Abstract
Old age, adiposity, and metabolic disorders are known as risk factors for chronic tendinopathy, which is a common problem in both athletes and the general population. However, the importance of these influencing factors has not yet been well understood. This study investigated alterations in gene expression and histology of Achilles tendons of young (10 weeks) and old (100 weeks) rats bred for low (low capacity runners, LCR) and high (high capacity runners, HCR) intrinsic aerobic exercise capacity. In this rat model, LCR displayed a phenotype of reduced exercise capacity, higher body weight, and metabolic dysfunctions compared to HCR. We hypothesized that the risk factors for tendinopathy in old LCR could lead to more pronounced impairments in Achilles tendon tissue. In quantitative real-time PCR (qPCR), age-related downregulation of tenocyte markers e.g., tenomodulin, genes related to matrix modeling and remodeling (e.g., collagens, elastin, biglycan, fibronectin, tenascin C) as well as transforming growth factor beta 3 (Tgfb3) have been detected. Inflammation marker cyclooxygenase 2 (Cox2) was downregulated in old rats, while microsomal prostaglandin E synthase 2 (Ptges2) was upregulated in old HCR and old LCR. In all groups, interleukin 6 (Il6), interleukin 1 beta (Il1b), and tumor necrosis factor alpha (Tnfa) showed no significant alteration. In histological evaluation, tendons of old rats had fewer and more elongated tenocyte nuclei than young rats. Even though a higher content of glycosaminoglycans, a sign of degeneration, was found in old HCR and LCR, no further signs of tendinopathy were detectable in tendons of old rats by histological evaluation. Low intrinsic aerobic exercise capacity and the associated phenotype did not show significant effects on gene expression and tendon histology. These findings indicate that aging seems to play a prominent role in molecular and structural alterations of Achilles tendon tissue and suggests that other risk factors associated with intrinsic aerobic exercise capacity are less influential in this rat model.
Highlights
This article is an open access articleAchilles tendinopathy is a common disease among athletes, especially runners [1].it occurs among non-athletes [2] and is present in aged patients [3].Tendinopathy is a clinical diagnosis characterized by a combination of pain, swelling, and impaired performance [4] in which overuse is one of the main risk factors for the occurrence in the Achilles tendon [5,6,7]
Old rats of both breeds had a higher tendon weight compared to young rats, whereas RNA quantity as an approximation for cell number was significantly lower in old rats compared to young rats (Table 1)
Upregulation of prostaglandin E synthase 2 (Ptges2) indicates the presence of inflammation in aged Achilles tendons, but inflammation does not seem to be a major feature in the investigated tendons
Summary
This article is an open access articleAchilles tendinopathy is a common disease among athletes, especially runners [1].it occurs among non-athletes [2] and is present in aged patients [3].Tendinopathy is a clinical diagnosis characterized by a combination of pain, swelling, and impaired performance [4] in which overuse is one of the main risk factors for the occurrence in the Achilles tendon [5,6,7]. Achilles tendinopathy is a common disease among athletes, especially runners [1]. It occurs among non-athletes [2] and is present in aged patients [3]. Because Scx, Mkx, and Tnmd were found to be downregulated in aged flexor digitorum longus tendons of mice, alteration in tenocyte markers might promote tendon degeneration [18]. While collagen type 1 (COL1A1), collagen type 3 (COL3A1), and collagen type 5 (COL5A2) are often found to be altered in tendinopathy and chronic ruptures of human Achilles tendons [20,21], aging seems to be associated with the downregulation of collagens in mice and rats [18,22]. Inflammatory mediators seem to trigger matrix degradation as interleukin 1 beta (IL1b) induces the expression of matrix degrading enzymes such as MMP1, MMP3, and other inflammatory markers such as COX2 and prostaglandin E2
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