Gill surface area allometry does not constrain the body mass scaling of maximum oxygen uptake rate in the tidepool sculpin, Oligocottus maculosus.
Derek A SomoKen ChuJeffrey G RichardsPublished in: Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology (2023)
The gill oxygen limitation hypothesis (GOLH) suggests that hypometric scaling of metabolic rate in fishes is a consequence of oxygen supply constraints imposed by the mismatched growth rates of gill surface area (a two-dimensional surface) and body mass (a three-dimensional volume). GOLH may, therefore, explain the size-dependent spatial distribution of fish in temperature- and oxygen-variable environments through size-dependent respiratory capacity, but this question is unstudied. We tested GOLH in the tidepool sculpin, Oligocottus maculosus, a species in which body mass decreases with increasing temperature- and oxygen-variability in the intertidal, a pattern consistent with GOLH. We statistically evaluated support for GOLH versus distributed control of [Formula: see text] allometry by comparing scaling coefficients for gill surface area, standard and maximum [Formula: see text] ([Formula: see text] ,Standard and [Formula: see text] ,Max , respectively), ventricle mass, hematocrit, and metabolic enzyme activities in white muscle. To empirically evaluate whether there is a proximate constraint on oxygen supply capacity with increasing body mass, we measured [Formula: see text] ,Max across a range of Po 2 s from normoxia to P crit , calculated the regulation value (R), a measure of oxyregulatory capacity, and analyzed the R-body mass relationship. In contrast with GOLH, gill surface area scaling either matched or was more than sufficient to meet [Formula: see text] demands with increasing body mass and R did not change with body mass. Ventricle mass (b = 1.22) scaled similarly to [Formula: see text] ,Max (b = 1.18) suggesting a possible role for the heart in the scaling of [Formula: see text] ,Max . Together our results do not support GOLH as a mechanism structuring the distribution of O. maculosus and suggest distributed control of oxyregulatory capacity.