BackgroundMyoblast differentiation requires metabolic reprogramming driven by increased mitochondrial biogenesis and oxidative phosphorylation. The canonical GH-GHR-IGFs axis in liver exhibits a great complexity in response to somatic growth. However, the underlying mechanism of whether localGHRacts as a control valve to regulate mitochondrial function through mitochondrial biogenesis during myoblast differentiation remains unknown.MethodsWe manipulated theGHRexpression in chicken primary myoblast to investigate its roles in mitochondrial biogenesis and function during myoblast differentiation.ResultsWe reported thatGHRis induced during myoblast differentiation. LocalGHRpromoted mitochondrial biogenesis during myoblast differentiation, as determined by the fluorescence intensity of Mito-Tracker Green staining and MitoTimer reporter system, the expression of mitochondrial biogenesis markers (PGC1α,NRF1,TFAM) and mtDNA encoded gene (ND1,CYTB,COX1,ATP6), as well as mtDNA content. Consistently, localGHRenhanced mitochondrial function during myoblast differentiation, as determined by the oxygen consumption rate, mitochondrial membrane potential, ATP level and ROS production. We next revealed that the regulation of mitochondrial biogenesis and function byGHRdepends onIGF1. In terms of the underlying mechanism, we demonstrated thatIGF1regulates mitochondrial biogenesis via PI3K/AKT/CREB pathway. Additionally,GHRknockdown repressed myoblast differentiation.ConclusionsIn conclusion, our data corroborate that localGHRacts as a control valve to enhance mitochondrial function by promoting mitochondrial biogenesis via IGF1-PI3K/AKT/CREB pathway during myoblast differentiation.Video AbstractSupplementary InformationThe online version contains supplementary material available at 10.1186/s12964-023-01166-5.