The Effect of Age and Intrinsic Aerobic Exercise Capacity on the Expression of Inflammation and Remodeling Markers in Rat Achilles Tendons

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.

Advanced Artificial Intelligence and Big Data Algorithm in Aerobics Formation Transformation Route Simulation Research

“…Chronic joint damage, old age, obesity, and metabolic diseases have been linked to an increased risk, with low. e structural and molecular changes appear primarily caused by age; AI suggests that other risk factors related to intrinsic aerobic formation in route simulation can have less of an impact in this rat model, according to these facts [11]. ere is a lack of understanding of ways physical exercise AF programs might improve academic achievement.…”

Genetic architecture and polygenic risk score prediction of degenerative suspensory ligament desmitis (DSLD) in the Peruvian Horse

“…Development of tendinopathy likely represents a failure to repair or remodel extracellular matrix after repetitive micro-injury. In this regard, poor healing has been associated with loss of TGFB receptors from diseased matrix ( Fenwick et al, 2001 ) and downregulation of TGFB3 is found with aging, particularly in tendons exposed to mechanical overload ( Kinitz et al, 2021 ). The Indian hedgehog signaling pathway, which includes the transcription factors GLI1 / GLI2/GLI3 , is known to modulate matrix responses to load and healing in tendon injury, particularly at bone attachment sites ( Liu et al, 2022 ).…”

Age and Intrinsic Fitness Affect the Female Rotator Cuff Tendon Tissue

“…In a 2021 published study, the histological and molecular alteration in the Achilles tendon of this rat model were investigated [ 56 ]. An age-dependent effect was seen with down-regulation of ECM and inflammatory factors in the old rats.…”