1. As a first approximation, whole-body metabolic rate can be considered as the sum of metabolic rates of constituent cells. Yet, among several current explanations of metabolic rate scaling, only two explicitly invoke cell architecture of organisms: (1) the Metabolic Theory of Ecology, which predicts size invariance of metabolically active cells, such as erythrocytes and (2) the cell metabolism hypothesis postulating partial dependence of metabolic scaling on the cell size (CS), which is mediated by nucleus/genome size variation.
2. Here, we tested (1) and (2) by comparing standard metabolic rate (SMR), erythrocyte size (used as a proxy of CS) and nucleus size (NS) between diploid and triploid individuals of a small fish (body mass of c. 3 g) belonging to the Cobitis taenia hybrid complex.
3. We demonstrated a positive correlation of CS with genome/nucleus size and an inverse relationship between those traits and SMR. SMR scaled to body mass with a 0·92 ± 0·05 exponent, which significantly differed from the ¾ value, while CS scaled with body mass with an allometric exponent of 0·05 ± 0·007, which significantly differed from 0. Ploidy level explained c. 85% of CS variation.
4. Our results provide empirical support for CS and genome/nucleus size being important determinants of metabolic rate variation and consequently, its allometric scaling. They call attention to the significance of a long-neglected integration of cellular and organismal perspectives in studies of body size–metabolic rate relationships and their consequences for energy utilization in the wild.