The Efficacy of Re-Warm-Up Practices during Half-Time: A Systematic Review

Background and Objectives: The passive nature of rest breaks in sport could reduce athletes' performance and even increase their risk of injury. Re-warm-up activities could help avoid these problems, but there is a lack of research on their efficacy. This systematic review aimed at analyzing the results of those randomized controlled trials (RCTs) that provided information on the effects of re-warm-up strategies. Materials and Methods: Four electronic databases (Web of Science, Scopus, PubMed, and SPORTDiscus) were searched from their inception to January 2021, for RCTs on the effects of re-warm-up activities on sports performance. Interventions had to be implemented just after an exercise period or sports competition. Studies that proposed activities that were difficult to replicate in the sport context or performed in a hot environment were excluded. Data were synthesized following PRISMA guidelines, while the risk of bias was assessed following the recommendations of the Cochrane Collaboration. Results: A total of 14 studies (178 participants) reporting data on acute or short-term effects were analyzed. The main outcomes were grouped into four broad areas: physiological measures, conditional abilities, perceptual skills, and sport efficiency measures. The results obtained indicated that passive rest decreases physiological function in athletes, while re-warm-up activities could help to improve athletes' conditional abilities and sporting efficiency, despite showing higher fatigue levels in comparison with passive rest. The re-warm-up exercise showed to be more effective than passive rest to improve match activities and passing ability. Conclusions: Performing re-warm-up activities is a valuable strategy to avoid reducing sports performance during prolonged breaks. However, given that the methodological quality of the studies was not high, these relationships need to be further explored in official or simulated competitions

Do you even exercise, ref? Exploring habits of Spanish basketball referees during practice and matches

Abstract Background: Basketball referees are a vital part of the organised competition system, although they remain an "outgroup" in sport. While physical development and fitness programming are deemed necessary for basketball officiating excellence, there is a paucity of literature exploring strategies for physical fitness management in this population. Methods: This research was a nationwide cross-sectional, self-administered online survey conducted in 2021. A sample of 628 (531 males, 97 females) referees from 18 regional referee organisations in Spain provided individual responses to gather information on demographic details, level of participation in refereeing, physical fitness practices, and match-day exercise-based regimens. The data were described using summary statistics, and the associations of the assessed variables were subsequently calculated using contingency tables. Results: Our findings reveal that a large fraction of the Spanish basketball referee population focuses on aerobic (83%) and strength (73.6%) activities, while less attention is paid to speed (36.9%) and flexibility (23.2%), and agility, coordination, and balance tasks are somewhat overlooked. No significant differences were observed among the referee categories regarding weekly training days or session duration, with most training for 15-60 min per session. Elite referees were more likely to hire personal trainers and engage in strength and flexibility exercises. Sub-elite referees showed a higher tendency to perform stretching and joint mobility activities post-match, while regional referees did so less frequently. Approximately 30.7% of referees across all competitive levels engaged in re-warm-up (RW-U) activities, with stretching and joint mobility being the most prevalent. Conclusions: Spanish basketball referees participate in routine physical exercise and fitness practices, irrespective of their competition level. While warm-up activities are prevalent, some sub-elite and regional referees do not consistently perform them, and re-warm-up routines are not extensively embraced

The effectiveness of a practical half-time re-warm-up strategy in youth female basketball players

Problem Statement: Passive rest during basketball games could reduce athletes’ performance and increase the risk of injury during the second half of the game due to loss of muscle temperature. Approach: The re-warm-up activities during half-time could help avoid this problem, but there is a lack of research on their efficacy, especially in basketball. Purpose: This study aimed to assess the influence of two half-time re-warm-up strategies (that do not demand additional equipment) on measures of performance and the physical, sports and perceptual response during a basketball simulated match. Methods: Ten female basketball players U16 completed a traditional intervention and alternative strategy based on bouncing, in which participants completed two 40-minute games (4 x 10-minute periods with a 10-minute half-time interspersing the third and fourth periods) separated by four days. The traditional trial comprised a passive 6-minute period followed by 3 minutes of shooting wheel, whilst the alternative trial comprised a passive 6-minute period, followed by 1 minute of bouncing and 2 minutes of shooting wheel. The re-warm-up protocols were completed 1 minute before the beginning of the second half. Results: The re-warm-up did not show significant effects on jump performance and rating of perceived exertion immediately after half-time and after the second half of the basketball simulated match. No significant changes were identified for heart rate and locomotory responses during the game, except for the distance covered at a very light speed which was significantly higher in the traditional group. Conclusions: These data support that adding a bouncing exercise to a classic re-warm-up during half-time does not lead to additional improvement in young female basketball players

Physiological Responses to, and Athlete and Coach Perceptions of Exertion During Small-sided Basketball Games

This study describes heart rate (HR) responses during different small sided games (SSGs) in junior basketball players, and identifies the level of agreement between athlete and coach perceptions of internal training load calculated using the in-task rating of perceived exertion (RPE) method. Over a 6 week period, 12 male junior basketball players who played in the Spanish national under-18 League, played 7 games of one-a-side (1v1), 6 games of two-aside (2v2), 8 games of five-a-side (5v5), and 5 games of superiority (3v2) situations. During 1v1, 2v2, 5v5, and 3v2 peak heart rates were 90.27 ± 3.37%, 92.68 ± 3.29%, 92.01 ± 3.48%, and 88.74 ± 5.77% of HRmax respectively. These differences were statistically significant between 1v1 and 2v2 (P<0.01), 1v1 and 5v5 (P<0.05), 2v2 and 3v2 (P<0.001), and 5v5 and 3v2 (P<0.001). Mean heart rate was 79.5 ± 4.4%, 83.1 ± 4.2%, 91.2 ± 4.7%, and 78.5 ± 7.5% of HRmax during 1v1, 2v2, 5v5, and 3v2, respectively, and differences were observed between 1v1 and 2v2 (P<0.001), 2v2 and 3v2 (P<0.001), and 5v5 and 3v2 (P<0.05). There were differences in athletes and coaches in-task RPE in all SSGs (all P<0.0001 apart from 5x5 P=0.0019). The 2v2 format elicited a higher mean in-task RPE in comparison to all other SSGs (P<0.001), possibly because 2v2 imposes a greater cognitive load

NOA36 Protein Contains a Highly Conserved Nucleolar Localization Signal Capable of Directing Functional Proteins to the Nucleolus, in Mammalian Cells

NOA36/ZNF330 is an evolutionarily well-preserved protein present in the nucleolus and mitochondria of mammalian cells. We have previously reported that the pro-apoptotic activity of this protein is mediated by a characteristic cysteine-rich domain. We now demonstrate that the nucleolar localization of NOA36 is due to a highly-conserved nucleolar localization signal (NoLS) present in residues 1–33. This NoLS is a sequence containing three clusters of two or three basic amino acids. We fused the amino terminal of NOA36 to eGFP in order to characterize this putative NoLS. We show that a cluster of three lysine residues at positions 3 to 5 within this sequence is critical for the nucleolar localization. We also demonstrate that the sequence as found in human is capable of directing eGFP to the nucleolus in several mammal, fish and insect cells. Moreover, this NoLS is capable of specifically directing the cytosolic yeast enzyme polyphosphatase to the target of the nucleolus of HeLa cells, wherein its enzymatic activity was detected. This NoLS could therefore serve as a very useful tool as a nucleolar marker and for directing particular proteins to the nucleolus in distant animal species

Loss of mitochondrial Ndufs4 in striatal medium spiny neurons mediates progressive motor impairment in a mouse model of leigh syndrome

Altres ajuts: Juan del la Cierva (IJCI-2015-24576)Inability of mitochondria to generate energy leads to severe and often fatal myoencephalopathies. Among these, Leigh syndrome (LS) is one of the most common childhood mitochondrial diseases; it is characterized by hypotonia, failure to thrive, respiratory insufficiency and progressive mental and motor dysfunction, leading to early death. Basal ganglia nuclei, including the striatum, are affected in LS patients. However, neither the identity of the affected cell types in the striatum nor their contribution to the disease has been established. Here, we used a mouse model of LS lacking Ndufs4, a mitochondrial complex I subunit, to confirm that loss of complex I, but not complex II, alters respiration in the striatum. To assess the role of striatal dysfunction in the pathology, we selectively inactivated Ndufs4 in the striatal medium spiny neurons (MSNs), which account for over 95% of striatal neurons. Our results show that lack of Ndufs4 in MSNs causes a non-fatal progressive motor impairment without affecting the cognitive function of mice. Furthermore, no inflammatory responses or neuronal loss were observed up to 6 months of age. Hence, complex I deficiency in MSNs contributes to the motor deficits observed in LS, but not to the neural degeneration, suggesting that other neuronal populations drive the plethora of clinical signs in LS

Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case-control study

Introduction: Approximately 100 loci have been definitively associated with rheumatoid arthritis (RA) susceptibility. However, they explain only a fraction of RA heritability. Interactions between polymorphisms could explain part of the remaining heritability. Multiple interactions have been reported, but only the shared epitope (SE) × protein tyrosine phosphatase nonreceptor type 22 (PTPN22) interaction has been replicated convincingly. Two recent studies deserve attention because of their quality, including their replication in a second sample collection. In one of them, researchers identified interactions between PTPN22 and seven single-nucleotide polymorphisms (SNPs). The other showed interactions between the SE and the null genotype of glutathione S-transferase Mu 1 (GSTM1) in the anti-cyclic citrullinated peptide-positive (anti-CCP+) patients. In the present study, we aimed to replicate association with RA susceptibility of interactions described in these two high-quality studies. Methods: A total of 1,744 patients with RA and 1,650 healthy controls of Spanish ancestry were studied. Polymorphisms were genotyped by single-base extension. SE genotypes of 736 patients were available from previous studies. Interaction analysis was done using multiple methods, including those originally reported and the most powerful methods described. Results: Genotypes of one of the SNPs (rs4695888) failed quality control tests. The call rate for the other eight polymorphisms was 99.9%. The frequencies of the polymorphisms were similar in RA patients and controls, except for PTPN22 SNP. None of the interactions between PTPN22 SNPs and the six SNPs that met quality control tests was replicated as a significant interaction term the originally reported finding or with any of the other methods. Nor was the interaction between GSTM1 and the SE replicated as a departure from additivity in anti-CCP+ patients or with any of the other methods. Conclusions: None of the interactions tested were replicated in spite of sufficient power and assessment with different assays. These negative results indicate that whether interactions are significant contributors to RA susceptibility remains unknown and that strict standards need to be applied to claim that an interaction exists

Lack of replication of interactions between polymorphisms in rheumatoid arthritis susceptibility: case–control study

[Abstract] INTRODUCTION: Approximately 100 loci have been definitively associated with rheumatoid arthritis (RA) susceptibility. However, they explain only a fraction of RA heritability. Interactions between polymorphisms could explain part of the remaining heritability. Multiple interactions have been reported, but only the shared epitope (SE) × protein tyrosine phosphatase nonreceptor type 22 (PTPN22) interaction has been replicated convincingly. Two recent studies deserve attention because of their quality, including their replication in a second sample collection. In one of them, researchers identified interactions between PTPN22 and seven single-nucleotide polymorphisms (SNPs). The other showed interactions between the SE and the null genotype of glutathione S-transferase Mu 1 (GSTM1) in the anti-cyclic citrullinated peptide-positive (anti-CCP+) patients. In the present study, we aimed to replicate association with RA susceptibility of interactions described in these two high-quality studies. METHODS: A total of 1,744 patients with RA and 1,650 healthy controls of Spanish ancestry were studied. Polymorphisms were genotyped by single-base extension. SE genotypes of 736 patients were available from previous studies. Interaction analysis was done using multiple methods, including those originally reported and the most powerful methods described. RESULTS: Genotypes of one of the SNPs (rs4695888) failed quality control tests. The call rate for the other eight polymorphisms was 99.9%. The frequencies of the polymorphisms were similar in RA patients and controls, except for PTPN22 SNP. None of the interactions between PTPN22 SNPs and the six SNPs that met quality control tests was replicated as a significant interaction term--the originally reported finding--or with any of the other methods. Nor was the interaction between GSTM1 and the SE replicated as a departure from additivity in anti-CCP+ patients or with any of the other methods. CONCLUSIONS: None of the interactions tested were replicated in spite of sufficient power and assessment with different assays. These negative results indicate that whether interactions are significant contributors to RA susceptibility remains unknown and that strict standards need to be applied to claim that an interaction exists.Instituto de Salud Carlos III; 11/01048Instituto de Salud Carlos III; 12/01909Instituto de Salud Carlos III; RD12/0009/000

Evaluation of 12 GWAS-drawn SNPs as biomarkers of rheumatoid arthritis response to TNF inhibitors. A potential SNP association with response to etanercept

Research in rheumatoid arthritis (RA) is increasingly focused on the discovery of biomarkers that could enable personalized treatments. The genetic biomarkers associated with the response to TNF inhibitors (TNFi) are among the most studied. They include 12 SNPs exhibiting promising results in the three largest genome-wide association studies (GWAS). However, they still require further validation. With this aim, we assessed their association with response to TNFi in a replication study, and a meta-analysis summarizing all nonredundant data. The replication involved 755 patients with RA that were treated for the first time with a biologic drug, which was either infliximab (n = 397), etanercept (n = 155) or adalimumab (n = 203). Their DNA samples were successfully genotyped with a single-base extension multiplex method. Lamentably, none of the 12 SNPs was associated with response to the TNFi in the replication study (p > 0.05). However, a drug-stratified exploratory analysis revealed a significant association of the NUBPL rs2378945 SNP with a poor response to etanercept (B = -0.50, 95% CI = -0.82, -0.17, p = 0.003). In addition, the metaanalysis reinforced the previous association of three SNPs: rs2378945, rs12142623, and rs4651370. In contrast, five of the remaining SNPs were less associated than before, and the other four SNPs were no longer associated with the response to treatment. In summary, our results highlight the complexity of the pharmacogenetics of TNFi in RA showing that it could involve a drug-specific component and clarifying the status of the 12 GWAS-drawn SNPsThis work was supported by the Instituto de Salud Carlos III (ISCIII, Spain) through grants PI14/01651, PI17/01606 and RD16/0012/0014 to AG and PI12/01909 to JJG-R. These grants are partially financed by the European Regional Development Fund of the EU (FEDER

Evaluation of 12 GWAS-drawn SNPs as biomarkers of rheumatoid arthritis response to TNF inhibitors. A potential SNP association with response to etanercept

Research in rheumatoid arthritis (RA) is increasingly focused on the discovery of biomarkers that could enable personalized treatments. The genetic biomarkers associated with the response to TNF inhibitors (TNFi) are among the most studied. They include 12 SNPs exhibiting promising results in the three largest genome-wide association studies (GWAS). However, they still require further validation. With this aim, we assessed their association with response to TNFi in a replication study, and a meta-analysis summarizing all non-redundant data. The replication involved 755 patients with RA that were treated for the first time with a biologic drug, which was either infliximab (n = 397), etanercept (n = 155) or adalimumab (n = 203). Their DNA samples were successfully genotyped with a single-base extension multiplex method. Lamentably, none of the 12 SNPs was associated with response to the TNFi in the replication study (p > 0.05). However, a drug-stratified exploratory analysis revealed a significant association of the NUBPL rs2378945 SNP with a poor response to etanercept (B = -0.50, 95% CI = -0.82, -0.17, p = 0.003). In addition, the meta-analysis reinforced the previous association of three SNPs: rs2378945, rs12142623, and rs4651370. In contrast, five of the remaining SNPs were less associated than before, and the other four SNPs were no longer associated with the response to treatment. In summary, our results highlight the complexity of the pharmacogenetics of TNFi in RA showing that it could involve a drug-specific component and clarifying the status of the 12 GWAS-drawn SNP