Effects of genetic strain and nutrition on muscle satellite cell function and the development of Wooden Breast myopathy in broilers

Abstract

Wooden Breast (WB) myopathy is one of the most significant muscle disorders affecting the Pectoralis major (PM) of modern commercial broiler chickens, resulting in impaired meat quality and substantial economic losses to the poultry industry. Although the condition has been closely associated with rapid genetic selection for growth and breast muscle yield, the biological mechanisms responsible for its development remain incompletely understood, particularly the contribution of muscle satellite cells (SC) during early post-hatch muscle growth. Therefore, the objective of this dissertation was to investigate the effects of genetic growth potential and early dietary nutrient reduction on skeletal muscle development, SC function, extracellular matrix remodeling, and inflammatory cell infiltration during the onset and progression of WB. Female broilers representing fast-growing (FG) and slow-growing (SG) genetic strains were reared under controlled conditions, with FG birds receiving either a conventional starter diet or a nutrient-reduced starter diet. Birds were evaluated daily from 7 to 25 days of age to characterize growth performance, breast muscle development, WB incidence and severity, muscle fiber morphology, SC heterogeneity, myogenic fusion-associated cell populations, collagen deposition, and macrophage abundance using histological and immunofluorescence approaches. Fast-growing broilers consistently showed greater body weight and breast muscle development than SG birds throughout the study. Wooden Breast myopathy first appeared in FG broilers at 17 days of age and progressed rapidly thereafter, with birds receiving the conventional control diet developing the greatest WB severity. In contrast, no WB was detected in SG broilers during the experimental period. As WB severity increased, breast muscle fibers became progressively larger while fiber density reduced, indicating accelerated hypertrophic growth preceding the development of severe myopathy. Daily characterization of SC populations demonstrated dynamic changes in myogenic regulatory factor expression throughout early muscle development. Slow-growing broilers maintained a greater proportion of activated myogenic cell populations and smaller muscle fibers, whereas FG broilers had alterations in SC heterogeneity that became more pronounced with increasing WB severity. Populations associated with SC maintenance, activation, and differentiation (Pax7, MyoD, and Myomixer) decreased as the WB progressed, suggesting reduced regenerative potential despite continued muscle hypertrophy. Concurrently, collagen deposition and macrophage abundance increased with WB severity, demonstrating progressive extracellular matrix remodeling and inflammatory cell infiltration during the onset of the myopathy. Collectively, these findings demonstrate that genetic growth rate is the primary determinant of early WB development, whereas starter diet nutrient reduction has been shown to delay but not completely prevent its onset and progression. More importantly, this work establishes a comprehensive experimental model that identifies the temporal relationship among muscle fiber hypertrophy, SC dynamics, fibrosis, and inflammation before and during the onset of WB. These results provide new understanding into the cellular mechanisms underlying impaired skeletal muscle regeneration in modern broilers to understand the biological events driving WB development, providing a foundation for future nutritional, genetic, and management strategies aimed to improve muscle health and reducing the incidence of this economically important meat quality defect in broiler chickens.