Impact of Weekly Training-Load Structure and Content on the Risk of Injury in Professional Rugby Union Match-Play.

ABSTRACT: Chéradame, J, Loursac, R, Piscione, J, Carling, C, Decq, P, and Jacqmin-Gadda, H. Impact of weekly training-load structure and content on the risk of injury in professional Rugby Union match-play. J Strength Cond Res XX(X): 000-000, 2024-The aim of this study was to investigate the impact of different components of daily training load during the week preceding the match on the risk of sustaining a match injury in professional rugby union. A cohort of 72 players from a single professional French club participated. Global positioning system-derived data including total distance (TD) and high-speed distance in addition to ratings of perceived effort (RPE) for both on- and off-pitch (gym-based strength conditioning work) training were collected for each training session over 3 seasons (2017-2020). The association between the daily measures of external and internal training load over the week preceding the day of the match (MD) and the subsequent risk of injury in match-play was estimated using a mixed-effects logistic model adjusted for contextual and individual factors. A total of 184 injuries were sustained in 128 matches (incidence: 81.2 injuries per 1,000 player hours). Higher RPE values for the strength conditioning session on MD-5 (p < 0.001) and for the on-pitch session on MD-1 (p = 0.04) were associated with an increased risk of injury in matches. On MD-2, a higher TD covered and that run at high speed (>MAS) were, respectively, associated with a higher (p = 0.03) and lower risk (p = 0.02) of injury in matches played. This study in professional rugby union shows that different components of external and internal load had varying influences on injury risk and particularly in relation to the day on which these were performed in the week leading up to the next match. At MD-2, training load favoring intensity rather than volume could reduce the risk of match-play injury.

Prediction of dementia risk from multimodal repeated measures: The added value of brain MRI biomarkers.

Abstract: The utility of brain magnetic resonance imaging (MRI) for predicting dementia is debated. We evaluated the added value of repeated brain MRI, including atrophy and cerebral small vessel disease markers, for dementia prediction. We conducted a landmark competing risk analysis in 1716 participants of the French population-based Three-City Study to predict the 5-year risk of dementia using repeated measures of 41 predictors till year 4 of follow-up. Brain MRI markers improved significantly the individual prediction of dementia after accounting for demographics, health measures, and repeated measures of cognition and functional dependency (area under the ROC curve [95% CI] improved from 0.80 [0.79 to 0.82] to 0.83 [0.81 to 0.84]). Nonetheless, accounting for the change over time through repeated MRIs had little impact on predictive abilities. These results highlight the importance of multimodal analysis to evaluate the added predictive abilities of repeated brain MRI for dementia and offer new insights into the predictive performances of various MRI markers. Highlights: We evaluated whether repeated brain volumes and cSVD markers improve dementia prediction.The 5-year prediction of dementia is slightly improved when considering brain MRI markers.Measures of hippocampus volume are the main MRI predictors of dementia.Adjusted on cognition, repeated MRI has poor added value over single MRI for dementia prediction.We utilized a longitudinal analysis that considers error-and-missing-prone predictors, and competing death.

Genetic Complexities of Cerebral Small Vessel Disease, Blood Pressure, and Dementia.

Importance: Vascular disease is a treatable contributor to dementia risk, but the role of specific markers remains unclear, making prevention strategies uncertain. Objective: To investigate the causal association between white matter hyperintensity (WMH) burden, clinical stroke, blood pressure (BP), and dementia risk, while accounting for potential epidemiologic biases. Design, Setting, and Participants: This study first examined the association of genetically determined WMH burden, stroke, and BP levels with Alzheimer disease (AD) in a 2-sample mendelian randomization (2SMR) framework. Second, using population-based studies (1979-2018) with prospective dementia surveillance, the genetic association of WMH, stroke, and BP with incident all-cause dementia was examined. Data analysis was performed from July 26, 2020, through July 24, 2022. Exposures: Genetically determined WMH burden and BP levels, as well as genetic liability to stroke derived from genome-wide association studies (GWASs) in European ancestry populations. Main Outcomes and Measures: The association of genetic instruments for WMH, stroke, and BP with dementia was studied using GWASs of AD (defined clinically and additionally meta-analyzed including both clinically diagnosed AD and AD defined based on parental history [AD-meta]) for 2SMR and incident all-cause dementia for longitudinal analyses. Results: In 2SMR (summary statistics-based) analyses using AD GWASs with up to 75 024 AD cases (mean [SD] age at AD onset, 75.5 [4.4] years; 56.9% women), larger WMH burden showed evidence for a causal association with increased risk of AD (odds ratio [OR], 1.43; 95% CI, 1.10-1.86; P = .007, per unit increase in WMH risk alleles) and AD-meta (OR, 1.19; 95% CI, 1.06-1.34; P = .008), after accounting for pulse pressure for the former. Blood pressure traits showed evidence for a protective association with AD, with evidence for confounding by shared genetic instruments. In the longitudinal (individual-level data) analyses involving 10 699 incident all-cause dementia cases (mean [SD] age at dementia diagnosis, 74.4 [9.1] years; 55.4% women), no significant association was observed between larger WMH burden and incident all-cause dementia (hazard ratio [HR], 1.02; 95% CI, 1.00-1.04; P = .07). Although all exposures were associated with mortality, with the strongest association observed for systolic BP (HR, 1.04; 95% CI, 1.03-1.06; P = 1.9 × 10-14), there was no evidence for selective survival bias during follow-up using illness-death models. In secondary analyses using polygenic scores, the association of genetic liability to stroke, but not genetically determined WMH, with dementia outcomes was attenuated after adjusting for interim stroke. Conclusions: These findings suggest that WMH is a primary vascular factor associated with dementia risk, emphasizing its significance in preventive strategies for dementia. Future studies are warranted to examine whether this finding can be generalized to non-European populations.