1. Life‐history theory predicts that high reproductive investment alters self‐maintenance. Several mechanisms underlying the cost of reproduction have been previously suggested, but how parental effort may impact cell and organism maintenance remains largely unknown. The effects of oxidative stress – the imbalance between oxidative damage and defences – on telomere dynamics may underlie this relationship. Indeed, oxidative stress is associated with costly activities like breeding, and impacts telomere length that is known to predict survival in birds. According to life‐history theory, long‐lived species are expected to minimize the adverse effects of current reproduction on their body maintenance and should therefore enhance their antioxidant capacity and preserve their telomeres when breeding workload increases.

2. In this study, we tested this hypothesis by determining experimentally how the oxidative status and telomere length were modified when long‐lived Adélie penguins (Pygoscelis adeliae) faced a costly reproductive event. The breeding workload was increased through a handicapping procedure that increased the cost of foraging and therefore chick‐provisioning.

3. In agreement with our hypothesis, Adélie penguins substantially increased their antioxidant defences during a costly breeding effort, while oxidative damage and telomere length remained unchanged.

4. As expected in long‐lived species, Adélie penguins subjected to increased breeding constraints appear to prioritize self‐maintenance as shown by their increased antioxidant capacity. Moreover, the absence of effects of our experimental procedure on telomere length suggests no apparent impact of breeding workload on the senescence of this long‐lived bird. However, to better understand the role of the couple ‘oxidative status/telomeres’ in the regulation of life‐history strategies, further studies should examine: (i) the nature and the cost of additional antioxidant protection; (ii) the changes in the oxidative status of animals throughout their annual cycle and the consequences on telomere dynamics; and (iii) the repartition of antioxidant resources between young and parents.