Meeting Abstract
Acquired resources must be allocated to a combination of reproductive output, as well as traits that enhance survival. Whole-organism performance traits are key for survival, but they are also energetically expensive. Previous work with green anoles showed that aerobic exercise (endurance training) forces allocation of resources to enhanced performance at the cost of current reproduction and immunocompetence. In general, aerobic exercise elicits the same response from all vertebrates, both mammalian and non-mammalian, which is an increase in hematocrit and heart size, as well as metabolic changes. In mammals, gene expression is often dramatically altered, and can be done so to increase mitochondria biogenesis for more ATP production, helping with sustained muscle contraction. However, it is unknown if non-mammals use these same molecular pathways to increase aerobic performance. In our study, we experimentally manipulated 48 male green anole lizards that were split among four treatment groups, with endurance training and a supplement as the two balanced factors. The supplement, pyrroloquinoline quinone (PQQ), stimulates the expression of PGC-1a, which in-turn enhances mitochondria biogenesis. We expected PQQ to increase mitochondria densities in muscles and enhance aerobic performance. We recorded time for each lizard to reach exhaustion, both before and after the treatments. We found that training increased endurance, but supplemented lizards did not have further increased endurance. Training alone decreased standard metabolic rates (SMR), but supplemented lizards had significantly increased SMR, suggesting a higher number of mitochondria. Our results suggest that enhanced endurance due to endurance training is likely not due to increased mitochondrial numbers, but instead mitochondrial efficiency.
