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Predicting oxygen availability in Atlantic salmon farms is challenging, but digital simulations that couple bioenergetics and hydrodynamics show great promise. Robust simulations depend on reliable estimates of oxygen demand, yet previous empirical models offer limited accuracy. Here, we present a refined fundamental model for Atlantic salmon oxygen consumption rate (MO 2 ) as a function of three readily measurable parameters: body weight, water temperature, and relative swimming speed. Retaining the established framework of Grøttum and Sigholt (1998), we refined the model through an improved coefficient estimation approach and a methodologically rigorous dataset derived from group swim tunnel respirometry measurements on 718 fish across seven experiments. Model coefficients were re-estimated using log-linear regression fitted via nonlinear mixed-effects, substantially improving parameterisation and yielding a model that explains 80% of the observed variation in MO 2 : , where MO 2 is oxygen consumption rate (mg O 2 kg − 1 h − 1 ), W is body weight (kg), T is water temperature (°C), and U is relative swimming speed (body lengths s − 1 ). Our model delivers reliable estimates of Atlantic salmon oxygen demand across relevant farming conditions (0.2–3.4 kg, 3–18 °C, 0.3–2.8 body lengths s − 1 ). With broad utility in both research and industry, our model supports the development of more precise, data-driven strategies for modern salmon aquaculture.

Infant and childhood growth are dynamic processes with large changes in BMI during development. By performing genome-wide association studies of BMI at 12 time points from birth to eight years (9286 children, 74,105 measurements) in the Norwegian Mother, Father, and Child Cohort Study, replicated in 5235 children, we identify a transient effect in the leptin receptor ( LEPR ) locus: no effect at birth, increasing effect in infancy, peaking at 6–12 months (rs2767486, P 6m   =  2.0 × 10 −21 , β 6m  = 0.16 sd-BMI), and little effect after age five. We identify a similar transient effect near the leptin gene ( LEP) , peaking at 1.5 years (rs10487505, P 1.5y  = 1.3 × 10 −8 , β 1.5y  = 0.079 sd-BMI). Both signals are protein quantitative trait loci for soluble-LEPR and LEP in plasma in adults independent from adult traits mapped to the respective genes, suggesting key roles of common variation in the leptin signaling pathway for healthy infant growth. Changes in body mass index (BMI) during infancy and childhood follow a well-characterized pattern. Here, Helgeland et al. perform genome-wide association studies for BMI at 12 time points between birth and 8 years of age and find transient associations at the LEP and LEPR loci.

Infant and childhood growth are dynamic processes characterized by drastic changes in fat mass and body mass index (BMI) at distinct developmental stages. To elucidate how genetic variation influences these processes, we performed the first genome-wide association study (GWAS) of BMI measurements at 12 time points from birth to eight years of age (9,286 children, 74,105 measurements) in the Norwegian Mother and Child Cohort Study (MoBa) with replication in 5,235 children (41,502 measurements). We identified five loci associated with BMI at distinct developmental stages with different patterns of association. Notably, we identified a novel transient effect in the leptin receptor (LEPR) locus, with no effect at birth, increasing effect on BMI in infancy, peaking at 6-12 months (rs2767486, P6m = 2.0 × 10−21, β6m = 0.16) and little effect after age five. A similar transient effect was found near the leptin gene (LEP), peaking at 1.5 years of age (rs10487505, P1.5y = 1.3 × 10−8, β1.5y = 0.079). Both signals are protein quantitative trait loci (pQTLs) for soluble LEPR and LEP in plasma in adults and independent from signals associated with other adult traits mapped to the respective genes, suggesting novel key roles of common variation in the leptin signaling pathway for healthy infant growth. Hence, our longitudinal analysis uncovers a complex and dynamic influence of common variation on BMI during infant and early childhood growth, dominated by the LEP-LEPR axis in infancy.