Elite sport policies and international sporting success: A panel data analysis of European women’s national football team performance

Research question: While national sporting governing bodies are encouraged to implement programmes which seek to enhance their international sporting success, comparative studies on elite sport policies have provided limited empirical evidence in support of the relationship between such programmes and the achievement of sporting outcomes. Following the SPLISS framework, this study examines the longitudinal impact of four programme-level factors - financial support, human resources, coaching provision and foundation phase activity - on the international success of women’s national football teams. Research methods: Data from 55 Union of European Football Associations’ (UEFA) members were collected over a seven-year-period (2011-2017). The associations between programme-level factors and FIFA ranking points are verified through panel regression analyses. Controls for economic, talent pool, political, socio-cultural, climate and men’s football legacy variables are included. Results and Findings: The results reveal that highly specialised coaching provision has a significant and positive impact on international success in women’s football, while our proxies for financial support, human resources and foundation phase activity have no notable explanatory power for the success of women’s national teams. A country’s economic development, talent pool, climate and men’s football legacy are significant predictors of its women’s football performance level. Implications: This paper offers practical insights into the organisation and management of women’s football in UEFA nations and contributes to the theoretical debate on comparative analysis of the sporting performance of countries. This article confirms that an exclusively quantitative approach does not permit definitive conclusions to be drawn on the complex relationship between elite sport policies and international sporting outcomes

Is prioritisation of funding in elite sport effective? An analysis of the investment strategies in 16 countries

Abstract Research question: This paper explores the extent to which nations prioritise elite sport funding; whether such nations are more successful than those whose funding is more diversified; and, if the sports that receive the most funding are also the most successful. Research methods: Data on public expenditure for elite sport programmes (2011/2012) were collected on a sport-specific basis in 16 nations (n=445 funded sports). The Herfindahl index and concentration ratios of the four/eight most funded sports (CR4/CR8) are used as proxies for prioritization. Success was measured using top 3 and top 8 places during the Olympic Games and World Championships. Descriptive analysis and linear regression are applied to identify the relationship between the distribution of funding and success. Results and findings: Generally, all sample nations are prioritisers. Nations with smaller total elite sport budgets tended to prioritise more. There is a slight negative association between the distribution of funding within a country and subsequent success, indicating that the sample countries that prioritise more tended to be less successful. Sample nations that diversify their funding more, are found to be successful in a wider range of sports. In addition, the data illustrated only low allocative efficiency for some nations. Implications: The study produced ambiguous conclusions that prioritisation as a deliberate strategic choice is an efficient way to invest funding. The findings have important implications for high performance managers and suggests that a more diverse resource allocation policy may help to avoid unintended negative consequences. Keywords: Targeted funding; elite sport policy; allocative efficiency; prioritisation; SPLIS

Convergence and divergence of elite sport policies: is there a one-size-fits-all model to develop international sporting success?

This study is based on a detailed international comparison of the elite sport policies of 15 nations as part of the SPLISS (Sports Policy Factors Leading to International Sporting Success) study. It aims to provide deeper insights into the phenomena of convergence and divergence of elite sport policies. The research uses a mixed methods approach based on document reviews, interviews with high performance directors and surveys of 3142 athletes, 1376 coaches and 246 performance directors. There appears to be no generic blueprint for achieving international sporting success. Nations that perform well in international competition show varying patterns of relative strengths and weaknesses across nine pillars, 96 critical success factors, and 750 sub-factors. While the basic raw ingredients of the recipe might be common in broad terms, the combinations in which they are mixed are diverse. Much of this diversity appears to be driven by social, cultural and political factors

The (non) determinants of Olympic success

This paper empirically examines the determinants of Summer Olympic success during the period 1996-2016. By modifying the panel Tobit estimator using the Mundlak transform, the results find that population size and the host effect are the only statistically significant determinants of Olympic attainment. We also show that participating in front of a home crowd will stimulate athletic performance equally for each gender, but the impact of population differs between the sexes. These findings are confirmed using a hurdle estimator. This relaxes the assumption that the factors determining Olympic success are the same as those that influence the quantity of success

The Anticancer Plant Triterpenoid, Avicin D, Regulates Glucocorticoid Receptor Signaling: Implications for Cellular Metabolism

Avicins, a family of apoptotic triterpene electrophiles, are known to regulate cellular metabolism and energy homeostasis, by targeting the mitochondria. Having evolved from “ancient hopanoids,” avicins bear a structural resemblance with glucocorticoids (GCs), which are the endogenous regulators of metabolism and energy balance. These structural and functional similarities prompted us to compare the mode of action of avicin D with dexamethasone (Dex), a prototypical GC. Using cold competition assay, we show that Avicin D competes with Dex for binding to the GC receptor (GR), leading to its nuclear translocation. In contrast to Dex, avicin-induced nuclear translocation of GR does not result in transcriptional activation of GC-dependent genes. Instead we observe a decrease in the expression of GC-dependent metabolic proteins such as PEPCK and FASN. However, like Dex, avicin D treatment does induce a transrepressive effect on the pro-inflammatory transcription factor NF-κB. While avicin's ability to inhibit NF-κB and its downstream targets appear to be GR-dependent, its pro-apoptotic effects were independent of GR expression. Using various deletion mutants of GR, we demonstrate the requirement of both the DNA and ligand binding domains of GR in mediating avicin D's transrepressive effects. Modeling of avicin-GR interaction revealed that avicin molecule binds only to the antagonist confirmation of GR. These findings suggest that avicin D has properties of being a selective GR modulator that separates transactivation from transrepression. Since the gene-activating properties of GR are mainly linked to its metabolic effects, and the negative interference with the activity of transcription factors to its anti-inflammatory and immune suppressive effects, the identification of such a dissociated GR ligand could have great potential for therapeutic use

Keratinocyte-Targeted Overexpression of the Glucocorticoid Receptor Delays Cutaneous Wound Healing

Delayed wound healing is one of the most common secondary adverse effects associated to the therapeutic use of glucocorticoid (GC) analogs, which act through the ligand-dependent transcription factor GC-receptor (GR). GR function is exerted through DNA-binding-dependent and –independent mechanisms, classically referred to as transactivation (TA) and transrepression (TR). Currently both TA and TR are thought to contribute to the therapeutical effects mediated by GR; however their relative contribution to unwanted side effects such as delayed wound healing is unknown. We evaluated skin wound healing in transgenic mice with keratinocyte-restricted expression of either wild type GR or a mutant GR that is TA-defective but efficient in TR (K5-GR and K5-GR-TR mice, respectively). Our data show that at days (d) 4 and 8 following wounding, healing in K5-GR mice was delayed relative to WT, with reduced recruitment of granulocytes and macrophages and diminished TNF-α and IL-1β expression. TGF-β1 and Kgf expression was repressed in K5-GR skin whereas TGF-β3 was up-regulated. The re-epithelialization rate was reduced in K5-GR relative to WT, as was formation of granulation tissue. In contrast, K5-GR-TR mice showed delays in healing at d4 but re-established the skin breach at d8 concomitant with decreased repression of pro-inflammatory cytokines and growth factors relative to K5-GR mice. Keratinocytes from both transgenic mice closed in vitro wounds slower relative to WT, consistent with the in vivo defects in cell migration. Overall, the delay in the early stages of wound healing in both transgenic models is similar to that elicited by systemic treatment with dexamethasone. Wound responses in the transgenic keratinocytes correlated with reduced ERK activity both in vivo and in vitro. We conclude that the TR function of GR is sufficient for negatively regulating early stages of wound closure, while TA by GR is required for delaying later stages of healing

Is there a role for glucocorticoid receptor beta in asthma?

Glucocorticoids (GCs) are routinely used as anti-inflammatory drugs in the treatment of asthma. They act through binding to glucocorticoid receptor α (GRα), which represses numerous genes encoding pro-inflammatory mediators. A hormone binding deficient GR isoform named GRβ has been isolated in humans. When overexpressed by transfection, GRβ may function as a dominant negative modulator of GRα. However, to act as such, GRβ has to be more abundant than GRα, and conflicting data have been obtained concerning the relative levels of the two isoforms in cell lines and freshly isolated cells. Moreover, the dominant negative effect was not confirmed by independent laboratories. In GC-resistant asthmatics, GRβ was expressed by an increased number of peripheral blood mononuclear cells (PBMCs), airway T cells, and cells found in skin biopsies of tuberculin responses. However, the relative amounts of GRα and GRβ in these cells were not determined. In GC-dependent asthmatics, PBMCs expressed GRα predominantly. No cells containing higher levels of GRβ than GRα have yet been reported in asthmatics. Even if the existence of such cells is demonstrated, the role of GRβ in asthma will remain a matter of controversy because functional studies have given discrepant data

Compound A, a Dissociated Glucocorticoid Receptor Modulator, Inhibits T-bet (Th1) and Induces GATA-3 (Th2) Activity in Immune Cells

Background: Compound A (CpdA) is a dissociating non-steroidal glucocorticoid receptor (GR) ligand which has antiinflammatory properties exerted by down-modulating proinflammatory gene expression. By favouring GR monomer formation, CpdA does not enhance glucocorticoid (GC) response element-driven gene expression, resulting in a reduced side effect profile as compared to GCs. Considering the importance of Th1/Th2 balance in the final outcome of immune and inflammatory responses, we analyzed how selective GR modulation differentially regulates the activity of T-bet and GATA-3, master drivers of Th1 and Th2 differentiation, respectively. Results: Using Western analysis and reporter gene assays, we show in murine T cells that, similar to GCs, CpdA inhibits T-bet activity via a transrepressive mechanism. Different from GCs, CpdA induces GATA-3 activity by p38 MAPK-induction of GATA-3 phosphorylation and nuclear translocation. CpdA effects are reversed by the GR antagonist RU38486, proving the involvement of GR in these actions. ELISA assays demonstrate that modulation of T-bet and GATA-3 impacts on cytokine production shown by a decrease in IFN-c and an increase in IL-5 production, respectively. Conclusions: Taken together, through their effect favoring Th2 over Th1 responses, particular dissociated GR ligands, fo