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This study examined pathomorphological changes and meat quality alterations associated with Wooden Breast Myopathy (WB) in total of 192 broiler chickens divided into Ross 308 (n=96) and Cobb 500 (n=96) heavy hybrids at ages 42, 60, and 70 days. WB occurrence remained consistently high (>73%) across periods, peaking on day 70 (83% for Ross, 90% for Cobb). Cobb broilers had better production results and carcass traits parameters after day 42 and day 60 of the experiment (p≤0.05). Genotype did not affect WB occurrence or severity, while slaughter age influenced severe cases WB occurrence, increasing from 11.67% on day 42 to 36.67% on day 70 (p=0.003). The presence of WB was associated with higher ultimate pH, lightness (L*), redness (a*), and yellowness (b*) of the muscle (p

This study was conducted on chicken pectoralis major muscle with different wooden breast severity in combination with different sampling locations to investigate the effects of wooden breast syndrome on protein traits and total myofiber area, and their associations. Contents of sarcoplasmic, salt-soluble myofibrillar and salt-insoluble protein and proportion of total myofiber area significantly declined with increasing severity in the superficial part of muscle, whereas the amount of heat-soluble/insoluble collagen and protein denaturation as well as the area of degenerated myofibers, connective tissue and cellular infiltrates increased. Myofibril protein content indicators showed strong positive correlations to total myofiber area. Moreover, PCA results indicated that severe wooden breast is positively linked to muscle collagen content and to protein denaturation. Our results suggest that decrease in sarcoplasmic and myofibrillar proteins is associated with reduction of myofiber area. In turn, the muscle fibers are replaced by connective tissue, accompanied by excessive myofibrillar and sarcoplasmic protein denaturation. [ABSTRACT FROM AUTHOR]

Summary: A descriptive case report of the management of a miniature pony presenting to a UK equine veterinary hospital with marked trismus and increased masseter muscle size. Diagnosis of masseter myodegeneration (MM) was aided by the use of computed tomography and excisional biopsy. Hyperlipaemia was diagnosed as a sequelae of MM. Treatment included nonsteroidal anti‐inflammatories, parenteral nutrition and fluid therapy in addition to supportive care. The gelding was discharged from the hospital 30 days after admission, having made a full recovery. MM in the horse is a rare condition that appears to be physiologically distinct from canine masticatory muscle myositis which is primarily immune mediated. [ABSTRACT FROM AUTHOR]

Summary: Regional and systemic disorders of myopathic or neurogenic cause affecting the masticatory muscles have been reported or suspected in horses. The primary masticatory muscles include the masseter, temporalis, lateral and medial pterygoid muscles. The masseter muscle is the largest of the primary masticatory muscles and the most affected based on sporadic reports. This is a brief review of disorders involving the masseter muscle. [ABSTRACT FROM AUTHOR]

BACKGROUND: White striping (WS) is a myopathy of breast muscle (Pectoralis major) that affects the quality and consumer acceptance of breast fillets of broiler chickens. Previous studies have shown that intermittent dilution of dietary nutrients suppresses the development of WS on the breast muscle of broiler chickens. However, the mechanism by which these interventions reduce the occurrence of WS remains inconclusive. In this study, we adopted intermittent reduction of dietary digestible lysine (dLys) density or metabolizable energy (ME) and amino acid (AA) density using chemical and fatty acid composition of breast fillets, and blood metabolites to understand the mechanism while histopathology and immunohistochemistry of breast muscles were used for confirmation. RESULTS: Occurrence of WS was lower in broiler chickens fed 85% dLys diets in comparison with other groups. Crude protein and ether extract in breast meat of 85% dLys groups were greater (P < 0.001) and lower (P = 0.010), respectively. Serum concentrations of lipid metabolites and enzymes were lower in broiler chickens fed 85% dLys diets than control group (P < 0.05). Feeding 85% dLys diets had low degree of myodegeneration and necrosis, inflammation, lipid deposition, infiltration of T‐lymphocyte (CD3+) and macrophages (Iba‐1+), and low expression of heat‐shock protein 70 (HSP70) than other groups (P < 0.001). CONCLUSION: Dilution of dietary dLys to 85% of the required quantities reduces the development of WS in broiler chickens by slowing the growth, lipid synthesis, and muscle damage confirmed by lower extent of histopathological lesions. © 2022 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

This study was conducted on chicken pectoralis major muscle with different wooden breast severity in combination with different sampling locations to investigate the effects of wooden breast syndrome on protein traits and total myofiber area, and their associations. Contents of sarcoplasmic, salt-soluble myofibrillar and salt-insoluble protein and proportion of total myofiber area significantly declined with increasing severity in the superficial part of muscle, whereas the amount of heat-soluble/insoluble collagen and protein denaturation as well as the area of degenerated myofibers, connective tissue and cellular infiltrates increased. Myofibril protein content indicators showed strong positive correlations to total myofiber area. Moreover, PCA results indicated that severe wooden breast is positively linked to muscle collagen content and to protein denaturation. Our results suggest that decrease in sarcoplasmic and myofibrillar proteins is associated with reduction of myofiber area. In turn, the muscle fibers are replaced by connective tissue, accompanied by excessive myofibrillar and sarcoplasmic protein denaturation.

Polyphasic myodegeneration potentially causes severe physiological and metabolic disorders in the breast muscle of fast-growing broiler chickens. To date, the etiology of recent muscle myopathies, such as the white striping (WS) phenotype, is still unknown. White striping–affected breast meats compromise the water holding capacity and predispose muscle to poor vascular tone, leading to the deterioration of meat qualities. Herein, this review article provides insight on the complexities around chicken breast myopathies: (i) the etiologies of WS occurrence in chicken; (ii) the metabolic changes that occur in WS defect in pectoralis major; and (iii) the interactions between breast muscle physiology and vascular tone. It also addressed the effects of nutritional supplements on muscle myopathies on chicken breast meats. Moreover, the review explored breast muscle biology focusing on the early preparation of satellite and vascular cells in fast-growth chicken breeds. Transcriptomics and histological analyses revealed poor vascularity in breast muscle of fast growth chickens. Thus, we suggest in ovo feeding of nutrients promoting vascularization and satellite cells replenishment as a potential strategy to enhance endothelium-derived nitric oxide availability to promote vascularization in the pectoralis major muscle region.

Case history: Data were collected from 47 outbreaks of dropped hock syndrome (DHS) that were reported by veterinarians in New Zealand to the Ministry for Primary Industries between October 2012 and August 2017. There were 181 affected dairy cows from 44 farms. Of those with records, all 86 were aged between 2–3 years-old, and 4/94 (4%) were Friesian, 56/94 (60%) were Jersey and 33/94 (35%) were Jersey/Friesian cross. Of the 47 outbreaks, 45 (96%) occurred during winter and 37 (79%) in the South Island. Clinical findings: Of 151 cases with records, hindlimb weakness (117 cows), shortened gait (112 cows) and dropped hocks (106 cows) were most commonly reported, with 110 cases being bilaterally affected. The level of diagnostic work-up and the data recorded by veterinarians for each outbreak were highly variable. Creatine kinase and aspartate aminotransferase activities were reported for 22 cases and were within normal ranges for cows with mild disease but increased in cows with severe disease. Concentrations of Cu in serum and liver were below normal for 13/22 and 9/10 cows, respectively, from six outbreaks. Of 41 cows with records for clinical outcomes, 12 had complete resolution, 18 had partial resolution, and 11 had no resolution. Pathological findings: Post-mortem data were available from 26 cases. Muscle necrosis and haemorrhage of the origin of the gastrocnemius muscle were the key gross findings. In 14 cows with records for muscle histopathology, myodegeneration and recent haemorrhage were observed, and connective tissue pathology was reported to predate muscular pathology in seven cases. Diagnosis: DHS appeared to be a degenerative rather than inflammatory condition primarily affecting the connective tissue of the hind limb, especially at the dense collagen interfaces of the gastrocnemius. Although no evidence of neuropathy was found, this cannot definitively be ruled out as a potential cause. Clinical relevance: A more standardised and systematic approach to investigating cases and recording case data is required to make robust inferences about the aetiology, risk factors, and treatment interventions for DHS. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the effects of aging on the quality of breast meat from broilers affected of wooden breast. Samples that were classified as normal (control), moderate (hardness verified only in one region of breast fillet), and severe (hardness verified in all the extension of breast fillet) were evaluated fresh and after three and seven days of aging. Normal samples and samples with a moderate degree of myopathy showed greater water-holding capacity, which may benefit the processing industry of poultry meat. During the aging process, increase was observed in total collagen concentration (from 0.41% in normal samples to 0.56% in samples with severe degree). Samples of chicken breast affected by moderate degree showed higher myofibril fragmentation index (MFI = 115) than normal chicken samples (95.65). Although chicken samples affected with severe degree of wooden breast myopathy are more tender than normal chicken breasts, they produce more exudate, which can be detrimental to the processing of poultry meat. The aging process may improve the reduction of cooking weight loss and protein loss in exudation of broilers’ breasts affected by wooden breast myopathy.

The purposes of the study were to investigate the effects of Wooden Breast (WB) myodegeneration on poultry meat quality and to give a contribution in typing lesions morphology. At a poultry meat cutting facility, 474 carcasses of a high-breast-yield hybrid chickens were inspected for WB condition, and 30 normal (N) and 30 affected (WB) breast fillets (Pectoralis major) were randomly selected. The WB condition represented 53.2% of the examined carcasses. Weight, cross sectional area (CSA), pH, L*, a*, b* colour values, water-holding capacity, and Warner-Bratzler shear force were determined. Samples were also visually and histologically evaluated. Affected samples were heavier, thicker, paler (P < 0.001), and characterized by palpatory hardness and lower water holding capacity (P < 0.05). Macroscopically, abnormalities were primarily localized in the cranial portion of the fillet and defined by the presence of bulges, petechiae, fluid and clear exudate, and higher pH. Microscopically, the WB condition was characterized by muscle fibres with greater CSA (P < 0.001) and higher giant fibres prevalence (P < 0.01). Data suggest a relationship between breast weight and WB condition.

This study aimed to characterize the effects of wooden breast myopathy (WBM) on quality of broiler chicken breast meat. Normal samples (absence of myopathy), moderate-degree samples (hardness only in one area of the breast fillet) and severe-degree samples (hardness throughout the breast fillet) were classified. In macroscopic analysis, the pectoral muscle affected by the WBM showed, in general, pale color with stiff, irregular and reddish regions (suffusions and petechiae), with the presence of white striations. In microscopic analysis, the myopathy was characterized by loss of the polygonal aspect of the muscle fibers. Samples with moderate degree of the myopathy showed greater (p = 0.0266) water retention capacity. There was an increase (p = 0.004) in total collagen concentration in samples from the severe-degree group 0.29% in normal samples to 0.43% and 0.48% in samples from moderate- and severe-degree groups, respectively. Samples of chicken breast affected by the severe-degree WBM showed lower (p < 0.0001) myofibrillar fragmentation index (64.51) and lower (p = 0.0002) fat concentration (2.17%) than normal chicken samples (80.45 and 3.79%, respectively). Samples affected by WBM are larger and heavier and present poorer physical quality when compared to normal chicken meat. Histologically it is possible to observe loss of the polygonal aspect of muscle fibers.

Skeletal muscle utilizes both free fatty acids (FFAs) and glucose that circulate in the blood stream. When blood glucose levels acutely increase, insulin stimulates muscle glucose uptake, oxidation, and glycogen synthesis. Under these conditions, skeletal muscle preferentially oxidizes glucose while the oxidation of fatty acids (FAs) oxidation is reciprocally decreased. In metabolic disorders associated with insulin resistance, such as diabetes and obesity, both glucose uptake, and utilization muscle are significantly reduced causing FA oxidation to provide the majority of ATP for metabolic processes and contraction. Although the causes of this metabolic inflexibility or disrupted “glucose-fatty acid cycle” are largely unknown, a diet high in fat and sugar (HFS) may be a contributing factor. This metabolic inflexibility observed in models of obesity or with HFS feeding is detrimental because high rates of FA oxidation in skeletal muscle can lead to the buildup of toxic metabolites of fat metabolism and the accumulation of pro-inflammatory cytokines, which further exacerbate the insulin resistance. Further, HFS leads to skeletal muscle atrophy with a decrease in myofibrillar proteins and phenotypically characterized by loss of muscle mass and strength. Overactivation of ubiquitin proteasome pathway, oxidative stress, myonuclear apoptosis, and mitochondrial dysfunction are some of the mechanisms involved in muscle atrophy induced by obesity or in mice fed with HFS. In this review, we will discuss how HFS diet negatively impacts the various physiological and metabolic mechanisms in skeletal muscle.

Skeletal muscle utilizes both free fatty acids (FFAs) and glucose that circulate in the blood stream. When blood glucose levels acutely increase, insulin stimulates muscle glucose uptake, oxidation, and glycogen synthesis. Under these conditions, skeletal muscle preferentially oxidizes glucose while the oxidation of fatty acids (FAs) oxidation is reciprocally decreased. In metabolic disorders associated with insulin resistance, such as diabetes and obesity, both glucose uptake, and utilization muscle are significantly reduced causing FA oxidation to provide the majority of ATP for metabolic processes and contraction. Although the causes of this metabolic inflexibility or disrupted "glucose-fatty acid cycle" are largely unknown, a diet high in fat and sugar (HFS) may be a contributing factor. This metabolic inflexibility observed in models of obesity or with HFS feeding is detrimental because high rates of FA oxidation in skeletal muscle can lead to the buildup of toxic metabolites of fat metabolism and the accumulation of pro-inflammatory cytokines, which further exacerbate the insulin resistance. Further, HFS leads to skeletal muscle atrophy with a decrease in myofibrillar proteins and phenotypically characterized by loss of muscle mass and strength. Overactivation of ubiquitin proteasome pathway, oxidative stress, myonuclear apoptosis, and mitochondrial dysfunction are some of the mechanisms involved in muscle atrophy induced by obesity or in mice fed with HFS. In this review, we will discuss how HFS diet negatively impacts the various physiological and metabolic mechanisms in skeletal muscle. [ABSTRACT FROM AUTHOR]

Background: Improvements in poultry production within the past 50 years have led to increased muscle yield and growth rate, which may be contributing to an increased rate and development of new muscle disorders in chickens. Previously reported muscle disorders and conditions are generally associated with poor meat quality traits and have a significant negative economic impact on the poultry industry. Recently, a novel myopathy phenotype has emerged which is characterized by palpably "hard" or tough breast muscle. The objective of this study is to identify the underlying biological mechanisms that contribute to this emerging muscle disorder colloquially referred to as "Wooden Breast", through the use of RNA-sequencing technology. Methods: We constructed cDNA libraries from five affected and six unaffected breast muscle samples from a line of commercial broiler chickens. After paired-end sequencing of samples using the Illumina Hiseq platform, we used Tophat to align the resulting sequence reads to the chicken reference genome and then used Cufflinks to find significant changes in gene transcript expression between each group. By comparing our gene list to previously published histology findings on this disorder and using Ingenuity Pathways Analysis (IPA®), we aim to develop a characteristic gene expression profile for this novel disorder through analyzing genes, gene families, and predicted biological pathways. Results: Over 1500 genes were differentially expressed between affected and unaffected birds. There was an average of approximately 98 million reads per sample, across all samples. Results from the IPA analysis suggested "Diseases and Disorders" such as connective tissue disorders, "Molecular and Cellular Functions" such as cellular assembly and organization, cellular function and maintenance, and cellular movement, "Physiological System Development and Function" such as tissue development, and embryonic development, and "Top Canonical Pathways" such as, coagulation system, axonal guidance signaling, and acute phase response signaling, are associated with the Wooden Breast disease. Conclusions: There is convincing evidence by RNA-seq analysis to support localized hypoxia, oxidative stress, increased intracellular calcium, as well as the possible presence of muscle fiber-type switching, as key features of Wooden Breast Disease, which are supported by reported microscopic lesions of the disease. [ABSTRACT FROM AUTHOR]

The article discusses a study that examines capillary and myofiber density in the pectoralis major muscles of rapidly growing, high-yield broiler chickens during increased heat stress. Myofiber hypertrophy can increase after hatch by assimilation of satellite cell nuclei into myofibers, while myofiber formation is complete at hatching. Data shows that myofiber diameter increased with age while the absolute numbers of capillaries, blood vessels, and myofibers decreased.

A myopathy affecting the pectoralis major muscle of the commercial broiler has emerged creating remarkable economic losses as well as a potential welfare problem of the birds. We here describe the macroscopic and histologic lesions of this myopathy within 10 pectoralis major muscles of 5- to 6-week-old broilers in Finland. Following macroscopic evaluation and palpation of the muscles, a tissue sample of each was fixed in formalin, processed for histology, and histologically evaluated. The muscles that were macroscopically hard, outbulging, pale, and often accompanied with white striping histologically exhibited moderate to severe polyphasic myodegeneration with regeneration as well as a variable amount of interstitial connective tissue accumulation or fibrosis. All affected cases also exhibited perivenular lymphocyte accumulation. The etiology of this myodegenerative lesion remains yet open. Polyphasic myodegeneration is associated with several previously known etiologies, but palpatory hardness focusing on the pectoralis major, together with perivenular lymphocytes, has not been described in relation to them. The results of this study provide the pathological basis for further studies concerning the etiology of the currently described myopathy. [ABSTRACT FROM PUBLISHER]

Inclusion body myositis (IBM) is a slowly progressive muscle disease affecting ageing individuals. IBM presents with a distinctive pattern of weakness involving the quadriceps and finger flexor muscles, although other muscles including pharyngeal muscles become affected over time. Pathological hallmarks of IBM include autoimmune features, including endomysial infiltration by highly differentiated T cells, as well as degenerative features marked by intramyofibre protein aggregates organised into inclusion bodies. Despite some progress in understanding the cellular pathways involved in IBM, it remains untreatable, and the progression of the disease leads to progressive weakness, disability, wheelchair dependency and loss of independence. Therefore, there is an urgent need to improve our understanding of the underlying mechanisms and pathways involved in this disease to identify new treatment targets. Here, we discuss the current understanding of aetiopathogenesis, the interrelationship between autoimmunity and degeneration, and how ageing is a major influencer of both these features., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The article discusses the case of an adult veiled chameleon, Chameleo calyptratus, that has been suffering from decreased ability to open its mouth for a year. The chameleon is 4 years old and weighs 210 grams. The chameleon also presented inability to use tongue, weakness and circling. After histopathologic examination, the animal was found to have generalized, subacute to chronic skeletal myopathy which was suspected to have been caused by deficiency in vitamin E and selenium as seen in mammals.

Abstract: There is now compelling evidence that sporadic inclusion body myositis (sIBM) is a muscle-specific autoimmune disease in which both T and B-cells play a part and in which both cytotoxic muscle fibre necrosis and degeneration occur. However the factors responsible for breakdown of immune tolerance and the nature of the target antigens expressed by muscle fibres remain unknown. Genetic factors are known to contribute to susceptibility, in particular MHC haplotyes which may influence antigenic presentation, and could also operate through genetic variations in muscle fibre constituents or immune effector mechanisms. Viral infection may act as a trigger mechanism, as in cases of HIV-associated sIBM. Our understanding of the mechanisms leading to the degenerative changes in muscle fibres is still incomplete. Protein misfolding and proteasomal dysfunction rather than defective transcriptional control is likely to underlie the abnormal accumulation of multiple proteins in the muscle fibre inclusions. However, aberrant transcription is thought to be the basis for the accumulation of potentially toxic mutant protein forms (e.g. UBB+1). The origin of the multiple clonally expanded somatic mtDNA mutations in COX-negative segments of muscle fibres remains uncertain but may be linked to the effects of oxidative stress. It is proposed that the disproportionate involvement of certain muscles in sIBM may be due to the existence of muscle group-specific transcriptomes which are differentially affected by the disease process and that the male predominance of the disease may indicate the influence of genes preferentially expressed in males. There is a need to develop better animal models of sIBM in which the relationship between the inflammatory and degenerative components of the disease as well as the gender difference in susceptibility and differential vulnerability of different muscle groups can be more critically investigated. [Copyright &y& Elsevier]

Simple Summary: The study of meat quality of modern birds and their respective myopathies is important to understand the responses of myopathy to the meat quality of these birds. Aging enters as an alternative to avoid losses that this myopathy generates in the poultry industry, with discards of chickens affected by the different degrees of myopathy in wooden breast. The constant genetic evolution that birds have suffered and still suffer during these years is the most plausible cause of the onset of this myopathy. This study aimed to evaluate the effects of aging on the quality of breast meat from broilers affected of wooden breast. Samples that were classified as normal (control), moderate (hardness verified only in one region of breast fillet), and severe (hardness verified in all the extension of breast fillet) were evaluated fresh and after three and seven days of aging. Normal samples and samples with a moderate degree of myopathy showed greater water-holding capacity, which may benefit the processing industry of poultry meat. During the aging process, increase was observed in total collagen concentration (from 0.41% in normal samples to 0.56% in samples with severe degree). Samples of chicken breast affected by moderate degree showed higher myofibril fragmentation index (MFI = 115) than normal chicken samples (95.65). Although chicken samples affected with severe degree of wooden breast myopathy are more tender than normal chicken breasts, they produce more exudate, which can be detrimental to the processing of poultry meat. The aging process may improve the reduction of cooking weight loss and protein loss in exudation of broilers' breasts affected by wooden breast myopathy. [ABSTRACT FROM AUTHOR]

Simple Summary: Wooden breast myopathy is a muscle abnormality resulting from the genetic improvement practiced by the poultry industry and which is widespread throughout the planet. Recent research has tried to unravel this myopathy for years and how the quality of the meat is affected, in search of its etiology and the solution to this problem. Unfortunately, the problems related to the myopathies of the affected birds will only be solved when the cause of the abnormality is in fact unveiled and controlled; in the meantime, it is up to us researchers to contribute scientifically to research on this type of meat that is fit for consumption but that, for often presenting non-standard appearance for sale in the form of whole fillets, is discarded. This study aimed to characterize the effects of wooden breast myopathy (WBM) on quality of broiler chicken breast meat. Normal samples (absence of myopathy), moderate-degree samples (hardness only in one area of the breast fillet) and severe-degree samples (hardness throughout the breast fillet) were classified. In macroscopic analysis, the pectoral muscle affected by the WBM showed, in general, pale color with stiff, irregular and reddish regions (suffusions and petechiae), with the presence of white striations. In microscopic analysis, the myopathy was characterized by loss of the polygonal aspect of the muscle fibers. Samples with moderate degree of the myopathy showed greater (p = 0.0266) water retention capacity. There was an increase (p = 0.004) in total collagen concentration in samples from the severe-degree group 0.29% in normal samples to 0.43% and 0.48% in samples from moderate- and severe-degree groups, respectively. Samples of chicken breast affected by the severe-degree WBM showed lower (p < 0.0001) myofibrillar fragmentation index (64.51) and lower (p = 0.0002) fat concentration (2.17%) than normal chicken samples (80.45 and 3.79%, respectively). Samples affected by WBM are larger and heavier and present poorer physical quality when compared to normal chicken meat. Histologically it is possible to observe loss of the polygonal aspect of muscle fibers. [ABSTRACT FROM AUTHOR]

Polyphasic myodegeneration potentially causes severe physiological and metabolic disorders in the breast muscle of fast-growing broiler chickens. To date, the etiology of recent muscle myopathies, such as the white striping (WS) phenotype, is still unknown. White striping–affected breast meats compromise the water holding capacity and predispose muscle to poor vascular tone, leading to the deterioration of meat qualities. Herein, this review article provides insight on the complexities around chicken breast myopathies: (i) the etiologies of WS occurrence in chicken; (ii) the metabolic changes that occur in WS defect in pectoralis major; and (iii) the interactions between breast muscle physiology and vascular tone. It also addressed the effects of nutritional supplements on muscle myopathies on chicken breast meats. Moreover, the review explored breast muscle biology focusing on the early preparation of satellite and vascular cells in fast-growth chicken breeds. Transcriptomics and histological analyses revealed poor vascularity in breast muscle of fast growth chickens. Thus, we suggest in ovo feeding of nutrients promoting vascularization and satellite cells replenishment as a potential strategy to enhance endothelium-derived nitric oxide availability to promote vascularization in the pectoralis major muscle region. [ABSTRACT FROM AUTHOR]