Ageing is associated with a decline in skeletal muscle mass and function, partially attributed to an impaired ability of muscle to repair and regenerate following mechanical stress. This decline has been associated, in part, with decreased muscle stem cell function (Sousa-Victor et al., 2015). A potential mechanism underpinning this is cellular senescence, by which cells undergo proliferative arrest and release senescence-associated secretory phenotype (SASP) factors (Campisi, 2013). However, it is unclear whether this mechanism is a prominent issue affecting skeletal muscle (myogenic) stem cells. Thereby, the present study aimed to compare markers of cellular senescence in human primary myogenic cell populations that had been obtained from older hip fracture (HF) patients (n=6, 70+ yrs) with those obtained from young (YO) healthy male donors (n=6, 22±1 yrs) at early passage in cell culture. Samples were obtained from the vastus lateralis either during surgery (HF) or using the Bergström needle technique with applied suction following local anesthesia (2% lidocaine, YO). Samples were purified using CD56+ve magnetic activated cell sorting (Agley et al., 2015). Due to slow HF cell expansion rate, an average of Day 30 in culture had to be used to compare YO and HF data. All samples were examined for myogenic purity (% Desmin), senescence associated-β-galactosidase (SA-β-gal), p16, and γH2AX protein expression using immunocytochemistry. mRNA expression of a small panel of known SASP factors were investigated using qRT-PCR. Unpaired T-tests tested for statistical significance between HF and YO samples (p<0.05). Desmin-positive cells from HF patients displayed elevated SA-β-gal expression compared to YO (n=3, 81 ± 2.6% vs. n=5, 28 ± 2.3% positive cells, p<0.001), and increased γH2AX expression (integrated density n=6, 95380 ± 11148 vs. n=6, 55709 ± 8543, p<0.05). SASP factor mRNA expression are given as fold change compared to YO, early passage (Day 10 in culture) populations. HF cells displayed increased fold change expression of several SASP Factors compared to YO: CXCL5 (n=3, 13.77 ± 15.31 vs. n=6, 1.62 ± 1.53, p<0.05), IL-8 (n=3, 20.38 ± 18.19 vs n=6, 1.39 ± 1.41, p<0.05), and IGFBP-3 (n=3, 10.81 ± 6.29 vs. n=6, 1.75 ± 2.15, p<0.01). Despite senescence markers having to be investigated at relatively late passage in YO to align with the slowly expanding HF cell populations, significant differences were observed between the young and older populations when exposed to similar times in culture. However, as these data were obtained from older HF patients, as opposed to healthy older individuals, it is not possible to conclude if the increases seen in senescent marker expression can solely be attributed to an inherent ageing process.