, at the molecular level, in nonhuman models. Knowledge about Val66- and Met66-variant differences, to date, has been achieved at the protein level using either cell culture or animal models. Thus, the purpose of our study was to analyze the impact of the Val66Met polymorphism on BDNF expression in healthy humans and compare the allele-specific responses to metabolic stress. Muscle biopsies from 13 male recreational athletes (34 ± 9 years, 1.80 ± 0.08 m, 76.4 ± 10.5 kg) were obtained before and immediately following a VO2max test. Allele-specific BDNF mRNA concentrations were quantified by droplet digital PCR (ddPCR) in heterozygous and homozygous subjects. The results indicated that BDNF expression levels were influenced by the genotype according to the presence of the polymorphism. BDNF expression from the Met66-coding alleles, in heterozygotes, was 1.3-fold lower than that from the Val66-coding alleles. Total BDNF mRNA levels in these heterozygotes remained below the whole sample’s mean. A partial dominance was detected for the Val66-coding variant on the Met66-coding’s. BDNF expression levels decreased by an average of 1.8-fold following the VO2max test, independent of the individual’s genotype. The results of this study indicate that metabolic stress downregulates BDNF expression but not plasma BDNF concentrations. No correlation between expression level and plasma BDNF concentrations was found.

Background: Obesity and being overweight have been described as potential causes of neurological disorders. Leptin, a peptide expressed in fat tissue, importantly participates in energy homeostasis and storage and has recently been identified for its signaling receptors in neuronal circuits of the brain. Aim: To elucidate whether the endogenous modulation of leptin can be a protection against neuropsychiatric disorders. Method: A systematic review was performed in accordance with the PRISMA-P method, and reports of studies containing data of leptin concentrations in healthy individuals with or without obesity were retrieved from the PubMed database, using the combinations of Mesh terms for “Leptin” and “Metabolism”. Results: Forty-seven randomized and non-randomized controlled trials, dating from 2000 to 2021, were included in the qualitative synthesis. Discussion and conclusions: Leptin secretion displays a stabilizing pattern that is more sensitive to a negative energy intake imbalance. Leptin levels influence body weight and fat mass as a pro-homeostasis factor. However, long-term exposure to elevated leptin levels may lead to mental/behavioral disorders related to the feeding and reward systems.

Background: Literature reports indicate changes in the expression of genes encoding proinflammatory factors are observed as a result of physical exercise. The stress changes caused by high-intensity loads and adaptive changes induced by the planned long-term training are less studied. The aim of this study was to determine the impact of intense anaerobic effort in people adapted to regular trainings and in non-trained persons on the expression levels of the TNFA gene.Material and methods: 50 experienced soccer players and 50 non-trained participants were recruited for the study. Anaerobic capacity was measured by means of the Wingate Anaerobic Test. To evaluate the expression of TNFA gene, a QRT-PCR was applied.Results: A comparison of the TNFA expression profiles between well-trained athletes and non-trained controls revealed that transcript levels were higher in non-trained participants when compared with soccer players in all the studied time points, with the exception of the second post-test; however, this difference was the only one that was statistically insignificant. Conclusions:The TNFA mRNA expression characteristic described in our study indicated a significant downregulation of the TNFA expression observed in the course of time in experienced athletes reflecting molecular adaptation to physical effort caused by long-term training regime.