Acta chirurgiae orthopaedicae et traumatologiae Cechoslovaca · 2026
Impact of Treadmill Running Intensity on Lubricin Levels in Rat Achilles Tendons.
СтатьяНазвание и аннотация: Перевод в очереди
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Shu-Fen L I, Song Cheng-Xian, Liu Sheng-Yao, Liu Wei, Shao-Yong X U
Аннотация
PURPOSE OF THE STUDY: The Achilles tendon is crucial for transferring force from the calf muscles to the heel bone. Lubricin, a key glycoprotein, ensures smooth tendon gliding. This study investigated the effects of different treadmill running intensities on lubricin levels in rat Achilles tendons and explored the associated molecular mechanisms.
MATERIAL AND METHODS: Eighteen rats were divided into three groups: Strenuous Treadmill Running (STR), Moderate Treadmill Running (MTR), and a sedentary Control group (CON). The running protocols were conducted over eight weeks. Post-intervention, tendon samples were analyzed for histological changes (collagen fiber integrity and cell count), lubricin levels, and the expression of TGF-β1 (a growth factor involved in tendon healing) and IL-1 (a pro-inflammatory cytokine).
RESULTS: The STR group exhibited significantly greater collagen fiber damage compared to the other groups. In contrast, the MTR group showed higher cell proliferation, elevated lubricin levels, and increased TGF-β1 expression. The STR group had reduced lubricin levels, likely due to elevated IL-1 expression.
DISCUSSION: MTR enhances tendon health by upregulating TGF-β1, increasing lubricin production, and improving load transmission. Conversely, STR may promote tendon degeneration by elevating IL-1, reducing lubricin levels, and increasing the risk of tendinopathy. These findings support previous research indicating that moderate mechanical loading maintains tendon homeostasis, whereas excessive loading leads to inflammation and structural damage.
CONCLUSIONS: Moderate-intensity treadmill running boosts lubricin levels via TGF-β1 regulation, supporting tendon function, while strenuous running decreases lubricin due to IL-1 upregulation, increasing tendon injury risk. These results emphasize the importance of optimal exercise intensity in preventing tendinopathies and maintaining tendon health. The findings could guide exercise recommendations for athletes and rehabilitation programs. Future research should explore therapeutic strategies targeting the TGF-β1 and IL-1 pathways.
MATERIAL AND METHODS: Eighteen rats were divided into three groups: Strenuous Treadmill Running (STR), Moderate Treadmill Running (MTR), and a sedentary Control group (CON). The running protocols were conducted over eight weeks. Post-intervention, tendon samples were analyzed for histological changes (collagen fiber integrity and cell count), lubricin levels, and the expression of TGF-β1 (a growth factor involved in tendon healing) and IL-1 (a pro-inflammatory cytokine).
RESULTS: The STR group exhibited significantly greater collagen fiber damage compared to the other groups. In contrast, the MTR group showed higher cell proliferation, elevated lubricin levels, and increased TGF-β1 expression. The STR group had reduced lubricin levels, likely due to elevated IL-1 expression.
DISCUSSION: MTR enhances tendon health by upregulating TGF-β1, increasing lubricin production, and improving load transmission. Conversely, STR may promote tendon degeneration by elevating IL-1, reducing lubricin levels, and increasing the risk of tendinopathy. These findings support previous research indicating that moderate mechanical loading maintains tendon homeostasis, whereas excessive loading leads to inflammation and structural damage.
CONCLUSIONS: Moderate-intensity treadmill running boosts lubricin levels via TGF-β1 regulation, supporting tendon function, while strenuous running decreases lubricin due to IL-1 upregulation, increasing tendon injury risk. These results emphasize the importance of optimal exercise intensity in preventing tendinopathies and maintaining tendon health. The findings could guide exercise recommendations for athletes and rehabilitation programs. Future research should explore therapeutic strategies targeting the TGF-β1 and IL-1 pathways.