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N C Stickland

Publications and source records attributed to N C Stickland.

At least 37 records · Page 2Linked to original sources

The effect of undernutrition in the early postnatal period on skeletal muscle tissue.

Guinea-pigs were undernourished from birth by first, cross-fostering in groups of six (in pairs for control animals) and then by feeding a diet of 60% of ad lib. intake from 2 to 6 weeks. The changing characteristics of muscle fibre types in the biceps brachii and soleus muscles were monitored by histochemistry. Undernutrition appeared to delay maturation of muscle fibres. Fibre cross-sectioned area was reduced in all fibres of the 60% of ad lib. intake group. Fibres of the biceps brachii were more affected than those of the soleus. Fibre area vulnerability was partly associated with a high relative growth rate in biceps brachii at this time. Total protein content in the semitendinosus muscle was depressed in the undernourished group compared with the control group. DNA concentrations were initially higher in the control group but decreased in both groups to similar levels by 6 weeks. RNA concentration increased up to 5 weeks in the control group and then decreased, but decreased after 2 weeks in the undernourished group.

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Muscle cellularity and postnatal growth in the pig.

Fast-growing strains of pigs and of other animals tend to have more muscle fibers than do slow-growing strains. The relationship between fiber number and growth rate was extended by examining pigs within the same strain. Seven litters of pigs (n = 66) were weighted at monthly intervals from birth to approximately 80 kg. The semitendinosus muscle was removed and an estimation of total fiber number, total primary fiber number, and mean secondary:primary fiber number (S:P) ratio was made for each animal. Pig growth was divided into three approximately linear phases: birth to 6 kg, 6 to 25 kg, and 25 kg to slaughter weight. Average daily gain in the first two phases was correlated with birth weight (r = .3614, P < .05 and r = .5873, P < .001, respectively) but was not correlated with total muscle fiber number. In the third growth phase ADG was correlated with muscle fiber number (r = .4149, P < .001) and was not correlated with birth weight. The gain:feed ratio was also calculated for each pig during the third growth phase and was found to be correlated with fiber number (r = .4191, P < .001). These results suggest that muscle fiber number is an important determinant of postnatal growth such that pig littermates with a high fiber number tend to grow faster and more efficiently than littermates with a lower fiber number.

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Satellite cell content in muscles of large and small mice.

Quantitative analyses of the satellite cell content in the biceps brachii muscle of mice genetically selected for high (QL) and low (QS) bodyweight showed that selection alters the total number of satellite cell nuclei rather than the relative proportions of nuclei in the myofibre and satellite cell populations. These findings are in accordance with those previously published for other tissues of these mice and support the hypothesis that regulatory mechanisms remain unaltered by selection pressure. Size at birth, however, is a reflection of nutritional status as well as genetic background, and comparisons between differently sized littermates within each of the lines showed a significant increase in satellite cell density in larger compared with smaller individuals. These differences between littermates were not accompanied by any alteration in myofibre nuclear density. It is therefore suggested that whilst both genetic and nutritional factors exert their effects on muscle growth through an influence on satellite cell division, both do so at different stages during the programme of satellite cell differentiation.

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Does the anatomical location of a muscle affect the influence of undernutrition on muscle fibre number?

Nutritional restriction during muscle fibre number development invariably has a more detrimental effect on the biceps brachii than on the soleus. The difference may be due to the relative proportions of fibre types in the muscles or the anatomical location of the muscles. To distinguish between the effects of location and fibre type the biceps (fast, cranial and proximal), soleus (slow, caudal and distal), and extensor digitorum longus (EDL) (fast, caudal and distal) were examined from control and undernourished guinea pig neonates. A 40% reduction in maternal intake resulted in a reduction in neonate body and muscle weights (P < 0.005), biceps (P < 0.05) and EDL fibre numbers (P < 0.005), but did not affect soleus fibre number. At birth the ratio of fast fibres to slow was 7.5 for the biceps, 7.0 for the EDL, and 1.5 for the soleus. The effect of undernutrition on muscle fibre number therefore seems to be a function of the fibre types in that muscle.

Adenosine Triphosphatases↗

The effect of maternal undernutrition on the growth and development of the guinea pig placenta.

Fetal growth is known to be correlated with the size of the placenta and the exchange surface area. Reduction in the growth of the materno-fetal exchange surface areas may be a mechanism by which the effects of maternal undernutrition on fetal growth are mediated. In the compact placenta of the guinea pig the exchange surface is equivalent to the peripheral labyrinth. The effect of a 40% reduction in maternal feed intake on the growth of the peripheral labyrinth was investigated in pregnant guinea pigs between gestational days 25 and 65. Fetal and placental weights were significantly reduced in the last trimester by 32% and 38% respectively (P < 0.01). Placental efficiency in early gestation was significantly impaired in restricted animals but equivalent to ad lib. fed controls by the last trimester. The volume of the peripheral labyrinth increased as a percentage of the total placental volume with gestational age. Restricted placentae tended to be composed of a smaller volume of peripheral labyrinth tissue in early gestation. It is suggested that maternal undernutrition results in an impaired or delayed expansion of the peripheral labyrinth in early gestation causing a reduction in placental efficiency. By the last trimester the weight of the peripheral labyrinth of restricted animals was reduced by 33% (P < 0.05). The weight of the peripheral labyrinth was also significantly correlated with fetal weight is limited by the size of the peripheral labyrinth in the later stages of gestation.

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The effects of maternal undernutrition on maternal and fetal serum insulin-like growth factors, thyroid hormones and cortisol in the guinea pig.

The insulin-like growth factors (IGF-I and -II) are potential mediators of the effects of maternal undernutrition on fetal growth and muscle development. The effects of a 40% reduction in maternal feed intake on serum levels of the IGFs, the thyroid hormones and cortisol, were investigated for the last two trimesters (day 25 to birth). This level of undernutrition is known to cause a 35% reduction in fetal and placental weights, and a 20-25% reduction in muscle fibre number. Maternal IGF-I level was greater than non-pregnant levels on day 25 gestation, in both control and restricted dams, and declined with gestational age. The increase in IGF-I level in the 40% restricted group was approximately two-thirds that of control animals. Fetal serum IGF-I was also reduced in undernourished fetuses throughout gestation. Maternal IGF-II did not change with gestational age and was unaffected by undernutrition. Fetal IGF-II reached a peak at day 55 of gestation, this peak was greatly diminished by maternal feed restriction. Both IGF-I and IGF-II tended to be related to fetal, placental and muscle weights at day 65 of gestation. Thyroid hormone concentration declined in maternal serum and increased in fetal serum with increasing gestational age. Levels were not significantly affected by undernutrition. Both triiodothyronine (T3) and thyroxine (T4) were correlated with IGF-I in maternal serum (P < 0.05), but not in fetal serum. Cortisol levels were elevated by undernutrition in both maternal and fetal serum, and increased with gestational age. Cortisol was inversely correlated with serum IGF-I in both maternal and fetal serum. Maternal serum IGF-I may mediate the effects of undernutrition on fetal growth by affecting the growth and establishment of the feto-placental unit in mid-gestation. Fetal IGF-I may mediate the effects on muscle growth, whereas IGF-II seems to be related to hepatic glycogen deposition. Cortisol may play a role via its effect on the IGFs, but the thyroid hormones are unlikely to be important until the late gestation/early postnatal period.

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Why are slow and fast muscles differentially affected during prenatal undernutrition?

The biceps brachii and soleus muscles (fast and slow twitch muscles, respectively) were taken from guinea-pig fetuses, undernourished via maternal dietary intake to 60% of ad lib, and examined for differences from their controls. At birth, muscle fiber number was found to be reduced by 26% in the biceps brachii but was unaltered in the soleus muscle. An examination of the muscles at ages through gestation revealed that any reduction in fiber number was associated with a reduction in the secondary/primary fiber ratio. There was a stage in soleus myogenesis at which fiber number was significantly lower than the control. The deficit was corrected by the continuation of secondary fiber hyperplasia beyond the time of usual cessation. A similar delay was found in the biceps brachii but it did not enable recovery to a full complement of fibers. The difference between the 2 muscles was thought to be related to the relative proportions of primary fibers in the muscles, primary fiber development being apparently unaffected by undernutrition in utero.

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The effect of temperature on myogenesis in embryonic development of the Atlantic salmon (Salmo salar L.).

From fertilisation to hatching one group of salmon embryos was reared at ambient temperatures (fluctuating around 1.6 degrees C) and another at 10 degrees C. At Gorodilov stages 28, 30 and 33 transverse sections of whole embryos were obtained for light and electron microscopy. Total cross-sectional areas, fibre numbers, fibre diameters and myofibrillar areas of the white muscle of m. lateralis were measured. At hatching (stage 33, which occurred much earlier at the higher temperature), the higher temperature embryos had significantly larger (P less than 0.01) but fewer (P less than 0.05) muscle fibres. These larger fibres contained significantly more myofibrillar material (P less than 0.05) than the smaller fibres of the lower temperature embryos. Lesser differences were found at pre-hatching stages. Higher temperatures caused myofibre hypertrophy to increase at a greater rate than hyperplasia. Hence, the cellularity of the tissue produced under the different temperature regimes was quite different.

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Relationship between motoneuron number and myofibre number in the pig.

A segment (at level T1) of spinal cord and a midbelly slice of the m. semitendinosus were removed from the largest- and smallest-birthweight littermate of each of 12 Large White pig litters sacrificed at various ages. When the ratio of myofibre numbers for large to small littermate within each litter was related to the ratio of motoneuron numbers then a significant correlation (r = 0.638, p less than 0.05) was observed. It is suggested that in utero growth retardation causes a reduction in myofibre numbers (within a litter), which in turn reduces motoneuron survival rate.

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The growth and differentiation of porcine skeletal muscle fibre types and the influence of birthweight.

Muscle growth and development was studied in 49 Large White pigs from a total of 17 litters. Representative large (mean birthweight of 1544 g), small (1144 g) and runt (776 g) littermates were selected and slaughtered at the same age, ages ranging from birth to 128 days. Fresh frozen, serial transverse sections taken from the semi-tendinosus and trapezius muscles of these animals were stained for the histochemical demonstration of acid and alkaline pre-incubated adenosine triphosphatase, succinate dehydrogenase and glycogen phosphorylase. Profiles of the muscle fibre types were compiled for each animal. In both muscles the number of slow oxidative (SO) fibres, that were arranged together in groups within 'metabolic bundles', increased with growth. The transverse sectional area (TSA) of the semitendinosus muscle increased with the 2/3 power of liveweight whereas the area occupied by SO fibres increased at a rate significantly greater than 1.0 (P less than 0.01). Regression analysis revealed that the area of this muscle occupied by SO fibres was greater (P less than 0.001) in runt and small littermates relative to their large littermates when they were compared at an equal liveweight. This greater TSA of the semitendinosus classified as 'SO' in lower birthweight pigs was the result of a combination of higher percentages (P less than 0.05) of SO fibres and significantly greater (P less than 0.001) SO fibre mean TSAs. The mean TSAs of all myofibre types were similar between littermates of the same age but most types were of greater TSA in the lower birthweight littermates when compared (by regression analysis) at the same liveweight suggesting that fibre TSA was age- rather than weight-related. The higher percentage of SO fibres in the low birthweight pigs, when compared at an equivalent liveweight to their large littermates, appeared to be related to their affected secondary/primary fibre number ratio. This phenomenon, plus the data on the number of slow fibres per metabolic bundle, indicated that it was apparently the number of slow fibres per metabolic bundle which was regulated with liveweight gain rather than the resultant percentage of slow fibres within the muscle.

Adenosine Triphosphatases↗

The effects of low birthweight on the ultrastructural development of two myofibre types in the pig.

An ultrastructural investigation of the postnatal development of oxidative and non-oxidative fibres from the deep and superficial portions of the semitendinosus muscle, respectively, was undertaken on 32 pure bred Large White pigs from a total of 11 litters. This study quantifies the changes in mitochondrial, lipid droplet and myofibrillar content of these two myofibre types between birth and 84 days of age, and evaluates differences between the largest male (mean birthweight of 1559 g), smallest normal male (1147 g), and runt (758 g) littermates. The oxidative and non-oxidative fibres, as well as possessing different complements of mitochondria, lipid droplets and myofibrils, showed different rates of myofibrillar accumulation. The relatively small postnatal change in the percentage volume of myofibrils of oxidative fibres, as opposed to the high change within the non-oxidative fibres, presented a cytological basis by which to explain the differential effects of growth retardation on these fibre types. The ultrastructural composition of myofibres was not impaired by reduced birthweight except when, as in two extreme cases, birthweight was severely reduced. In these instances the myofibrillar percentage volume of the non-oxidative fibres was greatly affected.

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"Giant" muscle fibres in skeletal muscle of normal pigs.

Observations made during a growth and development study of the semitendinosus and trapezius muscles of 49 purebred Large White pigs between birth and 128 days of age revealed the presence of giant fibres. The occurrence, histochemical and ultrastructural properties of these giant fibres were investigated. A high proportion of the pigs (85 per cent) contained giant fibres in their muscles but these giant fibres usually represented less than 1 per cent of the total myofibre population. Giant fibres possessed enhanced adenosine triphosphatase activity and a high capacity for oxidative metabolism (indicated by succinate dehydrogenase activity) which was reflected ultrastructurally by the greatly heightened electron density of myofibrils and by an abnormally high percentage of mitochondria and lipid droplets. These deviations from normal muscle fibre composition, together with the reduced percentage volume of sarcoplasmic reticulum, were consistent with changes seen in functionally over-loaded muscle. It appears that giant fibre anomalies occur through increased activity stimulated in occasional muscle fibres, perhaps by a structural defect, such as an inadequate amount of sarcoplasmic reticulum, which causes hyper-contractile activity within the fibres and associated compensatory adaptations. Giant fibres did not appear to represent fibres undergoing degenerative changes.

Adenosine Triphosphatases↗

The numbers and types of muscle fibres in large and small breeds of pigs.

M. semitendinosus and m. trapezius (portion) were removed from eight miniature pigs ranging from 21 to 160 days of age and eight age-control as well as eight weight-control commercial Large White pigs. Complete transverse frozen sections were obtained for each muscle sample and stained for various enzyme activities including myosin adenosine triphosphatase activity which enabled the identification of 'metabolic bundles'. This in turn enabled conclusions to be made about the prenatal development of the muscle in terms of primary and secondary myofibres. The Large White pigs contained 173% more muscle fibres in m. semitendinosus than did the miniature pigs. Primary myofibre number was found to be about four times more important than secondary to primary myofibre ratios in determining myofibre number in the two breeds of pigs. Both primary myofibre number and secondary to primary myofibre ratios were, however, significantly greater in Large White than in miniature pigs. When the age- and weight-control Large Whites were compared with the miniature pigs it was found that at any given live weight the miniature pigs had thicker myofibres whereas at the same age there was no significant difference. The total area of m. semitendinosus occupied by slow myofibres was about three times greater in the Large White pigs; the functional aspects of this are discussed. It was concluded that genetically smaller animals develop fewer muscle fibres in their muscles by a different mechanism to that exhibited by animals which are smaller due to nutritional deprivation in utero.

Adenosine Triphosphatases↗

Placental growth in the pig.

The growth of the porcine placenta from 38 days until term is described. Measurements were made of its area, circumference and in situ length. Placental area increased during the period of study due to increases in the uterine circumference at the sites of conceptuses. No change was found in uterine horn length or placental length with age. Fetal weight correlated well with placental area but poorly with the other parameters. Placental length was shorter in more crowded horns and showed a U shaped distribution with position within uterine horns. These results are discussed in terms of competition for space within the uterus as a cause of the within litter variation in fetal size.

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Muscle development in large and small pig fetuses.

The largest and smallest littermates were chosen by weight from litters of 38 days' gestation to 1 day post partum. Complete frozen sections of the semitendinosus muscle were used to provide a qualitative and quantitative account of the development of the primary and secondary generations of muscle fibres. The results showed that the time of formation of primary and secondary fibres, and the numbers of primary fibres formed, were the same in both large and small littermates. The number of secondary fibres formed, however, was lower in the smaller fetuses and resulted in there being a 17% difference in total fibre number at birth. Primary fibres in small fetuses were smaller, due to the smaller central myofibril-free region. This small size may have restricted the available surface area for secondary fibre formation. Fibre hyperplasia was found to cease between 85 and 95 days' gestation, and so the fibre number difference is likely to be permanent.

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Growth and development of muscle fibres in the rainbow trout (Salmo gairdneri).

The growth of red and white muscle was investigated in the rainbow trout, using fish from 2.2 cm to 71 cm in length. In the white muscle, fibre hyperplasia, initially, accounted for all muscle growth but its relative contribution decreased as the contribution from fibre hypertrophy increased. At and above about 65 cm there was no hyperplasia, and this corresponded approximately to the stage when there were no more fibres in the smallest size class (less than 20 microns). The results for the red muscle are more variable and hence more difficult to assess. Although red fibre hyperplasia may continue throughout growth, at 34 cm there are no fibres in the smallest size class, which possibly indicates no new fibre formation beyond this stage.

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The arrangement of muscle fibers and tendons in two muscles used for growth studies.

The arrangement of muscle fibres and tendons was examined in the soleus muscle of rats from 6 to 175 days post partum. The muscle was seen to change from a simple structure, with mean fibre length of approximately 90% of complete muscle length, to a unipennate structure, with mean fibre length of only about 60% of muscle length. The dog pectineus muscle was also investigated and found to have a bipennate structure throughout postnatal growth. The arrangement of muscle fibres in both these muscles is such that it might be difficult (particularly in the older animals) to cut a transverse section through all the fibres contained in the muscle; some fibres might not enter the plane of section. Results on muscle fibre number in these muscles at different ages may therefore be misleading.

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Scanning electron microscopy of prenatal muscle development in the mouse.

Scanning electron microscopy was used to study prenatal muscle development in mouse fetuses ranging from 12 days to 18 days gestation. Some transmission electron micrographs were also used for comparison. At 12 days no myofibres were evident although at 13 days long fibres surrounded by many mononucleated cells could be seen. At 14 days bundles of primary myofibres were observed with new myofibres forming in crevices between adjacent fibres. At 16 days the primary myofibres had separated but smaller secondary myofibres could be seen forming along their surfaces. The myofibres were very compact at 18 days and often appeared fused but this was due to the basal lamina ensheathing clusters of primary myofibres with their secondaries. The scanning electron micrographs appeared to illustrate the theories of muscle development which have arisen out of the various studies employing sectioning techniques.

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