New insights into sodium phenylbutyrate as a pharmacotherapeutic option for neurological disorders.

Neurological disorders (NDs) are diseases of the central and peripheral nervous systems that affect more than one billion people worldwide. The risk of developing an ND increases with age due to the vulnerability of the different organs and systems to genetic, environmental, and social changes that consequently cause motor and cognitive deficits that disable the person from their daily activities and individual and social productivity. Intrinsic factors (genetic factors, age, gender) and extrinsic factors (addictions, infections, or lifestyle) favor the persistence of systemic inflammatory processes that contribute to the evolution of NDs. Neuroinflammation is recognized as a common etiopathogenic factor of ND. The study of new pharmacological options for the treatment of ND should focus on improving the characteristic symptoms and attacking specific molecular targets that allow the delay of damage processes such as neuroinflammation, oxidative stress, cellular metabolic dysfunction, and deregulation of transcriptional processes. In this review, we describe the possible role of sodium phenylbutyrate (NaPB) in the pathogenesis of Alzheimer's disease, hepatic encephalopathy, aging, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis; in addition, we describe the mechanism of action of NaPB and its beneficial effects that have been shown in various in vivo and in vitro studies to delay the evolution of any ND.

A critical role for Macrophage-derived Cysteinyl-Leukotrienes in HIV-1 induced neuronal injury.

Macrophages (MΦ) infected with human immunodeficiency virus (HIV)-1 or activated by its envelope protein gp120 exert neurotoxicity. We found previously that signaling via p38 mitogen-activated protein kinase (p38 MAPK) is essential to the neurotoxicity of HIVgp120-stimulated MΦ. However, the associated downstream pathways remained elusive. Here we show that cysteinyl-leukotrienes (CysLT) released by HIV-infected or HIVgp120 stimulated MΦ downstream of p38 MAPK critically contribute to neurotoxicity. SiRNA-mediated or pharmacological inhibition of p38 MAPK deprives MΦ of CysLT synthase (LTC4S) and, pharmacological inhibition of the cysteinyl-leukotriene receptor 1 (CYSLTR1) protects cerebrocortical neurons against toxicity of both gp120-stimulated and HIV-infected MΦ. Components of the CysLT pathway are differentially regulated in brains of HIV-infected individuals and a transgenic mouse model of NeuroHIV (HIVgp120tg). Moreover, genetic ablation of LTC4S or CysLTR1 prevents neuronal damage and impairment of spatial memory in HIVgp120tg mice. Altogether, our findings suggest a novel critical role for cysteinyl-leukotrienes in HIV-associated brain injury.

Chronic resveratrol administration reduces oxidative stress and brain cell loss and improves memory of recognition in old rats.

The cognitive functions of people over 60 years of age have been diminished, due to the structural and functional changes that the brain has during aging. The most evident changes are at the behavioral and cognitive level, with decreased learning capacity, recognition memory, and motor incoordination. The use of exogenous antioxidants has been implemented as a potential pharmacological option to delay the onset of brain aging by attenuating oxidative stress and neurodegeneration. Resveratrol (RSVL) is a polyphenol present in various foods, such as red fruits, and drinks, such as red wine. This compound has shown great antioxidant capacity due to its chemical structure. In this study, we evaluated the effect of chronic RSVL treatment on oxidative stress and cell loss in the prefrontal cortex, hippocampus, and cerebellum of 20-month-old rats, as well as its impact on recognition memory and motor behavior. Rats treated with RSVL showed an improvement in locomotor activity and in short- and long-term recognition memory. Likewise, the concentration of reactive oxygen species and lipid peroxidation decreased significantly in the group with RSVL, coupled with an improvement in the activity of the antioxidant system. Finally, with the help of hematoxylin and eosin staining, it was shown that chronic treatment with RSVL prevented cell loss in the brain regions studied. Our results demonstrate the antioxidant and neuroprotective capacity of RSVL when administered chronically. This strengthens the proposal that RSVL could be an important pharmacological option to reduce the incidence of neurodegenerative diseases that affect older adults.

Diminished Neuronal ESCRT-0 Function Exacerbates AMPA Receptor Derangement and Accelerates Prion-Induced Neurodegeneration.

Endolysosomal defects in neurons are central to the pathogenesis of prion and other neurodegenerative disorders. In prion disease, prion oligomers traffic through the multivesicular body (MVB) and are routed for degradation in lysosomes or for release in exosomes, yet how prions impact proteostatic pathways is unclear. We found that prion-affected human and mouse brain showed a marked reduction in Hrs and STAM1 (ESCRT-0), which route ubiquitinated membrane proteins from early endosomes into MVBs. To determine how the reduction in ESCRT-0 impacts prion conversion and cellular toxicity in vivo, we prion-challenged conditional knockout mice (male and female) having Hrs deleted from neurons, astrocytes, or microglia. The neuronal, but not astrocytic or microglial, Hrs-depleted mice showed a shortened survival and an acceleration in synaptic derangements, including an accumulation of ubiquitinated proteins, deregulation of phosphorylated AMPA and metabotropic glutamate receptors, and profoundly altered synaptic structure, all of which occurred later in the prion-infected control mice. Finally, we found that neuronal Hrs (nHrs) depletion increased surface levels of the cellular prion protein, PrPC, which may contribute to the rapidly advancing disease through neurotoxic signaling. Taken together, the reduced Hrs in the prion-affected brain hampers ubiquitinated protein clearance at the synapse, exacerbates postsynaptic glutamate receptor deregulation, and accelerates neurodegeneration.SIGNIFICANCE STATEMENT Prion diseases are rapidly progressive neurodegenerative disorders characterized by prion aggregate spread through the central nervous system. Early disease features include ubiquitinated protein accumulation and synapse loss. Here, we investigate how prion aggregates alter ubiquitinated protein clearance pathways (ESCRT) in mouse and human prion-infected brain, discovering a marked reduction in Hrs. Using a prion-infection mouse model with neuronal Hrs (nHrs) depleted, we show that low neuronal Hrs is detrimental and markedly shortens survival time while accelerating synaptic derangements, including ubiquitinated protein accumulation, indicating that Hrs loss exacerbates prion disease progression. Additionally, Hrs depletion increases the surface distribution of prion protein (PrPC), linked to aggregate-induced neurotoxic signaling, suggesting that Hrs loss in prion disease accelerates disease through enhancing PrPC-mediated neurotoxic signaling.

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Prions induce an early Arc response and a subsequent reduction in mGluR5 in the hippocampus.

Synapse dysfunction and loss are central features of neurodegenerative diseases, caused in part by the accumulation of protein oligomers. Amyloid-ß, tau, prion, and α-synuclein oligomers bind to the cellular prion protein (PrPC), resulting in the activation of macromolecular complexes and signaling at the post-synapse, yet the early signaling events are unclear. Here we sought to determine the early transcript and protein alterations in the hippocampus during the pre-clinical stages of prion disease. We used a transcriptomic approach focused on the early-stage, prion-infected hippocampus of male wild-type mice, and identify immediate early genes, including the synaptic activity response gene, Arc/Arg3.1, as significantly upregulated. In a longitudinal study of male, prion-infected mice, Arc/Arg-3.1 protein was increased early (40% of the incubation period), and by mid-disease (pre-clinical), phosphorylated AMPA receptors (pGluA1-S845) were increased and metabotropic glutamate receptors (mGluR5 dimers) were markedly reduced in the hippocampus. Notably, sporadic Creutzfeldt-Jakob disease (sCJD) post-mortem cortical samples also showed low levels of mGluR5 dimers. Together, these findings suggest that prions trigger an early Arc response, followed by an increase in phosphorylated GluA1 and a reduction in mGluR5 receptors.

Transcriptomic and Genetic Profiling of HIV-Associated Neurocognitive Disorders.

Early in the HIV pandemic, it became evident that people living with HIV (PLWH) develop a wide range of neurological and neurocognitive complications. Even after the introduction of combination antiretroviral therapy (cART), which dramatically improved survival of PLWH, the overall number of people living with some form of HIV-associated neurocognitive disorders (HAND) seemed to remain unchanged, although the incidence of dementia declined and questions about the incidence and diagnosis of the mildest form of HAND arose. To better understand this complex disease, several transcriptomic analyses have been conducted in autopsy samples, as well as in non-human primates and small animal rodent models. However, genetic studies in the HIV field have mostly focused on the genetic makeup of the immune system. Much less is known about the genetic underpinnings of HAND. Here, we provide a summary of reported transcriptomic and epigenetic changes in HAND, as well as some of the potential genetic underpinnings that have been linked to HAND, and discuss future directions with hurdles to overcome and angles that remain to be explored.

Comprehensive review of lipocalin 2-mediated effects in lung inflammation.

Lipocalin-2 (LCN2) is an inflammatory mediator best known for its role as an innate acute-phase protein. LCN2 mediates the innate immune response to pathogens by sequestering iron, thereby inhibiting pathogen growth. Although LCN2 and its bacteriostatic properties are well studied, other LCN2 functions in the immune response to inflammatory stimuli are less well understood, such as its role as a chemoattractant and involvement in the regulation of cell migration and apoptosis. In the lungs, most studies thus far investigating the role of LCN2 in the immune response have looked at pathogenic inflammatory stimuli. Here, we compile data that explore the role of LCN2 in the immune response to various inflammatory stimuli in an effort to differentiate between protective versus detrimental roles of LCN2.

Influence of the Craniocervical Posture on Tongue Strength and Endurance.

Tongue strength has an important role in the swallowing process, and previous research has suggested that tongue position, concerning the craniomandibular region, could affect the oral function. This study aimed to evaluate the strength and endurance of three areas of the tongue in three experimentally induced craniocervical postures. A cross-sectional study with a nonprobabilistic sample of 37 participants (mean age: 3.85 ± 3.64 years; 20 men, 17 women) was performed. Tongue strength and endurance were assessed using a pressure device entitled Iowa Oral Performance Instrument (IOPI), in three different craniocervical positions: neutral head position (NHP), anterior head translation-or forward head position (FHP), and posterior head translation-or retracted head position (RHP). Measurements taken using the IOPI system showed significant differences in tongue strength for the anterior (p = 0.015) and middle areas of the tongue (p = 0.01). Significant differences were observed in analysis of variance (ANOVA) in the FHP (p = 0.02) and NHP (p = 0.009). The results of tongue endurance measurements showed statistically significant differences for FHP (p = 0.001), NHP (p = 0.00), and RHP (p = 0.007). The craniocervical position influences tongue strength, especially in the anterior and middle tongue areas, concerning the posterior, and, in the anterior and neutral head posture, regarding the retracted position. No differences were found in tongue resistance between the various craniocervical positions, but differences were found in resistance between the different tongue areas.

A pivotal role for Interferon-α receptor-1 in neuronal injury induced by HIV-1.

BACKGROUND: HIV-1 infection remains a major public health concern despite effective combination antiretroviral therapy (cART). The virus enters the central nervous system (CNS) early in infection and continues to cause HIV-associated neurocognitive disorders (HAND). The pathogenic mechanisms of HIV-associated brain injury remain incompletely understood. Since HIV-1 activates the type I interferon system, which signals via interferon-α receptor (IFNAR) 1 and 2, this study investigated the potential role of IFNAR1 in HIV-induced neurotoxicity. METHODS: We cross-bred HIVgp120-transgenic (tg) and IFNAR1 knockout (IFNAR1KO) mice. At 11-14 months of age, we performed a behavioral assessment and subsequently analyzed neuropathological alterations using deconvolution and quantitative immunofluorescence microscopy, quantitative RT-PCR, and bioinformatics. Western blotting of brain lysates and an in vitro neurotoxicity assay were employed for analysis of cellular signaling pathways. RESULTS: We show that IFNAR1KO results in partial, sex-dependent protection from neuronal injury and behavioral deficits in a transgenic model of HIV-induced brain injury. The IFNAR1KO rescues spatial memory and ameliorates loss of presynaptic terminals preferentially in female HIVgp120tg mice. Similarly, expression of genes involved in neurotransmission reveals sex-dependent effects of IFNAR1KO and HIVgp120. In contrast, IFNAR1-deficiency, independent of sex, limits damage to neuronal dendrites, microgliosis, and activation of p38 MAPK and restores ERK activity in the HIVgp120tg brain. In vitro, inhibition of p38 MAPK abrogates neurotoxicity caused similarly by blockade of ERK kinase and HIVgp120. CONCLUSION: Our findings indicate that IFNAR1 plays a pivotal role in both sex-dependent and independent processes of neuronal injury and behavioral impairment triggered by HIV-1.

Lipocalin-2 mediates HIV-1 induced neuronal injury and behavioral deficits by overriding CCR5-dependent protection.

People living with HIV (PLWH) continue to develop HIV-associated neurocognitive disorders despite combination anti-retroviral therapy. Lipocalin-2 (LCN2) is an acute phase protein that has been implicated in neurodegeneration and is upregulated in a transgenic mouse model of HIV-associated brain injury. Here we show that LCN2 is significantly upregulated in neocortex of a subset of HIV-infected individuals with brain pathology and correlates with viral load in CSF and pro-viral DNA in neocortex. However, the question if LCN2 contributes to HIV-associated neurotoxicity or is part of a protective host response required further investigation. We found that the knockout of LCN2 in transgenic mice expressing HIVgp120 in the brain (HIVgp120tg) abrogates behavioral impairment, ameliorates neuronal damage, and reduces microglial activation in association with an increase of the neuroprotective CCR5 ligand CCL4. In vitro experiments show that LCN2 neurotoxicity also depends on microglia and p38 MAPK activity. Genetic ablation of CCR5 in LCN2-deficient HIVgp120tg mice restores neuropathology, suggesting that LCN2 overrides neuroprotection mediated by CCR5 and its chemokine ligands. RNA expression of 168 genes involved in neurotransmission reveals that neuronal injury and protection are each associated with genotype- and sex-specific patterns affecting common neural gene networks. In conclusion, our study identifies LCN2 as a novel factor in HIV-associated brain injury involving CCR5, p38 MAPK and microglia. Furthermore, the mechanistic interaction between LCN2 and CCR5 may serve as a diagnostic and therapeutic target in HIV patients at risk of developing brain pathology and neurocognitive impairment.

Diesel Exhaust Extract Exposure Induces Neuronal Toxicity by Disrupting Autophagy.

The vast majority of neurodegenerative disease cannot be attributed to genetic causes alone and as a result, there is significant interest in identifying environmental modifiers of disease risk. Epidemiological studies have supported an association between long-term exposure to air pollutants and disease risk. Here, we investigate the mechanisms by which diesel exhaust, a major component of air pollution, induces neurotoxicity. Using a zebrafish model, we found that exposure to diesel exhaust particulate extract caused behavioral deficits and a significant decrease in neuron number. The neurotoxicity was due, at least in part, to reduced autophagic flux, which is a major pathway implicated in neurodegeneration. This neuron loss occurred alongside an increase in aggregation-prone neuronal protein. Additionally, the neurotoxicity induced by diesel exhaust particulate extract in zebrafish was mitigated by co-treatment with the autophagy-inducing drug nilotinib. This study links environmental exposure to altered proteostasis in an in vivo model system. These results shed light on why long-term exposure to traffic-related air pollution increases neurodegenerative disease risk and open up new avenues for exploring therapies to mitigate environmental exposures and promote neuroprotection.

Effect of Manual Therapy and Therapeutic Exercise Applied to the Cervical Region on Pain and Pressure Pain Sensitivity in Patients with Temporomandibular Disorders: A Systematic Review and Meta-analysis.

OBJECTIVE: To assess the effectiveness of cervical manual therapy (MT) on patients with temporomandibular disorders (TMDs) and to compare cervico-craniomandibular MT vs cervical MT. DESIGN: Systematic review and meta-analysis (MA). METHODS: A search in PubMed, EMBASE, PEDro, and Google Scholar was conducted with an end date of February 2019. Two independent reviewers performed the data analysis, assessing the relevance of the randomized clinical trials regarding the studies' objectives. The qualitative analysis was based on classifying the results into levels of evidence according to the Grading of Recommendations, Assessment, Development and Evaluation (GRADE). RESULTS: Regarding cervical MT, MA included three studies and showed statistically significant differences in pain intensity reduction and an increase in masseter pressure pain thresholds (PPTs), with a large clinical effect. In addition, the results showed an increase in temporalis PPT, with a moderate clinical effect. MA included two studies on cervical MT vs cervico-craniomandibular MT interventions and showed statistically significant differences in pain intensity reduction and pain-free maximal mouth opening, with a large clinical effect. CONCLUSIONS: Cervical MT treatment is more effective in decreasing pain intensity than placebo MT or minimal intervention, with moderate evidence. Cervico-craniomandibular interventions achieved greater short-term reductions in pain intensity and increased pain-free MMO over cervical intervention alone in TMD and headache, with low evidence.

Perception and self-assessment of digital skills and gaming among youth: A dataset from Spain.

The present article offers a dataset of how young Spanish people perceive and evaluate their digital skills, showing the confidence level of their Social skills, Mobile skills, Information/navigation skills, Operational skills, and Creative skills. It also provides data on the use and the typology of video games in which youth are involved. This data demonstrates how young people evaluate their relationship with interactive and digital media, and supports knowledge to understand such interaction in the context of skills and abilities. It also presents socio-demographic and socio-economic characteristics, including gender, age, marital status, education, occupation and, community/residence for the Spanish population between 16 and 35 years old. This data was acquired by interviewing 1012 individuals using computer-assisted telephone interviews (CATI) in May 2017.

Is aerobic exercise helpful in patients with migraine? A systematic review and meta-analysis.

PURPOSE: To assess the effects of aerobic exercise (AE) on patients with migraine in terms of pain intensity, frequency and duration of migraine, and quality of life. METHODS: A systematic review and meta-analysis of randomized controlled trials were conducted. Standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated for relevant outcomes and were pooled in a meta-analysis using the random-effects model. RESULTS: A total of 10 articles from 1950 to 2019 were included, involving 508 patients. The meta-analysis showed statistically significant differences in the decrease in pain intensity (five studies, n = 166; SMD = 1.25; 95% CI 0.47-2.04), frequency (six studies, n = 214; SMD = 0.76; 95% CI 0.32-1.2) and duration of migraine (four studies, n = 106; SMD = 0.41; 95% CI 0.03-0.8), in the short-term. In addition, the meta-analysis showed statistically significant differences in the increase in quality of life (four studies, n = 150; SMD = 2.7; 95% CI 1.17-4.24), even though the Egger's test suggested significant evidence of publication bias for the analysis of quality of life (intercept = 5.81; t = 6.97; P = .02). CONCLUSIONS: There is low- and moderate-quality evidence that in patients with migraine AE can decrease the pain intensity, frequency and duration of migraine and can also increase quality of life.

The Effects of Two Different Resisted Swim Training Load Protocols on Swimming Strength and Performance.

This study used a power rack device to evaluate the effects of 2 different approaches to resisted swim training loads on swimming strength and performance. Sixteen male, youth national-level swimmers (mean age, 16.22 ± 2.63 years; body height, 169 ± 10.20 cm; body mass, 61.33 ± 9.90 kg) completed a 6-week specific strength-training program, and were then randomly assigned to one of the two groups: a standard training group (GS, n = 8) and a flat pyramid-loading pattern group (GP, n = 8). Strength and power tests along with specific swimming tests (50-m crawl and 50-m competition-style time trials) were conducted at baseline (pre-test), before the third week (mid-test), and after 6 weeks of intervention (post-test). Isokinetic swim bench tests were conducted to obtain measurements of force production and power, and 1RM tests with the power rack system were conducted to measure the maximum drag load (MDL) and specific swimming power. Following 6 weeks of intervention, the mean MDL increased (p < 0.05) by 13.94%. Scores for the 50-m competition style and 50-m crawl time trials improved by 0.32% and 0.78%, respectively, in the GP; however, those changes were not statistically significant. The GS significantly increased their time in the 50-m competition style by 2.59%, and their isokinetic force production decreased by 14.47% (p < 0.05). The 6-week strength-training program performed with the power rack device in a pyramidal organization was more effective than a standard linear load organization in terms of producing improvements in the MDL; however, it did not produce significant improvements in performance. The use of a strength-training program with a pyramidal organization can be recommended for specific strength-training in young swimmers during a preparatory period. However, in our study, that program did not produce significant changes in 50-m crawl and main competition style performance.

CXCL12-induced neurotoxicity critically depends on NMDA receptor-gated and L-type Ca2+ channels upstream of p38 MAPK.

BACKGROUND: The chemokine receptor CXCR4 (CD184) and its natural ligand CXCL12 contribute to many physiological processes, including decisions about cell death and survival in the central nervous system. In addition, CXCR4 is a co-receptor for human immunodeficiency virus (HIV)-1 and mediates the neurotoxicity of the viral envelope protein gp120. However, we previously observed that CXCL12 also causes toxicity in cerebrocortical neurons but the cellular mechanism remained incompletely defined. METHODS: Primary neuronal-glial cerebrocortical cell cultures from rat were exposed to a neurotoxicity-inducing CXCL12 concentration for different times and the activity of the stress-associated mitogen-activated protein kinase p38 (p38 MAPK) was assessed using an in vitro kinase assay. Neurotoxicity of CXCL12 and cellular localization of p38 MAPK was analyzed by immunofluorescence microscopy. Pharmacological inhibition of NMDA-type glutamate receptor-gated ion channels (NMDAR) of L-type Ca2+ channels was employed during 12- and 24-h exposure to neurotoxic amounts of CXCL12 to study the effects on active p38 MAPK and neuronal survival by Western blotting and microscopy, respectively. Neurotoxicity of CXCL12 was also assessed during pharmacological inhibition of p38 MAPK. RESULTS: Here, we show that a neurotoxic amount of CXCL12 triggers a significant increase of endogenous p38 MAPK activity in cerebrocortical cells. Immunofluorescence and Western blotting experiments with mixed neuronal-glial and neuron-depleted glial cerebrocortical cells revealed that the majority of active/phosphorylated p38 MAPK was located in neurons. Blockade of NMDAR-gated ion channels or L-type Ca2+ channels both abrogated an increase of active p38 MAPK and toxicity of CXCL12 in cerebrocortical neurons. Inhibition of L-type Ca2+ channels with nimodipine kept the active kinase at levels not significantly different from baseline while blocking NMDAR with MK-801 strongly reduced phosphorylated p38 MAPK below baseline. Finally, we confirmed that directly blocking p38 MAPK also abrogated neurotoxicity of CXCL12. CONCLUSIONS: Our findings link CXCL12-induced neuronal death to the regulation of NMDAR-gated ion channels and L-type Ca2+ channels upstream of p38 MAPK activation.

Effects of Continuous and Interval Training on Running Economy, Maximal Aerobic Speed and Gait Kinematics in Recreational Runners.

The purpose of this study was to evaluate the effects on running economy (RE), V[Combining Dot Above]O2max, maximal aerobic speed (MAS), and gait kinematics (step length [SL] and frequency, flight and contact time [CT]) in recreational athletes, with 2 different training methods, Interval and Continuous (CON). Eleven participants were randomly distributed in an interval training group (INT; n = 6) or CON training group (CON; n = 5). Interval training and CON performed 2 different training programs (95-110% and 70-75% of MAS, respectively), which consisted of 3 sessions per week during 6 weeks with the same external workload (%MAS × duration). An incremental test to exhaustion was performed to obtain V[Combining Dot Above]O2max, MAS, RE, and gait variables (high speed camera) before and after the training intervention. There was a significant improvement (p ≤ 0.05) in RE at 60 and 90% of MAS by the CON group; without changes in gait. The INT group significantly increased MAS and higher stride length at 80, 90, and 100% of MAS and lower CT at 100% of MAS. As expected, training adaptations are highly specific to the overload applied with CON producing improvements in RE at lower percentage of MAS whereas INT produces improvements in MAS. The significantly increased stride length and decreased CT for the INT group are an important outcome of favorable changes in running gait.

Enhancing physical performance in elite junior tennis players with a caffeinated energy drink.

The aim of this study was to investigate the effectiveness of a caffeinated energy drink to enhance physical performance in elite junior tennis players. In 2 different sessions separated by 1 wk, 14 young (16 ± 1 y) elite-level tennis players ingested 3 mg caffeine per kg body mass in the form of an energy drink or the same drink without caffeine (placebo). After 60 min, participants performed a handgrip-strength test, a maximal-velocity serving test, and an 8 × 15-m sprint test and then played a simulated singles match (best of 3 sets). Instantaneous running speed during the matches was assessed using global positioning (GPS) devices. Furthermore, the matches were videotaped and notated afterward. In comparison with the placebo drink, the ingestion of the caffeinated energy drink increased handgrip force by ~4.2% ± 7.2% (P = .03) in both hands, the running pace at high intensity (46.7 ± 28.5 vs 63.3 ± 27.7 m/h, P = .02), and the number of sprints (12.1 ± 1.7 vs 13.2 ± 1.7, P = .05) during the simulated match. There was a tendency for increased maximal running velocity during the sprint test (22.3 ± 2.0 vs 22.9 ± 2.1 km/h, P = .07) and higher percentage of points won on service with the caffeinated energy drink (49.7% ± 9.8% vs 56.4% ± 10.0%, P = .07) in comparison with the placebo drink. The energy drink did not improve ball velocity during the serving test (42.6 ± 4.8 vs 42.7 ± 5.0 m/s, P = .49). The preexercise ingestion of caffeinated energy drinks was effective to enhance some aspects of physical performance of elite junior tennis players.

Isokinetic leg strength and power in elite handball players.

Isokinetic strength evaluation of the knee flexion and extension in concentric mode of contraction is an important part of the comprehensive evaluation of athletes. The aims of this study were to evaluate the isokinetic knee peak torque in both the extension and flexion movement in the dominant and non-dominant leg, and the relationship with jumping performance. Twelve elite male handball players from the top Spanish handball division voluntary participated in the study (age 27.68 ± 4.12 years; body mass 92.89 ± 12.34 kg; body height 1.90 ± 0.05 m). The knee extensor and flexor muscle peak torque of each leg were concentrically measured at 60º/s and 180º/s with an isokinetic dynamometer. The Squat Jump and Countermovement Jump were performed on a force platform to determine power and vertical jump height. Non-significant differences were observed between legs in the isokinetic knee extension (dominant= 2.91 ± 0.53 Nm/kg vs non-dominant = 2.70 ± 0.47 Nm/kg at 60º/s; dominant = 1.90 ± 0.31 Nm/kg vs non-dominant = 1.83 ± 0.29 Nm/kg at 180º/s) and flexion peak torques (dominant = 1.76 ± 0.29 Nm/kg vs non-dominant = 1.72 ± 0.39 Nm/kg at 60º/s; dominant = 1.30 ± 0.23 Nm/kg vs non-dominant = 1.27 ± 0.35 Nm/kg at 180º/s). Low and non-significant correlation coefficients were found between the isokinetic peak torques and vertical jumping performance (SJ = 31.21 ± 4.32 cm; CMJ = 35.89 ± 4.20 cm). Similar isokinetic strength was observed between the legs; therefore, no relationship was found between the isokinetic knee flexion and extension peak torques as well as vertical jumping performance in elite handball players.