Behavioral problems and emotional stress in children with bruxism

Bruxism has a multifactorial etiology, and psychosocial factors have been considered to increase the risk of occurrence of this parafunction. The aim of this study was to evaluate the behavior profile of a group of children diagnosed with bruxism. Eighty 7-11-year-old children of both genders (mean age 8.8 years) first recruited as eligible participants. Twenty-nine children (18 males and 11 females) whose parents/guardians reported to present frequent episodes of tooth grinding/clenching while awake or during sleep (at least 3 nights a week) in the previous 3 months were enrolled in the study. The diagnosis of bruxism was established based on the parents/guardians' report about the children's behavior, habits and possible discomforts in the components of the stomatognathic system allied to the presence of signs and symptoms such as pain on the masticatory muscles, masseter muscle hypertrophy, wear facets, fractures of restorations, dental impressions on the cheek mucosa and tongue. As part of the psychological evaluation, the Rutter's Child Behavior Scale-A2 was applied to the parents/caregivers (one for each child) and the Child Stress Scale was applied to the children. Data were analyzed descriptively based on the frequency of each studied variable. Twenty-four (82.76%) children needed psychological or psychiatric intervention; 17 of them presented neurotic disorders and 7 children presented antisocial disorders. Six (20.70%) children presented significant physical and psychological manifestations of stress. The findings of the present study suggest that behavioral problems and potential emotional problems can be risk factors to bruxism in children.

Myostatin: genetic variants, therapy and gene doping

Since its discovery, myostatin (MSTN) has been at the forefront of muscle therapy research because intrinsic mutations or inhibition of this protein, by either pharmacological or genetic means, result in muscle hypertrophy and hyperplasia. In addition to muscle growth, MSTN inhibition potentially disturbs connective tissue, leads to strength modulation, facilitates myoblast transplantation, promotes tissue regeneration, induces adipose tissue thermogenesis and increases muscle oxidative phenotype. It is also known that current advances in gene therapy have an impact on sports because of the illicit use of such methods. However, the adverse effects of these methods, their impact on athletic performance in humans and the means of detecting gene doping are as yet unknown. The aim of the present review is to discuss biosynthesis, genetic variants, pharmacological/genetic manipulation, doping and athletic performance in relation to the MSTN pathway. As will be concluded from the manuscript, MSTN emerges as a promising molecule for combating muscle wasting diseases and for triggering wide-ranging discussion in view of its possible use in gene doping.

Serum free testosterone, leptin and soluble leptin receptor changes in a 6-week strength-training programme

[EN] Strength training is usually associated with a reduction in fat mass and with muscle hypertrophy. The aim of the present study was to examine whether the serum free leptin index (FLI), measured by the molar excess of soluble leptin receptor (sOB-R) over leptin, is increased by 6 weeks of strength training. Eighteen male, physical education students were randomly assigned to two groups: a strength-training (n 12) and a control group (n 6). Body composition (lean body mass and body fat) determined by dual-energy X-ray absorptiometry (DXA), muscle performance and leptin, sOB-R, total testosterone and free testosterone concentrations were determined before and after training. Fat mass was reduced by 1 kg with strength training (P<0.05). Lean body mass of trained extremities was increased by 3% (P<0.05), while the concentration of free testosterone in serum was reduced by 17% (P<0.05) after training. However, despite the reduction in fat mass and free testosterone, serum leptin concentration was not significantly affected by strength training, even after accounting for the differences in body fat. By contrast, for a given fat mass, the sOB-R was increased by 13% (P<0.05) at the end of the strength-training programme, although the molar excess of sOB-R over leptin remained unchanged. Therefore, the quantity of free leptin available to bind to the target tissues was not significantly affected by the short strength-training programme, which elicited a 7% reduction in fat mass.

Strength training combined with plyometric jumps in adults: sex differences in fat-bone axis adaptations

[EN] Leptin and osteocalcin play a role in the regulation of the fat-bone axis and may be altered by exercise. To determine whether osteocalcin reduces fat mass in humans fed ad libitum and if there is a sex dimorphism in the serum osteocalcin and leptin responses to strength training, we studied 43 male (age 23.9 2.4 yr, mean +/- SD) and 23 female physical education students (age 23.2 +/- 2.7 yr). Subjects were randomly assigned to two groups: training (TG) and control (CG). TG followed a strength combined with plyometric jumps training program during 9 wk, whereas the CG did not train. Physical fitness, body composition (dual-energy X-ray absorptiometry), and serum concentrations of hormones were determined pre- and posttraining. In the whole group of subjects (pretraining), the serum concentration of osteocalcin was positively correlated (r = 0.29-0.42, P < 0.05) with whole body and regional bone mineral content, lean mass, dynamic strength, and serum-free testosterone concentration (r = 0.32). However, osteocalcin was negatively correlated with leptin concentration (r = -0.37), fat mass (r = -0.31), and the percent body fat (r = -0.44). Both sexes experienced similar relative improvements in performance, lean mass (+4-5%), and whole body (+0.78%) and lumbar spine bone mineral content (+1.2-2%) with training. Serum osteocalcin concentration was increased after training by 45 and 27% in men and women, respectively (P < 0.05). Fat mass was not altered by training. Vastus lateralis type II MHC composition at the start of the training program predicted 25% of the osteocalcin increase after training. Serum leptin concentration was reduced with training in women. In summary, while the relative effects of strength training plus plyometric jumps in performance, muscle hypertrophy, and osteogenesis are similar in men and women, serum leptin concentration is reduced only in women. The osteocalcin response to strength training is, in part, modulated by the muscle phenotype (MHC isoform composition). Despite the increase in osteocalcin, fat mass was not reduced.

Exercise and bone mass in adults

[EN] There is a substantial body of evidence indicating that exercise prior to the pubertal growth spurt stimulates bone growth and skeletal muscle hypertrophy to a greater degree than observed during growth in non-physically active children. Bone mass can be increased by some exercise programmes in adults and the elderly, and attenuate the losses in bone mass associated with aging. This review provides an overview of cross-sectional and longitudinal studies performed to date involving training and bone measurements. Cross-sectional studies show in general that exercise modalities requiring high forces and/or generating high impacts have the greatest osteogenic potential. Several training methods have been used to improve bone mineral density (BMD) and content in prospective studies. Not all exercise modalities have shown positive effects on bone mass. For example, unloaded exercise such as swimming has no impact on bone mass, while walking or running has limited positive effects.

Hemizygous deletion of COL3A1, COL5A2, and MSTN causes a complex phenotype with aortic dissection: a lesson for and from true haploinsufficiency

Aortic dilatation/dissection (AD) can occur spontaneously or in association with genetic syndromes, such as Marfan syndrome (MFS; caused by FBN1 mutations), MFS type 2 and Loeys-Dietz syndrome (associated with TGFBR1/TGFBR2 mutations), and Ehlers-Danlos syndrome (EDS) vascular type (caused by COL3A1 mutations). Although mutations in FBN1 and TGFBR1/TGFBR2 account for the majority of AD cases referred to us for molecular genetic testing, we have obtained negative results for these genes in a large cohort of AD patients, suggesting the involvement of additional genes or acquired factors. In this study we assessed the effect of COL3A1 deletions/duplications in this cohort. Multiplex ligation-dependent probe amplification (MLPA) analysis of 100 unrelated patients identified one hemizygous deletion of the entire COL3A1 gene. Subsequent microarray analyses and sequencing of breakpoints revealed the deletion size of 3,408,306 bp at 2q32.1q32.3. This deletion affects not only COL3A1 but also 21 other known genes (GULP1, DIRC1, COL5A2, WDR75, SLC40A1, ASNSD1, ANKAR, OSGEPL1, ORMDL1, LOC100129592, PMS1, MSTN, C2orf88, HIBCH, INPP1, MFSD6, TMEM194B, NAB1, GLS, STAT1, and STAT4), mutations in three of which (COL5A2, SLC40A1, and MSTN) have also been associated with an autosomal dominant disorder (EDS classical type, hemochromatosis type 4, and muscle hypertrophy). Physical and laboratory examinations revealed that true haploinsufficiency of COL3A1, COL5A2, and MSTN, but not that of SLC40A1, leads to a clinical phenotype. Our data not only emphasize the impact/role of COL3A1 in AD patients but also extend the molecular etiology of several disorders by providing hitherto unreported evidence for true haploinsufficiency of the underlying gene.

Efeitos da Imunocastração e de agonistas beta-adrenérgicos sobre a qualidade da carne de bovinos

Os agonistas beta-adrenérgicos (βAA) são conhecidos por aumentar a hipertrofia muscular e lipólise, neste caso uma maneira de se reduzir o efeito da lipólise seria a imunocastração. Dessa forma, o objetivo deste projeto foi avaliar o efeito dos βAA e da imunocastração sobre a qualidade da carne de bovinos Nelore. Foram utilizados noventa e seis bovinos Nelore, sendo que metade dos animais (n=48) receberam uma dose da vacina de imunocastração, e após 30 dias receberam a segunda dose. A outra metade dos animais (n=48) não recebeu nenhuma dose da vacina. Durante 70 dias os animais foram alimentados com uma dieta padrão composta de 24% volumoso e 76% de concentrado. Após 70 dias de confinamento os animais foram divididos em três grupos, dentro de bloco (peso inicial) e condição sexual e foram alimentados por 30 dias, com umas das seguintes dietas: CON - dieta padrão utilizada na fase anterior, sem a adição de βAA; ZIL - dieta padrão acrescida de 80 mg/dia Cloridrato de Zilpaterol; RAC - dieta padrão acrescida de 300 mg/dia Cloridrato de Ractopamina. Ao final desse período os animais foram abatidos e colhidas amostras do músculo Longissimus dorsi para as avaliações de qualidade de carne, lipídeos totais, perfil de ácidos graxos, análise sensorial do consumidor, perfil morfométrico muscular, expressão dos genes calpaína e calpastatina, comprimento de sarcômero. Para a maioria das características avaliadas não foram observadas interações entre os tratamentos. Ao avaliar o efeito da condição sexual, os animais imunocastrados apresentaram maiores intensidades de cor L, a e b, lipídios totais, ácidos oleico, palmítico e total de monoinsaturados e maior frequência para as fibras oxidativas (FO) e glicolíticas (FG) em relação aos não-castrados. Contudo, os animais não-castrados tiveram uma tendência a apresentarem uma carne mais macia na análise sensorial e obtiveram maior frequência das fibras oxidativasglicolíticas (FOG) em relação aos imunocastrados. Quanto ao efeito dos βAA, o grupo ZIL apresentaram uma carne menos macia na força de cisalhamento, maiores concentrações de ácidos heptadecanoico, linoleico, araquidonico ácido C20:3 N6C8C11C14, ômega 6, maior frequência para as FO e menor para FG em comparação ao grupo RAC e CON. No entanto, os animais do grupo CON e ZIL apresentaram maior área para as FO em comparação ao grupo RAC, enquanto que para as FOG, os animais do grupo CON tiveram maior área do que os animais do grupo RAC e ZIL. Na análise sensorial, os grupos RAC e ZIL receberam menores notas para os atributos textura e qualidade global em relação ao CON. Não foi observado efeito da condição sexual e dos βAA sobre a expressão dos genes e comprimento de sarcômero. Conclui-se que a condição sexual e a suplementação com os βAA podem alterar a qualidade da carne, perfil de ácidos graxos e morfométrico muscular, sem, contudo, alterar a expressão dos genes e do comprimento de sarcômero.

Efeito de diferentes intensidades do treinamento de força nos ganhos de força máxima e hipertrofia muscular

O presente estudo investigou o efeito de diferentes intensidades do treinamento de força (TF), aplicadas com volume total de treino (VTT) equalizado, nos ganhos de força dinâmica máxima (1RM) e massa muscular dos membros superiores e inferiores. Trinta voluntários do sexo masculino, com idade entre 18 e 30 anos, participaram de 12 semanas de TF com uma frequência semanal de duas sessões. Foi utilizado um protocolo de treinamento unilateral com um dos lados do corpo realizando o exercício com intensidade equivalente a 20% 1RM (G20) e o lado contralateral utilizando uma das três intensidades 40%, 60% ou 80% 1RM (G40, G60 e G80, respectivamente). O grupo G20 realizava três séries compostas de repetições até a falha concêntrica e o VTT era calculado e replicado para os demais grupos. A força dinâmica máxima e a área de secção transversa (AST) dos músculos flexores do cotovelo e do vasto lateral foram avaliadas nos momentos pré, 6 semanas e pós-treinamento. Os resultados demonstraram que os grupos G40, G60 e G80 apresentaram ganhos similares de AST (25%, 25,1% e 25%, flexores do cotovelo e 20,5%, 20,4% e 19,5% vasto lateral, respectivamente, p<0,05). Somente o grupo G80 demonstrou diferença significante com o grupo G20 na comparação do período pós-treinamento (25% e 14,4%, respectivamente para os flexores do cotovelo e 19,5% e 7,9%, respectivamente para vasto lateral, p<0,05). Para os ganhos de 1RM o grupo G80 demonstrou maiores aumentos após 12 semanas de TF para a flexão unilateral do cotovelo na posição em pé (54,2% p<0,05) e para o leg press 45º os grupos G60 e G80 demonstraram os maiores aumentos (55,4% e 45,7%, respectivamente, p<0,05). Assim, quando o VTT foi equalizado entre diferentes intensidades (40, 60 e 80% 1RM) os ganhos da AST tanto dos flexores do cotovelo quanto o vasto lateral foram semelhantes e a intensidade de 20% 1RM não causou aumento significante da AST. No que diz respeito a força muscular as intensidades mais elevadas (60% e 80% 1RM) foram superiores em promover ganhos de força do que as demais intensidades utilizadas. Esses dados sugerem que ao equalizar o VTT os ganhos de massa muscular são semelhantes para as intensidades de treinamento entre 40- 80% 1RM. Além disso, a intensidade de 20% 1RM, mesmo com o VTT equalizado com as intensidades maiores, não promove aumentos de massa muscular para ambos os segmentos corporais. Por outro lado, intensidades altas de treinamento produzem os maiores ganhos de força máxima em membros superiores e inferiores

O uso da percepção subjetiva do esforço da sessão no controle da progressão da carga do treinamento de força: uma alternativa ao modelo tradicional

O objetivo deste estudo foi investigar se a progressão da carga do treinamento de força (TF) de acordo com a monitoração da percepção subjetiva do esforço da sessão (PSE da sessão) pode ser mais eficaz no desenvolvimento da força motora e hipertrofia muscular em relação ao modelo tradicional de prescrição do TF baseado apenas na carga externa do treinamento. Métodos: Vinte sujeitos do sexo masculino com experiência prévia em treinamento de força (5,4± 4,1 anos) foram submetidos a seis semanas de TF no exercício agachamento (2x/sem.). Os sujeitos foram separados em dois grupos: i) grupo progressão linear da carga de treinamento (PL, n=10), que seguiu um modelo pré-determinado de progressão da carga do TF, com incrementos realizados a cada duas semanas de treino, partindo do protocolo A em direção ao protocolo C (protocolo A= 2x12-15RM; protocolo B= 4x8-10RM e protocolo C= 6x4-6RM) e; ii) grupo PSE (PSE, n=10), que progrediu a carga do TF de acordo com os escores da PSE da sessão partindo do protocolo A, na primeira sessão de treino, com incremento de carga (i.e., do protocolo A para protocolo B ou do protocolo B em direção ao protocolo C) quando os escores de PSE da sessão estivessem abaixo de 6 (i.e., <=5). Mantendo o protocolo do próximo treino caso os escores da PSE da sessão estivessem entre 6 e 8 e diminuindo em uma série o protocolo da sessão seguinte caso os escores da PSE da sessão estivessem por duas vezes consecutivas acima de 8 (i.e., >=9) até que a resposta perceptiva voltasse as classificações entre 6 e 8. As avaliações de força máxima dinâmica (1-RM) e de área de secção transversa muscular (ASTM) foram realizadas antes (pré) a pós o período experimental (pós). Resultados: Ambos os grupos aumentaram de forma semelhante os valores de 1-RM (PL: p<0,0001 e PSE: p<0,0001) a ASTM (PL: p<0,0001 e PSE: p=0,0032). Entretanto, o grupo PSE chegou a estes resultados realizando um número menor de sessões nos protocolos com cargas de treinamento mais altas (protocolos B: p=0,0028 e C: p=0,004) ao mesmo tempo em que realizaram um número maior de sessões no protocolo de treinamento com cargas mais baixas (i.e., protocolo A) (p<0,0001) quando comparado ao grupo PL. De forma interessante, o subgrupo composto (a posteriori) pelos indivíduos do grupo PSE que não progrediram a carga do TF além do protocolo A (SubPSE, n =6), obtiveram ganhos de força motora e hipertrofia muscular semelhantes àqueles observados no grupo PL (1-RM p=0,0003; ASTM: p=0,0212 respectivamente) realizando de um volume total menor de treinamento (p=0,0258). Conclusão: O controle da progressão da carga do TF por meio da PSE da sessão proporcionou ajustes mais eficientes da carga de treinamento possibilitando aumentos de força motora e hipertrofia muscular similares aos obtidos através do modelo de progressão tradicional por meio de protocolos de treinamento menos intensos e de menor volume. Adicionalmente, quando considerados os dados do subgrupo SubPSE, observou-se as mesmas adaptações funcionais e morfológicas por meio de um menor volume total de treinamento

Salmeterol enhances the cardiac response to gene therapy in Pompe disease.

Enzyme replacement therapy (ERT) with recombinant human (rh) acid α-glucosidase (GAA) has prolonged the survival of patients. However, the paucity of cation-independent mannose-6-phosphate receptor (CI-MPR) in skeletal muscle, where it is needed to take up rhGAA, correlated with a poor response to ERT by muscle in Pompe disease. Clenbuterol, a selective β2 receptor agonist, enhanced the CI-MPR expression in striated muscle through Igf-1 mediated muscle hypertrophy, which correlated with increased CI-MPR (also the Igf-2 receptor) expression. In this study we have evaluated 4 new drugs in GAA knockout (KO) mice in combination with an adeno-associated virus (AAV) vector encoding human GAA, 3 alternative β2 agonists and dehydroepiandrosterone (DHEA). Mice were injected with AAV2/9-CBhGAA (1E+11 vector particles) at a dose that was not effective at clearing glycogen storage from the heart. Heart GAA activity was significantly increased by either salmeterol (p<0.01) or DHEA (p<0.05), in comparison with untreated mice. Furthermore, glycogen content was reduced in the heart by treatment with DHEA (p<0.001), salmeterol (p<0.05), formoterol (p<0.01), or clenbuterol (p<0.01) in combination with the AAV vector, in comparison with untreated GAA-KO mice. Wirehang testing revealed that salmeterol and the AAV vector significantly increased performance, in comparison with the AAV vector alone (p<0.001). Similarly, salmeterol with the vector increased performance significantly more than any of the other drugs. The most effective individual drugs had no significant effect in absence of vector, in comparison with untreated mice. Thus, salmeterol should be further developed as adjunctive therapy in combination with either ERT or gene therapy for Pompe disease.

Altération de la régénération musculaire dans la maladie pulmonaire obstructive chronique

Altération de la régénération musculaire dans la maladie pulmonaire obstructive chronique. La maladie pulmonaire obstructive chronique (MPOC) est caractérisée par une obstruction bronchique irréversible et progressive. L’atrophie musculaire périphérique y est fréquente et a un impact négatif sur la capacité fonctionnelle et la survie des sujets atteints. Toutefois, on ignore si une altération du processus de régénération musculaire est un processus ayant cours dans l’atrophie musculaire périphérique. Le but de la présente thèse était donc d’étudier les cellules satellites, principales cellules responsables de la régénération musculaire dans les muscles périphériques de patients ayant une MPOC. Dans un premier temps, nous avons évalué l’historique de réplication du tissu musculaire et la sénescence des cellules satellites. Les changements morphologiques ayant lieu dans le muscle au cours de la progression de la maladie rendent le muscle plus susceptible aux dommages, induisant un raccourcissement prématuré des télomères. Un raccourcissement des télomères chez les sujets ayant une MPOC avec atrophie est concomitant avec une augmentation du nombre de cellules satellites sénescentes et de l’épuisement du potentiel de régénération compromettant le maintien de la masse musculaire chez ces sujets. Dans un deuxième et troisième temps, nous avons étudié les étapes amenant une cellule satellite vers une cellule musculaire dans les muscles périphériques et respiratoires de patients ayant une MPOC comparativement à des sujets contrôles. Les cellules satellites sont impliquées dans la réparation du tissu musculaire. Dans les cellules satellites provenant des sujets ayant une MPOC, une altération de la prolifération et de la différentiation a été observée. Ces résultats sont compatibles avec une altération de la régénération musculaire pouvant conduire à l’atrophie musculaire dans la MPOC. Le quatrième volet de ce projet s’intéressait à l’impact d’un entraînement en résistance sur l’activité des cellules satellites et le rôle joué par la myostatine dans ce contexte. La littérature montre que l’exercice en résistance est bien toléré et aide les patients ayant une MPOC à retrouver une meilleure qualité de vie. Cependant, il semble qu’ils n’y répondent pas tous aussi bien que les sujets contrôles. La capacité de réponse des cellules satellites à un entraînement en résistance semble inadéquate, suggérant ainsi un défaut de leur activation. Dans la dernière étude de cette thèse, nous avons voulu évaluer l’impact de l’inflammation systémique en étudiant SAA1, une protéine de phase aiguë et p21, une protéine du cycle cellulaire dans la dégradation des protéines des cellules musculaires. Les liens de causalité entre l’affection primaire et les différentes comorbidités demeurent nébuleux dans la MPOC. SAA1 et p21 sont augmentés dans les muscles squelettiques des patients ayant une MPOC et par ailleurs, SAA1 est capable d’induire la dégradation des protéines musculaires. Cette thèse expose les premiers éléments impliquant l’altération de la régénération musculaire avec la dysfonction musculaire observée chez les patients ayant une MPOC. Ces résultats vont certainement contribuer au développement de nouvelles thérapies et stratégies d’intervention dans le but d’améliorer la qualité de vie des personnes atteintes d’une MPOC. En somme, les travaux effectués dans le cadre de la présente thèse montrent que plusieurs mécanismes agissent de concert avec l’inactivité physique afin d’induire le phénotype dysfonctionnel dans les muscles des patients ayant une MPOC.

ms1, a novel stress-responsive, muscle-specific gene that is up-regulated in the early stages of pressure overload-induced left ventricular hypertrophy

We have identified and characterised a cDNA encoding a novel gene, designated myocyte stress 1 (ms1), that is up-regulated within 1 h in the left ventricle following the application of pressure overload by aortic banding in the rat. The deduced ms1 protein of 317 amino acids contains several putative functional motifs, including a region that is evolutionarily conserved. Distribution analysis indicates that rat ms1 mRNA expression is predominantly expressed in striated muscle and progressively increases in the left ventricle from embryo to adulthood. These findings suggest that rust may be important in striated muscle biology and the development of pressure-induced left ventricular hypertrophy. (C) 2002 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.

Muscle-specific growth hormone receptor (GHR) overexpression induces hyperplasia but not hypertrophy in transgenic zebrafish

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Myosin heavy chain expression and atrophy in rat skeletal muscle during transition from cardiac hypertrophy to heart failure

The purpose of this investigation was to determine whether changes in myosin heavy chain (MHC) expression and atrophy in rat skeletal muscle are observed during transition from cardiac hypertrophy to chronic heart failure (CHF) induced by aortic stenosis (AS). AS and control animals were studied 12 and 18 weeks after surgery and when overt CHF had developed in AS animals, 28 weeks after the surgery. The following parameters were studied in the soleus muscle: muscle atrophy index (soleus weight/body weight), muscle fibre diameter and frequency and MHC expression. AS animals presented decreases in both MHC1 and type I fibres and increases in both MHC2a and type IIa fibres during late cardiac hypertrophy and CHF. Type IIa fibre atrophy occurred during CHF. In conclusion, our data demonstrate that skeletal muscle phenotype changes occur in both late cardiac hypertrophy and heart failure; this suggests that attention should be given to the fact that skeletal muscle phenotype changes occur prior to overt heart failure symptoms.