Medical Journal of Mashhad university of Medical Sciences

Medical Journal of Mashhad university of Medical Sciences

Resistance Training-Induced Muscle Damage: Induction of MMP-2/9 Expression as a Key Step in Extracellular Matrix Remodeling

Document Type : Research Paper

Authors
1 n
2 Department of Sport Sciences, Na.C., Islamic Azad University, NajafAbad, Iran
3 Department of Sport Sciences, Na.C., Islamic Azad University, Najafabad, Iran
Abstract
Background and Aim: Exercise-induced muscle damage is a physiological stimulus for initiating extracellular matrix (ECM) recovery. Creatine kinase (CK) is a key marker of sarcolemmal damage, and matrix metalloproteinases (MMP-2 and MMP-9) are key ECM-degrading enzymes. This study aimed to investigate the hypothesis that muscle damage induced by resistance training (indicated by elevated CK) is the main trigger for increased MMP-2 and MMP-9 gene expression.
Methods: In this quasi-experimental study, 30 healthy active men were randomly divided into training (n=15) and control (n=15) groups. The training group performed progressive resistance training for 12 weeks (3 sessions/week). Blood samples were taken 48 hours after the last session. Serum CK was measured by ELISA and MMP-2/MMP-9 gene expression in white blood cells by Real-time PCR. Data were analyzed using MANCOVA and Pearson's correlation.
Results: Resistance training led to a significant increase in serum CK (47.2% increase) and the gene expression of both MMP-2 (16.21% increase) and MMP-9 (12.77% increase) compared to the control group. Furthermore, a significant positive correlation was observed between serum CK levels and the expression of both MMP-2 (r=0.61, P=0.004) and MMP-9 (r=0.57, P=0.008) genes.
Conclusion: Muscle damage induced by resistance training (marked by increased CK) is a strong signal for inducing MMP-2 and MMP-9 expression. This coordinated molecular response is a key step in repairing damaged ECM and preparing the substrate for muscle regeneration and hypertrophy.
Keywords


Articles in Press, Accepted Manuscript
Available Online from 08 November 2026