Author(s): HELDER, T., LEWIS, N., MCEWEN, T., LANCASTER, M., BREEN, D., MILES, E., BARTLETT, D., HILL, J., PEDLAR, C. , Institution: ST MARY'S UNIVERSITY, Country: UNITED KINGDOM, Abstract-ID: 1572

INTRODUCTION:
Professional rugby union is characterised by repeated high-intensity efforts and collisions that challenge physiological homeostasis. Although acute perturbations in inflammatory and stress-related biomarkers have been reported, evidence for integrated inflammatory, redox, endocrine, and immune responses across in-season match cycles remains limited. Recent reports of clinically elevated C-reactive protein in rugby players have raised concern about potential sustained inflammatory load (1). This study therefore aimed to characterise post-match biomarker changes and examine associations with match exposure and positional grouping in elite rugby union players.
METHODS:
In this single-team case study, data were collected across six professional matches. Biomarkers (high-sensitivity C-reactive protein [hs-CRP], Free Oxygen Radicals Testing [FORT], Free Oxygen Radicals Defence [FORD], Oxidative Stress Ratio [OSI], cortisol, and immune cell counts/ratios) were measured pre-match and post-match at either game day (GD) +2 or GD+3. Match exposure was quantified using minutes played and contact counts; positional groups were also compared. Analyses were performed using mixed-effects models (player-level random intercept), with additional sensitivity regressions.
RESULTS:
hs-CRP increased from pre-match to GD+2 and trended back toward baseline by GD+3. Players with ≥60 min of match exposure had higher hs-CRP than those with <60 min (2.50 vs 0.89 mg·L⁻¹ ; ~181%; p = 0.001). In mixed-effects models, neither game time nor contacts was independently associated with biomarkers. In sensitivity analyses, contact counts were inversely associated with monocyte-to-lymphocyte ratio (β = −0.00178; p = 0.029). Redox markers and cortisol showed no time effects; positional differences were observed for cortisol, FORT, and haemoglobin. Immune indices showed no recovery-day effects in mixed models; however, pooled pre–post comparisons indicated higher lymphocyte and monocyte counts (1.9 to 2.2, ~15.8%, p = 0.040; 0.2 to 0.3, ~50%, p < 0.001), lower neutrophil-to-lymphocyte ratio (1.28 to 1.12, ~12.5%, p = 0.033), and higher monocyte-to-lymphocyte ratio (0.120 to 0.133, ~10.8%, p = 0.002).
CONCLUSION:
Match-play elicited a delayed, transient inflammatory response typically resolving within ~72 h. While prior rugby studies have reported persistently elevated or clinically high CRP, this pattern was not observed in the present cohort. hs-CRP elevations appear to have a short-lived exposure threshold, and alongside immune indices suggest a rapid resolution of inflammatory insult. Whether this rapid resolution is a prerequisite for improved game performance remains unknown. This case study contributes valuable pilot data to inform the design of larger, multi-team studies in rugby union.

1. McHugh C, Hind K, Kelly A, et al. Cardiovascular risk and systemic inflammation in male professional rugby: a cross-sectional study. BMJ Open Sport Exerc Med. 2023;9(4):e001636.