The Contact Sport Brain: What the Evidence Actually Says (And How to Protect Yours)

For a lot of retired players, it isn't the knees or the shoulders that keep them awake at night. It's the smaller things: losing a word mid-sentence, walking into a room and forgetting why, a flatness or fog that wasn't there a decade ago. Underneath it all sits the concerning question: is this just getting older, or is this what all those seasons of contact left behind?

It's a fair question, and as a researcher in the Neurovascular Research Laboratory (NVRL) at the University of South Wales, it's one I get asked all too frequently. It deserves a proper answer, not a headline, and not blanket reassurance either.

Here, we will use rugby as the primary example, as it is the focus of my PhD thesis. To read more about our ongoing project, or to sign up as a participant, click here

Rust in the Pipes

Immediately obvious to any player or spectator is that rugby players get hit a lot. Rugby union players absorb around 600 substantial head impacts per season from matches alone (King et al., 2015), not factoring in training. The overwhelming majority of these impacts, of course, are still far shy of causing a concussion.

For years, sports science mostly counted concussions (which make up a very small slice of the impact pie chart) and left it there. My colleagues and I at the NVRL wanted to know what all those smaller, sub-concussive knocks were doing beneath the surface, specifically to the blood vessels that feed the brain.

Before I had joined the NVRL, my colleagues conducted a season-long study of professional rugby union players from pre- to post-season and found a significant decrease in cognition after just a single season. These differences were most evident in forwards, who are typically involved in more numerous and more forceful tackles (Owens et al., 2021).

We could trace the decline back to disrupted “redox” balance in the vessels themselves. In plain terms: repeated contact was generating unstable molecules called free radicals faster than the body's antioxidant defences could mop them up, and the blood vessels supplying the brain were bearing the brunt of it. If you want the fuller picture of how that free radical process works, I've written about it here.

This isn't unique to rugby, either. A comparable pattern of impaired cerebral blood flow regulation has since turned up in footballers with a heavy heading history (Marley et al., 2021), which tells us the mechanism isn't sport-specific. It's about repeated sub-concussive load on the vascular system, whichever code you play.

What We Found in Retired Players

This is where I have to be careful not to overstate things, because the picture for retired players is genuinely more mixed than either the panicked headlines or the "it's all fine" reassurances suggest.

A systematic review pooling data from over 670 retired rugby players found inconsistent results across the board: some studies picked up fine motor and self-reported cognitive changes, others found no meaningful difference from population norms, and the reviewers were candid about how much the field's methodological limitations restrict any firm conclusions (Cunningham et al., 2018). One caveat I will put on this, however, is that a mountain of new evidence on rugby players has arisen since January 2018, which was the cut-off period for the papers examined in this review. Read on to hear about some of this newer research. Later, a separate large-scale cohort study found former international rugby players carried roughly 2.7 times the risk of a neurodegenerative disease diagnosis compared with matched non-players, though that risk was concentrated in specific conditions like motor neurone disease rather than spread evenly across the board (Russell et al., 2022).

Where we've measured cerebrovascular function directly, rather than inferring it from questionnaires, the picture sharpens. In our own follow-up study, retired players with a history of concussion showed reduced nitric oxide bioactivity and lower blood flow to the brain compared with players without that history (Owens et al., 2023). Nitric oxide is your blood vessels' natural "open" signal: it's what lets them widen and deliver oxygen where it's needed most. When its availability drops, the brain simply gets less blood exactly when it's working hardest.

A study of 146 retired elite rugby players found no overall association between self-reported concussion count and cognitive function, with a measurable effect only showing up in older players who had reported three or more concussions (Gallo et al., 2022). 

However, it's worth being precise about what one of the larger studies in this space actually compared. The "no concussion" group here wasn't a non-rugby-playing control group. Every participant was a former elite player with a broadly similar length of career, so even those who never recalled a diagnosed concussion may still have likely accumulated a serious volume of sub-concussive trauma along the way. 

The finding tells us something useful: that concussion count on its own doesn't cleanly predict cognitive outcomes within a population of former players. However, this study itself can't tell us whether rugby exposure itself carries a cost relative to people who never played, simply because of this lack of a baseline group. 

The CTE Question

What none of this supports is the idea that CTE is a foregone conclusion for anyone who's played contact sport. Despite well over a decade of intense research attention, CTE still can't be diagnosed in a living person (only inferred clinically and confirmed at autopsy), and the field's own diagnostic criteria remain openly contested among researchers (Mavroudis et al., 2023). The honest summary is this: the risk is real, unevenly distributed, and still being actively mapped. It is not a fixed sentence.

Risk Isn't Destiny

This is where the framing matters most. None of the above means a switch has already been flipped. The underlying vascular and inflammatory systems we're talking about are modifiable, and there's a solid evidence base for how.

Cardiovascular fitness is itself a lever on brain blood flow. A systematic review and meta-analysis found that people with higher cardiorespiratory fitness showed measurably better cerebrovascular resistance and reactivity than less fit counterparts (Smith et al., 2021). Cardiorespiratory fitness is separately one of the strongest predictors of long-term mortality risk identified in large-scale clinical data, tracked across more than 120,000 patients in one Cleveland Clinic cohort (Mandsager et al., 2018). 

In simple terms: cardiovascular fitness protects your brain’s function throughout your lifespan, and decreases your risk of just about every disease. 

Sleep carries similar weight. The brain's glymphatic system, its internal “power-washing network” to clear cellular waste products (such as harmful proteins that can otherwise accumulate), relies on quality sleep to clear the same class of metabolic waste products implicated in neurodegenerative disease, and disrupted sleep is consistently associated with impaired clearance (Chong et al., 2022). For a super informative podcast episode on sleep, and some best practices for optimising sleep, check out this episode of Andrew Huberman’s podcast with Dr Matt Walker

Finally, chronic low-grade inflammation, one of the suspected mechanisms compounding the vascular strain of repeated contact, responds reliably to regular aerobic exercise. Meta-analyses show meaningful reductions in markers like CRP and IL-6 with consistent aerobic training (Zheng et al., 2019).

Three Things to Do This Week

  1. Get an actual measure of your cardiovascular fitness. Even a submaximal test gives you a number to track, not a guess. This can be done with many fitness wearables, or you can book in for a laboratory standard VO2 max test with our lab (I do not run these tests, nor receive any money/commission if you purchase them).

  2. Protect seven to eight hours of sleep, particularly the earlier, deeper stages of the night, when glymphatic clearance does its heaviest lifting. Again, wearable devices are a great asset here to monitor your sleep quality and quantity.

  3. Build two to three sessions of moderate aerobic work into your week, not for aesthetics, but because it's one of the few interventions consistently shown to lower your inflammatory load.

The Bottom Line

The vascular strain of a career in contact sport is real, measurable, and, in our own data, still detectable years after retirement. But detectable isn't the same as irreversible. The same systems that took the hit (blood flow regulation, inflammation, oxidative balance) are also the systems that respond fastest to fitness, sleep, and consistent aerobic training.

If you want to know where you actually stand rather than estimate it, that's exactly what a proper assessment is for: turning "am I okay?" into an answer built on your own data, not population averages. Get in touch here if you'd like to talk through what that would look like for you.

Further Reading

For more on the sleep principles above, Matt Walker (Professor of Neuroscience at UC Berkeley and author of Why We Sleep) lays out his QQRT framework, quantity, quality, regularity, and timing, in his own words:

References

Chong, P.L.H., Garic, D., Shen, M.D., Lundgaard, I. and Schwichtenberg, A.J. (2022) 'Sleep, cerebrospinal fluid, and the glymphatic system: A systematic review', Sleep Medicine Reviews, 61, 101572. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC8821419/

Cunningham, J., Broglio, S.P. and Wilson, F. (2018) 'Influence of playing rugby on long-term brain health following retirement: a systematic review and narrative synthesis', BMJ Open Sport & Exercise Medicine, 4(1), e000356. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC5926651/

Gallo, V., McElvenny, D.M., Seghezzo, G., et al. (2022) 'Concussion and long-term cognitive function among rugby players—The BRAIN Study', Alzheimer's & Dementia, 18(6), pp. 1164–1176. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9298292/

King, D., Hume, P.A., Brughelli, M. and Gissane, C. (2015) 'Instrumented mouthguard acceleration analyses for head impacts in amateur rugby union players over a season of matches', American Journal of Sports Medicine, 43(3), pp. 614–624. Available at: https://pubmed.ncbi.nlm.nih.gov/25535096/

Mandsager, K., Harb, S., Cremer, P., Phelan, D., Nissen, S.E. and Jaber, W. (2018) 'Association of cardiorespiratory fitness with long-term mortality among adults undergoing exercise treadmill testing', JAMA Network Open, 1(6), e183605. Available at: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2707428

Marley, C.J., Owens, T.S., Tsukamoto, H., Stacey, B.S., Corkill, R. and Bailey, D.M. (2021) 'Impaired cerebral blood flow regulation and cognition in male football players', Scandinavian Journal of Medicine & Science in Sports, 31(10), pp. 1908–1913. Available at: https://onlinelibrary.wiley.com/doi/10.1111/sms.14018

Mavroudis, I., Balmus, I.-M., Ciobica, A., Luca, A.-C., Gorgan, D.L., Dobrin, I. and Gurzu, I.L. (2023) 'A review of the most recent clinical and neuropathological criteria for chronic traumatic encephalopathy', Healthcare, 11(12), 1689. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC10298260/

Owens, T.S., Calverley, T.A., Stacey, B.S., et al. (2021) 'Contact events in rugby union and the link to reduced cognition: evidence for impaired redox-regulation of cerebrovascular function', Experimental Physiology, 106(9), pp. 1971–1980. Available at: https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP089330

Owens, T.S., Marley, C.J., Calverley, T.A., et al. (2023) 'Lower systemic nitric oxide bioactivity, cerebral hypoperfusion and accelerated cognitive decline in formerly concussed retired rugby union players', Experimental Physiology, 108(8), pp. 1029–1046. Available at: https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP091195

Russell, E.R., Mackay, D.F., Lyall, D., et al. (2022) 'Neurodegenerative disease risk among former international rugby union players', Journal of Neurology, Neurosurgery & Psychiatry, 93(12), pp. 1262–1268. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC9669247

Smith, E.C., Pizzey, F.K., Askew, C.D., Mielke, G.I., Ainslie, P.N., Coombes, J.S. and Bailey, T.G. (2021) 'Effects of cardiorespiratory fitness and exercise training on cerebrovascular blood flow and reactivity: a systematic review with meta-analyses', American Journal of Physiology-Heart and Circulatory Physiology, 321(1), pp. H59–H76. Available at: https://journals.physiology.org/doi/full/10.1152/ajpheart.00880.2020

Zheng, G., Qiu, P., Xia, R., Lin, H., Ye, B., Tao, J. and Chen, L. (2019) 'Effect of aerobic exercise on inflammatory markers in healthy middle-aged and older adults: A systematic review and meta-analysis of randomized controlled trials', Frontiers in Aging Neuroscience, 11, 98. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6497785/

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