Achilles tendon structure differs between competitive distance runners and nonrunners despite no clinical signs or symptoms of midsubstance tendinopathy.
Academic Article
Overview
abstract
Achilles tendinopathy affects many running athletes and often leads to chronic pain and functional deficits. Although changes in tendon structure have been linked with tendinopathy, the effects of distance running on tendon structure are not well understood. Therefore, the purpose of this study was to characterize structural differences in the Achilles tendons in healthy young adults and competitive distance runners using quantitative ultrasound analyses. We hypothesized that competitive distance runners with no clinical signs or symptoms of tendinopathy would have quantitative signs of tendon damage, characterized by decreased collagen alignment and echogenicity, in addition to previous reports of thicker tendons. Longitudinal ultrasound images of the right Achilles tendon midsubstance were acquired in competitive distance runners and recreationally active adults. Collagen organization, mean echogenicity, and tendon thickness were quantified using image processing techniques. Clinical assessments confirmed that runners had no signs or symptoms of tendinopathy, and controls were only included if they had no history of Achilles tendon pain or injuries. Runner tendons were 40% less organized, 48% thicker, and 41% less echogenic compared with the control tendons ( P < 0.001). Young adults engaged in competitive distance running have structurally different tendons than recreationally active young adults. NEW & NOTEWORTHY In this study, we quantified the Achilles tendon substructure in distance runners, and a control group of young adults, to determine whether distance running elicits structural adaptations of the tendon. We found that competitive distance runners have structurally compromised Achilles tendons despite not showing any clinical signs or symptoms of tendon injury. These findings suggest that distance running may stimulate structural changes as a protective mechanism against tendon pain and dysfunction.
