Rethinking Neurophysiology of Delayed Onset Muscle Soreness (DOMS): Updated Concepts and Mechanisms for Mitigation across Endurance, Resistance, and Plyometric Exercise

Delayed-onset muscle soreness (DOMS) is a physiological response to intense eccentric exercise across endurance, resistance, and plyometric training. Although traditionally attributed primarily to structural muscle damage and inflammation, accumulating evidence indicates that DOMS is a multifactorial neurophysiological response involving complex interactions between peripheral tissue responses, inflammatory signalling, neural sensitisation, proprioceptive alterations, and central nervous system adaptations. Objective: This review aimed to synthesise current evidence on the neurophysiological mechanisms underlying DOMS across endurance, resistance, and plyometric exercise within an integrated neurophysiological framework. It further examined the mechanisms underpinning therapeutic interventions, critically evaluated current approaches to DOMS assessment, and explored their implications for personalised recovery strategies, providing key-take-home to help clinicians and field partitioners. Methods: This systematic review with narrative synthesis followed PRISMA 2020 guidelines and registered with the International Prospective Register of Systematic Reviews (PROSPERO). 1,183 articles, including clinical trials examining DOMS neurophysiology and therapeutic interventions across exercise modalities were screened. Results: The evidence indicates that DOMS cannot be explained by a single biological mechanism. Rather, distinct exercise modalities activate overlapping but different combinations of inflammatory, neural, metabolic, and proprioceptive pathways that influence symptom development and recovery. The findings further indicate that different exercise modalities elicit unique neuromuscular adaptations, with endurance training leading to cumulative inflammatory responses, resistance training inducing nociceptor sensitization, and plyometric exercise disrupting proprioceptive control. Endurance exercise produces IL-6 increase within 48 h but shows inflammation reduction after repeated bouts. Resistance training causes strength loss with Group III/IV nociceptor activation. Plyometric exercise disrupts proprioception alongside C-fiber sensitization. Recovery interventions show DOMS reduction: compression garments SMD = −0.44, acupuncture SMD = −0.89, foam rolling SMD = −0.34, but majority of studies lack extractable effect sizes preventing meta-analysis. Intervention efficacy appeared to vary according to exercise modality, exercise load, and individual neurophysiological responses, suggesting a dose-response influence on recovery outcomes. Conclusion: Collectively, the evidence supports the concept that DOMS should be regarded as a multifactorial neurophysiological response rather than simply a consequence of muscle damage. Exercise-specific recovery optimizes DOMS management: active recovery for endurance, compression/photobiomodulation for resistance, foam rolling/acupuncture for plyometric. Chronic training reduces DOMS through repeated bout adaptation. Future research should prioritise standardised outcome reporting together with mechanistic biomarkers and adequately designed longitudinal studies to strengthen the evidence base. This review highlights the need for individualized and exercise-specific recovery strategies to optimize DOMS mitigation, post-exercise recovery, and requires rehabilitation protocols based on neural and biochemical markers. Recovery interventions should also consider the dose-response relationship between exercise load and neurophysiological stress, as treatment effectiveness may vary according to DOMS severity and training demands. Given the variability in individual responses, integrating multiple assessment tools enhances accuracy and reliability in both research and clinical settings.