C N Yen, M D Zumbaugh, J C Wicks, M Beline, J S Bodmer, E C Roth, L A Rimmer, A Wivell, S D Gerrard, S L Silva, S Materneh, D E Gerrard
Skeletal muscle growth is often viewed through the lens of maximal cellular energy production, with oxidative phosphorylation thought mandatory for optimal support of anabolic growth processes. However, efficient lean tissue accretion is also subjected to the economy of carbon sequestration, as oxidative metabolism irreversibly releases carbon as CO₂. Herein, we propose skeletal muscle in faster-growing, more efficient meat animals adopt a regulated, Warburg-like metabolism that enhances efficiency of lean tissue accretion. Drawing on evidence from long-term selection, growth promotant use, and naturally occurring gene mutations, we propose that rapid muscle growth may be facilitated by increased glycolytic capacity, selective remodeling of mitochondrial function, and improved carbon retention for biosynthetic processes. Although direct evidence linking these processes causally to lean tissue accretion remains limited, this framework integrates numerous observations reported across livestock species into a testable metabolic hypothesis. Although an absolute causality for this occurrence remains largely unexplored in skeletal muscle, this configuration mirrors core features of Warburg metabolism observed in many types of cancer cells that prioritize glycolysis in the presence of oxygen and enhance biosynthetic flux to support nucleotide synthesis and redox homeostasis. By reframing muscle growth as an issue of carbon allocation in addition to ATP production, this hypothesis integrates long-standing consistent observations in the field of muscle growth with cutting-edge concepts of metabolic reprogramming and offers a framework to interpret gains in growth efficiency alongside potential trade-offs in metabolic health, robustness, and meat quality development.