Improving meat quality of the broiler chicken: integrated mechanistic frameworks linking pre-slaughter determinants, postmortem transformations, and multi-omics technology

Abstract

Broiler meat quality is governed by complex biological interactions spanning genetic, nutritional, environmental, and management factors, yet current literature remains fragmented across disciplinary silos. Most studies focus independently on pre-slaughter conditions or postmortem processes, limiting mechanistic understanding of how upstream determinants collectively shape meat quality outcomes. This review addresses this gap by proposing a unified mechanistic framework that integrates pre-slaughter factors, muscle metabolism at slaughter, and postmortem biochemical transformations as interconnected components governing final meat quality traits, with multi-omics approaches enabling system-level resolution. The framework identifies key mechanistic hubs, including muscle energy metabolism, mitochondrial function, oxidative balance, calcium homeostasis, and proteolytic systems, which act as central regulators linking pre-slaughter influences on postmortem conversion dynamics. These processes collectively determine pH decline kinetics, protein degradation, lipid oxidation, and structural integrity during postmortem transformation, ultimately shaping tenderness, water-holding capacity, color stability, flavor development, and susceptibility to quality defects such as pale, soft, exudative and dark, firm, dry meat. A key feature of the synthesis is resolution of persistent trade-offs in the literature, including growth efficiency versus meat quality, oxidative stability versus nutritional enrichment, and rapid muscle accretion versus myopathy susceptibility. The review further integrates multi-omics technologies, linking genomic variants, proteomic pathways, and metabolomic signatures with physiological and phenotypic outcomes, thereby enabling predictive modeling of meat quality traits across production stages. This system level integration provides a foundation for integrated precision management strategies to highlight the coordinated control of pre-slaughter conditions, muscle metabolism, and postmortem processes in commercial broiler systems to achieve improved quality broiler meat production.

Introduction

Broiler meat quality has emerged as a major scientific, economic, and industrial priority due to its direct influence on consumer acceptance, processing efficiency, nutritional value, and global poultry market sustainability (Dinasarki et al., 2024). Modern poultry production systems have achieved remarkable improvements in growth rate, feed efficiency, and breast muscle yield through intensive genetic selection, precision nutrition, and advanced management practices (Naeem et al., 2026). However, these production gains have also intensified the incidence of quality defects, including pale, soft, exudative (PSE) meat, dark, firm, dry (DFD) conditions, woody breast, white striping, reduced water-holding capacity (WHC), oxidative instability, and inconsistent tenderness (Warner, 2017; Huang and Ahn, 2018). Increasing consumer demand for high-quality, minimally processed, nutritionally enhanced poultry meat has further emphasized the need to understand the biological mechanisms governing muscle-to-meat conversion (Choi et al., 2023). Consequently, improving broiler meat quality now requires a systems-level understanding that integrates pre-slaughter physiology, postmortem biochemistry, and molecular regulatory mechanisms rather than focusing solely on isolated production traits or individual interventions (Zampiga et al., 2019).

Despite extensive research on genetic, nutritional, environmental, and postmortem determinants of meat quality, current literature remains highly fragmented. Most studies investigate individual factors independently, including dietary additives, muscle fiber characteristics, stress physiology, processing conditions, or postmortem ageing, without sufficiently addressing how these components interact within an integrated biological framework (Ismail and Joo, 2017; Soglia et al., 2020). Similarly, genomics, proteomics, metabolomics, and physiological studies are frequently presented as isolated analytical domains rather than interconnected regulatory layers governing muscle metabolism and postmortem transformation (Yigitturk et al., 2025; Naeem, 2026). This compartmentalized approach has contributed to contradictory findings regarding growth-performance trade-offs, oxidative stability, lipid enrichment strategies, and stress responsiveness, limiting the development of predictive and mechanistically unified models of meat quality (Liu et al., 2021). As a result, the field lacks a coherent framework capable of explaining how diverse pre-slaughter inputs converge to regulate postmortem biochemical trajectories and final meat quality phenotypes (Petracci and Cavani, 2011; Zampiga et al., 2019).

A growing body of evidence indicates that muscle metabolic status at slaughter represents the central integrative node linking pre-slaughter interventions with postmortem biochemical transformations and ultimate meat quality outcomes (Weng et al., 2022). At the time of slaughter, muscle tissue reflects the cumulative effects of genetics, nutrition, environmental stressors, health status, and management practices through coordinated regulation of glycogen reserves, mitochondrial efficiency, oxidative balance, calcium homeostasis, muscle fiber composition, intramuscular fat deposition, endocrine stress responses, and proteolytic preparedness (Xing et al., 2021) . These interconnected metabolic and structural determinants collectively govern postmortem glycolysis, ATP depletion, pH decline kinetics, rigor mortis development, proteolysis, oxidative deterioration, and structural remodelling, which subsequently determine tenderness, WHC, color stability, flavor, shelf life, and susceptibility to myopathies and meat quality defects (Nawaz et al., 2021; Bordignon et al., 2022). Accordingly, understanding broiler meat quality requires recognition of muscle metabolism as a dynamic systems-level regulator that mechanistically connects pre-slaughter biology with postmortem conversion processes.

Integrated mechanistic framework

Broiler meat quality results from a continuous biological continuum in which genetics, nutrition, environment, and welfare collectively determine the metabolic state of muscle at slaughter and thereby shape postmortem transformation and final product attributes (Yigitturk et al., 2025) (Fig. 1). Genetic selection for rapid growth and increased breast yield alters muscle fiber composition, mitochondrial density, glycolytic capacity, and oxidative stability, establishing the intrinsic metabolic potential of the tissue (Ikusika et al., 2020). Nutritional inputs further regulate this system by influencing glycogen storage, lipid profile, antioxidant defenses, and cellular energy balance, thereby modifying metabolic resilience prior to slaughter (Alagawany et al., 2022). Environmental and welfare-related stressors such as heat exposure, high stocking density, handling, and transport impose physiological strain that disrupts endocrine regulation, accelerates glycogen depletion, and elevates oxidative stress (Wu et al., 2025). These interacting factors converge to define the pre-slaughter muscle metabolic status, characterized by glycogen availability, ATP reserves, mitochondrial function, calcium regulation, and redox balance, which critically determines postmortem biochemical behavior (Yang et al., 2020). After slaughter, oxygen deprivation initiates anaerobic glycolysis, resulting in lactic acid accumulation and progressive pH decline, where the rate and extent of acidification govern protein denaturation, water distribution, and color development (Mir et al., 2017a). Concurrently, calcium dysregulation activates endogenous proteolytic systems such as calpains, leading to degradation of key structural proteins that regulate tenderization, while oxidative reactions affecting lipids and proteins compromise membrane integrity, flavor stability, and shelf life (Chevet et al., 2015; Kuttappan et al., 2016). These biochemical events collectively drive structural muscle transformation, including sarcomere shortening, cytoskeletal disorganization, myofibrillar fragmentation, and extracellular matrix remodelling, which ultimately determine functional meat quality traits such as water-holding capacity, tenderness, color stability, flavor, storage life, and susceptibility to myopathies like woody breast and white striping, reflecting the integrated outcome of a single interconnected physiological and biochemical system (Song et al., 2025).

Fig. 1.

A unified mechanistic, systems-level, conceptual framework integrating pre-slaughter determinants, muscle metabolic status and postmortem biochemical transformations for improving meat quality in broiler chicken.

Pre-slaughter modulators

Pre-slaughter determinants regulate broiler meat quality primarily through their collective influence on muscle metabolic status before slaughter (Okon et al., 2026) (Suppl. Table 1-23). Genetic architecture establishes the foundational biological framework governing muscle fiber programming, hypertrophic growth, vascularization, mitochondrial density, and metabolic phenotype (Petracci and Cavani, 2011; Hussein et al., 2019). Modern selection for rapid growth and increased breast yield has shifted muscle toward highly glycolytic phenotypes characterized by enlarged fibers, reduced capillary density, impaired oxygen diffusion, and limited mitochondrial capacity. Although these adaptations improve feed efficiency and muscle accretion, they simultaneously increase susceptibility to metabolic overload, oxidative stress, hypoxia, fibrosis, and postmortem acidification abnormalities (Weng et al., 2022; Gu et al., 2024). Reduced vascularization and mitochondrial efficiency impair ATP buffering and oxidative resilience, predisposing muscle to accelerated glycolysis, calcium dysregulation, and reactive oxygen species accumulation before slaughter (Liao et al., 2022) (Table 1). Muscle fiber composition further modulates these responses, where glycolytic fibers favor rapid growth but increase vulnerability to protein denaturation and water loss, while oxidative fibers support metabolic flexibility and redox stability at the expense of maximal hypertrophic efficiency (Zampiga et al., 2019; Yue et al., 2024). Thus, pre-slaughter muscle biology should be interpreted as a dynamic balance between growth-oriented metabolism and physiological resilience rather than as isolated structural traits (El-Senousey et al., 2013; Song et al., 2025).

Table 1.

Integrated mechanistic relationships between pre-slaughter determinants, muscle metabolic regulation, postmortem biochemical transformation, and final meat quality outcomes in broiler chicken.

Pre-slaughter determinants	Primary biological targets	Core mechanistic pathways	Effects on muscle metabolic status	Postmortem biochemical consequences	Final meat quality outcomes	Major associated defects	Mechanistic interpretations
AI-assisted monitoring and smart sensors	Real-time stress and environmental regulation	Continuous optimization of welfare and metabolism	Reduced metabolic fluctuations	More controlled biochemical transformation	Consistent meat quality outcomes	Reduced quality variability	Precision technologies improve dynamic metabolic regulation
Arginine	Nitric oxide signaling and blood flow regulation	Improved vascular function and mitochondrial respiration	Enhanced oxygen delivery and metabolic efficiency	Stabilized glycolysis and proteolysis	Improved tenderness and reduced myopathy risk	Reduced woody breast incidence	Arginine improves metabolic resilience through vasodilation and mitochondrial support
Arginine supplementation	Nitric oxide synthesis and mitochondrial respiration	Improved vasodilation and oxygen delivery	Enhanced oxygen utilization and metabolic resilience	Controlled glycolysis and reduced oxidative stress	Improved WHC and reduced myopathy susceptibility	Excessive supplementation may alter metabolic balance	Arginine supports mitochondrial energetic efficiency
Balanced omega-6: omega-3 ratio	Inflammatory signaling and membrane biology	Regulation of eicosanoid synthesis	Reduced inflammatory stress and oxidative burden	Stabilized lipid oxidation kinetics	Improved oxidative stability and sensory quality	Imbalanced ratios promote inflammation	Fatty acid balance influences systemic inflammatory status
Catching, loading, transport duration	Catecholamine release and glycogen metabolism	Muscular activity and stress-induced glycogen depletion	Reduced glycogen reserves and metabolic exhaustion	Abnormal pH decline kinetics	Poor WHC and color defects	PSE-like or DFD-like outcomes	Stress duration determines glycolytic trajectory
Coenzyme Q10, L-carnitine	Mitochondrial respiration and fatty acid oxidation	Improved ATP generation and reduced ROS leakage	Enhanced energetic stability and oxidative balance	Reduced mitochondrial-driven oxidative deterioration	Improved tenderness and shelf life	Limited large-scale validation	Mitochondrial nutrients enhance energetic efficiency and redox control
Cold stress	Energy metabolism and thermoregulation	Increased metabolic demand and glycogen utilization	Altered energetic reserves	Delayed rigor development	Variable tenderness and color	Stress-related quality variability	Thermoregulatory stress alters pre-slaughter energy balance
Controlled atmosphere stunning	Stress hormone regulation and oxygen availability	Reduced struggling and stress responses	Stabilized metabolic status	Controlled glycolysis and pH decline	Improved carcass uniformity and WHC	Lower haemorrhagic defects	Reduced pre-slaughter stress improves metabolic stability
Controlled feeding programs	Metabolic efficiency and oxidative adaptation	Reduced metabolic overload and oxidative stress	Improved mitochondrial function and metabolic balance	Stabilized rigor development and oxidation	Improved texture and reduced myopathy incidence	Excess restriction may reduce productivity	Moderate restriction enhances metabolic resilience
Delayed chilling	Protein denaturation and oxidation	Prolonged high-temperature glycolysis	Accelerated pH-temperature interaction	Enhanced denaturation and membrane damage	Reduced WHC and tenderness	PSE-like conditions	Temperature and pH interaction critically regulate protein integrity
Dynamic nutrient delivery	Energetic synchronization and antioxidant support	Precision adjustment of nutrient supply	Improved metabolic efficiency	Controlled glycolytic and oxidative responses	Enhanced consistency of WHC and tenderness	Reduced metabolic collapse	Precision feeding stabilizes biological variability
Dynamic nutrient delivery	Real-time energetic and antioxidant adjustment	Continuous optimization of nutrient availability	Reduced metabolic fluctuation and stress	Stabilized biochemical transformation postmortem	Enhanced meat quality consistency	Technological complexity and infrastructure costs	Precision feeding minimizes metabolic variability
Electrical stunning	Membrane depolarization and muscle contraction	Intense contraction and ATP depletion	Accelerated energetic exhaustion	Rapid rigor onset and altered proteolysis	Variable tenderness and haemorrhage incidence	Structural damage and blood splash	Stunning intensity determines metabolic disruption severity
Electrolytes and osmolytes	Cellular hydration and acid-base balance	Maintenance of osmotic stability and stress adaptation	Reduced corticosterone and metabolic disruption	Improved pH stability and reduced oxidation	Reduced heat-induced quality deterioration	Effectiveness varies with stress severity	Electrolytes improve physiological resilience during thermal stress
Extended pre-slaughter fasting	Glycogen reserves and energy balance	Reduced muscle glycogen availability	Energetic depletion	Limited lactic acid production	Darker meat and altered tenderness	DFD-like characteristics	Glycogen exhaustion impairs normal rigor development
Formic acid, citric acid, butyric acid	Intestinal pH and microbial ecology	Pathogen suppression and nutrient utilization enhancement	Reduced inflammatory burden and improved digestion	Stabilized postmortem glycolytic trajectory	Improved carcass quality consistency	Over-acidification may impair feed intake	Organic acids improve metabolic efficiency and gut health
Glycolytic muscle fiber predominance	Anaerobic glycolysis and glycogen metabolism	High glycolytic flux and rapid ATP turnover	Increased glycogen dependence and ROS susceptibility	Accelerated pH decline and protein denaturation	Higher drip loss and reduced WHC	PSE-like conditions	Glycolytic fibers favor growth efficiency but reduce metabolic flexibility
Heat stress	Mitochondrial function and endocrine balance	ROS generation, protein denaturation, corticosterone elevation	Glycogen depletion and oxidative imbalance	Accelerated glycolysis or glycogen exhaustion	PSE-like or DFD-like conditions	Severe oxidative deterioration	Heat stress destabilizes energetic and redox homeostasis
High breast-yield selection	Muscle architecture and extracellular matrix remodelling	Disproportionate muscle accretion and impaired capillary development	Hypoxia and metabolic stress	Enhanced oxidative deterioration and fibrosis	Texture abnormalities and structural rigidity	Woody breast and spaghetti meat	Muscle enlargement exceeds adaptive metabolic and circulatory capacity
High stocking density	Stress physiology and inflammatory signaling	Increased corticosterone and reduced welfare	Elevated oxidative stress and muscular fatigue	Enhanced protein denaturation and oxidation	Reduced tenderness and WHC	Higher drip loss	Chronic stress impairs metabolic stability
High-energy diets	Glycogen storage and lipid deposition	Increased glycolytic substrate availability	Enhanced glycogen reserves and metabolic load	Accelerated postmortem glycolysis	Increased risk of rapid pH decline	Elevated PSE-like susceptibility	Excess energy promotes glycolytic dominance
Insect meal, algae, plant proteins	Amino acid balance and lipid metabolism	Alteration of protein and fatty acid composition	Modified muscle metabolic pathways	Changes in oxidation susceptibility and flavor development	Variable effects on texture and sensory quality	Inconsistent responses among protein sources	Alternative proteins influence both metabolism and membrane composition
Integrated environmental adaptation	Multi-stressor resilience	Combined thermal, nutritional, and welfare regulation	Improved physiological adaptability	Stabilized postmortem biochemical trajectory	Sustainable meat quality consistency	Reduced climate-associated defects	Integrated adaptation strategies improve long-term resilience
Leucine, isoleucine, valine	Muscle protein metabolism and mTOR signaling	Regulation of anabolic and energetic pathways	Improved metabolic efficiency and muscle integrity	Stabilized postmortem proteolysis	Improved tenderness and muscle structure	Nutrient imbalance may reduce efficiency	BCAA regulate muscle anabolic signaling and recovery
Lysine optimization	Muscle protein accretion	Regulation of myofibrillar protein synthesis	Improved muscle growth and protein turnover	Enhanced structural protein preservation	Improved texture and carcass yield	Excessive growth pressure may increase myopathy risk	Balanced lysine improves lean tissue deposition efficiency
Methionine	Glutathione synthesis and methyl metabolism	Improved antioxidant capacity and protein turnover	Reduced oxidative stress and enhanced cellular repair	Reduced protein oxidation	Improved WHC and protein stability	Lower oxidative damage	Methionine supports redox homeostasis and structural integrity
Methionine supplementation	Glutathione synthesis and methyl metabolism	Enhanced antioxidant capacity and protein synthesis	Improved cellular repair and redox homeostasis	Reduced protein oxidation and denaturation	Improved protein stability and tenderness	Imbalanced levels may impair nutrient utilization	Methionine maintains structural and antioxidant integrity
Nutrigenomic feeding strategies	Gene-expression regulation and metabolic pathways	Targeted modulation of growth and stress-response genes	Improved metabolic synchronization and adaptive capacity	Controlled glycolytic and oxidative responses	Consistent WHC, tenderness, and shelf life	Requires genotype-specific optimization	Precision nutrition aligns nutrient supply with molecular regulation
Omega-3 fatty acid supplementation	Membrane phospholipid composition	Anti-inflammatory signaling and membrane remodelling	Altered membrane fluidity and oxidative susceptibility	Modified oxidation kinetics	Improved flavor profile and lipid quality	Increased oxidation susceptibility if antioxidants insufficient	PUFA enrichment improves nutritional value but may elevate oxidative risk
Omega-3 fatty acid supplementation	Membrane phospholipid composition	Anti-inflammatory lipid remodelling	Altered membrane fluidity and reduced inflammation	Modified oxidation susceptibility and membrane stability	Improved nutritional value and flavor profile	Increased oxidation risk without antioxidant support	PUFA enrichment improves functionality but elevates oxidative sensitivity
Oxidative muscle fiber predominance	Mitochondrial respiration and oxygen utilization	Enhanced aerobic metabolism and antioxidant defense	Stable ATP generation and ROS regulation	Slower pH decline and reduced oxidation	Improved tenderness and color stability	Reduced susceptibility to PSE-like conditions	Oxidative fibers improve metabolic resilience but may compromise growth rate
Perches, activity stimulation, natural lighting	Muscle conditioning and oxidative metabolism	Enhanced activity and oxidative adaptation	Improved mitochondrial efficiency and muscle integrity	Stabilized postmortem metabolism	Improved texture and reduced myopathies	Lower incidence of structural defects	Physical activity promotes oxidative muscle phenotype
Phytase, protease, xylanase	Nutrient digestibility and metabolic efficiency	Enhanced nutrient release and reduced anti-nutritional effects	Improved energy utilization and reduced metabolic waste	Reduced oxidative stress and metabolic instability	Improved growth efficiency and carcass quality	Enzyme efficacy depends on feed composition	Improved digestibility reduces metabolic burden
Polyphenols, flavonoids, essential oils	Nrf2 signaling, inflammatory pathways	Antioxidant and anti-inflammatory regulation	Reduced oxidative stress and inflammatory burden	Stabilized protein integrity and oxidation kinetics	Improved tenderness, shelf life, and color retention	Variable responses depending on source and dose	Phytobiotics modulate redox-sensitive signaling pathways
Poor litter quality	Immune activation and locomotion	Increased inflammatory burden and reduced mobility	Metabolic inefficiency and oxidative stress	Impaired postmortem proteolysis	Reduced texture quality	Increased myopathy susceptibility	Chronic inflammatory stress affects muscle biology
Prebiotics	Beneficial microbial fermentation	Promotion of favorable intestinal microbial populations	Improved nutrient absorption and immune modulation	Controlled glycolysis and reduced oxidative stress	Improved carcass consistency and shelf life	Effectiveness depends on diet composition	Prebiotics indirectly influence muscle metabolism through microbial metabolites
Probiotics	Gut microbiota composition and immune signaling	Enhanced SCFA production and intestinal integrity	Reduced systemic inflammation and oxidative stress	Stabilized glycogen metabolism and reduced oxidation	Improved WHC, tenderness, and shelf life	Reduced stress-induced deterioration	Gut microbiota regulates systemic metabolic and inflammatory pathways
Probiotics	Gut microbiota composition and immune signaling	Enhanced SCFA production and intestinal integrity	Reduced systemic inflammation and oxidative stress	Stabilized glycogen utilization and postmortem metabolism	Improved WHC, tenderness, and oxidative stability	Responses vary by microbial strain	Gut microbiota regulates host metabolic and inflammatory pathways
Rapid chilling	Sarcomere shortening and rigor progression	Cold-induced contraction before rigor completion	Structural tension and reduced proteolysis	Shortened sarcomeres and altered aging	Increased toughness	Cold shortening	Excessively rapid chilling disrupts normal rigor development
Rapid-growth commercial broiler strains	Muscle fiber development, mitochondrial density, vascularization	Accelerated hypertrophy, glycolytic fiber dominance, oxygen diffusion limitation	Reduced oxidative capacity, mitochondrial overload, glycogen instability	Rapid glycolysis, excessive lactate accumulation, oxidative stress	Reduced WHC, poor tenderness, color instability	Woody breast, white striping, PSE-like meat	Selection for growth efficiency increases metabolic burden beyond vascular and oxidative support capacity
Selenium supplementation	Glutathione peroxidase system	Enhancement of endogenous antioxidant defense	Improved ROS detoxification	Reduced oxidative cascade progression	Improved oxidative stability and tenderness	Reduced oxidative deterioration	Selenium-dependent GPx activity preserves membrane integrity
Selenium supplementation	Glutathione peroxidase system and redox enzymes	Enhancement of endogenous antioxidant defense pathways	Improved ROS detoxification and mitochondrial protection	Reduced oxidative deterioration and membrane disruption	Improved oxidative stability and structural integrity	Lower oxidative damage under heat stress	Selenium-dependent GPx activity preserves cellular redox balance
Synbiotics	Combined probiotic-prebiotic interactions	Synergistic enhancement of microbial ecosystem stability	Enhanced metabolic resilience and antioxidant capacity	Stabilized pH decline and oxidative balance	Improved tenderness and reduced drip loss	Variable synergistic responses	Synbiotics strengthen gut-muscle metabolic communication
Synbiotics and prebiotics	Microbial fermentation and nutrient utilization	Improved microbial balance and nutrient absorption	Enhanced metabolic efficiency and immune modulation	Controlled postmortem glycolysis	Improved carcass consistency	Reduced inflammatory stress	Gut-derived metabolites influence muscle metabolic stability
Vitamin C + Vitamin E	Redox cycling and ROS detoxification	Synergistic antioxidant regeneration	Enhanced oxidative defense and mitochondrial stability	Reduced lipid and protein oxidation	Improved shelf life and color retention	Excess supplementation may disrupt redox signaling	Combined antioxidant systems improve cellular protection
Vitamin E supplementation	Lipid membranes and antioxidant systems	Lipid radical scavenging and membrane stabilization	Reduced oxidative damage and preserved mitochondrial integrity	Lower lipid oxidation and protein denaturation	Improved shelf life, WHC, and color retention	Reduced rancidity and discoloration	Antioxidants stabilize redox balance during pre- and postmortem phases
Vitamin E supplementation	Cellular membranes, phospholipids, myoglobin stability	Lipid radical scavenging and membrane stabilization	Reduced ROS accumulation and preserved mitochondrial integrity	Lower lipid oxidation and protein denaturation	Improved WHC, color stability, shelf life, tenderness	Reduced rancidity and discoloration	Vitamin E interrupts oxidative chain reactions during pre- and postmortem phases
Zinc, copper, manganese	Antioxidant enzymes and immune regulation	Cofactor support for SOD and metabolic enzymes	Improved enzymatic antioxidant activity	Reduced oxidative deterioration	Improved oxidative stability and structural quality	Mineral imbalance may impair metabolism	Trace minerals support endogenous defense systems

Nutritional and environmental factors further modify this metabolic framework by influencing oxidative balance, mitochondrial function, glycogen dynamics, inflammatory signaling, and stress adaptability (Pečjak Pal et al., 2024). Antioxidant-supportive strategies involving vitamin E, selenium, and phytogenic polyphenols consistently demonstrate strong mechanistic robustness through stabilization of membrane integrity, reduction of lipid peroxidation, and preservation of mitochondrial function, although phytogenic efficacy remains highly context dependent (El-Tarabany et al., 2022). Gut-muscle axis modulation through probiotics, synbiotics, and organic acids influences systemic metabolism by improving intestinal barrier integrity, microbial balance, nutrient utilization, and inflammatory regulation, yet reproducibility varies according to strain composition, diet, and environmental conditions (Mayulu et al., 2019; Abd El-Samee et al., 2019) (Fig. 2). Environmental metabolic stress including heat exposure, transport, stocking density, and poor litter quality converges mechanistically on glycogen depletion, oxidative overload, mitochondrial dysfunction, and inflammatory activation, thereby destabilizing postmortem metabolism and increasing myopathy risk (Nawaz et al., 2021; Hong et al., 2024). Precision poultry technologies (Fig. 4) such as thermal imaging, biosensors, and AI-assisted monitoring systems offer potential for real-time metabolic assessment, but most remain at proof-of-concept or intermediate Technology Readiness Levels.

Fig. 2.

Integrated conceptual framework of the gut-muscle axis linking dietary interventions, microbiota modulation, immune regulation and oxidative homeostasis for improvement of broiler meat quality.

Fig. 4.

Precision management framework for improving meat quality of the broiler chicken.

Muscle metabolic programming

The metabolic and structural condition of skeletal muscle immediately before slaughter represents the central determinant of postmortem biochemical progression and final broiler meat quality (Okon et al., 2026). Rather than functioning as isolated influences, pre-slaughter genetic, nutritional, environmental, and managerial factors converge to establish a highly integrated muscle metabolic state that governs the entire muscle to meat conversion process (Yigitturk et al., 2025). This state is defined by glycogen availability, mitochondrial efficiency, oxidative balance, muscle fiber composition, calcium regulation, lipid metabolism, and proteolytic readiness (Xing et al., 2021; Nagasao et al., 2022). Together, these variables determine how effectively muscle transitions from aerobic homeostasis to anaerobic metabolism after exsanguination. This transition shapes ATP depletion patterns, glycolytic intensity, pH decline kinetics, oxidative reactions, and structural remodelling processes (Wang et al., 2023; Wu et al., 2025). Consequently, key quality attributes such as tenderness, water-holding capacity, color stability, flavor development, and shelf life are pre-determined to a large extent before slaughter occurs (Abd El-Samee et al., 2019; Idowu et al., 2026). Moreover, major quality defects including pale soft exudative meat, woody breast, white striping, and dark firm dry conditions emerge as direct consequences of imbalanced pre-slaughter muscle metabolism and impaired physiological resilience under intensive production systems (Praud et al., 2020; Bošković Cabrol et al., 2025).

Among all determinants, glycogen reserves and glycolytic potential function as the primary regulators of postmortem acidification dynamics. Glycogen serves as the principal substrate for anaerobic glycolysis following death, and its concentration directly controls lactate production and ultimate pH decline (Dashdorj et al., 2015; Majdeddin et al., 2018). When muscles possess abundant glycogen stores combined with high glycolytic enzyme activity, postmortem glycolysis proceeds rapidly while carcass temperature remains elevated. This results in excessive proton accumulation, rapid protein denaturation, reduced water retention, pale coloration, and soft texture, collectively associated with pale soft exudative conditions (Kaya et al., 2024). In contrast, chronic stress, heat exposure, prolonged feed withdrawal, or transport stress can deplete glycogen reserves prior to slaughter. Under these conditions, limited lactate production leads to insufficient acidification, elevated ultimate pH, darker meat color, firmer texture, and altered microbial stability typical of dark firm dry conditions (Xing et al., 2017; Wu et al., 2024). Thus, glycogen dynamics act as a metabolic bridge linking pre-slaughter energy balance to postmortem biochemical outcomes, and any disruption in this system directly alters meat quality trajectory (Yigitturk et al., 2025).

Mitochondrial function and oxidative balance are central regulators of metabolic stability before slaughter, controlling ATP production, redox homeostasis, and calcium buffering capacity. Efficient mitochondria maintain energy supply and delay metabolic collapse, whereas mitochondrial dysfunction accelerates ATP depletion, increases reactive oxygen species generation, and disrupts membrane and ionic stability (Xing et al., 2021; Wu et al., 2025). Oxidative stress promotes lipid peroxidation, protein oxidation, and myoglobin instability, reducing color stability, tenderness development, and water-holding capacity (Liao et al., 2022). Muscle fiber type also influences these processes, where fast glycolytic fibers favor rapid acidification and higher defect susceptibility, while oxidative fibers enhance metabolic stability but may reduce growth efficiency (Weng et al., 2022; Mo et al., 2023). Calcium imbalance further accelerates rigor development and structural contraction, impairing tenderness (Sayre, 1970; Ismail and Joo, 2017). Lipid metabolism contributes to sensory quality but increases oxidative risk when unsaturated fat levels are high (Adegoke et al., 2024). Proteolytic system efficiency determines the extent of postmortem protein breakdown, influencing final tenderness and texture (Song et al., 2025). Collectively, these interconnected mechanisms confirm that meat quality is fundamentally programmed by pre-slaughter muscle metabolism rather than determined only by postmortem events (Doherty et al., 2007).

Systems biology of myopathies

Modern broiler myopathies emerge from a tightly interconnected systems-level disruption in muscle growth regulation, vascular architecture, metabolic homeostasis, oxidative balance, inflammatory signaling, and extracellular matrix remodelling (Barbut et al., 2024). Intense genetic selection for rapid hypertrophic breast muscle accretion produces enlarged glycolytic fibers that outpace capillary development, thereby generating vascular insufficiency, local hypoxia, impaired nutrient diffusion, and reduced oxygen delivery (Bordignon et al., 2022). This metabolic mismatch destabilizes mitochondrial function, compromises oxidative phosphorylation, and promotes excessive reactive oxygen species generation, leading to lipid peroxidation, protein oxidation, calcium dysregulation, and sarcoplasmic reticulum stress (Nawaz et al., 2021; Hong et al., 2024). Oxidative injury subsequently activates inflammatory cascades involving macrophage infiltration, cytokine release, and stress-responsive signaling pathways that further exacerbate myofibre degeneration and necrosis (Chevet et al., 2015; Kuttappan et al., 2016). Concurrently, chronic tissue injury stimulates fibroblast activation and extracellular matrix deposition, resulting in fibrosis, collagen accumulation, reduced muscle elasticity, and altered water-holding capacity (El-Senousey et al., 2013; Roy and Bruce, 2024). Progressive extracellular matrix remodelling also disrupts muscle ultrastructure and impairs intracellular communication between metabolic, vascular, and structural compartments (Ismail and Joo, 2017; Soglia et al., 2020). As mitochondrial dysfunction intensifies, ATP depletion, impaired ion homeostasis, and metabolic collapse accelerate the transition from reversible cellular stress to irreversible myo-degeneration. Collectively, these interconnected events establish an integrated pathogenesis model in which hypertrophic growth pressure initiates cascading vascular, oxidative, inflammatory, fibrotic, and metabolic failures that ultimately determine the severity and phenotypic expression of broiler myopathies (Praud et al., 2020; Bošković Cabrol et al., 2025).

Emerging precision technologies

Parallel to phenotyping advances, multi-omics integration is redefining systems-level understanding of muscle development and postmortem conversion by connecting genomic variation with transcript, protein, metabolite, and lipid level regulation (Hong et al., 2024) (Table 2; Fig. 3). However, current analyses frequently remain compartmentalized, limiting interpretation of cross level regulatory control (Doherty et al., 2007; Kuttappan et al., 2016). Integrated frameworks are needed to link genetic determinants of energy metabolism, mitochondrial efficiency, and proteolytic regulation with downstream molecular outputs such as lactate accumulation, ATP degradation, oxidative stress markers, and lipid oxidation products (Yigitturk et al., 2025; Naeem, 2026). This linkage enables explanation of how molecular networks translate into structural outcomes including fiber stability, proteolysis, and oxidative deterioration that ultimately determine tenderness, water retention, color stability, and myopathy susceptibility (Fig. 5), shifting omics from descriptive profiling to predictive biological modelling (Hong et al., 2024; Ma et al., 2024).

Table 2.

Integrated multi-omics molecular signatures, biological functions, metabolic regulatory mechanisms, postmortem biochemical consequences, and translational biomarker applications associated with broiler meat quality determination.

Omics layer	Molecular signatures	Primary biological functions	Mechanistic link to muscle metabolism	Associated postmortem effects	Major meat quality outcomes	Integrated systems interpretations	Translational potentials
Genomics	QTLs associated with pH decline	Regulation of glycolytic capacity and stress responsiveness	Determines glycogen storage and metabolic intensity before slaughter	Alters lactate accumulation and rigor kinetics	WHC, tenderness, PSE susceptibility	Establishes inherited metabolic trajectory	Genomic selection for meat quality
Genomics	SNPs linked to muscle hypertrophy	Muscle growth and vascular regulation	Excessive hypertrophy reduces oxygen diffusion and mitochondrial efficiency	Accelerated oxidative stress and impaired proteolysis	Woody breast, white striping	Explains growth-quality trade-offs	Precision breeding programs
Genomics	Myogenic regulatory genes (MyoD, Myf5, Myogenin)	Muscle fiber development	Determines fiber type composition and metabolic phenotype	Influences glycolytic versus oxidative metabolism	Texture and color stability	Connects developmental biology with meat quality	Marker-assisted selection
Transcriptomics	Glycolytic pathway genes	Regulation of anaerobic metabolism	Controls postmortem glycolytic flux	Rapid or delayed pH decline	PSE-like or DFD-like conditions	Links stress signaling with postmortem biochemistry	Early stress prediction
Transcriptomics	Oxidative stress-responsive genes	Cellular antioxidant defense	Regulates ROS detoxification and redox homeostasis	Reduced lipid and protein oxidation	Shelf life and color stability	Indicates metabolic resilience	Nutritional targeting
Transcriptomics	Heat shock protein expression	Cellular stress adaptation	Protects proteins and mitochondria during stress	Stabilizes structural proteins postmortem	Improved tenderness and oxidative stability	Biomarker of adaptive stress resistance	Stress-monitoring systems
Transcriptomics	Inflammatory cytokine signaling	Immune and fibrosis regulation	Promotes extracellular matrix remodelling and metabolic disruption	Chronic inflammatory degeneration	Woody breast and fibrosis	Integrates inflammation with myopathy development	Therapeutic intervention targets
Proteomics	Glycolytic enzymes	ATP depletion and lactate production	Reflects energetic status at slaughter	Alters rigor development and pH kinetics	WHC and drip loss	Functional indicators of metabolic flux	Precision phenotyping
Proteomics	Calpain system proteins	Postmortem proteolysis	Regulates cytoskeletal degradation	Determines tenderization efficiency	Tenderness variability	Central regulator of structural remodelling	Processing optimization
Proteomics	Cytoskeletal proteins	Muscle structural integrity	Maintains sarcomere organization and membrane stability	Structural degradation during aging	Texture and water retention	Links structural biology with meat quality	Biomarker-assisted grading
Proteomics	Heat shock proteins	Protein protection and folding	Stabilizes cellular proteins under thermal and oxidative stress	Reduces denaturation and oxidation	Improved oxidative stability	Protective adaptation network	Commercial stress biomarkers
Proteomics	Mitochondrial respiratory proteins	Cellular bioenergetics	Controls oxidative phosphorylation and ATP synthesis	Influences ROS generation and oxidative collapse	Color stability and shelf life	Central energetic regulatory hub	Mitochondrial-targeted nutrition
Metabolomics	Lactate accumulation	Indicator of glycolytic intensity	Reflects glycogen utilization and anaerobic metabolism	Rapid pH decline and protein denaturation	PSE-like meat and WHC loss	Direct biochemical marker of metabolic stress	Slaughter optimization
Metabolomics	ATP degradation metabolites	Rigor mortis progression	Indicates energetic depletion and contraction status	Accelerates rigor development	Texture and tenderness variation	Connects energy metabolism with structural transformation	Postmortem quality prediction
Metabolomics	ROS-associated metabolites	Oxidative deterioration	Reflects imbalance between ROS generation and antioxidant defense	Lipid and protein oxidation	Discoloration and rancidity	Central indicator of redox instability	Antioxidant intervention assessment
Metabolomics	Amino acid metabolic signatures	Protein turnover and flavor precursor generation	Influences muscle protein integrity and flavor development	Proteolysis and volatile compound formation	Flavor and tenderness	Connects metabolism with sensory quality	Functional nutrition design
Lipidomics	PUFA oxidation products	Membrane oxidation susceptibility	Determines oxidative stability of phospholipids	Membrane destabilization and aldehyde formation	Rancidity and reduced shelf life	Integrates nutrition with oxidation biology	Precision lipid nutrition
Lipidomics	Phospholipid remodelling signatures	Membrane fluidity and integrity	Alters mitochondrial and cellular membrane stability	Changes oxidation kinetics	Color and oxidative stability	Links membrane biology with meat deterioration	Shelf-life optimization
Microbiomics	SCFA-producing bacterial taxa	Gut-muscle metabolic communication	Enhances mitochondrial efficiency and anti-inflammatory signaling	Stabilized postmortem metabolism	Improved WHC and tenderness	Demonstrates gut-muscle axis regulation	Precision probiotic strategies
Microbiomics	Dysbiosis-associated microbial profiles	Inflammatory and oxidative signaling	Promotes immune activation and metabolic disruption	Increased oxidative deterioration	Poor texture and reduced shelf life	Integrates gut health with muscle quality	Microbiota-directed interventions
Integrated multi-omics	Glycolysis-centered molecular networks	Coordinated energetic regulation	Integrates genomic, proteomic, and metabolomic control of glycolysis	Predicts pH decline trajectory	WHC and PSE susceptibility	Unified model of postmortem metabolism	Predictive quality algorithms
Integrated multi-omics	Oxidative stress interaction hubs	Redox systems integration	Connects antioxidant genes, proteins, and metabolites	Controls oxidation-mediated deterioration	Shelf life and color stability	Central convergence mechanism	Precision antioxidant strategies
Integrated multi-omics	Fiber type-associated regulatory networks	Metabolic phenotype coordination	Links myogenic signaling with mitochondrial function	Determines oxidative versus glycolytic balance	Texture and myopathy susceptibility	Resolves contradictory fiber-type findings	Precision breeding and management
Integrated multi-omics	Fibrosis-associated molecular signatures	Extracellular matrix remodelling	Integrates inflammatory signaling and structural degeneration	Progressive connective tissue accumulation	Woody breast and white striping	Systems-level myopathy mechanism	Early diagnostic biomarker panels
Integrated multi-omics	AI-assisted predictive biomarker models	Systems-level phenotype prediction	Integrates omics layers with environmental and physiological datasets	Predicts metabolic collapse and quality defects	Overall meat quality performance	Enables precision poultry systems biology	Commercial precision meat quality platforms

Fig. 3.

Multi-omics integration network for improving meat quality of the broiler chicken.

Fig. 5.

Systems biology framework of broiler myopathies: integrated metabolic, oxidative, fibrotic, and mitochondrial interactions.

Recent advances in poultry production are shifting toward data driven systems that connect real time animal monitoring with underlying muscle biology, although most applications remain partially disconnected from mechanistic understanding of muscle metabolism and postmortem transformation (Brassó et al., 2025). Precision phenotyping platforms, including thermal imaging, computer vision, wearable biosensors, and artificial intelligence based behavioral analytics, now enable continuous measurement of locomotion, feeding activity, respiration, thermal profiles, and physiological variability that collectively reflect metabolic stability (Brassó et al., 2025) (Table 3). These indicators can indirectly capture early disruptions in energy metabolism, oxidative balance, mitochondrial performance, calcium regulation, and stress physiology that precede meat quality defects (Apalowo et al., 2024; Di Luca et al., 2024). For instance, heat stress associated behavioral and thermal deviations often align with accelerated glycolytic flux and increased risk of pale soft exudative conditions, whereas prolonged behavioral suppression and altered activity rhythms may reflect glycogen depletion linked to dark firm dry phenotypes (Aslam et al., 2021).

Table 3.

Mechanistic evaluation of precision intervention strategies targeting muscle metabolic stability, postmortem biochemical regulation, and meat quality optimization in broiler production systems.

Intervention strategy	Mechanistic target	Core biological mechanisms	Evidence strength	Technology readiness	Major advantages	Current limitations	Commercial applicability
Precision feeding systems	Nutrient synchronization and metabolic optimization	Dynamic adjustment of amino acid, energy, and antioxidant supply to stabilize muscle metabolism	High	High	Improved feed efficiency, reduced metabolic stress, enhanced consistency of meat quality	Requires automated infrastructure and real-time data integration	Commercially feasible in intensive systems
Precision antioxidant supplementation	Oxidative stress regulation	Enhancement of endogenous antioxidant defenses through vitamin E, selenium, polyphenols, and phytobiotics	High	High	Improved oxidative stability, shelf life, color retention, and WHC	Dose-dependent responses and ingredient variability	Widely applicable
Gut microbiota modulation	Gut-muscle axis regulation	Modulation of microbial metabolites, inflammatory signaling, and nutrient absorption	High	High	Reduced inflammation, improved oxidative balance, enhanced tenderness and WHC	Strain-specific variability and inconsistent field responses	Increasing industrial adoption
Precision amino acid nutrition	Mitochondrial efficiency and protein turnover	Optimization of arginine, methionine, lysine, and branched-chain amino acid metabolism	Moderate to high	High	Improved muscle growth efficiency and metabolic resilience	Interaction effects with genetics and environment	Commercially practical
Environmental control systems	Thermal stress and metabolic stability	Regulation of temperature, humidity, ventilation, and air quality to reduce physiological stress	High	High	Stabilized glycogen reserves and reduced PSE-like conditions	High energy and infrastructure costs	Widely used commercially
Precision thermal management	Heat stress mitigation	Dynamic environmental adaptation using automated cooling and ventilation systems	Moderate to high	Moderate	Reduced ROS generation and improved mitochondrial stability	Sensor calibration and operational complexity	Expanding commercial relevance
Controlled atmosphere stunning	Stress minimization during slaughter	Reduction of struggle and catecholamine release through hypoxia or hypercapnia	High	High	Improved carcass uniformity, WHC, and welfare outcomes	Equipment investment and gas management challenges	Commercially established
Precision slaughter optimization	Postmortem glycolytic regulation	Optimization of stunning voltage, chilling rate, and carcass handling	Moderate to high	High	Improved pH decline kinetics and tenderness	Parameter standardization remains inconsistent	Highly feasible industrially
Smart sensor monitoring	Real-time physiological stress detection	Continuous monitoring of activity, temperature, respiration, and welfare indicators	Moderate to high	Moderate	Early detection of stress and metabolic imbalance	Data interpretation complexity	Emerging commercial implementation
Hyperspectral imaging systems	Non-invasive meat quality prediction	Optical detection of biochemical and structural changes in muscle	Moderate	Moderate	Rapid carcass grading and quality prediction	Calibration variability among production systems	Pilot-scale industrial use
AI-assisted predictive modeling	Integrated quality prediction	Machine learning integration of environmental, metabolic, and omics datasets	Emerging	Moderate	Predictive identification of quality defects and optimization opportunities	Requires large, validated datasets	Rapidly developing
Multi-omics biomarker platforms	Precision phenotyping	Integration of genomics, proteomics, metabolomics, and microbiomics	Emerging	Low to moderate	Mechanistic understanding and early quality prediction	High analytical cost and computational complexity	Primarily research-stage
Genomic selection platforms	Genetic improvement of metabolic resilience	Selection for favorable QTLs, stress tolerance, and muscle quality traits	Moderate to high	Moderate	Long-term improvement in meat quality consistency	Complex polygenic interactions	Expanding rapidly
Mitochondrial-targeted nutritional strategies	Energetic stability and ROS control	Enhancement of mitochondrial respiration and antioxidant capacity	Emerging	Moderate	Reduced metabolic collapse and oxidative deterioration	Limited validation across commercial strains	Experimental but promising
Wearable biosensors	Dynamic welfare and stress assessment	Continuous physiological monitoring of broilers	Emerging	Low	Real-time precision management capability	Limited field-scale validation	Proof-of-concept stage
Digital twin systems	Integrated production simulation	Virtual modeling of growth, metabolism, and environmental interactions	Emerging	Low	Predictive systems-level optimization	High computational and data requirements	Early developmental stage
Early myopathy prediction systems	Prevention of woody breast and white striping	Detection of fibrosis-associated metabolic and inflammatory biomarkers	Emerging	Low to moderate	Enables preventive management strategies	Biomarker validation remains incomplete	Mostly experimental
Precision lighting programs	Circadian and muscle metabolic regulation	Modulation of photoperiod and wavelength to influence stress and muscle growth	Moderate	Moderate to high	Improved oxidative status and behavioral welfare	Variable genotype responses	Increasing commercial adoption
Precision enrichment systems	Stress reduction and muscle conditioning	Enhancement of activity and welfare through environmental enrichment	Moderate	Moderate	Reduced myopathy incidence and improved muscle structure	Standardization challenges	Expanding in welfare-oriented production
Integrated climate-resilient production systems	Multi-stressor adaptation	Simultaneous regulation of heat, ventilation, nutrition, and welfare stressors	Emerging but promising	Moderate	Improved sustainability and meat quality consistency under climate stress	Complex implementation and cost	Future-oriented commercial potential

Artificial intelligence and machine learning further extend this framework by integrating heterogeneous datasets from omics, sensors, and environmental systems to capture nonlinear relationships governing meat quality traits (Brassó et al., 2025). These models can predict tenderness, drip loss, oxidative stability, and myopathy risk prior to slaughter, while digital twin approaches simulate postmortem biochemical trajectories under varying management conditions (Dehau et al., 2022; Brassó et al., 2025). However, limited biological interpretability remains a key constraint, emphasizing the need to couple computational outputs with validated physiological mechanisms (Almeida et al., 2015). Dynamic biomarkers such as circulating metabolites, oxidative stress indicators, hormonal profiles, and muscle derived vesicles may enhance early detection of metabolic imbalance, enabling continuous regulation of muscle physiology across production stages for improved meat quality (Domínguez et al., 2019; Abd El-Samee et al., 2019).

Translational precision strategies

Translational strategies for optimizing meat quality require direct alignment with the integrated metabolic, oxidative, vascular, and structural processes that govern muscle to meat conversion (Naeem, 2026). Central to this framework is strengthening metabolic resilience through improved mitochondrial efficiency, balanced energy partitioning, regulated calcium homeostasis, and adaptive stress responses that collectively reduce susceptibility to metabolic failure during postmortem transition (Wu et al., 2025). Redox regulation strategies focus on maintaining oxidative equilibrium by limiting reactive oxygen species accumulation, protecting membrane and protein integrity, and suppressing inflammatory amplification pathways that accelerate muscle degeneration and quality loss (Domínguez et al., 2019). Precision nutrition approaches further refine metabolic control through targeted nutrient timing, optimized amino acid supply, antioxidant supplementation, and microbiome modulation to regulate glycolysis, lipid metabolism, muscle growth, and vascular function (Biswas et al., 2021; Alagawany et al., 2022). In parallel, smart environmental management integrates real time physiological and behavioral monitoring to minimize chronic stress, enhance thermal adaptation, and stabilize muscle homeostasis during critical growth phases (Costa et al., 2021; Apalowo et al., 2024). Early detection systems for myopathies combine imaging, circulating biomarkers, omics signatures, and machine learning models to identify metabolic instability before irreversible tissue damage occurs (Brassó et al., 2025; Bošković Cabrol et al., 2025). Collectively, these strategies converge into an integrated control framework where phenotyping, analytics, nutrition, environment, and molecular targeting function as interconnected regulatory layers to preserve muscle integrity and optimize meat quality under intensive production systems.

Postmortem biochemical cascades

The postmortem biochemical cascade determines whether skeletal muscle is converted into high quality meat or progresses toward structural and metabolic deterioration characterized by poor texture, excessive drip loss, discoloration, oxidative instability, and defects such as pale soft exudative or dark firm dry conditions (Ijaz et al., 2024) (Fig. 6; Table 4; Suppl. Table 24). Importantly, postmortem reactions are not inherently beneficial or harmful; rather, meat quality depends on the rate, coordination, and metabolic balance of these interconnected processes (Debut et al., 2003; Che et al., 2023). Optimal meat quality emerges when ATP depletion, glycolysis, pH decline, calcium release, proteolysis, oxidative activity, and structural remodelling proceed in a synchronized and physiologically regulated manner (Bowker and Zhuang, 2015; Coria et al., 2018). When these processes are properly aligned, muscles undergo controlled conversion with preservation of protein functionality, membrane integrity, and water distribution (Warner, 2017). In contrast, disruption in timing or intensity of any step produces biochemical imbalance, leading to protein denaturation, impaired water retention, structural collapse, and reduced sensory and functional quality (Huang and Ahn, 2018; Domínguez et al., 2019). Thus, meat quality should be interpreted as an emergent outcome of integrated postmortem metabolism rather than a consequence of isolated biochemical reactions (Bonnieu et al., 2023).

Fig. 6.

A unified mechanistic model of postmortem energy depletion, glycolytic flux, proteolysis, oxidative deterioration, and structural remodelling regulating development of meat quality in broiler chicken.

Table 4.

Integrated regulatory nodes governing muscle metabolic stability, postmortem biochemical transformation, and meat quality determination in broiler chickens.

Regulatory nodes	Primary upstream drivers	Core biological functions	Mechanistic pathways	Effects on muscle metabolic status	Postmortem biochemical consequences	Final meat quality outcomes	Major associated defects	Integrated mechanistic interpretations
Glycogen reserves	Genetics, nutrition, heat stress, transport stress, feed withdrawal	Primary substrate for anaerobic glycolysis	Regulation of ATP generation and lactate production	Determines energetic capacity and glycolytic potential	Controls rate and extent of postmortem pH decline	WHC, tenderness, color stability	PSE-like or DFD-like meat	Glycogen availability determines the entire postmortem metabolic trajectory
Mitochondrial function	Muscle fiber type, oxidative stress, rapid growth, hypoxia	ATP production and ROS regulation	Oxidative phosphorylation and energetic homeostasis	Maintains metabolic flexibility and oxygen utilization	Influences oxidative stability and ATP depletion rate	Shelf life, tenderness, oxidative stability	Woody breast and oxidative deterioration	Mitochondria represent the central energetic hub linking pre-slaughter stress with postmortem quality
Oxidative balance	ROS generation, antioxidants, inflammation, thermal stress	Cellular redox regulation	Antioxidant defense and oxidative signaling	Determines membrane stability and metabolic resilience	Controls lipid and protein oxidation intensity	Color stability, shelf life, tenderness	Rancidity and discoloration	Redox imbalance accelerates structural and biochemical deterioration
Reactive oxygen species accumulation	Heat stress, mitochondrial overload, inflammatory activation	Oxidative signaling and molecular damage	Lipid peroxidation and protein oxidation	Induces mitochondrial dysfunction and membrane instability	Accelerates oxidation and protein denaturation	Reduced WHC and oxidative stability	PSE-like conditions and myopathies	Excess ROS drive metabolic collapse and structural degeneration
Calcium homeostasis	ATP depletion, membrane damage, stress-induced ion imbalance	Muscle contraction and protease activation	Sarcoplasmic reticulum calcium release and leakage	Alters contraction intensity and energetic demand	Activates calpain-mediated proteolysis	Tenderness and rigor development	Toughness and structural instability	Calcium dysregulation coordinates rigor mortis and proteolytic remodelling
Calpain proteolytic system	Calcium availability, pH decline, oxidative stress	Postmortem protein degradation	Cytoskeletal and myofibrillar proteolysis	Influences structural protein integrity	Determines tenderization efficiency during aging	Tenderness and texture quality	Excessive toughness or over-softening	Calpain activity is the principal driver of postmortem tenderization
Muscle fiber phenotype	Genetics, activity level, growth selection	Metabolic specialization of muscle tissue	Oxidative versus glycolytic metabolic programming	Determines oxygen demand and glycolytic capacity	Influences pH decline kinetics and oxidation susceptibility	Texture, color, and WHC	Growth-quality trade-offs	Fiber composition explains variability in metabolic resilience and quality outcomes
ATP depletion dynamics	Stunning systems, glycogen reserves, temperature	Energy transfer and rigor progression	ATP hydrolysis and rigor onset	Determines timing of rigor mortis	Regulates contraction intensity and sarcomere shortening	Texture and tenderness	Cold shortening and rigor defects	ATP depletion links energy metabolism with structural transformation
Glycolytic rate	Glycogen concentration, stress hormones, muscle type	Anaerobic ATP generation	Conversion of glycogen to lactate	Determines metabolic intensity after slaughter	Controls acidification kinetics	WHC and drip loss	PSE-like conditions	Excessively rapid glycolysis destabilizes protein structure
pH decline kinetics	Glycolysis, chilling rate, carcass temperature	Acid-base regulation during rigor development	Lactic acid accumulation and protein denaturation	Alters protein solubility and membrane stability	Influences rigor progression and enzyme activity	WHC, tenderness, and color	Pale color and exudative meat	The interaction between pH and temperature critically determines meat quality
Protein denaturation	Rapid pH decline, elevated muscle temperature	Structural destabilization of proteins	Loss of protein-water interactions	Reduces water-binding capacity	Impairs membrane and myofibrillar integrity	Reduced WHC and texture quality	PSE-like meat	Denaturation is a major mechanism underlying drip loss
Lipid oxidation	PUFA abundance, ROS accumulation, antioxidant depletion	Membrane deterioration and flavor instability	Peroxidation of phospholipids	Alters membrane fluidity and mitochondrial integrity	Generates aldehydes and oxidative metabolites	Reduced shelf life and flavor quality	Rancidity and discoloration	Lipid oxidation connects oxidative stress with sensory deterioration
Protein oxidation	ROS accumulation and inflammatory signaling	Structural and enzymatic damage	Oxidative modification of amino acid residues	Impairs enzymatic and structural protein functions	Reduces proteolytic susceptibility	Toughness and reduced tenderness	Structural rigidity	Protein oxidation interferes with normal postmortem tenderization
Membrane integrity	Antioxidant capacity, oxidative stress, phospholipid stability	Cellular compartmentalization	Regulation of ion transport and water retention	Preserves mitochondrial and cellular stability	Influences calcium leakage and drip formation	WHC and oxidative stability	Excessive drip loss	Membrane disruption accelerates postmortem deterioration
Sarcomere shortening	ATP depletion, chilling rate, calcium release	Muscle contraction regulation	Actomyosin cross-bridge formation	Determines structural tension in muscle fibers	Influences rigor shortening and tenderness	Texture and tenderness	Cold shortening and toughness	Sarcomere length directly affects perceived tenderness
Myoglobin chemistry	Oxidative status, oxygen availability, pH	Meat color regulation	Oxymyoglobin and metmyoglobin conversion	Influences oxygen-binding stability	Alters color development during storage	Consumer color acceptability	Discoloration	Myoglobin oxidation determines visual quality perception
Inflammatory signaling	Heat stress, gut dysbiosis, hypoxia	Immune activation and fibrosis	Cytokine-mediated oxidative and structural damage	Promotes metabolic instability and tissue degeneration	Accelerates fibrosis and oxidative deterioration	Reduced tenderness and structural quality	Woody breast and white striping	Chronic inflammation links stress physiology with myopathy development
Extracellular matrix remodelling	Fibrosis, chronic oxidative stress, inflammatory activation	Connective tissue restructuring	Collagen deposition and fibrosis progression	Reduces muscular flexibility and oxygen diffusion	Impairs proteolysis and structural remodelling	Increased hardness and rigidity	Woody breast	Fibrotic remodelling alters both metabolism and texture
Heat shock proteins	Thermal stress, oxidative stress	Cellular protection and protein folding	Stabilization of damaged proteins and mitochondria	Enhances stress adaptation and metabolic resilience	Reduces denaturation and oxidative damage	Improved oxidative stability	Inadequate response increases stress susceptibility	Heat shock proteins function as adaptive protective regulators
Gut-muscle axis signaling	Microbiota composition, dietary modulation	Immune and metabolic communication	SCFA production and inflammatory regulation	Improves energetic stability and redox balance	Stabilizes glycolysis and oxidative processes	Improved WHC and tenderness	Dysbiosis-associated quality deterioration	Gut-derived metabolites regulate systemic muscle metabolism
Hormonal stress responses	Corticosterone, catecholamines, transport stress	Energy mobilization and stress adaptation	Glycogen mobilization and oxidative activation	Promotes metabolic exhaustion and ROS accumulation	Alters glycolytic trajectory	Reduced carcass quality consistency	Stress-related quality defects	Neuroendocrine stress responses shape pre-slaughter metabolic state
Vascularization capacity	Growth rate, muscle hypertrophy	Oxygen and nutrient delivery	Capillary density regulation	Determines oxygen availability and waste removal	Influences oxidative metabolism and hypoxia risk	Texture and myopathy incidence	Woody breast and hypoxic degeneration	Insufficient vascularization creates metabolic overload conditions
Mitochondrial ROS leakage	Rapid growth, hypoxia, oxidative imbalance	Oxidative injury propagation	Electron transport chain instability	Amplifies oxidative stress and energetic dysfunction	Accelerates oxidation and structural deterioration	Reduced shelf life and tenderness	Severe oxidative collapse	Mitochondrial dysfunction is a central driver of metabolic degeneration
Integrated metabolic resilience	Genetics, nutrition, environment, management	Systems-level adaptive capacity	Coordination of energetic, oxidative, and inflammatory pathways	Maintains metabolic stability under stress	Stabilizes postmortem biochemical transformation	Consistent high-quality meat production	Reduced incidence of metabolic defects	Meat quality ultimately reflects the integrated resilience of the muscle metabolic system

ATP depletion and glycolysis initiate the conversion of muscle into meat by shifting energy metabolism from aerobic respiration to anaerobic pathways immediately after slaughter. ATP is essential for maintaining membrane integrity, ion transport, and structural stability in living muscle, and its gradual decline enables orderly rigor mortis development (Debut et al., 2003; Warner, 2017). Simultaneously, glycogen is converted into lactate through anaerobic glycolysis, generating the acidification required for postmortem maturation (Bowker and Zhuang, 2015; Coria et al., 2018). When these processes occur at moderate rates, they support controlled pH decline while preserving protein structure, resulting in desirable tenderness and water holding capacity (Abdullah et al., 2025). However, excessively rapid glycolysis leads to accelerated lactate accumulation at high carcass temperature, causing protein denaturation, membrane damage, pale coloration, and high drip loss typical of pale soft exudative meat (Huang and Ahn, 2018). In contrast, insufficient glycolytic activity due to glycogen depletion prevents adequate acidification, resulting in high ultimate pH, dark coloration, firm texture, and reduced shelf stability associated with dark firm dry conditions (Dadgar et al., 2010; Aslam et al., 2021). Therefore, balanced glycolytic progression is essential for maintaining equilibrium between energy depletion and structural preservation during early postmortem transformation (Dashdorj et al., 2015; Bonnieu et al., 2023).

The kinetics of pH decline, calcium regulation, proteolysis, oxidative balance, and structural remodelling collectively govern the quality outcome of postmortem muscle. pH directly regulates enzyme activity, protein solubility, and water binding, where gradual decline preserves structural integrity and improves tenderness, while rapid acidification at high temperature causes protein denaturation and fluid loss (Debut et al., 2003; Alnahhas et al., 2017). Calcium accumulation following ATP depletion drives rigor mortis and activates calpain systems, but excessive calcium induces strong contraction, reduced water holding capacity, and tougher texture (Ismail and Joo, 2017). Proteolysis mediated by calpains is essential for tenderization through degradation of structural proteins, yet its efficiency depends on pH, calcium balance, and oxidative conditions (Coria et al., 2018; Bonnieu et al., 2023). Oxidative stress promotes lipid and protein oxidation, impairing membrane stability, color retention, and enzyme activity, while also accelerating flavor deterioration (Amaral et al., 2018; Domínguez et al., 2019; Abd El-Samee et al., 2019). Structural remodelling and water redistribution ultimately determine juiciness and texture through interactions among myofibrillar shrinkage, cytoskeletal degradation, and extracellular matrix changes (El-Senousey et al., 2013; Soglia et al., 2020). When these processes are coordinated, meat exhibits improved tenderness, color stability, and shelf life; when dysregulated, they collectively drive protein denaturation, water loss, and quality defects (Aslam et al., 2021).

Resolution of trade-offs

Intensive genetic selection for accelerated growth rate and high breast muscle yield has substantially improved production efficiency; however, these gains are often accompanied by metabolic and structural instability within skeletal muscle (Yimiletey et al., 2026). Rapid hypertrophic growth shifts muscle toward glycolytic fiber predominance characterized by high glycogen turnover, lower mitochondrial density, reduced capillarization, and diminished oxidative capacity (Berri et al., 2007; Alnahhas et al., 2017). As muscle accretion outpaces vascular and metabolic adaptation, intracellular hypoxia, oxidative stress, and calcium dysregulation become increasingly pronounced (Table 5). These disturbances impair mitochondrial efficiency and promote fibrosis, inflammatory infiltration, and myo-degeneration (Di Luca et al., 2024), thereby predisposing broilers to woody breast, white striping, and PSE conditions despite superior carcass yield (Bordignon et al., 2022). Thus, the apparent contradiction between productivity and quality reflects a biological imbalance in resource allocation, where metabolic resilience and structural integrity are sacrificed to maximize protein accretion and growth efficiency.

Table 5.

Systems-level synthesis of convergent mechanisms, mechanistic trade-offs, and integrated regulatory pathways governing broiler meat quality from pre-slaughter metabolic programming to postmortem biochemical transformation.

Major biological domains	Consistent cross-study patterns	Central mechanistic interpretations	Major regulatory nodes	Context-dependent trade-offs	Postmortem consequences	Final meat quality outcomes
Genetic selection and growth intensification	Rapid-growth genotypes consistently exhibit higher breast yield but increased susceptibility to myopathies and quality instability	Accelerated hypertrophic growth increases anabolic demand beyond vascular and mitochondrial adaptive capacity	Muscle hypertrophy, oxygen diffusion, mitochondrial efficiency, vascularization	Enhanced production efficiency versus metabolic resilience	Accelerated glycolysis, oxidative stress, impaired proteolysis	Woody breast, white striping, reduced WHC, texture defects
Muscle fiber metabolic phenotype	Oxidative fibers improve oxidative stability and tenderness, whereas glycolytic fibers improve growth efficiency and carcass yield	Fiber-type specialization determines oxygen utilization, glycogen metabolism, mitochondrial density, and stress resilience	Fiber plasticity, mitochondrial density, glycogen dynamics	Oxidative stability versus production efficiency	Variable pH decline and proteolytic activity	Differences in tenderness, color stability, oxidative stability
Glycogen reserve dynamics	Both excessive and depleted glycogen reserves impair quality through different mechanisms	Glycogen availability determines glycolytic intensity and postmortem acidification kinetics	Glycogen turnover, glycolysis, ATP availability	Energy reserve sufficiency versus excessive glycolytic acceleration	Rapid or insufficient pH decline	PSE-like or DFD-like meat conditions
Mitochondrial metabolic capacity	Mitochondrial dysfunction consistently associates with oxidative damage and myopathies	Impaired oxidative phosphorylation promotes reactive oxygen species accumulation and energetic collapse	Mitochondrial respiration, ATP synthesis, oxidative phosphorylation	Rapid growth demand versus energetic stability	Membrane destabilization and oxidative deterioration	Reduced shelf life, discoloration, impaired WHC
Oxidative stress and redox imbalance	Excessive reactive oxygen species consistently correlate with poor meat quality and fibrosis	Oxidative imbalance destabilizes proteins, lipids, mitochondria, and calcium regulation	ROS threshold, antioxidant defense, lipid peroxidation	Adaptive oxidative signaling versus oxidative collapse	Protein oxidation, membrane damage	Reduced tenderness, discoloration, oxidative rancidity
Calcium regulation and proteolysis	Dysregulated calcium homeostasis alters rigor mortis progression and tenderness development	Calcium leakage activates calpain-mediated proteolysis and cytoskeletal degradation	Calcium channels, calpain system, sarcoplasmic reticulum	Controlled proteolysis versus excessive structural damage	Altered sarcomere shortening and protein degradation	Variability in tenderness and texture
Nutritional antioxidant interventions	Vitamin E, selenium, and polyphenols consistently improve oxidative stability under stress conditions	Antioxidant interventions preserve membrane integrity and mitochondrial stability	Nrf2 signaling, GPx, SOD, catalase	Protective antioxidant effects depend on stress intensity and dosage	Reduced oxidative deterioration	Improved shelf life, color stability, WHC
Gut-muscle axis modulation	Probiotics and synbiotics frequently improve metabolic resilience and oxidative stability	Gut microbiota regulates inflammatory signaling, nutrient utilization, and oxidative metabolism	Microbial metabolites, immune signaling, mitochondrial regulation	Microbiome responses vary with diet, genetics, and environment	Stabilized glycolysis and inflammatory status	Improved tenderness, oxidative stability, reduced drip loss
Amino acid and fatty acid modulation	Functional nutrients influence mitochondrial energetics and muscle metabolism	Nutritional substrates alter ATP generation, membrane composition, and oxidative metabolism	Energy metabolism, fatty acid oxidation, membrane fluidity	Growth promotion versus oxidative susceptibility	Altered glycolytic and oxidative trajectories	Variability in WHC, texture, oxidative stability
Environmental metabolic stress	Heat stress, transport stress, stocking density, and poor welfare consistently impair metabolic stability	Environmental stress accelerates glycogen depletion and oxidative imbalance	Corticosterone signaling, ROS generation, mitochondrial dysfunction	Adaptive stress responses versus metabolic exhaustion	Altered glycolysis and membrane stability	Increased PSE-like meat and quality deterioration
Inflammatory activation and fibrosis	Chronic metabolic stress consistently promotes fibrosis and extracellular matrix remodeling	Inflammatory signaling links oxidative stress with structural degeneration	Cytokines, collagen remodeling, inflammatory pathways	Repair adaptation versus pathological fibrosis	Reduced proteolytic efficiency	Woody breast and texture abnormalities
Postmortem glycolytic trajectory	Rate and extent of glycolysis strongly determine downstream quality outcomes	Pre-slaughter metabolic state governs postmortem biochemical cascade	Glycolytic enzymes, lactate accumulation, ATP depletion	Rapid acidification versus insufficient acidification	Protein denaturation or impaired rigor development	PSE-like or DFD-like phenotypes
Proteolytic remodelling	Balanced proteolysis improves tenderness whereas dysregulation impairs structure	Cytoskeletal degradation determines structural softening during aging	Calpain-calpastatin system, sarcomere integrity	Structural remodeling versus excessive degradation	Variable tenderization efficiency	Tenderness variability
Water redistribution and protein denaturation	Protein denaturation strongly influences water retention and texture	Oxidative and acidification-induced structural changes alter protein functionality	Myofibrillar proteins, membrane integrity, pH decline	Structural stability versus denaturation	Reduced water-binding capacity	Drip loss, reduced WHC
Multi-omics convergence	Genomic, proteomic, and metabolomic alterations consistently converge on energetic metabolism and oxidative pathways	Cross-omics regulation governs muscle metabolic phenotype and postmortem transformation	QTL, glycolytic enzymes, metabolites, signaling networks	Molecular adaptation versus metabolic instability	Altered biochemical trajectory	Predictive biomarkers for meat quality
Systems biology of myopathies	Woody breast and white striping consistently emerge under intensified metabolic load	Myopathies represent systems-level metabolic collapse syndromes	Hypoxia, mitochondrial dysfunction, fibrosis, inflammation	Production intensity versus physiological adaptability	Structural degeneration and impaired remodeling	Severe texture and processing defects
Precision management and predictive biology	Real-time monitoring improves early detection of metabolic instability	Precision technologies enable proactive metabolic regulation	Sensors, biomarkers, AI-assisted prediction	Commercial feasibility versus technological complexity	Improved intervention timing	Enhanced quality consistency and sustainability

A similar mechanistic paradox exists in muscle fiber biology. Oxidative fibers are generally associated with enhanced tenderness, WHC, oxidative stability, and flavor development because of their higher mitochondrial content, greater capillary density, improved lipid metabolism, and slower postmortem glycolytic rate (Cherian, 2011; El-Senousey et al., 2013). Nevertheless, excessive reliance on oxidative metabolism may limit maximal hypertrophic growth and feed conversion efficiency, as greater metabolic resources are directed toward aerobic maintenance, mitochondrial biogenesis, and vascular support rather than rapid muscle enlargement (Dransfield and Sosnicki, 1999; Berri et al., 2007). In contrast, glycolytic fibers support rapid growth and improved carcass yield through accelerated glycolysis and fast protein deposition, but simultaneously increase susceptibility to rapid pH decline, protein denaturation, oxidative instability, and myopathic lesions (Alnahhas et al., 2017; Che et al., 2023). Consequently, neither oxidative nor glycolytic phenotypes are universally advantageous, and optimal meat quality likely depends on achieving a balanced metabolic phenotype capable of supporting both productive efficiency and postmortem biochemical stability (Dashdorj et al., 2015).

Enrichment with omega-3 polyunsaturated fatty acids (PUFAs) improves lipid profile, enhances human health, and modulates inflammatory signaling pathways (Alagawany et al., 2022); however, increased lipid unsaturation simultaneously elevates susceptibility to reactive oxygen species-mediated lipid peroxidation. This may accelerate oxidative rancidity, pigment oxidation, membrane destabilization, and deterioration of flavor and shelf life (Amaral et al., 2018; Domínguez et al., 2019). The ultimate outcome therefore depends heavily on the oxidative buffering capacity of the muscle, including antioxidant enzyme systems, mitochondrial efficiency, vitamin E status, selenium availability, and storage conditions (Cheng et al., 2016; Elkhateeb et al., 2024). Under adequate antioxidant protection, omega-3 enrichment may improve both nutritional and sensory quality, whereas insufficient redox buffering shifts the system toward oxidative deterioration (El-Tarabany et al., 2021). Similar context-dependent effects are observed with phytogenics, probiotics, and functional feed additives, where beneficial effects on gut health, immune modulation, and oxidative stability vary according to dosage, environmental stress intensity, diet composition, and genotype-specific metabolic responsiveness (Attia et al., 2020; Biswas et al., 2021; Abdel Baset et al., 2022).

Environmental stressors further illustrate the dynamic nature of meat quality trade-offs. Acute heat stress often accelerates glycogenolysis, glycolytic rate, and protein denaturation, promoting rapid pH decline and PSE-like characteristics (Apalowo et al., 2024). In contrast, chronic heat stress may severely deplete glycogen reserves before slaughter, limiting postmortem lactate production and resulting in elevated ultimate pH and DFD-like conditions (Dadgar et al., 2010; Aslam et al., 2021). Similarly, moderate environmental enrichment and physical activity may enhance muscle development, oxidative metabolism, and structural integrity, whereas excessive activity or chronic stress exposure can increase energy expenditure and reduce growth performance (Costa et al., 2021; Delanglez et al., 2025). These observations demonstrate that meat quality outcomes are strongly dependent on stress duration, severity, timing, and adaptive physiological capacity rather than on the stressor itself alone.

Trade-offs are equally important in postmortem processing interventions. Electrical stunning, for instance, may improve animal welfare and reduce handling stress when appropriately optimized (Xu et al., 2011; Huang et al., 2014), but excessive voltage or prolonged exposure can induce muscle haemorrhage, accelerated ATP depletion, calcium overload, and severe protein denaturation (Joseph et al., 2013; Alam et al., 2024). Conversely, insufficient stunning intensity fails to suppress stress-induced catecholamine release and excessive muscular activity, thereby exacerbating glycogen depletion and metabolic instability (Huang et al., 2014; Okon et al., 2026). Controlled atmosphere stunning systems may reduce physical struggle and improve carcass uniformity, yet transient hypercapnic stress responses during induction can temporarily elevate physiological stress markers (EFSA et al., 2017; Alam et al., 2024).

Collectively, these contradictions demonstrate that broiler meat quality is fundamentally governed by context-dependent metabolic regulation rather than simple unidirectional relationships. The balance among growth efficiency, oxidative resilience, mitochondrial capacity, glycogen dynamics, lipid metabolism, and proteolytic activity ultimately determines whether biological adaptations produce favorable quality outcomes or pathological deterioration. A systems-level mechanistic framework, therefore, provides a more accurate interpretation of apparently conflicting findings by recognizing muscle metabolic state at slaughter as the central integrative node through which genetic, nutritional, environmental, and management factors converge to regulate postmortem biochemical trajectories and final meat quality phenotypes.

Research gaps

Current progress in broiler meat quality research remains constrained by several critical conceptual and methodological limitations that prevent development of fully predictive and mechanistically integrated models. A major gap is the scarcity of longitudinal mechanistic studies capable of tracking dynamic transitions from live muscle physiology to postmortem biochemical conversion and ultimate meat quality outcomes across developmental, environmental, and processing stages. Existing research also suffers from inadequate integration across biological scales, where molecular findings are frequently disconnected from cellular architecture, tissue biomechanics, systemic physiology, and commercial phenotypes, thereby limiting causal interpretation. Furthermore, static endpoint measurements dominate the field despite the inherently dynamic nature of muscle metabolism, emphasizing the urgent need for real-time metabolic phenotyping approaches capable of capturing temporal fluctuations in mitochondrial activity, redox balance, vascular adaptation, and stress responsiveness. Translation into commercial production systems remains difficult because controlled experimental findings often fail to account for environmental variability, management heterogeneity, economic constraints, and scalability challenges encountered under intensive production conditions. In omics research, predictive associations frequently lack causal validation (Table 6), as many identified biomarkers remain correlative without functional confirmation of their mechanistic roles in muscle pathology or meat quality determination. Additionally, climate resilience and sustainability dimensions remain insufficiently integrated into meat quality frameworks despite increasing thermal stress, resource limitations, and environmental pressures influencing metabolic stability, animal welfare, production efficiency, and long-term sustainability of intensive poultry systems.

Table 6.

Mechanistic synthesis of cross-validated nutritional, nutrigenomic, proteomic, metabolomic, and gut-muscle axis strategies regulating metabolic resilience, postmortem biochemical stability, and broiler meat quality outcomes.

Functional intervention domains	Most consistent cross-validated strategies	Primary mechanistic targets	Dominant biological pathways affected	Convergent proteomic / metabolomic signatures	Contexts showing highest efficacy	Major limitations or contradictions	Overall mechanistic robustness for meat quality improvement
Antioxidant-supportive nutrition	Vitamin E + selenium co-supplementation	Oxidative stability and membrane protection	Nrf2 activation, GPx activity, lipid peroxide suppression, mitochondrial stabilization	Reduced malondialdehyde, preserved membrane proteins, reduced oxidative metabolites	Heat stress, fast-growing strains, prolonged storage conditions	Limited benefit under low oxidative challenge; excessive supplementation may reduce adaptive signaling	Very high
Polyphenol-rich phytogenics	Curcumin, oregano, rosemary, green tea polyphenols	Reactive oxygen species modulation and inflammatory attenuation	Antioxidant signaling, NF-κB suppression, mitochondrial protection	Reduced stress proteins, lower lipid oxidation markers, improved antioxidant enzyme abundance	Heat stress, transport stress, oxidative-prone genotypes	Bioavailability variability; inconsistent responses across doses and formulations	High
Gut-muscle axis modulation	Probiotics + synbiotics	Microbial metabolite-mediated metabolic stabilization	SCFA production, intestinal barrier integrity, immune modulation, mitochondrial regulation	Reduced inflammatory proteins, altered amino acid metabolism, improved energy metabolites	Early growth phase, environmental stress, dysbiosis-prone systems	Strain-specific effects; responses vary with diet composition and management	Very high
Organic acid supplementation	Butyrate, fumarate, citric acid	Energetic efficiency and gut integrity	Mitochondrial energy metabolism, intestinal pH regulation, nutrient absorption	Improved ATP-related metabolites, reduced inflammatory metabolites	High-density production systems and pathogen pressure	Responses weaker under optimal management conditions	Moderate to high
Functional amino acid nutrition	Methionine, arginine, glutamine	Redox balance and mitochondrial energetics	Glutathione synthesis, nitric oxide signaling, protein turnover, oxidative phosphorylation	Enhanced antioxidant enzyme abundance, altered amino acid flux, improved mitochondrial metabolites	Rapid growth phases and oxidative stress conditions	Excessive protein accretion may exacerbate metabolic load	High
Omega-3 and functional fatty acids	Omega-3 PUFA enrichment	Membrane fluidity and inflammatory regulation	Lipid metabolism, mitochondrial β-oxidation, inflammatory signaling	Altered phospholipid profiles, reduced inflammatory metabolites	Oxidative challenge and inflammatory conditions	Increased susceptibility to lipid oxidation if antioxidant support is insufficient	Moderate
Alternative protein sources	Insect meal, fermented proteins, algae-derived proteins	Nutrient sustainability and metabolic modulation	Amino acid metabolism, microbiota regulation, oxidative metabolism	Variable proteomic responses associated with energy metabolism	Sustainable production systems and feed-cost reduction strategies	Inconsistent digestibility and metabolomic responses across inclusion levels	Moderate
Nutrigenomic metabolic optimization	Antioxidant-cantered nutritional programming	Regulation of metabolic resilience genes	Oxidative defense genes, mitochondrial biogenesis, stress-response pathways	Coordinated antioxidant proteomic signatures and reduced oxidative metabolites	Heat stress and fast-growth systems	Strong genotype dependence	Very high
Nutrigenomic mitochondrial support strategies	Amino acid and energy-substrate optimization	Mitochondrial efficiency and ATP stability	Oxidative phosphorylation, glycolytic balance, mitochondrial adaptation	Improved ATP turnover metabolites and mitochondrial proteins	High-performance commercial broilers	Responses vary according to baseline metabolic status	High
Nutrigenomic gut-muscle regulation	Synbiotic-driven microbiome programming	Immune-metabolic coordination	Gut-derived metabolite signaling, inflammatory regulation, nutrient partitioning	SCFA-associated metabolic signatures and reduced inflammatory proteins	Stress-prone commercial systems	Strong microbiome dependency	Very high
Convergent proteomic hubs predictive of meat quality	Glycolytic enzymes, heat shock proteins, oxidative stress proteins, cytoskeletal proteins	Regulation of postmortem metabolic trajectory	Glycolysis, oxidative stress adaptation, cytoskeletal remodelling	Lactate accumulation, ATP degradation products, oxidative metabolites	Broadly consistent across multiple quality phenotypes	Temporal variability during postmortem aging	Very high
Convergent metabolomic indicators	Lactate, creatine, inosine monophosphate, oxidative metabolites	Energetic and oxidative status prediction	Energy metabolism, redox regulation, purine metabolism	Distinct metabolomic trajectories associated with WHC and tenderness	Early postmortem prediction models	High sensitivity to slaughter conditions	High
Most robust integrated intervention model	Antioxidant + probiotic/synbiotic + amino acid optimization	Simultaneous redox, mitochondrial, and inflammatory stabilization	Integrated metabolic resilience networks	Coordinated improvements in oxidative, energetic, and inflammatory biomarkers	High-intensity commercial systems under environmental challenge	Requires precision formulation and context-specific implementation	Highest overall evidence consistency

Conclusions

Pre-slaughter metabolic conditioning and post-slaughter biochemical transformation collectively constitute the fundamental biological continuum determining meat quality development. The physiological state of muscle prior to slaughter governs substrate availability, mitochondrial competence, vascular integrity, oxidative stability, and stress responsiveness, thereby shaping the metabolic susceptibility of tissue during postmortem transition. Following slaughter, a coordinated sequence of anaerobic glycolysis, ATP depletion, pH decline, rigor development, proteolysis, and oxidative modification progressively regulates muscle structural integrity, protein functionality, and water distribution. Meat quality therefore emerges from dynamic interactions between pre-existing metabolic status and postmortem biochemical kinetics rather than from isolated events occurring within either phase alone. Future progress will depend on integrative systems biology approaches capable of coupling pre-slaughter physiology with postmortem transformation within unified predictive frameworks. Precision multi-omics, real time phenotyping, and computational modeling are expected to accelerate this transition toward mechanistically informed and predictive meat quality biology.

CRediT authorship contribution statement

Md. Emran Hossain: Writing – review & editing, Supervision, Resources, Methodology, Investigation, Conceptualization. Nusrat Binte Amin: Writing – original draft, Visualization, Investigation.

Disclosures

We declare that there are no financial, commercial, or personal relationships that could be perceived as potential conflicts of interest with respect to the content of this review. No external funding was received specifically for the preparation of this manuscript. All sources of support, affiliations, and contributions have been disclosed in the acknowledgments where applicable.