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PubMed2000

The zebrafish slow-muscle-omitted gene product is required for Hedgehog signal transduction and the development of slow muscle identity.

Hedgehog proteins mediate many of the inductive interactions that determine cell fate during embryonic development. Hedgehog signaling has been shown to regulate slow muscle fiber type development. We report here that mutations in the zebrafish slow-muscle-omitted (smu) gene disrupt many developmental processes involving Hedgehog signaling. smu(-/-) embryos have a 99% reduction in the number of slow muscle fibers and a complete loss of Engrailed-expressing muscle pioneers. In addition, mutant embryos have partial cyclopia, and defects in jaw cartilage, circulation and fin growth. The smu(-/-) phenotype is phenocopied by treatment of wild-type embryos with forskolin, which inhibits the response of cells to Hedgehog signaling by indirect activation of cAMP-dependent protein kinase (PKA). Overexpression of Sonic hedgehog (Shh) or dominant negative PKA (dnPKA) in wild-type embryos causes all somitic cells to develop into slow muscle fibers. Overexpression of Shh does not rescue slow muscle fiber development in smu(-/-) embryos, whereas overexpression of dnPKA does. Cell transplantation experiments confirm that smu function is required cell-autonomously within the muscle precursors: wild-type muscle cells rescue slow muscle fiber development in smu(-/-) embryos, whereas mutant muscle cells cannot develop into slow muscle fibers in wild-type embryos. Slow muscle fiber development in smu mutant embryos is also rescued by expression of rat Smoothened. Therefore, Hedgehog signaling through Slow-muscle-omitted is necessary for slow muscle fiber type development. We propose that smu encodes a vital component in the Hedgehog response pathway.

Animals↗
PubMed1991

Nerve-dependent modulation of acetylcholine receptor epsilon-subunit gene expression.

The relative abundance of mRNAs encoding the gamma- and epsilon-subunits of acetylcholine receptor changes in opposite directions during mouse development. Both gamma- and epsilon-mRNAs are expressed early in muscle development in vivo, and in aneural embryonic muscle and myogenic cell lines in vitro, though gamma-mRNA is at least 20-fold more abundant than epsilon-mRNA in these circumstances. While during normal development, gamma-mRNA decreases to an undetectable level by postnatal day 12, epsilon-mRNA first increases 10-fold between day 2 and day 12-15, then decreases to the level characteristic of adult muscle. We have found that the transition form gamma- to epsilon-mRNA is influenced by the levels of thyroid hormones. Indeed, high and low levels of thyroid hormones, respectively, accelerated and delayed the switch between gamma- and epsilon-mRNAs. Neither the dramatic postnatal rise in epsilon-mRNA nor its sensitivity to thyroid hormones was observed in denervated newborn animals. By contrast, denervation was without effect on epsilon-mRNA expression in adult muscle. These results suggest that, although not required for the initial activation of the epsilon-gene nor its maintenance in adult muscle, the nerve plays a major role in the perinatal regulation of epsilon-gene transcription.

Aging↗
PubMed2006

The expression of the neonatal sarcoplasmic reticulum Ca2+ pump (SERCA1b) hints to a role in muscle growth and development.

The neonatal isoform of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 1 (SERCA1b) is a Ca2+ pump with a well-known developmentally regulated transcript level but an undefined protein expression and function. Specific antibodies were generated to show that SERCA1b is exclusively expressed in myoblasts and myotubes of cultured and regenerating muscle. However, the SERCA1b protein was not detectable in normal adult fast and slow muscles. Studies of the in vitro differentiating myogenic cell lines C2C12 and sol8 showed that SERCA1b is the main SERCA1 protein isoform induced during differentiation and that it is found in the myotubes. Remarkably in BC3H1 cells, which show incomplete differentiation and are reluctant to form myotubes, express the SERCA1b mRNA but not the corresponding protein. SERCA1b protein was also absent from stretched or denervated adult soleus, in spite of the fact that its mRNA level was upregulated. SERCA1b accounts for nearly the total of SERCA1 expression in the diaphragm of newborn mice, which suggests that the insufficient function and development of the diaphragm in the SERCA1 null mutant mice may be due to the lack of SERCA1b. Our studies point to an important regulation of SERCA1b expression at the protein level and hints to a role in the growth of the developing muscle.

Amino Acid Sequence↗
PubMed1996

Role of thyroid hormones in early postnatal development of skeletal muscle and its implications for undernutrition.

Energy intake profoundly influences many endocrine axes which in turn play a central role in development. The specific influence of a short period of mild hypothyroidism, similar to that induced by undernutrition, in regulating muscle development has been assessed in a large mammal during early postnatal life. Hypothyroidism was induced by providing methimazole and iopanoic acid in the feed of piglets between 4 and 14 d of age, and controls were pair-fed to the energy intake of their hypothyroid littermates. Thyroid status was evaluated, and myofibre differentiation and cation pump concentrations were then assessed in the following functionally distinct muscles: longissimus dorsi (l. dorsi), soleus and rhomboideus. Reductions in plasma concentrations of thyroxine (T4; 32%, P < 0.01), triiodothyronine (T3; 48%, P < 0.001), free T3 (58%, P < 0.001) and hepatic 5'-monodeiodinase (EC 1.11.1.8) activity (74%, P < 0.001) occurred with treatment. Small, although significant, increases in the proportion of type I slow-twitch oxidative fibres occurred with mild hypothyroidism, in l. dorsi (2%, P < 0.01) and soleus (7%, P < 0.01). Nuclear T3-receptor concentration in l. dorsi of hypothyroid animals compared with controls increased by 46% (P < 0.001), a response that may represent a homeostatic mechanism making muscle more sensitive to low levels of circulating thyroid hormones. Nevertheless, Na+, K(+)-ATPase (EC 3.6.1.37) concentration was reduced by 15-16% in all muscles (l. dorsi P < 0.05, soleus P < 0.001, rhomboideus P < 0.05), and Ca(2+)-ATPase (EC 3.6.1.38) concentration was significantly reduced in the two slow-twitch muscles: by 22% in rhomboideus (P < 0.001) and 23% in soleus (P < 0.05). It is concluded that during early postnatal development of large mammals a period of mild hypothyroidism, comparable with that found during undernutrition, induces changes in myofibre differentiation and a down-regulation of cation pumps in skeletal muscle. Such changes would result in slowness of movement and muscle weakness, and also reduce ATP hydrolysis with a concomitant improvement in energetic efficiency.

Animals↗
PubMed2003

Myosin heavy chain isoforms of the murine masseter muscle during pre- and post-natal development.

Masticatory muscles that are derived from the branchial arches express different compositions of myosin heavy chain (MHC) isoforms during the transitional phase from suckling to mastication. To clarify the developmental changes of murine masseter muscle, the composition of MHC isoforms was examined using immunohistochemical staining and competitive reverse transcription PCR. We found that MHC1 was expressed transiently in the pre and post-natal stages. In the compositional change of isoforms, the embryonic type MHCp was expressed consistently, whereas the adult isoforms increased with the developmental process. In particular, a significant change was observed between embryonic days 14 and 16, a stage when murine facial development is conspicuous. This suggests that the development of murine masseter muscle is closely associated with facial development.

Aging↗
PubMed1999

Repression by Notch is required before Wingless signalling during muscle progenitor cell development in Drosophila.

The larval muscles of Drosophila arise from the fusion of muscle founder cells, which give each individual muscle its identity, with myoblasts (reviewed in [1]). Muscle founder cells arise from the asymmetric division of muscle progenitor cells, each of which develops from a group of cells in the somatic mesoderm that express lethal of scute [2]. All the cells in a cluster can potentially form muscle progenitors, but owing to lateral inhibition, only one or two develop as such [2] [3] [4] [5]. Muscle progenitors, and the subsequent founder cells, then express transcription factors such as Krüppel, S59 and Even-skipped, which confer identity on the muscle [6] [7] [8]. Definition of some muscle progenitors, including three groups that express S59, depends on Wingless signalling [9]. Lateral inhibition requires Delta signalling through Notch and the transcription factor Suppressor of Hairless [3] [4] [5]. As the Wingless and lateral-inhibition signals are sequential [8], one might expect that muscle progenitors would fail to develop in the absence of Wingless signalling, regardless of the presence or absence of lateral-inhibition signalling. Here, we examine the development of the S59-expressing muscle progenitor cells in mutant backgrounds in which both Wingless signalling and lateral inhibition are disrupted. We show that progenitor cells failed to develop when both these processes were disrupted. Our analysis also reveals a repressive function of Notch, required before or concurrently with Wingless signalling, which is unrelated to its role in lateral inhibition.

Animals↗
PubMed1996

The significance of tumour grade in predicting disease progression in stage Ta transitional cell carcinoma of the urinary bladder.

OBJECTIVE: To determine the significance of tumour grade in predicting disease progression in stage Ta transitional cell carcinoma (TCC) of the urinary bladder. PATIENTS AND METHODS: From August 1975 to January 1991, 140 patients (121 men and 19 women, mean age 64.2 years, range 30-83) with stage Ta TCC of the urinary bladder were treated at the Veterans General Hospital-Taipei by transurethral resection and post-operative adjuvant intravesical chemotherapy. There were 48 patients (34%) with grade 1, 78 patients (56%) with grade 2 and 14 patients (10%) with grade 3 tumours. Disease progression and muscle invasion were assessed during a mean follow-up of 74.3 months and related to grade, urine cytology and the number and location of tumours. RESULTS: A total of 10 patients (7%) had tumour recurrence which invaded the muscle, of whom one had grade 1, six had grade 2 and three had grade 3 tumours. The patient with a grade 1 tumour developed muscle invasion within 16 months of surgery. The mean interval to the development of muscle invasion was 49.2 months in patients with grade 2 and 39.4 months with grade 3 tumour. In patients with stage Ta TCC, a grade 3 tumour was more likely to progress to muscle invasion (21%) than was a grade 1 (2.1%; P < 0.05) or grade 2 (7.7%; P < 0.05) tumour. One patient with a grade 2 and one patient with grade 3 tumour developed distant metastases without muscle invasion. Overall, the disease progression rate was 8.6% (12/140) in stage Ta TCC. Disease progression was more common with grade 3 (28.5%) than with grade 2 (9.0%; P < 0.05) and grade 1 (2.1%; P < 0.05) tumours. CONCLUSION: Tumour grade may be used to predict disease progression after resection of stage Ta urinary bladder cancer. A higher grade of tumour was associated with a higher incidence of disease progression.

Administration, Intravesical↗
PubMed1996

Developmental control of cathepsin B expression in bovine fetal muscles.

Expression of lysosomal cysteine proteinases was studied during fetal calf muscle development. The peptide cleaving activities of cathepsins B and L decreased strongly from 80 to 250 days of fetal age. This decrease in cathepsin activities occurred similarly in three muscles exhibiting different metabolic and contractile properties in adult animals. Cathepsin B from adult or fetal muscle revealed similar enzymatic properties, but presented a five- to sixfold lower concentration in adult muscle as indicated by active-site titration with L-3-carboxy-trans-2,3-epoxypropionyl-leucylamido-(4-guani din o)butane. During fetal growth, decreases in muscle cathepsin B specific activity and active enzyme concentration were associated with a parallel drop of cathepsin B mRNA levels. Bovine cathepsin B is encoded by two different transcripts resulting from alternative polyadenylation [Mordier, S. B., Béchet, D. M., Roux, M. P., Obled, A., and Ferrara, M. (1995) Eur. J. Biochem. 229, 35-44]. As revealed by ribonuclease protection assays, the two mRNAs encoding cathepsin B declined similarly during fetal muscle growth. This study indicates that lysosomal proteinases in skeletal muscle are under developmental control. The decrease of muscle cathepsins during fetal development appears sufficient to account for the low levels of these enzymes in adult muscles. In fetuses, high activities of lysosomal cysteine proteinases might be important for remodeling muscles during early development.

Aging↗
PubMed2003

Jelly belly protein activates the receptor tyrosine kinase Alk to specify visceral muscle pioneers.

The secreted protein Jelly belly (Jeb) is required for an essential signalling event in Drosophila muscle development. In the absence of functional Jeb, visceral muscle precursors are normally specified but fail to migrate and differentiate. The structure and distribution of Jeb protein implies that Jeb functions as a signal to organize the development of visceral muscles. Here we show that the Jeb receptor is the Drosophila homologue of anaplastic lymphoma kinase (Alk), a receptor tyrosine kinase of the insulin receptor superfamily. Human ALK was originally identified as a proto-oncogene, but its normal function in mammals is not known. In Drosophila, localized Jeb activates Alk and the downstream Ras/mitogen-activated protein kinase cascade to specify a select group of visceral muscle precursors as muscle-patterning pioneers. Jeb/Alk signalling induces the myoblast fusion gene dumbfounded (duf; also known as kirre) as well as org-1, a Drosophila homologue of mammalian TBX1, in these cells.

Anaplastic Lymphoma Kinase↗
PubMed2005

Potential roles for BMP and Pax genes in the development of iris smooth muscle.

The embryonic optic cup generates four types of tissue: neural retina, pigmented epithelium, ciliary epithelium, and iris smooth muscle. Remarkably little attention has focused on the development of the iris smooth muscle since Lewis ([1903] J. Am. Anat. 2:405-416) described its origins from the anterior rim of the optic cup neuroepithelium. As an initial step toward understanding iris smooth muscle development, I first determined the spatial and temporal pattern of the development of the iris smooth muscle in the chick by using the HNK1 antibody, which labels developing iris smooth muscle. HNK1 labeling shows that iris smooth muscle development is correlated in time and space with the development of the ciliary epithelial folds. Second, because neural crest is the only other neural tissue that has been shown to generate smooth muscle (Le Lievre and Le Douarin [1975] J. Embryo. Exp. Morphol. 34:125-154), I sought to determine whether iris smooth muscle development shares similarities with neural crest development. Two members of the BMP superfamily, BMP4 and BMP7, which may regulate neural crest development, are highly expressed by cells at the site of iris smooth muscle generation. Third, because humans and mice that are heterozygous for Pax6 mutations have no irides (Hill et al. [1991] Nature 354:522-525; Hanson et al. [1994] Nat. Genet. 6:168-173), I determined the expression of Pax6. I also examined the expression of Pax3 in the developing anterior optic cup. The developing iris smooth muscle coexpresses Pax6 and Pax3. I suggest that some of the eye defects caused by mutations in Pax6, BMP4, and BMP7 may be due to abnormal iris smooth muscle.

Actins↗
PubMed1995

Transcription factor families: muscling in on the myogenic program.

Embryonic skeletal muscle development has become a paradigm for understanding the molecular basis of how cell lineages are established and how cells differentiate into specialized structures. Most vertebrate muscles are derived from individual somites that produce two distinct muscle populations: the myotomal muscles that generate the axial and trunk musculature and a second migratory cell population that colonizes regions of the developing limbs. In both instances, muscle differentiation is accompanied by cell cycle arrest, fusion of individual myoblasts into multinucleate myotubes, and the transcriptional activation of muscle-specific genes. Recent experimental progress has led to greater understanding of the molecular mechanisms that control myogenesis in the embryo. Most of the advances have come from the identification and isolation of regulatory genes that are involved in controlling specific transcriptional events. In particular, the muscle regulatory factor (MRF) and myocyte enhancer factor 2 (MEF2) families have been implicated in establishing the myogenic lineage as well as controlling terminal differentiation. Two additional transcription factors, Pax-3 and MLP, also appear to play a role in the production of a mature muscle cell. This review focuses on these four vertebrate transcription factor families and discusses the experimental evidence that these factors play important, non-overlapping roles in regulating skeletal muscle development.

Amino Acid Sequence↗
PubMed1987

Postnatal maturation of spindles in deafferented rat soleus muscles.

Whether the motor innervation can direct the morphological and histochemical differentiation of developing muscle spindles in the absence of sensory innervation was investigated by deafferentation of the soleus muscle in immature rats. Dorsal root ganglia containing the cell bodies of afferents from the soleus muscle were removed surgically at a stage of postnatal development when spindles already contain the full complement of intrafusal fibers innervated by both afferents and efferents, but when the fibers are histochemically and structurally immature. Experimental soleus muscles were excised one year after deafferentation and sectioned frozen at a thickness of 8 micron. Sections were stained for enzymes indicative of types of muscle fibers and sites of neuromuscular junctions, and were examined by light microscopy. Spindles of muscles that matured in the absence of sensory innervation were abnormal. They lacked the periaxial fluid space and contained fewer intrafusal fibers than did normal spindles. The morphological and histochemical profiles of the encapsulated fibers present in the deafferented spindles more closely resembled extrafusal rather than intrafusal muscle fibers. These observations suggest that deafferentation of the immature spindles induces disintegration of some intrafusal fibers and alters maturation of others. Moreover, motor axons terminated less frequently along muscle fibers in deafferented spindles than on intrafusal fibers of normal spindles. Thus, maintenance of a full complement of intrafusal fibers in the developing spindle, emergence of histochemical profiles typical of normal intrafusal fibers, and development of adult pattern of fusimotor innervation require intact sensory innervation.

Adenosine Triphosphatases↗
PubMed1977

Development of sarcoplasmic reticulum in cultured chicken muscle.

The development of sarcoplasmic reticulum membranes was studied in vivo and in tissue culture in chicken pectoralis muscle cells. The concentration of the calcium- and magnesium-activated ATPase measured by selective labeling of the enzyme with [32P]ATP in whole muscle homogenates was found to increase in developing chicken pectoralis muscle in vivo from 0.01 nmol/mg of protein in 12-day embryos to 0.3 to 0.4 nmol/mg of protein in 1-month-old chicks, where it constitutes about 3% of the total protein content of muscle. In cultured muscle cells the concentration of calcium-sensitive phosphoprotein increased from 0.015 nmol/mg of protein at 2 days to 0.04 to 0.05 nmol/mg of protein after 5 days of culture. This amount represents about 0.5% of the protein content of the muscle cells. The accumulation of Ca2+ transport ATPase began during fusion and continued with a linear rate during 8 days of culture. The density of 75 A intramembranous particles seen by freeze-etch electron microscopy on fracture faces of sarcoplasmic reticulum membranes is about 4,000/mum2 in adult chick pectoralis muscle but only 400/mum2 in cultured muscle cells in rough proportion to the concentration of Ca2+-sensitive phosphoprotein. The Ca2+, Na+, and K+ concentration of the medium and addition of ouabain, caffeine, or the calcium ionophores A23187 and X537A sharply influence the concentration of calcium transport ATPase in cultured muscle cells, parallel with their effect upon cell fusion and growth. These observations are consistent with the proposition that the gene expression leading to the accumulation of Ca2+ transport ATPase during development in culture may be regulated by intracellular ion concentrations.

Aging↗
PubMed1996

Muscle growth and muscle function: a molecular biological perspective.

Molecular biological methods are pervading all biomedical fields and it is likely that they will soon introduce new techniques to veterinary diagnostics and have a major impact on food and fibre production in animal agriculture. The ability to manipulate muscle growth and phenotype will present new ethical problems, particularly if the techniques are used to manipulate muscle development in greyhounds and racehorses where the financial rewards could be very substantial. Muscle has been a useful tissue for the study of the molecular control of tissue development because terminal differentiation results in the production of large quantities of highly specialised proteins. Now that the functional anatomy of structural genes in muscle is being elucidated, a coherent picture is beginning to emerge of the way in which post-natal muscle growth and phenotype are regulated at the gene level. The hormones and growth factors involved in regulating the quantitative and qualitative changes in gene expression are now better understood, together with the ability of the tissue to adapt to physical signals and hence new activity patterns. The myosin heavy chain isoform genes which encode the myosin cross-bridges (the force generators for muscular contraction) exist as a large multigene family. The contractility and other characteristics of muscle depend to a large extent on the differential expression of members of this and other gene families. Muscle fibres adapt for increased power output by expressing a subset of "fast' genes and for increased economy of action by expressing a slow subset of genes and producing more mitochondria. With the increasing understanding of gene expression in muscle, there are prospects for manipulating the mass, contractility and other characteristics of muscle and also to change its phenotype and understand certain disease states.

Agriculture↗
PubMed1999

Intrauterine growth retardation is associated with reduced cell cycle activity, but not myofibre number, in ovine fetal muscle.

Cellular development of muscle was studied in sheep fetuses at 85 days of gestation. Large and small fetuses were compared at 100, 115 and 130 days, and an additional group of large 130-day fetuses were studied following 7 days of maternal undernutrition. Myogenesis in the peroneus longus muscle was completed between 100 and 115 days of gestation, and myofibre number did not differ between small and large fetuses. The proportion of myofibre-related nuclei identified as entering S-phase of the cell cycle was 1.7% per hour in 85-day fetuses. In large fetuses, subsequent rates were relatively constant (approximately 1.5% h(-1)), whereas in small fetuses cell cycle activity declined with age from 1.3 to 0.9% h(-1), and was 0.5% h(-1) in 130-day fetuses of restricted ewes. The constant rate of cell cycle activity in large fetuses was associated with an increasing estimated rate of muscle growth (peroneus longus (mg) = 0.831 x 10(0.024 x age [d]), r2 = 0.98), which contrasted with slow and relatively constant muscle accretion in small fetuses (8.4 mg day(-1)), and slower muscle accretion at 130 days in large fetuses from restricted ewes. Differences in DNA and RNA content in the semimembranosus muscle increased with age, large fetuses having 70% more muscle DNA, 108% more muscle RNA and 104% larger muscles than small fetuses at 130 days (all P<0.001). The results demonstrate that myonuclei accumulation, but not myofibre number, is associated with fetal growth in sheep and, therefore, with fetal nutrition during mid to late gestation.

Animals↗
PubMed2004

Gene discovery by microarray: identification of novel genes induced during growth factor-mediated muscle cell survival and differentiation.

Peptide growth factors regulate cell fate by activating distinct signal transduction pathways that ultimately influence gene expression. Insulin-like growth factors (IGFs) play central roles in controlling somatic growth and participate in skeletal muscle development and regeneration. In cultured muscle cells, IGF action is critical both for maintaining viability during the transition from proliferating to differentiating myoblasts and for facilitating differentiation. By contrast, platelet-derived growth factor (PDGF) can sustain cell survival but inhibits differentiation. Here we examine the genetic programs that accompany IGF and PDGF action in myoblasts. Through analysis of high-density oligonucleotide arrays containing approximately 36,000 mouse probe sets, we identify 90 transcripts differentially induced by IGF-I, including 28 muscle-specific genes and 33 previously unannotated mRNAs, and 55 transcripts specifically stimulated by PDGF, including 14 unknowns. Detailed study of one IGF-induced mRNA shows that it encodes a protein related to a recently characterized repulsive guidance molecule postulated to regulate neuronal targeting during development. Our results demonstrate the power of transcriptional profiling for gene discovery and provide opportunities for investigating new proteins potentially involved in different aspects of growth factor action in muscle.

Animals↗
PubMed1992

Fiber-type proportions in mammalian soleus muscle during postnatal development.

We analyzed the fiber-type composition of the soleus muscle in rats and mice to determine whether the adult proportion of fiber types is fixed soon after birth or whether it changes during postnatal maturation. We examined muscles from animals varying in age from 1 week to 1 year using monoclonal antibodies that distinguish between fast and slow isoforms of myosin heavy chains. In cross sections of unfixed muscle containing profiles of all myofibers in the muscle, we counted the fibers that stained with antibodies to fast myosin, and in adjacent sections, those that stained positive with an antibody to slow myosin. We also counted the total number of fibers in each section. Rat soleus contained about 2500 myofibers, and mouse about 1000 at all ages studied, suggesting that myogenesis ceases in soleus by 1 week after birth or sooner. In mouse soleus, the relative proportions of fibers staining positive with fast and slow myosin antibodies were similar at all ages studied, about 60%-70% being fast and 30%-40% slow. In rat soleus, however, the proportions of fast antibody-positive and slow antibody-positive fibers changed dramatically during postnatal maturation. At 1 week after birth, about 50% of rat soleus fibers stained with fast myosin antibodies, whereas between 1 and 2 months this value fell to about 10%. In mouse, about 10% of fibers at 1 week, but none at 1 year, reacted with both fast and slow antibodies, whereas in rat, fewer than 3% bound both antibodies to a significant degree at 1 week. It is puzzling why, in rat soleus, the majority of apparently fast fibers present at 1 week is converted to a slow phenotype, whereas in mouse soleus the predominant change appears to be the suppression of fast myosin expression in a subset of fibers that expresses both myosin types at 1 week. It is possible that this may be related to differences in size and the amount of body growth between these two species.

Animals↗
PubMed1997

The effect of training status on the serum creatine kinase response, soreness and muscle function following resistance exercise.

Untrained individuals develop muscle soreness and increased serum creatine kinase (CK) activity in the blood after strenuous, unaccustomed exercise. An unpublished observation in our laboratory revealed that trained weightlifters also experience considerable soreness after unaccustomed exercise, but may not show a dramatic CK response. This study examined the CK and soreness responses to strenuous exercise in weightlifters (TR, n = 10) and untrained subjects (UTR, n = 10). Trained subjects had a minimum of three years weightlifting experience, and regularly performed squats and leg presses. Untrained subjects had not participated in any regular resistance exercise for the past three years. Following two acclimation sessions, subjects reported to the lab on seven consecutive days and on the tenth day after knee extensor exercise. Weight training sessions occurred on day 1 for the knee extensors (KE) and day 2 for the knee flexors (KF). The weight training consisted of these exercises (sets): squat (5), leg press (3), leg extension and lunge (3) for the KE, double leg curls (6), single leg curls (3), stiff-legged deadlifts (4, TR group only) for the KF at 12 RM for all exercises. To document the stress due to exercise, the loss in strength (isometric peak torque, IPT) was assessed on a Biodex isokinetic dynamometer. Maximal voluntary IPT of the KE at 90 degrees and the KF at 80 degrees decreased 17-30% with no significant differences between groups. Muscle soreness during simulated squat leg curl movement was assessed by a 100 mm visual analog scale (VAS). Average peak KE soreness was 76 mm for TR and 58 mm for UTR, KF soreness was 60 mm for TR and 47 mm for UTR post-exercise. Serum CK levels were significantly different between groups with a peak of 1349 IU for TR and 3272 IU for the UTR (p < 0.01). Although the TR group experienced greater soreness than the UTR, peak serum CK activity was significantly lower, suggesting that trained individuals can develop severe soreness without the same degree of increase in serum CK activity observed in untrained individuals.

Adult↗