Exercise-induced muscle damage (EIMD) results in transient muscle inflammation, strength loss, muscle soreness (Damas et al., 2016) and can result in subsequent exercise avoidance. Omega-3 (n-3) supplementation has been proposed to minimise EIMD via its anti-inflammatory properties (Jakeman et al., 2017), however its action remains unclear. We aimed to examine the effects of n-3 supplementation on exercise-induced inflammatory response following muscle-damaging exercise. Physically active, healthy Caucasian males (n = 14, 25.07 ± 4.05 years) provided written informed consent, then were single blind randomised to either receive 3 g/day n-3 supplementation (N-3, n = 7) or placebo (PLA, n = 7). Following 4 weeks n-3 supplementation, a downhill running protocol (60 minutes at 65% VO2max, -10% gradient) was performed. Before supplementation (baseline), prior to EIMD, immediately after EIMD, and at 24, 48, and 72 hours post-EIMD, venous plasma was collected for creatine kinase (CK), interleukin (IL)-6 and tumour necrosis factor (TNF)-a, and maximal voluntary isometric contraction (MVIC), anaerobic power and perceived muscle soreness were also quantified. Results are presented here as ‘mean ± SD’. No significant differences in CK activity were found between N-3 and PLA group (p = 0.363), however, PLA showed a larger increase in CK levels (baseline- vs 24h post-EIMD) compared to N-3 (882.8% ±564.8 vs 496.1% ±275.4, respectively). PLA group showed a larger increase in IL-6 compared to N-3 immediately post-EIMD (162.3% ±68.6 vs 123.3% ±15.1, respectively), however, there was no significant difference between the two groups (p = 0.422). TNF-a showed a smaller increase for the N-3 group compared to the PLA, again, there were no significant differences between the two groups (p = 0.320). No significant difference in MVIC between N-3 and PLA group (p = 0.883) was found, however, there was a significant main effect for time (p = 0.008) with both groups showing a reduction in muscle strength immediately post-EIMD. No differences in peak power were found between N-3 and PLA group across time (p = 0.798). No significant difference in muscle soreness was found between N-3 and PLA (p = 0.3), however, the latter showed a larger increase in muscle soreness (pre- vs post-EIMD) compared to the N-3 group (>165.1% vs N-3). In this study, even though we recorded some reduction in the plasma markers for the N-3 group, there was no statistically significant decrease to allow us to draw any definitive conclusions about the n-3 supplementation. Additionally, there was no impact on muscle function nor power output. Future studies might compare the dosage and duration of n-3 supplementation on muscle function or examine the effect of n-3 supplementation on EIMD during ageing-associated muscle function loss, where increased basal inflammation is seen.