Determining the barriers to the use of post-match fatigue monitoring in the rugby codes: A Concept Mapping study.

Topics in Exercise Science and Kinesiology Volume 5: Issue 1, Article 3, 2024. The rugby codes (i.e., rugby union, rugby league, rugby sevens [termed ‘rugby’]) are team-sports that impose complex physical demands upon players which in-turn, leads to domain-specific fatigue (e.g., neuromuscular, cardio-autonomic). Quantifying post-match fatigue through various methods and metrics is important to monitor player fatigue status, which influences training readiness. The specific and general barriers limiting the use of post-match fatigue monitoring in rugby are not presently known. Therefore, the aims of this study were to identify specific and general barriers (clusters of specific barriers) to the use of post-match fatigue monitoring methods and metrics in rugby across the domains of neuromuscular performance, cardio-autonomic, tissue biomarker, and self-reported fatigue, and which of these specific barriers were considered important to overcome and feasible to overcome. An international cohort of subject matter experts (SME) in rugby completed a two-round online questionnaire survey (Round One; n = 42, Round Two; n = 13), with the responses collected and analysed using Concept Mapping. Specific barrier statements were generated based on the SME responses to Round One, which were structured and then rated by the SME for importance to overcome and feasibility to overcome in Round Two. Five clusters of specific barriers (representing the general barriers) were determined based on analyses of the SME responses: 1. ‘Budget and Equipment’, 2. ‘Data and Testing Considerations’, 3. ‘Player and Coach Perceptions’, 4. ‘Test Appropriateness’, and 5. ‘Time and Space’. For both importance to overcome and feasibility to overcome, the ‘Data and Testing Considerations’ had the highest overall rating and contained the largest number of specific barriers which rated highly. These findings should be considered when identifying which post-match fatigue monitoring methods and metrics to implement in rugby, and potentially other sports

Transient over-expression of estrogen receptor-α in breast cancer cells promotes cell survival and estrogen-independent growth

International audienceEstrogen receptor-α (ERα) positive breast cancer frequently responds to inhibitors of ERα activity, such as tamoxifen, and/or to aromatase inhibitors that block estrogen biosynthesis. However, many patients become resistant to these agents through mechanisms that remain unclear. Previous studies have shown that expression of ERα in ERα-negative breast cancer cell lines frequently inhibits their growth. In order to determine the consequence of ERα over-expression in ERα-positive breast cancer cells, we over-expressed ERα in the MCF-7 breast cancer cell line using adenovirus gene transduction. ERα over-expression led to ligand-independent expression of the estrogen-regulated genes pS2 and PR and growth in the absence of estrogen. Interestingly, prolonged culturing of these cells in estrogen-free conditions led to the outgrowth of cells capable of growth in cultures from ERα transduced, but not in control cultures. From these cultures a line, MLET5, was established which remained ERα-positive, but grew in an estrogen-independent manner. Moreover, MLET5 cells were inhibited by anti-estrogens showing that ERα remains important for their growth. Gene expression microarray analysis comparing MCF-7 cells with MLET5 highlighted apoptosis as a major functional grouping that is altered in MLET5 cells, such that cell survival would be favoured. This conclusion was further substantiated by the demonstration that MLET5 show resistance to etoposide-induced apoptosis. As the gene expression microarray analysis also shows that the apoptosis gene set differentially expressed in MLET5 is enriched for estrogen-regulated genes, our findings suggest that transient over-expression of ERα could lead to increased cell survival and the development of estrogen-independent growth, thereby contributing to resistance to endocrine therapies in breast cancer patients