Objectives This study examined the impact of a single season of rugby union – and subsequent exposure to head acceleration events (HAEs) – on functional connectivity in adolescent males compared to non-collision sport athletes.

Methods Resting-state functional MRI scans were acquired from 72 rugby players and 20 non-collision sport athletes. The rugby cohort were scanned longitudinally throughout the season. Voxel-wise maps of functional connectivity (FC) for 15 resting-state brain networks were generated for 178 datasets. Cross-sectional comparisons were performed between the rugby cohort at different stages of the season and the non-collision sport group. Longitudinal analyses were performed within the rugby cohort. An exposure analysis estimated HAE exposure based on the number of matches played.

Results No significant cross-sectional differences in FC were found between rugby and non-collision sport athletes or between rugby players with high versus low exposure to HAEs. Longitudinally, rugby players showed increased inter-network FC over the season, with strengthening of connectivity in the temporal, motor, secondary visual, and anterior intraparietal sulcus networks, and mid-season decreases in the cerebellar-visual network. No association was found between longitudinal FC changes and changes in self-reported symptoms.

Conclusions These findings suggest that participation in a season of rugby is associated with neuroplastic changes. These changes may reflect compensatory adaptations to preserve neurological function during periods of HAE exposure. Alternatively, they may also represent developmental changes or responses to physical activity and/or motor learning. This highlights the complexity of interpreting changes in FC in adolescent athletes participating in collision sports and the need for further research.

The authors have declared no competing interest.

The authors would like to acknowledge funding support provided by: the Ministry of Business, Innovation & Employment (MBIE) Catalyst Strategic Fund NZ-Singapore Data Science Research Programme (UOAX2001); the Hugh Green Foundation; the Neurological Foundation of New Zealand First Fellowship (2243 FFE); the New Zealand Health Research Council Explorer Grant (22-625-A); the Te Titoki Mataora Research Acceleration Programme Fund; and an anonymous donor.

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This work was conducted under ethical approval from the New Zealand Health and Disability Ethics Committee (Ethics Ref: 20/NTB/14/AM09) in accordance with the Declaration of Helsinki.

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