SUMMARYLife history theory suggests that investment in reproduction can trade off against growth, longevity and both reproduction and performance later in life. One possible reason for this trade-off is that reproduction directly causes somatic damage. Oxidative stress, an overproduction of reactive oxygen species in relation to cellular defences, can correlate with reproductive investment and has been implicated as a pathway leading to senescence. This has led to the suggestion that this aspect of physiology could be an important mechanism underlying the trade-off between reproduction and lifespan. We manipulated female reproductive investment to test whether oxidative stress increases with reproduction in mice. Each female's pups were cross-fostered to produce litters of either two or eight, representing low and high levels of reproductive investment for wild mice. No differences were observed between reproductive groups at peak lactation for several markers of oxidative stress in the heart and gastrocnemius muscle. Surprisingly, oxidative damage to proteins was lower in the livers of females with a litter size of eight than in females with two pups or non-reproductive control females. While protein oxidation decreased, activity levels of the antioxidant enzyme superoxide dismutase increased in the liver, suggesting this may be one pathway used to protect against oxidative stress. Our results highlight the need for caution when interpreting correlative relationships and suggest that oxidative stress does not increase with enhanced reproductive effort during lactation. Supplementary material available online at

Sexual conflict theory suggests that male and female interests often diverge, causing selection to favour sex‐specific reproductive strategies that maximize the fitness of an individual at the expense of its mate. Sexually antagonistic selection can lead to conflicts over the timing and frequency of mating events, mate choice and the delivery of parental care. This antagonistic view of reproduction has received little attention in discussions of the evolution of mammalian mating systems. Reproduction in mammals, more than in other organisms, is characterized by asymmetry in parental investment between the sexes. This asymmetry provides opportunities for sexual conflict to manifest itself. We highlight the potential for sexual conflict in mammalian mating systems by exploring why males and females are selected to mate with multiple partners and by considering the shared characteristics of mammalian reproductive biology that may lead to predictable patterns of conflict over parental investment. The degree to which sexual conflict is realized as sexually antagonistic adaptations may vary between species, depending on the strength of selection for multiple mating, paternity assurance and the amount of parental care required. Empirical evidence of sexual conflict in mammalian species is needed. Available genomic and phylogenetic tools, and the identification of mating, placentation, lactation and parental care as likely sites of conflict, make mammals a natural choice for research. Understanding the factors that influence the magnitude of the conflict and the ways in which conflict shapes male and female adaptations and counter‐adaptations should be priorities. The integration of sexual conflict theory into models of mammalian life history evolution will unify developments in behavioural ecology, physiology, genetics and genomics. This multidisciplinary approach may reveal novel ways in which sexual conflict can operate, and increase understanding of evolution.

The trade-off between reproductive investment and lifespan is the single most important concept in life-history theory. A variety of sources of evidence support the existence of this trade-off, but the physiological costs of reproduction that underlie this relationship remain poorly understood. The Free Radical Theory of Ageing suggests that oxidative stress, which occurs when there is an imbalance between the production of damaging Reactive Oxygen Species (ROS) and protective antioxidants, may be an important mediator of this trade-off. We sought to test this theory by manipulating the reproductive investment of female mice (Mus musculus domesticus) and measuring the effects on a number of life history and oxidative stress variables. Females with a greater reproductive load showed no consistent increase in oxidative damage above females who had a smaller reproductive load. The groups differed, however, in their food consumption, reproductive scheduling and mean offspring mass. Of particular note, females with a very high reproductive load delayed blastocyst implantation of their second litter, potentially mitigating the costs of energetically costly reproductive periods. Our results highlight that females use strategies to offset particularly costly periods of reproduction and illustrate the absence of a simple relationship between oxidative stress and reproduction.