Ageing has been purported to impair day-to-day muscle regeneration with muscle tissue inflammation being a putative culprit. Nonetheless, the impact of ageing on muscle function and inflammation at rest and following exercise in young (Y) vs. older (O) volunteers remains poorly defined. Here we investigated muscle functional and inflammatory responses to unilateral eccentric exercise (ECC) as a “muscle damage” stimulus in both Y and O men. Eight Y (22±1y, mean±SEM) and eight O (70±1y) healthy, exercise naïve men performed a single bout of unilateral ECC (7×10 repetitions at 80% of ECC one-repetition maximum). We assessed perceived leg muscle soreness and sensitivity to pain, in addition to peak muscle torque, power, plasma creatine kinase (CK) and muscle tumor necrosis factor alpha (TNF-a) and phospho NF-KappaB (p-NFkB) proteins at baseline (BL), immediately (0), 5, 24, 72 and 168h after exercise. As expected, Y exhibited greater BL peak torque compared to O (Y: 253±21 vs. O: 166±15Nm; P<0.05, two-way ANOVA). Declines in peak torque (compared to BL) were observed in Y and O at 0h (Y: 171.1±15.3, P<0.01; O: 128.5±11, P<0.05), which persisted until 24h in O (113±13, P<0.01) and 72h in the Y (201±24, P<0.01). No BL age-related differences were observed for power (Y: 228±32 vs. 179±26W), which declined immediately following ECC in Y (169±16, P<0.05), and persisted for 24h (150±24, P<0.01) but did not change in O. Sensitivity to pain heightened in Y and O at 5h post-ECC (Y: 11±2; O: 7±1lbs, P<0.05) compared to BL (Y: 13±1; O: 10±1) but remained heightened for 72h (11±1, P<0.05) in Y only. Muscle soreness was elevated immediately after ECC (6±1cm, P<0.01, one-way ANOVA) and persisted for 72h (4.9±0.8, P<0.01) in Y, and was elevated at 24h in O (6±1, P<0.01). Plasma CK was elevated at 24 and 72h in Y, and at 72h in O (P<0.05, Friedman’s one-way ANOVA) – confirming “muscle damage”. Interestingly, O displayed higher BL muscle TNF-a compared to Y (P<0.05, two-way ANOVA). Nonetheless, while TNF-a did not change post-ECC in O, it increased at 72h and remained elevated at 168h in Y (compared to BL, P<0.01). A similar, non-significant pattern was observed for p-NFKb. We report that ageing per se is associated with increased muscle TNF-a and reductions in muscle function, as shown previously (1). However, the data does not necessarily support the notion of a heightened induction of muscle inflammation and delayed recovery in response to “damaging” exercise in O, since Y exhibited a more sustained deficit in muscle function than O in tandem to the induction of muscle TNF-a. The absence of muscle mass and activation measures precluded investigation into differences in specific forces which could explain the apparent heightened susceptibility to ECC-induced muscle dysfunction in Y vs. O i.e. if Y lifted relatively more than O, heightening the stimulus.