Evaluation of muscular and functional inter-limb asymmetries during mid-season in young male soccer athletes.

BACKGROUND: To identify inter-limb asymmetries through the knee's muscular and lower limb functional performance in young male soccer athletes. METHODS: Twenty male soccer athletes aged 17 to 19 from an under-20 team performed isokinetic tests at 60°/s., 120°/s., 180°/s., and 240°/s. To assess the knee extensors and flexors muscles and functional tests (hop tests and Y-balance test). RESULTS: There were no significant differences between the dominant limb (DL) and non-dominant limb (NDL) in the knee extensors and flexors peak torque and hamstrings (H)/quadriceps(Q) conventional ratio. Moreover, no angular velocities observed inter-limb asymmetries seen by values higher than 10% in the isokinetic parameters. However, the H/Q conventional ratio shows borderline values in low angular velocities (60°/s. and 120°/s.). No significant changes were observed in the functional test performance between the DL and NDL. Furthermore, we did not see inter-limb asymmetries in both hop and Y-balance tests. On the contrary, the anterior distance reached was lower than found in the literature, and the composite score of the Y-balance test demonstrated values below the normative (>94%). CONCLUSION: The data demonstrated that soccer athletes have muscular and functional inter-limb symmetry. However, they tend to have knee muscle imbalance in low velocities and dynamic balance deficits that might increase the risk of musculoskeletal injury.

Locomotor Behavior and Memory Dysfunction Induced by 3-Nitropropionic Acid in Adult Zebrafish: Modulation of Dopaminergic Signaling.

Huntington's disease (HD) is a progressive neurodegenerative disease characterized by neuropsychiatric disturbance, cognitive impairment, and locomotor dysfunction. In the early stage (chorea) of HD, expression of dopamine D2 receptors (D2R) is reduced, whereas dopamine (DA) levels are increased. Contrary, in the late stage (bradykinesia), DA levels and the expression of D2R and dopamine D1 receptors (D1R) are reduced. 3-Nitropropionic acid (3-NPA) is a toxin that may replicate HD behavioral phenotypes and biochemical aspects. This study assessed the neurotransmitter levels, dopamine receptor gene expression, and the effect of acute exposure to quinpirole (D2R agonist) and eticlopride (D2R antagonist) in an HD model induced by 3-NPA in adult zebrafish. Quinpirole and eticlopride were acutely applied by i.p. injection in adult zebrafish after chronic treatment of 3-NPA (60 mg/kg). 3-NPA treatment caused a reduction in DA, glutamate, and serotonin levels. Quinpirole reversed the bradykinesia and memory loss induced by 3-NPA. Together, these data showed that 3-NPA acts on the dopaminergic system and causes biochemical alterations similar to late-stage HD. These data reinforce the hypothesis that DA levels are linked with locomotor and memory deficits. Thus, these findings may suggest that the use of DA agonists could be a pharmacological strategy to improve the bradykinesia and memory deficits in the late-stage HD.

Physical exercise prevents behavioral alterations in a reserpine-treated zebrafish: A putative depression model.

Major depressive disorder (MDD) has increasingly reached the world population with an expressive increase in recent years due to the COVID-19 pandemic. Here we used adult zebrafish (Danio rerio) as a model to verify the effects of reserpine on behavior and neurotransmitter levels. We observed an increase in the immobile time and time spent in the bottom zone of the tank in reserpine-exposed animals. The results demonstrated a decrease in distance traveled and velocity. Reserpine exposure did not induce changes in memory and social interaction compared to the control group. We also evaluated the influence of exposure to fluoxetine, a well-known antidepressant, on the behavior of reserpine-exposed animals. We observed a reversal of behavioral alterations caused by reserpine. To verify whether behavioral alterations in the putative depression model induced by reserpine could be prevented, the animals were subjected to physical exercise for 6 weeks. The results showed a protective effect of the physical exercise against the behavioral changes caused by reserpine in zebrafish. In addition, we observed a reduction in dopamine and serotonin levels and an increase in the 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the brain. Physical exercise was able to prevent the changes in dopamine and serotonin levels, reinforcing that the preventive effect promoted by physical exercise is related to the modulation of neurotransmitter levels. Our findings showed that reserpine was effective in the induction of a putative depression model in zebrafish and that physical exercise may be an alternative to prevent the effects induced by reserpine.

Two Years of COVID-19 Pandemic: How the Brazilian Serie A Championship Was Affected by Home Advantage, Performance and Disciplinary Aspects.

As a result of the COVID-19 pandemic, the Brazilian Serie A championship was played without crowds in 2020 and partially in the 2021 season. We verified if the home advantage (HA) was different between the 2018, 2019, 2020, and 2021 seasons. We also compared the HA, performance, and disciplinary aspects between the rounds with or without crowds and verified the association between the number of absent athletes because of health protocols and the HA in the 2020 and 2021 seasons. We calculated the HA using the Pollard method. The performance aspects were goals, corners, shots, and ball possession, and the disciplinary aspects were fouls, yellow cards, and red cards. The HA was higher in the 2018 season compared with the other seasons. The rounds with crowds showed higher HAs than the two previous seasons and the teams had more shots and scored more goals than in the rounds without crowds. There were 457 athletes in the 2020 season and 123 athletes in the 2021 season who were absent because of health protocols, and there was no association between absence and HA. The COVID-19 pandemic affected soccer in the two last seasons in different ways in the Brazilian Serie A championship.

Role of the nucleoside-metabolizing enzymes on pain responses in zebrafish larvae.

Purinergic signaling is a pathway related to pain underlying mechanisms. Adenosine is a neuromodulator responsible for the regulation of multiple physiological and pathological conditions. Extensive advances have been made to understand the role of adenosine in pain regulation. Here we investigated the effects of purinergic compounds able to modulate adenosine production or catabolism on pain responses induced by Acetic Acid (AA) in zebrafish larvae. We investigated the preventive role of the ecto-5'-nucleotidase inhibitor adenosine 5'-(α,ß-methylene)diphosphate (AMPCP) and adenosine deaminase inhibitor erythro-9-(2-Hydroxy-3-nonyl)-adenine (EHNA) on the AA-pain induced model. The pain responses were evaluated through exploratory and aversive behaviors in zebrafish larvae. The exploratory behavior showed a reduction in the distance covered by animals exposed to 0.0025% and 0.050% AA. The movement and acceleration were reduced when compared to control. The treatment with AMPCP or EHNA followed by AA exposure did not prevent behavioral changes induced by AA for any parameter tested. There were no changes in aversive behavior after the AA-induced pain model. After AA-induced pain, the AMP hydrolysis increased on zebrafish larvae. However, the AMPCP or EHNA exposure did not prevent changes in AMP hydrolysis induced by the AA-induced pain model in zebrafish larvae. Although AMPCP or EHNA did not show differences in the AA-induced pain model, our results revealed changes in AMP hydrolysis, suggesting the involvement of the purinergic system in zebrafish larvae pain responses.

Modulation of adenosine signaling reverses 3-nitropropionic acid-induced bradykinesia and memory impairment in adult zebrafish.

Huntington's disease (HD) is a neurodegenerative disorder, characterized by motor dysfunction, psychiatric disturbance, and cognitive decline. In the early stage of HD, occurs a decrease in dopamine D2 receptors and adenosine A2A receptors (A2AR), while in the late stage also occurs a decrease in dopamine D1 receptors and adenosine A1 receptors (A1R). Adenosine exhibits neuromodulatory and neuroprotective effects in the brain and is involved in motor control and memory function. 3-Nitropropionic acid (3-NPA), a toxin derived from plants and fungi, may reproduce HD behavioral phenotypes and biochemical characteristics. This study investigated the effects of acute exposure to CPA (A1R agonist), CGS 21680 (A2AR agonist), caffeine (non-selective of A1R and A2AR antagonist), ZM 241385 (A2AR antagonist), DPCPX (A1R antagonist), dipyridamole (inhibitor of nucleoside transporters) and EHNA (inhibitor of adenosine deaminase) in an HD pharmacological model induced by 3-NPA in adult zebrafish. CPA, CGS 21680, caffeine, ZM 241385, DPCPX, dipyridamole, and EHNA were acutely administered via i.p. in zebrafish after 3-NPA (at dose 60 mg/kg) chronic treatment. Caffeine and ZM 241385 reversed the bradykinesia induced by 3-NPA, while CGS 21680 potentiated the bradykinesia caused by 3-NPA. Moreover, CPA, caffeine, ZM 241385, DPCPX, dipyridamole, and EHNA reversed the 3-NPA-induced memory impairment. Together, these data support the hypothesis that A2AR antagonists have an essential role in modulating locomotor function, whereas the activation of A1R and blockade of A2AR and A1R and modulation of adenosine levels may reduce the memory impairment, which could be a potential pharmacological strategy against late-stage symptoms HD.

Purinergic Signaling in the Pathophysiology and Treatment of Huntington's Disease.

Huntington's disease (HD) is a devastating, progressive, and fatal neurodegenerative disorder inherited in an autosomal dominant manner. This condition is characterized by motor dysfunction (chorea in the early stage, followed by bradykinesia, dystonia, and motor incoordination in the late stage), psychiatric disturbance, and cognitive decline. The neuropathological hallmark of HD is the pronounced neuronal loss in the striatum (caudate nucleus and putamen). The striatum is related to the movement control, flexibility, motivation, and learning and the purinergic signaling has an important role in the control of these events. Purinergic signaling involves the actions of purine nucleotides and nucleosides through the activation of P2 and P1 receptors, respectively. Extracellular nucleotide and nucleoside-metabolizing enzymes control the levels of these messengers, modulating the purinergic signaling. The striatum has a high expression of adenosine A2A receptors, which are involved in the neurodegeneration observed in HD. The P2X7 and P2Y2 receptors may also play a role in the pathophysiology of HD. Interestingly, nucleotide and nucleoside levels may be altered in HD animal models and humans with HD. This review presents several studies describing the relationship between purinergic signaling and HD, as well as the use of purinoceptors as pharmacological targets and biomarkers for this neurodegenerative disorder.

Paternal exposure to excessive methionine altered behavior and neurochemical activities in zebrafish offspring.

An increase in plasma L-methionine (Met) levels, even if transitory, can cause important toxicological alterations in the affected individuals. Met is essential in the regulation of epigenetic mechanisms and its influence on the subsequent generation has been investigated. However, few studies have explored the influence of a temporary increase in Met levels in parents on their offspring. This study evaluated the behavioral and neurochemical effects of parental exposure to high Met concentration (3 mM) in zebrafish offspring. Adult zebrafish were exposed to Met for 7 days, maintained for additional 7 days in tanks that contained only water, and then used for breeding. The offspring obtained from these fish (F1) were tested in this study. During the early stages of offspring development, morphology, heart rate, survival, locomotion, and anxiety-like behavior were assessed. When these animals reached the adult stage, locomotion, anxiety, aggression, social interaction, memory, oxidative stress, and levels of amino acids and neurotransmitters were analyzed. F1 larvae Met group presented an increase in the distance and mean speed when compared to the control group. F1 adult Met group showed decreased anxiety-like behavior and locomotion. An increase in reactive oxygen species was also observed in the F1 adult Met group whereas lipid peroxidation and antioxidant enzymes did not change when compared to the control group. Dopamine, serotonin, glutamate, and glutathione levels were increased in the F1 adult Met group. Taken together, our data show that even a transient increase in Met in parents can cause behavioral and neurochemical changes in the offspring, promoting transgenerational effects.

Withdrawal Effects Following Methionine Exposure in Adult Zebrafish.

Methionine (Met) has important functions for homeostasis of various species, including zebrafish. However, the increased levels of this amino acid in plasma, a condition known as hypermethioninemia, can lead to cell alterations. Met is crucial for the methylation process and its excesses interfere with the cell cycle, an effect that persists even after the removal of this amino acid. Some conditions may lead to a transient increase of this amino acid with unexplored persistent effects of Met exposure. In the present study, we investigated the behavioral and neurochemical effects after the withdrawal of Met exposure. Zebrafish were divided into two groups: control and Met-treated group (3 mM) for 7 days and after maintained for 8 days in tanks containing only water. In the eighth day post-exposure, we evaluated locomotion, anxiety, aggression, social interaction, and memory, as well as oxidative stress parameters, amino acid, and neurotransmitter levels in the zebrafish brain. Our results showed that 8 days after Met exposure, the treated group showed decreased locomotion and aggressive responses, as well as impaired aversive memory. The Met withdrawal did not change thiobarbituric acid reactive substances, reactive oxygen species, and nitrite levels; however, we observed a decrease in antioxidant enzymes superoxide dismutase, catalase, and total thiols. Epinephrine and cysteine levels were decreased after the Met withdrawal whereas carnitine and creatine levels were elevated. Our findings indicate that a transient increase in Met causes persistent neurotoxicity, observed by behavioral and cognitive changes after Met withdrawal and that the mechanisms underlying these effects are related to changes in antioxidant system, amino acid, and neurotransmitter levels.

Influence of 3-nitropropionic acid on physiological and behavioral responses in zebrafish larvae and adults.

Long-term treatment with 3-nitropropionic acid (3-NPA), a toxin derived from plants and fungi, may reproduce symptoms and biochemical characteristics of Huntington's disease (HD). Our study evaluated the effects of 3-NPA on the physiological and behavioral responses in zebrafish larvae and adults. Larvae exposed to 0.1, 0.2, or 0.5 mM 3-NPA exhibited an increase in heart rate at 2- and 5-days post-fertilization (dpf). There was a decrease in the ocular distance at 5 dpf with 0.05 mM 3-NPA treatment. However, 3-NPA did not alter larval locomotor parameters. Adult zebrafish received 3-NPA intraperitoneal injections (a total of seven injections at doses 10, 20, or 60 mg/kg every 96 h) and showed a decrease in body weight , locomotion and aggressive behavior. No changes were observed in anxiety-like behavior and social interaction between 3-NPA-exposed animals and control groups. However, 3-NPA-treated animals (at 60 mg/kg) demonstrated impaired long-term aversive memory. Overall, 3-NPA exposure induced morphological and heart rate alterations in zebrafish larvae. Additionally, our study showed behavioral changes in zebrafish that were submitted to long-term 3-NPA treatment, which could be related to HD symptoms.

Tebuconazole alters morphological, behavioral and neurochemical parameters in larvae and adult zebrafish (Danio rerio).

In this study, we evaluated the effects of tebuconazole on morphology and exploratory larvae behavior and adult locomotion. Furthermore, we analyzed the effects of this fungicide on AChE activity and gene expression in zebrafish larvae and in the adult zebrafish brain. Tebuconazole (4 mg/L) increased the ocular distance in larvae and reduced the distance travelled, absolute turn angle, line crossing and time outside area in exposed larvae. Moreover, adult zebrafish that were exposed to this fungicide (4 and 6 mg/L) showed a decrease in distance travelled and mean speed when compared to the control group. However, tebuconazole did not alter the number of line crossings or time spent in the upper zone. Tebuconazole inhibited AChE activity at concentrations of 4 mg/L for larvae and 4 and 6 mg/L in the adult zebrafish brain. However, this fungicide did not alter AChE gene expression in the adult zebrafish brain but increased AChE mRNA transcript levels in larvae. These findings demonstrated that tebuconazole could modulate the cholinergic system by altering AChE activity and that this change may be associated with the reduced locomotion of these animals.

Manganese(II) chloride alters behavioral and neurochemical parameters in larvae and adult zebrafish.

Manganese (Mn) is an essential metal for organisms, but high levels can cause serious neurological damage. The aim of this study was to evaluate the effects of MnCl2 exposure on cognition and exploratory behavior in adult and larval zebrafish and correlate these findings with brain accumulation of Mn, overall brain tyrosine hydroxylase (TH) levels, dopamine (DA) levels, 3,4-dihydroxyphenylacetic acid (DOPAC) levels and cell death markers in the nervous system. Adults exposed to MnCl2 for 4days (0.5, 1.0 and 1.5mM) and larvae exposed for 5days (0.1, 0.25 and 0.5mM) displayed decreased exploratory behaviors, such as distance traveled and absolute body turn angle, in addition to reduced movement time and an increased number of immobile episodes in larvae. Adults exposed to MnCl2 for 4days showed impaired aversive long-term memory in the inhibitory avoidance task. The overall brain TH levels were elevated in adults and larvae evaluated at 5 and 7 days post-fertilization (dpf). Interestingly, the protein level of this enzyme was decreased in larval animals at 10dpf. Furthermore, DOPAC levels were increased in adult animals exposed to MnCl2. Protein analysis showed increased apoptotic markers in both the larvae and adult nervous system. The results demonstrated that prolonged exposure to MnCl2 leads to locomotor deficits that may be associated with damage caused by this metal in the CNS, particularly in the dopaminergic system.