Meeting Abstract
A central tenet of biology is that the costs of reproduction contribute to reduced future fecundity and earlier senescence, but the mechanisms that underlie such a tradeoff are unclear. We reasoned that this tradeoff is driven, in part, by variation in energetic responses of different organs to the demands of reproduction. Mitochondria are the major source of ATP production in the body, but during OXPHOS mitochondria also emit ROS. Thus, we predicted that differences in mitochondrial bioenergetics and redox state would influence both the amount of resources that a female can allocate to current reproduction and the relative cost of current reproduction to future reproduction and survival. To this end, we evaluated changes in liver and skeletal muscle mitochondrial function between non-reproductive and lactating house mice. We found that skeletal muscle of lactating house mice displayed substrate-sparing strategies, including a more efficient basal respiration rate, reduced antioxidant production, and fewer mitochondrial subunits. The liver of lactating mice, however, showed a mix of costly and substrate-sparing changes. Measured costs included increased tissue synthesis, increased basal respiratory rate, and greater lipid peroxidation. Substrate-sparing strategies included reduced antioxidant production and a higher maximum respiratory rate. These findings suggest that adaptations by both the skeletal muscle and liver are likely to play important roles in supporting nutrient allocation to the developing young. Because the strategy for supporting reproduction differs between organs, the costs of reproduction also appear to vary between organs. Based on our findings, the long-term impact of reproduction on skeletal muscle is predicted to be minimal, while damage incurred by the liver may contribute to the tradeoff between reproduction and longevity.
