The Utility of a Small Animal Grip Strength Measurement Device as a Model for Studying Exercise-Induced Muscle Damage

Exercise-induced muscle damage (EIMD) is characterized by structural muscle tissue damage and elevated biochemical markers following high-intensity or unaccustomed exercise. This study evaluated the utility of a small animal grip strength measurement device as a model for EIMD. Thirty-four male mice were divided into four groups: one control and three experimental groups, and sacrificed at 2, 4, and 7 days post-exercise. The exercise protocol involved 50 tail-pull contractions at 60 Hz using a forelimb grip strength device. Biochemical biomarkers, inflammatory gene expression, and oxidative stress markers from blood and muscle tissue were assessed at each sacrificial time point. Muscle damage marker, plasma aldolase activity, showed significant elevation at 4 days post-exercise (<i>p</i> < 0.01). Inflammatory gene expression in triceps brachii showed no significant changes. Oxidative stress analysis revealed significantly decreased biological antioxidant potential (BAP) at 7 days and a trend toward a significant increase in Diacron-reactive oxygen metabolites (d-ROMs) at 4 days. NF-kB expression showed a trend toward significance increase. The grip strength exercise model induced modest biochemical alterations suggesting possible involvement of oxidative stress. The early release of aldolase and subsequent oxidative stress suggest that this model replicates EIMD and may serve as a valuable tool for quantitative loading on muscles, studying EIMD mechanisms and facilitating EIMD-based interventions.