Congenital myopathy in Japanese Black calves

Two Japanese Black bull calves from a dam showed muscular weakness and became recumbent after birth. At necropsy, skeletal muscles, including face, neck, body and proximal and distal forelimb and hindlimb were extremely pale in color and edematous. Histopathological examination of skeletal muscles revealed degenerative changes as follows: replacement of muscle with fat, variation in muscle fiber diameter, internal nuclei, central core-like structures, and vacuolar and hyaline degeneration of muscle fibers. Ultrastructurally, the lesions were characterized by focal myofibrillar disorganization with streaming or irregularity of Z bands. The present cases seem to be classified as congenital myopathy based on pathological alterations and age of onset.     

A familial degenerative neuromuscular disease of Gelbvieh cattle.

A degenerative skeletal muscle disease with vascular, neurologic, and renal lesions and a probable familial distribution was identified in 4-20-month-old purebred Gelbvieh cattle. Thirteen affected animals were confirmed from 6 separate beef herds, with a mortality rate of 100%. Clinical signs in affected animals consisted of ataxia, weakness, and terminal recumbency. Gross and histologic muscle lesions were indicative of nutritional myopathy of ruminants, with a lack of myocardial lesions in most cases and only rare myocardial changes in a few animals. Acute to chronic lesions in most large skeletal muscle groups consisted of degeneration, necrosis, regeneration, fibrosis, and atrophy. Fibrinoid necrosis of arterioles was a common feature in multiple tissues. Lesions in the spinal cord white matter and peripheral nerves consisted of degeneration of the dorsal columns and axons, respectively. Changes in the kidneys consisted of chronic interstitial nephritis with fibrosis, hyaline droplet change and tubular epithelial vacuolar change and were most severe in the older calves. Intracytoplasmic myoglobin and iron were demonstrated within the hyaline droplets in degenerate renal cortical tubular epithelial cells. Vitamin E levels were deficient in most (6/7) of the animals tested. Investigation of the pedigree of affected animals revealed a common ancestry for all but 1 of the animals whose parentage could be traced. This investigation suggests that a hereditary metabolic defect, possibly involving antioxidant metabolism, could be responsible for this condition. Renal disease, possibly secondary to myoglobinuria, may be unique to this bovine condition.     

The toxicity of Castanospermum australe seeds for cattle

Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.     

Variability in limb malformations and possible significance in the pathogenesis of an inherited congenital neuromuscular disease of Charolais cattle (syndrome of arthrogryposis and palatoschisis)

Limb abnormalities in 30 calves with an inherited congenital neuromuscular disorder known as syndrome of arthrogryposis and palatoschisis were classified according to the range of severity of joint deformity in either flexion or extension, and restricted joint movement. Joint movement was variably affected; it was either normal, lax, restricted in the range of mobility, or occasionally, fixed. The characteristic findings were: bilateral hyperextension of the hind fetlock, flexion deformity of the forelimb that particularly involved the fetlock and the carpus, with restricted articular movement and complete rigidity in some cases. One-third of calves also had medial deviation of the forelimb due to angular deformity of articular surfaces in the carpus. All nine live calves were floppy due to marked generalized muscular hypotonia. Birth weight of deformed calves was reduced. In some calves muscle development was impaired as judged by muscle weight, and histological examination. In some calves the gross appearance, muscle weight and histological examination revealed no abnormal development and indicated that the effects on skeletal muscle were secondary. No lesions were found in the spinal cord of 23 of 24 calves examined histologically. The remaining calf had a localized cavitation in the dorsal white matter at T2-3. Based on the observations in calves in this study it is proposed that both primary and secondary factors contribute to the phenotypic expression of this congenital deformity. The primary lesion is considered to be a neurogenic abnormality of differentiation in the central nervous system. Cytogenetic analysis of 16 carrier cows and two deformed calves showed normal karyotypes. Serology for Akabane virus in 16 carrier cows was negative.     

Androgen and estrogen receptors in bovine skeletal muscle: relation to steroid-induced allometric muscle growth

The presence of free androgen (AR) and estrogen receptors (ER) was demonstrated in bovine skeletal muscle. Androgen receptor concentrations in neck muscle from cattle of different sexes and stages of development were related to hormonal status. In mature bulls (mean weight 600 kg), no free AR was detectable. Highest AR concentrations were measured in mature bulls (517 kg) castrated 24 h prior to slaughter (.85 +/- .21 fmol/mg protein). In female calves (155 kg), AR concentrations (.56 +/- .14 fmol/mg) were greater (P less than .01) than in male calves (.20 +/- .08 fmol/mg) of the same weight. Androgen receptors and ER in skeletal muscle of neck, shoulder, abdomen and hind leg of female and male calves were compared. There was no significant difference between AR concentrations in the neck, shoulder and hind leg, but concentrations were lower (P less than .05) in abdominal muscle. Estrogen receptor concentrations in neck, shoulder, abdomen and hind leg were not different between sexes (P less than .05). In male calves, ER content was lower (P less than .05) in abdominal than in other muscles. Estrogen receptor concentrations in muscles of female calves did not differ (P less than .05). The pronounced sensitivity to estrogens and androgens in the neck, shoulder, and hind leg of calves, being free of the respective hormone, may partly explain the characteristic conformation in calves treated with estrogenic and androgenic steroids and the sexual dimorphism of muscle growth.     

The physical state and plasma biochemical profile of young calves on arrival at a slaughter plant

AIM: To determine the welfare of calves arriving at a slaughter plant by assessing their physical state and plasma biochemical profile. METHODS: Calves (n=7,169) aged 4-10 days, were examined immediately after they were unloaded from trucks (n=20) and categorised on physical grounds as being in an 'unacceptable', 'marginal' or 'acceptable' state. 'Unacceptable' calves were lying down, unable to walk, extremely weak or seriously injured. 'Marginal' calves had a wet umbilicus, were hollow sided, apparently immature, or weak and slow and unsteady on their feet. 'Acceptable' calves were strong, walked freely, round-sided, bright and alert and had a dry umbilicus. After unloading, 27 'unacceptable', 306 'marginal' and 289 'acceptable' calves were weighed, examined clinically and a blood sample was taken from each. A second blood sample was taken from 118 of these calves, 12-15 hours later. The packed cell volume (PCV) and plasma concentrations of glucose, beta-hydroxybutyrate (BHB), total plasma proteins (TPP), gamma-glutamyl transferase (GGT), urea, creatine kinase (CK) and lactate were measured. RESULTS: Only 27 of the 7,169 calves examined (0.4%) were categorised as being in an 'unacceptable' state on arrival and these were euthanased shortly after unloading. Generally, the plasma biochemical profiles of the 'acceptable' calves were similar to those of 'marginal' animals. However the glucose concentration of 'marginal' calves was lower than that of 'acceptable' calves, suggesting that they had lower energy reserves. After 12-15 h in lairage, plasma glucose concentration decreased and the BHB concentration increased in both 'acceptable' and 'marginal' calves compared with concentrations measured on arrival. CONCLUSIONS: The percentage of calves presented for slaughter in an 'unacceptable' state was small (0.4%). However, 4% of calves were classified as 'marginal' and failed to meet all the requirements of the code of recommendations and minimum standards governing the welfare of young calves in New Zealand. The categorisation of calves by a physical assessment was supported by results of plasma biochemistry. As a result, plasma biochemical profiles are considered unnecessary for making decisions regarding the welfare status of calves arriving at a slaughter plant; an assessment of their physical state is sufficient.     

Histopathological characterization of the skeletal myopathy in rasH2 mice carrying human prototype c-Ha-ras gene

A skeletal myopathy is found in approximately 100% of rasH2 mice. To confirm detailed features of the rasH2 skeletal myopathy, the biceps femoris, diaphragm, triceps brachii, gastrocnemial (types I and II fiber-mixed muscles) and soleus muscle (type I fiber-dominant muscle) obtained from male rasH2 and non-transgenic littermates aged 10-13 and 34 weeks were examined. Variations in the muscle fiber size, early-scattered degeneration/necrosis and regeneration of muscle fibers were detected in 10-13-week-old rasH2 mice. The severity of the above muscular lesions was more prominent in older rasH2 mice. These lesions were noted in the type II myofiber dominant muscles (biceps femoris, triceps brachii and gastrocnemial). NADH-TR stain clearly demonstrated a disorganized intermyofibrillar network and necrotic change in muscle fibers. No specific morphological changes, like rod structure or tubular aggregation seen in some types of myopathy, were noted in Gomori trichrome and NADH-TR stains in the rasH2 mouse like in many types of muscular dystrophy. Electronmicroscopically, occasional muscle fiber degeneration/regeneration, invaded phagocytic cells, indistinct Z-band suggesting excessive contraction and dilatation of the sarcoplasmic reticulum were observed. In summary, the skeletal myopathy occurring in rasH2 mice is consistent with muscular dystrophy characterized morphologically by progressive degeneration and regeneration of myofibers. The myopathy is confined to the type II myofiber predominant muscles and is not associated with any pathognomonic lesions. These characteristics will provide us with a useful model for research in muscular dystrophy of diverse myofibers.     

Masseter myodegeneration as a cause of trismus or dysphagia in adult horses

The medical records of eight horses with histological evidence of myodegeneration of the masseter muscles were examined. While they were alive their most common clinical signs had included difficulty in eating or opening their mouths, weight loss, difficulty in moving, and noticeable atrophy of the masseter muscles. The serum activities of muscle enzymes were abnormally high in all of the horses. Whole blood and/or liver selenium and vitamin E concentrations were less than the reference ranges in some of the horses. The lesions varied with the stage of the disease and consisted of swelling and discoloration, or muscle atrophy and fibrosis. Histologically, the muscle changes ranged from acute to subacute degeneration, with regenerative changes accompanying ongoing degeneration, to chronic degeneration with fibrotic replacement of muscle tissue. There were changes in the masseter muscle of all the horses, but some had widespread lesions in skeletal muscle, and a few also had myocardial lesions.     

Clinical, diagnostic and biochemical features of generalised glycogenosis type II in Brahman cattle

SUMMARY Clinical, diagnostic and biochemical features of generalised glycogenosis are described In 96 Brahman-type calves. Typically the calves were presented when about 6 months of age, with III-thrift and muscular weakness as the most common signs. Acidic α-glucosidase activity was reduced in peripheral blood lymphocytes and skeletal muscle. Muscle glycogen concentration was consistently higher in affected animals than In clinically normal cattle. Other observations in affected calves Included elevation of serum aspartate amlnotransferase and creatine kinase activities and excessive amounts of high molecular weight oligosaccharides in urine. Fine cytoplasmic vacuolation of neurones In the brain and spinal cord, skeletal muscle, myocardlum and of Purkinje fibres were consistent histological observations. Periodic acid-Schlff staining revealed the presence of glycogen-like material In peripheral blood lymphocytes of all affected calves, Indicating that this is a useful aid for the diagnosis of glycogenosis. While 3 of the 96 calves showed somewhat different clinical signs, the similarity of pathology and the biochemical and clinical evidence in the remainder suggested that, In these animals, the disease was expressed as a single syndrome.     

Enterotoxigenic colibacillosis in colostrum-fed calves: pathologic changes.

Enterotoxigenic colibacillosis was experimentally produced in 8 of 9 colostrum-fed calves orally given 10(11) Escherichia coli. The eight calves developed profuse diarrhea accompanied by dehydration and depression. At 12 hours after exposure, all calves were euthanatized for necropsy and for collection of tissues for microscopic examination. Histopathologic changes included stunted villi in the jejunum and ileum, focal degeneration and exfoliation of absorptive epithelial cells at the tips of jejunal and ileal villi, and focal emigration of neutrophils which was especially prominent above the dome area of aggregated lymphatic follicles (Peyer's patches). A layer of E coli adhered to the epithelial surface of the jejunum and ileum. In the duodenum, lesions were minimal or absent and bacteria were not adhering to the mucosa. Histopathologic changes were not observed in other tissues. In two calves examined 24 hours after they were inoculated and in two calves euthanatized 24 to 36 hours after spontaneously developing enteric colibacillosis, lesions were similar to those observed in the calves at 12 hours after exposure.     

Leucine‐induced promotion of post‐absorptive EAA utilization and hepatic gluconeogenesis contributes to protein synthesis in skeletal muscle of dairy calves

The high rate of protein synthesis in skeletal muscle of dairy calves can benefit their first lactation even lifetime milk yield. Since the rate of protein synthesis is relatively low in the post‐absorptive state, the aim of this research was to determine whether leucine supplementation could increase the post‐absorptive essential amino acid (EAA) utilization and protein synthesis in the skeletal muscle. Ten male neonatal dairy calves (38 ± 3 kg) were randomly assigned to either the control (CON, no leucine supplementation, n = 5) or supplementation with 1.435 g leucine/L milk (LEU, n = 5). Results showed that leucine significantly increased the length and protein concentration in longissimus dorsi (LD) muscle, whereas it decreased creatinine concentration and glutamic‐oxalacetic transaminase (GOT) activity. Compared to the control group, leucine supplementation also reduced the glutamic‐pyruvic transaminase (GPT) activity. Supplementation of leucine improved the phosphorylation of mammalian target of rapamycin (mTOR), eukaryotic initiation factor 4E‐binding protein 1 (4EBP1) and substrates ribosomal protein S6 kinase 1 (p70S6K). Supplementation of leucine resulted in increased concentrations of glucose, methionine, threonine, histidine and EAAs and decreased concentration of arginine in serum. Liver glucose concentration was higher and pyranic acid was lower in LEU compared to CON. In conclusion, leucine supplementation can promote post‐absorptive EAA utilization and hepatic gluconeogenesis, which contributes to protein synthesis in skeletal muscle of dairy calves.     

Postnatal development of glucose transporter proteins in bovine skeletal muscle and adipose tissue.

Facilitated diffusion of glucose across the plasma membrane is mediated by a family of glucose transporter (GLUT). GLUT1 is ubiquitously present in all tissues and involved in cellular glucose uptake, while GLUT4 plays a key role in cellular glucose uptake stimulated by insulin in skeletal muscles and adipose tissue. To examine the postnatal change in the GLUTs of ruminants, the protein levels of GLUT1 and GLUT4 were measured by Western blot analysis of skeletal muscles, adipose tissue and brain of Holstein male calves aged from 0 to 12 months. Analysis of rumen short chain volatile fatty acids revealed that rumen fermentation increased around 2-3 months old. The GLUT1 level did not change in all tissues examined during the postnatal period, while the GLUT4 levels in skeletal muscle and subcutaneous adipose tissue decreased gradually, and at 12 month old, it was about 40% of those seen at 0 month old. These results are contrast to those in non-ruminant species, in which GLUT4 increases during postnatal development, and may be related to the insulin-resistance seen in adult ruminants.     

Pulmonary dysfunction and skeletal muscle changes in horses with RAO

BACKGROUND: Chronic pulmonary diseases (recurrent airway obstruction [RAO]) have been reported to alter skeletal muscle cells in humans. The purpose of this study was to evaluate a potential relationship between pulmonary and muscle variables in horses with a clinical diagnosis of RAO. Muscle biopsies from healthy horses and from horses with RAO were investigated and the relationship between the severity of lung disease and the degree of muscular changes was determined. HYPOTHESIS: We hypothesized that chronic pulmonary disease can lead to changes of the skeletal muscle in horses. ANIMALS: Fifteen healthy horses (control) and 50 horses with RAO were examined. METHODS: In a prospective clinical trial, a complete lung examination was performed in all horses. In all horses, muscle enzyme activity at rest and after exercise and muscle biopsies from the M. gluteus medius were examined. RESULTS: None of the horses had clinical or histologic signs of primary or neurogenic myopathies. According to the clinical, endoscopic, and radiographic findings and with a scoring system, the horses with RAO were grouped according to the severity of pulmonary findings (15 horses mild, 24 horses moderate, 11 horses severe RAO). Pathologic changes of the skeletal muscle (fiber atrophy or fiber hypertrophy, myofibrillar degeneration, hyperplasia of mitochondria, and ragged-red-like fibers) were identified in most horses with RAO but in only a few individual control horses. In addition, a marked depletion of muscle glycogen storage was evident in the RAO horses but not in the control group. Other pathologic changes of skeletal muscle such as centralized nuclei and regenerating fibers were rare, but were more frequent in horses with lung diseases than in the control group. The degree of muscle cell changes was also graded with a scoring system and correlated with the severity of pulmonary disease (r= 0.55). CONCLUSION: Chronic pulmonary disease in horses is associated with structural changes in skeletal muscle. CLINICAL IMPORTANCE: Because chronic pulmonary disease may affect muscles, early and effective therapy may prevent these changes. This finding could be of clinical importance but requires further studies.     

Vacuolar degeneration of skeletal muscle in transgenic mice overexpressing ORP150

ORP150 is a hypoxic stress-induced protein located in the endoplasmic reticulum. Transgenic mice overexpressing ORP150 (ORP-Tg) exhibit vacuolar degeneration in the heart. To determine whether vacuolization is present in skeletal muscle, we pathologically examined ORP-Tg mice. After 60 days of age, severe vacuolization was found in the soleus muscles of the hind legs of the ORP-Tg mice. Immunohistochemical staining of ORP150 revealed co-localization of ORP150 and vacuolization in the affected cells. Electron microscopy revealed a marked increase in the number of rough-surfaced endoplasmic reticula (rER) and distention of the cisterna. These findings suggest that overexpression of ORP150 causes accumulation of ORP150 in the rER, resulting in vacuolar degeneration in the skeletal muscle of ORP-Tg mice.     

Polymyositis in mice experimentally inoculated with Getah virus

Mice inoculated intracerebrally with parent, large-plaque (LP) and small-plaque (SP) strains of Kanagawa strain of Getah virus showed clinically recumbency and paralysis. The LP strain caused recumbency more rapidly and killed mice more early after inoculation than the parent and SP strains. Microscopically, skeletal muscles of the whole body were involved showing degenerative or inflammatory changes. In mice inoculated with the parent or SP strains, there were degeneration and necrosis of the muscle fibers with inflammatory cell infiltration and regenerative reaction. The lesions were particularly conspicuous in muscles of the hind legs. In mice inoculated with the LP strain, most of the muscle fibers revealed degeneration and necrosis, but reactive changes were poor. In addition, the periosteum and muscular connective tissue were thickened with karyorrhexis. Electron microscopically, virus particles were recognized mainly in cisternae of sarcoplasmic reticulum in skeletal muscle fibers of mice inoculated with the LP strain, while they were rare in those of animals injected with the parent and SP strains. From these finding, it was suggested that Kanagawa strain of Getah virus has the virulence to skeletal muscles of mice.     

Gross postmortem and histologic examination findings from abortion losses and calf mortalities in western Canadian beef herds

Production losses from abortions, stillbirths, and early calf mortality were described for the 2002 calf crop in 203 beef herds in western Canada. A total of 1689 calves were examined. A summary diagnosis was reported for 64% of aborted calves, 78% of stillborn calves, 88% of neonatal calves, and 94% of the calves > 3 d of age. Diagnoses for aborted calves included: thyroid gland lesions, pneumonia, developmental anomalies, placentitis, and myocardial necrosis or myopathy. For stillborn calves, diagnostic findings included: dystocia, thyroid gland lesions, myocardial necrosis or myopathy, developmental anomalies, and skeletal myopathy or necrosis. The most common diagnoses for neonatal calves (≤ 3 d) were: pneumonia, skeletal myopathy or necrosis, myocardial necrosis or myopathy, accident or trauma, and septicemia. For older calves (3 d to 3 mo), the most common diagnoses included: starvation, abomasal ulcer or perforation, enteritis or colitis, pneumonia, and intestinal volvulus, obstruction, or perforation.     

Myophosphorylase deficiency (glycogen storage disease Type V) in a herd of Charolais cattle in New Zealand: confirmation by PCR-RFLP testing

AIM: To describe a disease of muscle in Charolais calves and confirm the putative diagnosis of inherited myophosphorylase deficiency. METHODS: Variously stained paraffin sections of muscle prepared from affected calves were used to describe the lesions. A polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) test was developed and applied to affected calves, their sires, dams and other individuals. RESULTS: The lesions were those of rhabdomyolysis of skeletal muscles and sub-sarcolemmal spaces in normal fibres. The PCRRFLP test confirmed the expected mutation for phosphorylase deficiency of Charolais cattle in two affected calves. In addition, sires, dams and other closely-related individuals of four affected calves tested as heterozygous for the mutation. Other apparently unrelated animals also tested as heterozygous. CONCLUSIONS: The diagnosis of myophosphorylase deficiency was confirmed. The PCR-RFLP test is suitable for use in controlling this recessively-inherited disorder as it can diagnose heterozygous individuals that are otherwise clinically normal.     

Myophosphorylase deficiency (glycogen storage disease Type V) in a herd of Charolais cattle in New Zealand: Confirmation by PCR-RFLP testing

AIM: To describe a disease of muscle in Charolais calves and confirm the putative diagnosis of inherited myophosphorylase deficiency.

METHODS: Variously stained paraffin sections of muscle prepared from affected calves were used to describe the lesions. A polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) test was developed and applied to affected calves, their sires, dams and other individuals.

RESULTS: The lesions were those of rhabdomyolysis of skeletal muscles and sub-sarcolemmal spaces in normal fibres. The PCR-RFLP test confirmed the expected mutation for phosphorylase deficiency of Charolais cattle in two affected calves. In addition, sires, dams and other closely-related individuals of four affected calves tested as heterozygous for the mutation. Other apparently unrelated animals also tested as heterozygous.

CONCLUSIONS: The diagnosis of myophosphorylase deficiency was confirmed. The PCR-RFLP test is suitable for use in controlling this recessively-inherited disorder as it can diagnose heterozygous individuals that are otherwise clinically normal.     

Heavy metals in fluids and tissues of fetal calves and in young calves of nursing cows exposed or not exposed to anaerobically digested wastewater sludge

Fetal fluid, diaphragm muscle, heart, kidney, and liver from 14 four- to five-month-old calf fetuses were analyzed for Zn, Cu, Cd, Cr, Ni, Pb, and Fe. The same tissues and bone were examined from postparturient calves 30, 60, and 120 days of age. Weaned calves (8 to 9 months old) were necropsied and diaphragm muscle, heart, kidney, liver, brain, and bone were analyzed. Additional calves from cows exposed or not exposed to anaerobically digested sludge were placed in a feed yard at weaning for a feeding period of 150 days and then were killed and necropsied. Heavy metal content of the aforementioned tissues was compared with the same tissues obtained from peer calves weaned, killed, and necropsied 150 days earlier. Zinc, Cu, and Fe were up to 11 times higher in fetal livers than in control or exposed postparturient calves. These concentrations declined after birth and stabilized at approximately the concentrations observed in adult cattle at about 12 to 14 months of age. Cadmium accumulated to a greater extent in kidneys and livers of exposed calves than in control calves. However, the accumulation did not produce a detectable effect upon the functional or morphologic characteristics of the organs examined. Other metals were present at low levels and were generally not remarkably different in control and exposed animals.     

Plane of nutrition affects growth rate,organ size and skeletal muscle satellite cell activity in newborn calves

Plane of nutrition effects on body, tissue and cellular growth in the neonatal calf are poorly understood. The hypothesis that a low plane of nutrition (LPN) would limit skeletal muscle size by reducing fibre growth and muscle progenitor cell activity was tested. At birth, calves were randomly assigned to either a LPN (20% CP, 20% fat; GE=1.9 Mcal/days) or a high plane of nutrition (HPN; 27% CP, 10% fat, GE = 3.8 Mcal/days) in a 2 × 3 factorial design to test the impact of diet on neonatal calf growth, organ weight and skeletal muscle morphometry with time. Groups of calves (n = 4 or 5) were euthanised at 2, 4 and 8 week of age and organ and empty carcass weights were recorded. Body composition was measured by DXA. Longissimus muscle (LM) fibre cross‐sectional area (CSA), fibre/mm² and Pax7 were measured by immunohistology. Satellite cells were isolated at each time point and proliferation rates were measured by EdU incorporation. Calves fed a HPN had greater (p < 0.05) BW, ADG and hip height than those fed a LPN for 2, 4 or 8 weeks. HPN calves contained a greater (p < 0.05) percentage of fat tissue than LPN calves. Liver, spleen and thymus weights were less (p < 0.05) in LPN calves than HPN animals. Calves fed HPN had larger (p < 0.05) LM CSA at 8 weeks than LPN fed animals with no differences between the groups in numbers of satellite cells per fibre. Proliferation rates of satellite cells isolated from HPN fed calves were greater (p < 0.05) at 2 weeks than LPN fed animals, which exhibited greater (p < 0.05) proliferation rates at 4 weeks than HPN fed calves. We conclude a LPN diet reduces body growth and organ size and metabolically reprograms satellite cell activity.