The induction of haem oxygenase-1 (HO-1) is a general response to oxidant stress in mammalian cells (Keyse & Tyrrell, 1989) and has been shown to inhibit apoptosis in lymphocytes (Choi et al. 2004). Since exercise is a form of oxidative stress, cells taken from individuals who take part in regular exercise may respond differently to an exogenous oxidant challenge in comparison to cells taken from less active individuals. The aim of this investigation was to examine the relationship between HO-1 protein induction and cell death in response to hydrogen peroxide (H₂O₂) treatment and habitual physical activity. Twenty-four males (age 26 ± 4 years, height 180 ± 10 cm and body mass 77 ± 11 kg; mean ± S.D.) reported to the laboratory following an overnight fast. Mononuclear cells were isolated from peripheral blood and exposed to 50 μM H₂O₂ for 30 min at 37°C. HO-1 protein was analysed by flow cytometry at baseline and 48 h after recovery from treatment (Markovitch et al. 2005). Cell death was measured by flow cytometry at baseline and 18 h after H₂O₂ treatment using annexin/propidium iodide staining. Physical activity energy expenditure was estimated using a combined movement and heart rate (HR) monitor (Actiheart, CNT, Cambridge) which was worn for seven representative consecutive days (Brage et al. 2005; Thompson et al. 2006). Briefly, energy expenditure (EE) in low, moderate and vigorous intensity physical activity ( 6 Metabolic Equivalents; METs, respectively) was determined using a branched equation model for HR and accelerometer counts. Spearman’s rank order correlation was used to determine whether relationships existed between habitual physical activity (PA), HO-1 protein expression and cell death (basal and following H₂O₂ treatment). Weekly EE at moderate intensity or above (> 3 METs in bouts of 10 min or more) ranged between 373 and 7187 kilocalories. There were no relationships between EE and responses to H₂O₂, however, there was a modest positive relationship between basal HO-1 protein and EE (> 3 METs) in both lymphocytes (r = 0.397, P = 0.055) and monocytes (r = 0.443, P = 0.030). Furthermore, energy expended in moderate intensity physical activity was inversely related to basal apoptosis (r = -0.535, P = 0.007). These findings indicate that those individuals who expended a greater amount of energy through at least moderate intensity PA had higher levels of basal HO-1 expression and a lower level of apoptosis. The non-causal nature of these results does not allow firm conclusions. However, it is tempting to suggest that these results show that regular physical activity is associated with an improved profile at rest without compromising the ability of mononuclear cells to respond to an oxidant challenge. Further work is clearly required.