Effects of Exercise on Inflammatory Biomarkers and Brain-Derived Neurotrophic Factor in Individuals with Knee Osteoarthritis

سال انتشار: 1403
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 9

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شناسه ملی سند علمی:

SPORTU02_001

تاریخ نمایه سازی: 6 خرداد 1404

چکیده مقاله:

Background: Knee osteoarthritis (KOA) is a degenerative joint disease characterized by the breakdown of cartilage, with inflammatory mediators playing a significant role in its progression. Regular exercise therapy (ET) has been proposed as an effective intervention to alleviate symptoms and improve joint function in KOA patients. However, the exact mechanisms by which ET influences the immune response and modulates inflammation in these individuals remain unclear. Objectives: This systematic review aimed to explore both the baseline and immediate effects of ET on inflammatory biomarkers and brain-derived neurotrophic factor (BDNF) in individuals with KOA. Methods: A comprehensive search was conducted across databases including PubMed, Web of Science, and PEDro to identify relevant studies. The Cochrane ROB ۲.۰ or ROBINS-I tools were utilized to assess the risk of bias in the included studies. Results: Eight studies encompassing ۳۷۴ participants were analyzed. Among these, fifteen studies examined the baseline effects of exercise, four focused on acute effects, and two addressed both aspects. Biomarker evaluations involved synovial fluid (n=۴) and serum/plasma (n=۱۷). The meta-analysis indicated a significant reduction in C-reactive protein (CRP) levels in KOA patients after ۶-۱۸ weeks of ET (Mean Difference: -۰.۱۷; ۹۵% Confidence Interval: [-۰.۳۱; -۰.۰۳]). However, interleukin-۶ (IL-۶) and tumor necrosis factor-alpha (TNF-α) levels did not show significant changes. There was insufficient data for a meta-analysis on several biomarkers. Nevertheless, a low degree of evidence suggested decreases in IL-۶ (Effect Sizes: -۰.۵۹۶, -۰.۲۵۹, -۰.۵۱۳), an increase in soluble TNF receptors (sTNFR۱: ES: ۲.۳۲۵), a decrease in sTNFR۲ (ES: -۰.۹۹۷), and an increase in BDNF (ES: ۱.۴۱۲). Also, notable changes included an increase in intra-articular IL-۱۰ (ES: ۹.۱۶۳) and decreases in IL-۱β (ES: -۶.۱۹۹) and TNF-α (ES: -۲.۳۲۲) following ET. An acute exercise session prompted a myokine response with an increase in IL-۶ (ES: ۰.۳۱۴) and BDNF, but did not result in significant inflammatory changes for CRP or TNF-α. Conclusion: Exercise therapy can induce both circulatory and intra-articular anti-inflammatory effects among KOA patients. These findings underscore the importance of informing patients and healthcare providers about the beneficial impacts of ET on inflammation related to KOA management.

نویسندگان

Reza Farzizadeh

Department of Sports Physiology, Faculty of Educational Sciences and Psychology, University of Mohaghegh Ardabili, Ardabil, Iran.

Amir Nejah Hossein Hasini

Department of Sports Physiology, Faculty of Educational Sciences and Psychology, University of Mohaghegh Ardabili, Ardabil, Iran.