UEFA Women's Elite Club Injury Study: a prospective study on 1527 injuries over four consecutive seasons 2018/2019 to 2021/2022 reveals thigh muscle injuries to be most common and ACL injuries most burdensome.

OBJECTIVE: Injuries in women's football (soccer) have scarcely been investigated, and no study has been conducted in the highest competitive level involving club teams from different countries. Our aim was to investigate the time-loss injury epidemiology and characteristics among women's elite football players over four seasons. METHODS: 596 players from 15 elite women's teams in Europe were studied prospectively during the 2018/2019 to 2021/2022 seasons (44 team seasons). Medical staff recorded individual player exposure and time-loss injuries. Injury incidence was calculated as the number of injuries per 1000 playing hours and injury burden as the number of days lost per 1000 hours. RESULTS: 1527 injuries were recorded in 463 players with an injury incidence of 6.7 (95% CI 6.4 to 7.0) injuries per 1000 hours and a nearly fourfold higher incidence during match play compared with training (18.4, 95% CI 16.9 to 19.9 vs 4.8, 95% CI 4.5 to 5.1; rate ratio 3.8, 95% CI 3.5 to 4.2). Thigh muscle injuries (hamstrings 12%, 188/1527, and quadriceps 11%, 171/1527) were the most frequent injury, while anterior cruciate ligament (ACL) injury had the highest burden (38.0 days lost per 1000 hours, IQR 29.2-52.1) with median days lost of 292 (IQR 246-334) days. Concussions constituted 3% (47/1527) of all injuries, with more than half of them (55%, 26/47) due to ball-related impact. CONCLUSION: An elite women's football team can expect approximately 35 time-loss injuries per season. Thigh muscle injury was the most common injury and ACL injury had the highest injury burden.

Low adoption in women's professional football: teams that used the Nordic Hamstring Exercise in the team training had fewer match hamstring injuries.

Objectives: The primary objective was to study the reach, effectiveness, adoption, implementation and maintenance of the Nordic Hamstring Exercise (NHE) programme in women's elite teams in Europe in the 2020-21 season. The secondary objective was to compare hamstring injury rates between teams that used the NHE programme regularly in team training and teams that did not. Methods: Eleven teams participating in the Women's Elite Club Injury Study during the 2020-21 season provided data about injury rates and the implementation of the NHE programme. Results: One team (9%) used the full original NHE programme, and four teams used the programme in the team training during parts of the season (team training group, n=5). Five teams did not use the NHE, or used it only sporadically for individual players, and one team used NHE only for players with a previous or current hamstring injury (no team training group, n=6). The team training group had a lower incidence of hamstring injuries during match-play (1.4 vs 4.0, p=0.028) than the non-team training group while no difference between groups was shown for the hamstring injury incidence in training (0.6 vs 0.7, p=0.502). Conclusion: A low adoption of the NHE programme was reported during the 2020-21 season. However, teams that used NHE for the whole team or most players had a lower hamstring injury incidence at match-play than teams that did not use the NHE or used it for individual players only.

Most modifiable risk factors for hamstring muscle injury in women's elite football are extrinsic and associated with the club, the team, and the coaching staff and not the players themselves: the UEFA Women's Elite Club Injury Study.

PURPOSE: To describe the perceived importance of suggested hamstring injury risk factors according to chief medical officers (CMOs) of European women's professional football clubs. A secondary objective was to compare if these perceptions differed between teams with a lower-than-average and higher-than-average hamstring injury burden. METHODS: The CMOs of eleven European professional women's football clubs were initially asked to suggest modifiable risk factors for hamstring injury. These risk factors were rated in according with their perceived importance on a 5-graded Likert scale. Participating teams were divided in two groups depending on their hamstring injury burden during the 2020/21 season. The LOW group consisted of six teams that had a lower-than-average hamstring injury burden. The HIGH group consisted of five teams that had a higher-than-average hamstring injury burden. RESULTS: Twenty-one risk factors were suggested, most of which were extrinsic in nature, hence associated with the coaching staff, the team or the club organization rather than with the players themselves. The risk factors with the highest average importance were: "lack of communication between medical staff and coaching staff" and "load on players" (each with a weighted average of 3.9), followed by "lack of regular exposure to high-speed football actions during training" and "playing matches 2-3 times a week" (weighted average of 3.8 and 3.7). Differently from the LOW group, the HIGH group perceived the coaching factors (style of coach leadership, training/exercise surveillance by coaching staff) as more important. CONCLUSION: In accordance to the eleven CMOs recruited in this study, most risk factors for hamstring injuries are extrinsic in nature and associated with the club, the team, and the coaching staff, and not the players themselves. LEVEL OF EVIDENCE: Level III.

Influence of the COVID-19 Lockdown and Restart on the Injury Incidence and Injury Burden in Men's Professional Football Leagues in 2020: The UEFA Elite Club Injury Study.

BACKGROUND: Studies on football and the coronavirus disease 2019 (COVID-19) have mainly focused on the lockdown consequences for player fitness, the resumption of football training, and how to safely restart the league play, but injury data are scarce. OBJECTIVE: To describe the injury incidence and injury burden in men's professional football teams during the pandemic year of 2020. METHODS: Nineteen teams in 12 countries prospectively registered data on player-exposure and time-loss injuries throughout 2020. All major football leagues were paused as a direct response to the pandemic in March 2020 and were thereafter completely cancelled or restarted after a lockdown interval of at least two months. Historical data from 43 teams in the same cohort during the five preceding years (2015-2019) were used as reference. Between-season and within-season comparisons were made for injury incidence (number of injuries per 1000 h) and injury burden (number of absence days per 1000 h) with 95% confidence intervals and interquartile ranges. RESULTS: There was no increased match injury incidence or injury burden following the restart in 2020 compared with other time periods of 2020 and the corresponding periods 2015-2019. There was an increased training injury incidence and injury burden immediately during the lockdown in 2020, and they remained elevated also following the restart, being higher in 2020 compared with 2015-2019, respectively. The injury characteristics during the first months of the new 2020/21 season (August/September-December) were similar between the five teams that cancelled their 2019/20 season in March 2020 and the 14 teams that restarted their season in May/June 2020. CONCLUSIONS: There was no increased match injury incidence or injury burden following the COVID-19 lockdown and restart of the football season in 2020, but training injury incidence and injury burden were elevated and higher than in 2015-2019.

Hepatic expression of lipopolysaccharide-binding protein (Lbp) is induced by the gut microbiota through Myd88 and impairs glucose tolerance in mice independent of obesity.

OBJECTIVE: Gut-derived inflammatory factors can impair glucose homeostasis, but the underlying mechanisms are not fully understood. In this study, we investigated how hepatic gene expression is regulated by gut colonization status through myeloid differentiation primary response 88 (MYD88) and how one of the regulated genes, lipopolysaccharide-binding protein (Lbp), affects insulin signaling and systemic glucose homeostasis. METHODS: Liver transcriptomics analysis was conducted on four groups of mice fed a chow diet: conventionally raised (CONV-R) wild-type, germ-free (GF) wild-type, CONV-R Myd88 KO, and GF Myd88 KO. Primary hepatocytes were exposed to combinations of lipopolysaccharide (LPS), LBP, and the LBP-blocking peptide LBPK95A, and the effect on insulin signaling was determined. To assess how LBP affects glucose metabolism in vivo, two mouse models were applied: treatment with LBPK95A and hepatic knockdown of Lbp using CRISPR-CAS9. RESULTS: We showed that the colonization status regulates gene expression in the liver and that a subset of these genes, including Lbp, is regulated through MYD88. Furthermore, we demonstrated that LBP impairs insulin signaling in hepatocytes in the presence of low levels of LPS and that the effect of LBP is abolished by LBPK95A. We showed that both systemic pharmacological blocking of LBP by LBPK95A and CRISPR-CAS9-mediated downregulation of hepatic Lbp improve glucose homeostasis. CONCLUSIONS: Our results demonstrate that the gut microbiota regulates hepatic expression of Lbp through MYD88-dependent signaling. LBP potentiates LPS inhibition of insulin signaling in vitro and impairs systemic glucose homeostasis in vivo.

Simplified Intestinal Microbiota to Study Microbe-Diet-Host Interactions in a Mouse Model.

The gut microbiota can modulate human metabolism through interactions with macronutrients. However, microbiota-diet-host interactions are difficult to study because bacteria interact in complex food webs in concert with the host, and many of the bacteria are not yet characterized. To reduce the complexity, we colonize mice with a simplified intestinal microbiota (SIM) composed of ten sequenced strains isolated from the human gut with complementing pathways to metabolize dietary fibers. We feed the SIM mice one of three diets (chow [fiber rich], high-fat/high-sucrose, or zero-fat/high-sucrose diets [both low in fiber]) and investigate (1) how dietary fiber, saturated fat, and sucrose affect the abundance and transcriptome of the SIM community, (2) the effect of microbe-diet interactions on circulating metabolites, and (3) how microbiota-diet interactions affect host metabolism. Our SIM model can be used in future studies to help clarify how microbiota-diet interactions contribute to metabolic diseases.

Does Feeling Empathy Lead to Compassion Fatigue or Compassion Satisfaction? The Role of Time Perspective.

Research has shown that feeling empathy sometimes leads to compassion fatigue and sometimes to compassion satisfaction. In three studies, participants recalled an instance when they felt empathy in order to assess the role time perspective plays in how empathizers perceive the consequences of empathy. Study 1 revealed that college students perceive empathy as having more negative consequences in the short term, but more positive consequences in the long term. Study 2 showed that service industry professionals perceive the consequences of feeling empathy for customers who felt bad as less negative, and the consequences of feeling empathy for people who felt good as less positive, in the long as opposed to the short term. Because Studies 1 and 2 confounded time perspective with event specificity a third study was conducted in which event specificity was held constant across time perspectives. The same pattern of results emerged. The results of these studies indicate that perceptions of the effects of feeling empathy, whether positive or negative, become less extreme over time. These findings shed light on the relation between empathy and compassion fatigue and satisfaction by suggesting that situations that initially are experienced as stressful can over time make the empathizer stronger.

Regulation of body fat mass by the gut microbiota: Possible mediation by the brain.

New insight suggests gut microbiota as a component in energy balance. However, the underlying mechanisms by which gut microbiota can impact metabolic regulation is unclear. A recent study from our lab shows, for the first time, a link between gut microbiota and energy balance circuitries in the hypothalamus and brainstem. In this article we will review this study further.

Dietary Fiber-Induced Improvement in Glucose Metabolism Is Associated with Increased Abundance of Prevotella.

The gut microbiota plays an important role in human health by interacting with host diet, but there is substantial inter-individual variation in the response to diet. Here we compared the gut microbiota composition of healthy subjects who exhibited improved glucose metabolism following 3-day consumption of barley kernel-based bread (BKB) with those who responded least to this dietary intervention. The Prevotella/Bacteroides ratio was higher in responders than non-responders after BKB. Metagenomic analysis showed that the gut microbiota of responders was enriched in Prevotella copri and had increased potential to ferment complex polysaccharides after BKB. Finally, germ-free mice transplanted with microbiota from responder human donors exhibited improved glucose metabolism and increased abundance of Prevotella and liver glycogen content compared with germ-free mice that received non-responder microbiota. Our findings indicate that Prevotella plays a role in the BKB-induced improvement in glucose metabolism observed in certain individuals, potentially by promoting increased glycogen storage.

Return to play following muscle injuries in professional footballers.

This prospective cohort study described return-to-play (RTP) data for different types of muscle injuries in male elite-level football players in Europe. Eighty-nine European professional teams were followed between 2001 and 2013. Team medical staff recorded individual player exposure and time-loss injuries. A total of 17,371 injuries occurred, including 5603 (32%) muscle injuries. From 2007, we received results from 386 magnetic resonance imaging (MRI) examinations, and radiological grading was performed. A negative MRI was associated with shorter recovery time (6 ± 7 days). Lay-off days were correlated with MRI grading of thigh muscle injuries (P < 0.001). Among hamstring injuries, 83% occurred to the biceps femoris, 12% affected the semimembranosus and 5% the semitendinosus. Recurrence rate was higher among biceps femoris injuries (18%) compared with semitendinosus and semimembranosus injuries (2% together). Groin muscle injuries caused shorter median absence (9 days) than hamstring (13 days; P < 0.001), quadriceps (12 days; P < 0.001) and calf muscle (13 days; P < 0.001) injuries. Overall, we found that MRI was valuable for prognosticating RTP, with radiological grading associated with lay-off times after injury. Re-injuries were common in biceps femoris injuries but rare in semitendinosus and semimembranosus injuries.

The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon (Gcg) and brain-derived neurotrophic factor (Bdnf) in the central nervous system.

The gut microbiota contributes to fat mass and the susceptibility to obesity. However, the underlying mechanisms are not completely understood. To investigate whether the gut microbiota affects hypothalamic and brainstem body fat-regulating circuits, we compared gene expression of food intake-regulating neuropeptides between germ-free and conventionally raised (CONV-R) mice. We found that CONV-R mice had decreased expression of the antiobesity neuropeptide glucagon-like peptide-1 (GLP-1) precursor proglucagon (Gcg) in the brainstem. Moreover, in both the hypothalamus and the brainstem, CONV-R mice had decreased expression of the antiobesity neuropeptide brain-derived neurotrophic factor (Bdnf). CONV-R mice had reduced expression of the pro-obesity peptides neuropeptide-Y (Npy) and agouti-related protein (Agrp), and increased expression of the antiobesity peptides proopiomelanocortin (Pomc) and cocaine- and amphetamine-regulated transcript (Cart) in the hypothalamus. The latter changes in neuropeptide expression could be secondary to elevated fat mass in CONV-R mice. Leptin treatment caused less weight reduction and less suppression of orexigenic Npy and Agrp expression in CONV-R mice compared with germ-free mice. The hypothalamic expression of leptin resistance-associated suppressor of cytokine signaling 3 (Socs-3) was increased in CONV-R mice. In conclusion, the gut microbiota reduces the expression of 2 genes coding for body fat-suppressing neuropeptides, Gcg and Bdnf, an alteration that may contribute to fat mass induction by the gut microbiota. Moreover, the presence of body fat-inducing gut microbiota is associated with hypothalamic signs of Socs-3-mediated leptin resistance, which may be linked to failed compensatory body fat reduction.

Generating and Analyzing Germ-Free Mice.

The normal gut microbiota has evoked many investigators' interest over the years and the pioneering work of James Reyniers in the 1920s generated the first germ-free guinea pigs. Comparing the physiology between germ-free and conventionally raised animals has provided invaluable insights on how the gut microbiota affect host biology. Today we know that the gut microbiota modulate the immune system, epithelial cell proliferation, intestinal angiogenesis, hormone production, energy absorption, and behavior. Furthermore, recent data have demonstrated that obesity is associated with an altered gut microbiota, and a direct role for the microbiota in disease development was demonstrated by the use of germ-free mice. Here we are presenting protocols for maintaining and generating germ-free mice. Curr. Protoc. Mouse Biol. 2:307-316 © 2012 by John Wiley & Sons, Inc.

Role of a consensus AP-2 regulatory sequence within the Epstein-Barr virus LMP1 promoter in EBNA2 mediated transactivation.

The Epstein-Barr virus (EBV) tumor-associated latent membrane protein 1 (LMP1) gene expression is transactivated by EBV nuclear antigen 2 (EBNA2) in human B cells. We previously reported that an E-box element at the LMP1 regulatory sequence (LRS) represses transcription of the LMP1 gene through the recruitment of a Max-Mad1-mSin3A complex. In the present study, using deletion/mutation analysis, and electrophoretic mobility shift assays, we show that the promoter region adjacent to the E-box (-59/-67) is required for the full repression conferred by E-box binding proteins. The repressive effect of these factors was overcome by an inhibitor of histone deacetylation, Trichostatin A (TSA), concurring with the reports that histone deacetylation plays an important role in repression mediated by Max-Mad1-mSin3A complex. Furthermore, ChIP analyses showed that histones at the transcriptionally active LMP1 promoter were hyperacetylated, whereas in the absence of transcription they were hypoacetylated. EBNA2 activation of the promoter required a consensus AP-2 sequence in the -103/-95 LRS region. While EMSA results and the low level of AP-2 factors expression in B cells argue against known AP-2 factors binding to this site, several pieces of evidence point to a similar mechanism of promoter activation as seen by AP-2 factors. We conclude that an AP-2 site-binding factor and EBNA2 act in concert to overcome the repression of the LMP1 promoter via the consensus AP-2 site. This activation showed strong correlation with histone hyperacetylation at the promoter, indicating this to be a major mechanism for the EBNA2 mediated LMP1 transactivation.