The full article can be found here
Tell us more about yourself and the author team.
I am a postdoctoral researcher at Trinity College Dublin focusing on cardiovascular and exercise physiology in athlete populations. Following my Ph.D. and postdoctoral work at Trinity College Dublin, I was awarded a Fulbright Fellowship to work with Dr. Meagan Wasfy at Massachusetts General Hospital and Harvard University.
This project is a collaboration between researchers and clinicians from multiple disciplines within Trinity College Dublin, including physiotherapy, physiology, and immunology, and the cardiology division at Massachusetts General Hospital.
What is the story behind your study?
The cardiovascular benefits of routine moderate physical activity are well-established and robust. Similarly, routine engagement in moderate physical activity is considered a potent and long-lasting anti-inflammatory therapy. However, the dose-response relationship between cardiovascular health outcomes and inflammatory status, and exercise doses that exceed current recommendations remains unclear. Athletes routinely engage in high volumes of high-intensity exercise, well exceeding recommended levels. Additionally, athletes participating in contact sports, such as Rugby or American Football, often engage in intentional weight gain for performance benefit, high caloric diets, and are exposed to repetitive blunt trauma from collision tackling. This raises the question as to whether certain athletes are potentially exposed to levels of inflammation during their playing career that could be categorized as low-grade systemic inflammation, an early marker of endothelial dysfunction contributing to atherosclerosis progression.
In your own words, what did you find?
In this study, we found that in a group of rugby athletes. However, 26% were free from all cardiovascular risk factors, and a large proportion had risk factors, with 25% demonstrating increased cardiovascular risk (3-4 risk factors). Falling in line with previous research on rugby athletes, we found that rugby forwards had significantly higher levels of body fat and visceral fat compared to backs. In relation to biomarkers of low-grade systemic inflammation, compared to healthy controls, rugby players had higher levels of vascular adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1). Although rugby players had lower CRP than rheumatoid arthritis patients, one-third of rugby players (n=15) displayed equivalent ICAM-1 and VCAM-1 levels. With several studies showing an association between increased circulatory soluble ICAM-1 and VCAM-1 and cardiovascular risk, findings from our study support the need for further research to investigate the risk of low-grade systemic inflammation and subsequent prognostic implications in rugby athletes.
What was the main challenge you faced in your study?
No previous study has investigated low-grade systemic inflammation in a comparable cohort of athletes, therefore contextualizing findings related to biomarkers of low-grade systemic inflammation was always going to be a challenge. Therefore, we decided to include a small cohort of healthy controls and patients with an inflammatory disease, rheumatoid arthritis. Although our comparator groups are limited by not being matched for age or sex, we believe that the inclusion of this comparison enables a greater ability to put findings from rugby players into context.
If there is one take-home message from your study, what would that be?
Regular engagement in moderate levels of exercise is a potent and long-lasting anti-inflammatory therapy and is undoubtedly beneficial to improving cardiovascular health. Conversely, while regular engagement in high-intensity exercise improves athletes’ physiology and performance capacities, when coupled with high-body mass, high caloric diet, and repeated blunt trauma some athletes may be at risk for low-grade systemic inflammation and increased cardiovascular risk.