Abstract
BACKGROUND AND OBJECTIVE: Apart from mechanical dysfunction, low back pain (LBP) is also associated with underlying inflammatory and muscle-related biochemical changes. An increase in certain biomarkers, such as IL-10, a key anti-inflammatory cytokine, provides a positive objective indicator of underlying physiological responses to interventions in LBP beyond subjective clinical measures. This study assessed the effects of McKenzie Extension Protocol (MEP), Static Back Extension Endurance (SBEE), and Dynamic Back Extension Endurance (DBEE) on selected clinical outcomes and biomarkers of muscle status [creatine kinase (CK)] and inflammation (IL-4 and IL-10) in LBP. METHODS: A randomized controlled trial involving 76 patients with chronic LBP who were randomly assigned to MEP, SBEE, or DBEE groups was conducted. MEP involved a specific sequence of lumbosacral repeated movements in extension. SBEE involved five different back extensor muscle endurance protocols of increasing difficulty level. DBEE was a dynamic replica of the SBEE. Pain, CK, IL-4, and IL-10 were the primary outcomes. Functional disability and health-related quality of life were the secondary outcomes. Assessments were conducted at baseline, 3rd, and 6th week of the study. RESULTS: MEP and SBEE caused significant effects in all clinical and biochemical variables (p < 0.05) except IL-4 and IL-10 (p > 0.05). DBEE yielded no significant effects on IL-4 and IL-10 (p > 0.05). MEP had a significantly higher effect on pain (p < 0.05). SBEE had a greater impact on IL-4 (p < 0.05) and IL-10 (p < 0.05) at week 3. SBEE led to a higher impact on IL-4 (p < 0.05) and IL-10 (p < 0.05) at week 6. All interventions had comparable effects on other clinical parameters at week 6 (p > 0.05). CONCLUSION: MEP reduced pain more, while SBEE led to higher changes in IL-4 and IL-10 inflammatory biomarker levels. Serum CK levels rose in all groups without indicating muscle damage. The results suggest that these exercises show potential benefits in modulating inflammation and enhancing muscle status, potentially supporting tissue repair and reducing chronic LBP, and therefore should be incorporated as part of strategies targeting underlying inflammatory processes in the management of chronic LBP.