This study investigated whether the variability observed in the markers of exercise-induced muscle damage (EIMD) has a genetic etiology. Sixteen pairs of identical twins performed 24 maximal eccentric contractions (24MAX) using the elbow flexors. EIMD indicators were measured pre-24MAX and three days post-24MAX and included: post-exercise force deficit, maximal isometric force (ISO), plasma creatine kinase (CK), myoglobin (Mb), and joint range of motion. Force-time curves were recorded throughout the 24MAX. Twin siblings were alike for pre-exercise ISO (intraclass R = 0.89) and CK (R = 0.76) (p < 0.001), but were discordant for post-exercise force deficit (R = 0.29), CK (R = 0.15), and Mb (R = 0.17) (p > 0.05). In comparison with individuals minimally affected by the 24MAX, those who experienced the greatest force deficit 3 days post-exercise (> 50 %) were characterised by the greater application of eccentric force at longer muscle lengths (23.1 % vs 17.3 %) (p < 0.05). This study demonstrates that twins do not experience the same level of EIMD following identical exercise bouts. This suggests that the individual variability following high-force eccentric exercise cannot be attributed to genetic differences, refuting the idea that an inherited subclinical predisposition is responsible. From these results, a potential mechanism for the repeated bout effect is discussed.