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% V̇O2max, -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), peak power (PP) and perceived muscle soreness were also quantified.
Results are presented here as ‘median and interquartile range’ for CK, IL-6, TNF-a and perceived muscle soreness, and as ‘mean ± SD’ for MVIC and PP. Significant difference in CK activity was found between N-3 and PLA (p = 0.048) at 24 h post-EIMD, with PLA showing a larger increase in serum CK (baseline- vs 24h post-EIMD) compared to N-3 (677.4% vs 459.6%, respectively). PLA showed a larger increase in plasma IL-6 compared to N-3 immediately post-EIMD (143.9% vs 131.1%, respectively), however, there was no significant difference between groups at any time point (p > 0.05). TNF-a showed a smaller increase for the N-3 group compared to the PLA, again, there were no significant differences between groups at any time point (p > 0.05). Significant difference in muscle soreness was found between N-3 and PLA at 24 h post-EIMD (p = 0.034), with PLA showing a higher muscle soreness compared to N-3. A significant main effect for time was observed for MVIC with both groups showing a significant reduction in leg strength immediately post-EIMD. However, there were no significant differences between groups (p = 0.26) nor any group by time interactions (p = 0.90). A significant main effect for time was observed for PP, again, with PLA showing a larger reduction in PP at 24 h post-EIMD (pre- vs 24 h post-EIMD) compared to the N-3 (>96.6% vs N-3). However, there were no significant differences between groups (p = 0.31) nor any group by time interactions (p = 0.51).
N-3 supplementation may attenuate EIMD, however, n-3 supplementation had no impact on muscle function nor power output. Even though we recorded some reduction in the inflammatory 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 on exercise-induced muscle inflammation. 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.