Ten years ago, the occurrence of macroscopic defects in breasts muscles from fast‐growing broilers challenged producers and animal scientists to label and characterize myopathies wholly unknown. The distinctive white striations in breasts affected by white striping disorder, the presence of out‐bulging and pale areas of hardened consistency in the so‐called wooden breast, and the separation of the fiber bundles in breasts labelled as spaghetti meat, made these myopathies easily identified in chicken carcasses. Yet, the high incidence of these myopathies and the increasing concern by producers and retailers led to an unprecedented flood of questions on the causes and consequences of these abnormal chicken breasts. This review comprehensively collects the most relevant information from studies aimed to understand the pathological mechanisms of these myopathies, their physicochemical and histological characterization and their impact on meat quality and consumer's preferences. Today, it is known that the occurrence is linked to fast‐growth rates of the birds and their large breast muscles. The muscle hypertrophy along with an unbalanced growth of supportive connective tissue leads to a compromised blood supply and hypoxia. The occurrence of oxidative stress and mitochondrial dysfunction leads to lipidosis, fibrosis, and overall myodegeneration. Along with the altered appearance, breast muscles affected by the myopathies display poor technological properties, impaired texture properties, and reduced nutritional value. As consumer's awareness on the occurrence of these abnormalities and the concerns on animal welfare arise, efforts are made to inhibit the onset of the myopathies or alleviate the severity of the symptoms. The lack of fully effective dietary strategies leads scientists to propose whether “slow” production systems may alternatively provide with poultry meat free of these myopathies.

The objective of this work was to investigate the occurrence of pale, soft, exudative meat (PSE) in chicken by submitting birds to physical stress. Dietary supplementation of vitamin E was undertaken to overcome this syndrome. Postmortem muscle biochemical events and their consequence on meat properties were evaluated in samples with and without supplemented vitamin E. Our studies showed chickens were susceptible to heat stress which promoted changes in the glycolytic parameters causing the development of chicken PSE. Dietary vitamin E was capable of inhibiting the development of the syndrome hence improving meat functional properties.

a b s t r a c tThe biological cause of broiler PSE meat seems to be an excessive release of Ca 2+ , promoted by a genetic mutation of ryanodine receptors located in the sarcoplasmic reticulum of skeletal muscle cells. Excessive Ca 2+ , associated with protein denaturation in meat, enhances protease activity and influences the functional properties of PSE meat. Twenty-four-hour post-mortem Pectoralis major m. samples exhibited lower values for pH, water-holding capacity, and shear force than did control samples, in contrast to colour (L * ) and cooking loss values. Protease activity, measured as myofibril fragmentation index, presented higher values in PSE meat than in control samples. Ultrastructural examination revealed shrinking and depolymerisation of myofilaments and Z-lines disorganisation within the sarcomere in PSE meat. Intense calpain activity was also observed, indicating that the process may initiate at the filaments, because of protein denaturation, and spread through Z-lines, resulting in the collapse of the sarcomere structure.

The connections between the redox imbalance in post-mortem muscle, early protein oxidation and the onset of pale, soft and exudative (PSE) condition in chicken breast are studied. PSE was induced by incubation of post-mortem chicken carcasses at 37°C for 200min. PSE-induced muscle consistently had faster pH decline and lower pH at 200min (5.84 vs. 6.59) and 24h (5.69 vs. 5.96), higher L(∗) (54.4 vs. 57.3), and lower texture and water holding capacity (WHC) than normal meat. The activities of catalase, glutathione peroxidase and superoxide dismutase were significantly lower in PSE-induced samples than in the normal counterparts. PSE was more susceptible to proteolysis and protein oxidation than normal meat during succeeding chilled storage with more intense tryptophan and thiols depletion, higher protein carbonylation and more intense formation of protein cross-links. We provide plausible explanations to support the role of protein oxidation in the impaired quality PSE chicken.

The objective of this work was to investigate the influence of water spray treatment before broiler slaughtering on the quality of breast meat (Pectoralis major) and to observe ultrastructural changes promoted by the biochemical/physiological events during rigor mortis onset. Commercial Ross chickens were divided into two groups: Untreated Group (UG) (n = 608) and Treated Group (TG) (n = 611), without and with water shower treatment, respectively. Drip and cook losses, pH and color measured after 24 h postmortem demonstrated that antemortem water shower treatment inhibited PSE development in chicken breast meat. Histological studies of the PSE samples from UG birds after 72 h postmortem revealed under light microscopy a shrinking of muscle cell diameter by approximately 10% in relation to TG samples and an extracellular enlargement of endomysium and perimysium sheaths. By electron microscopy of PSE meat, Z‐lines appeared fragmented, A‐bands including the M‐line disappeared and a super‐contraction of sarcomeres was observed, indicating that proteins were adversely affected by heat stress.