Metabolic scaling is a widely recognised problem in biology. The underlying causes for the disproportionate relationship between the metabolic rate of an organism and its body size have long puzzled scientists, and continue to be controversial. In recent years this fascinating subject has been treated more than 25 times in Nature, Science and PNAS. However, the editorial (Hoppeler & Weibel, J Exp Biol, May 2005) summarises the state-of-the-art in the monograph on metabolic scaling as: ´There is only one c onsensus: There is scaling, but how and why?´ Our hypothesis is that scaling in teleost fishes is primarily demand-driven based on age-related control of mitochondrial metabolism and density in the differentiating tissues.
Most studies have simply remode led existing data, rather than investigating the underlying causes of metabolic scaling. The current proposal represents a new approach to the problem, and extends the results of Finn et al. (2002) and the solid pilot study of Finn and Cruz (2003). We aim to test our hypothesis that there is a single principle - but many exponents - underlying the cause of mass-metabolic scaling. We will do this by quantifying both the volume fractions of red and white muscle, and the change in mitochondrial density with development in these tissues (WP1). In WP2 we will determine intrinsic metabolic rates and substrate preferences of the red and white muscle mitochondria under varying substrate and temperature conditions. In WP3, gene manipulation experiments will be att empted in order to demonstrate the cause and effect relationship that altering the aerobic basis of muscle metabolism has on metabolic scaling.
The project includes salary for the principal investigator, and is designed to attract students with diverse i nterests at the MSc and PhD levels.