Introduction Regular physical activity is generally associated with reduced colorectal cancer (CRC) risk. However, extreme endurance exercise may produce repetitive gastrointestinal stress through splanchnic hypoperfusion, ischemia–reperfusion injury, mucosal inflammation and occult gastrointestinal bleeding.
Introduction
Regular physical activity is generally associated with reduced colorectal cancer (CRC) risk. However, extreme endurance exercise may produce repetitive gastrointestinal stress through splanchnic hypoperfusion, ischemia–reperfusion injury, mucosal inflammation and occult gastrointestinal bleeding. Whether chronic exposure to these physiologic insults influences colorectal neoplasia risk remains poorly understood.
Problem Statement
Although gastrointestinal bleeding and ischemic colitis are recognized complications of endurance running, data linking high-volume endurance exercise with colorectal adenomas or advanced neoplasia are lacking. Understanding whether endurance athletes harbor increased rates of premalignant colorectal lesions could influence screening and evaluation strategies, particularly in younger individuals with post-exercise rectal bleeding.
Summary
This prospective hypothesis-generating study evaluated colonoscopic findings in endurance runners aged 35–50 years with substantial marathon or ultramarathon exposure. Adenomas were identified in over 40% of participants, while advanced adenomas were detected in 15%, substantially exceeding historical screening benchmarks for average-risk younger adults. Importantly, no colorectal cancers were identified. Most advanced lesions were right-sided and frequently exhibited high-risk features including large size, tubulovillous histology or sessile serrated morphology. Post-exercise rectal bleeding was significantly more common among runners with advanced adenomas, suggesting that gastrointestinal bleeding after endurance exercise should not be routinely dismissed as benign “runner’s colitis.” Notably, advanced adenomas were also detected in asymptomatic runners without bleeding, indicating that clinically silent lesions may occur in this population. Despite the observed adenoma burden, the study did not demonstrate a clear relationship between training intensity and lesion prevalence, underscoring the exploratory nature of the findings. The authors propose several biologically plausible mechanisms including repetitive ischemia–reperfusion injury, oxidative stress, microbiome alterations and mucosal regenerative hyperproliferation. However, the study’s single-arm design, modest sample size and potential selection bias preclude causal inference. Overall, the findings generate an important hypothesis that extreme endurance running may be associated with increased prevalence of advanced colorectal precursor lesions and support larger controlled studies evaluating colorectal neoplasia risk in endurance athletes.
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