29 resultados para FORÇA MUSCULAR

em Deakin Research Online - Australia


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Developing a lean muscular figure for the purposes of sports and/or appearance has become a central issue for males. Concern has been raised because the desire to develop such a body build may lead to the adoption of numerous health-threatening behaviors. Consequently, this review presents a comprehensive analysis of the physical and psychological consequences that result from the use of steroids (legal and illegal), ephedrine, and deleterious dieting strategies specific to males. Putative risk factors for these behaviors will be identified, and the clinical disorder associated with the extreme abuse of these behaviors, muscle dysmorphia, will be examined.


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Objectives
To elicit descriptive data about limited joint range of motion (ROM) in subjects with type II or III spinal muscular atrophy (SMA) and to examine the relation between the number of motions with limited range and both age and functional ability.
Design
Descriptive cross-sectional study.
Setting
Neurologic pediatric outpatient clinic at a hospital in Taiwan.
Participants
Twenty-seven subjects with SMA type II (mean age, 9.8±6.5y) and 17 with SMA type III (mean age, 12.2±8.7y).
Intervention
Measurement with transparent goniometers of joint ROM bilaterally of the shoulder, elbow, wrist, hip, knee, and ankle.
Main outcome measures
The proportion of participants with each ROM limitation compared with all participants with the same SMA type, age distribution of the participants with each ROM limitation, mean range loss of each motion limitation, and the contracture index (risk index of joint contracture).
Results
Eighty-nine percent of the participants with SMA type II experienced knee extension limitation. Approximately 50% of the participants with both types of SMA had ankle dorsiflexion limitation. The motions of knee and hip extension and ankle dorsiflexion also had a relatively high contracture index. The number of motions with limited range positively correlated (P<.001) with age and upper-extremity functional grade (the higher the functional grade, the poorer the functional ability) for SMA type II.
Conclusions
We found varying degrees of joint ROM limitation. Certain motions were noted to be high risks for the development of contractures. This risk was higher mostly in younger children.

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Duchenne muscular dystrophy (DMD) is a severe and progressive muscle wasting disorder caused by mutations in the dystrophin gene that result in the absence of the membrane-stabilizing protein dystrophin1, 2, 3. Dystrophin-deficient muscle fibres are fragile and susceptible to an influx of Ca2+, which activates inflammatory and muscle degenerative pathways4, 5, 6. At present there is no cure for DMD, and existing therapies are ineffective. Here we show that increasing the expression of intramuscular heat shock protein 72 (Hsp72) preserves muscle strength and ameliorates the dystrophic pathology in two mouse models of muscular dystrophy. Treatment with BGP-15 (a pharmacological inducer of Hsp72 currently in clinical trials for diabetes) improved muscle architecture, strength and contractile function in severely affected diaphragm muscles in mdx dystrophic mice. In dko mice, a phenocopy of DMD that results in severe spinal curvature (kyphosis), muscle weakness and premature death7, 8, BGP-15 decreased kyphosis, improved the dystrophic pathophysiology in limb and diaphragm muscles and extended lifespan. We found that the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA, the main protein responsible for the removal of intracellular Ca2+) is dysfunctional in severely affected muscles of mdx and dko mice, and that Hsp72 interacts with SERCA to preserve its function under conditions of stress, ultimately contributing to the decreased muscle degeneration seen with Hsp72 upregulation. Treatment with BGP-15 similarly increased SERCA activity in dystrophic skeletal muscles. Our results provide evidence that increasing the expression of Hsp72 in muscle (through the administration of BGP-15) has significant therapeutic potential for DMD and related conditions, either as a self-contained therapy or as an adjuvant with other potential treatments, including gene, cell and pharmacological therapies.

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New Findings What is the central question of this study? The Notch signalling pathway plays an important role in muscle regeneration, and activation of the pathway has been shown to enhance muscle regeneration in aged mice. It is unknown whether Notch activation will have a similarly beneficial effect on muscle regeneration in the context of Duchenne muscular dystrophy (DMD). What is the main finding and its importance? Although expression of Notch signalling components is altered in both mouse models of DMD and in human DMD patients, activation of the Notch signalling pathway does not confer any functional benefit on muscles from dystrophic mice, suggesting that other signalling pathways may be more fruitful targets for manipulation in treating DMD. Abstract In Duchenne muscular dystrophy (DMD), muscle damage and impaired regeneration lead to progressive muscle wasting, weakness and premature death. The Notch signalling pathway represents a central regulator of gene expression and is critical for cellular proliferation, differentiation and apoptotic signalling during all stages of embryonic muscle development. Notch activation improves muscle regeneration in aged mice, but its potential to restore regeneration and function in muscular dystrophy is unknown. We performed a comprehensive examination of several genes involved in Notch signalling in muscles from dystrophin-deficient mdx and dko (utrophin- and dystrophin-null) mice and DMD patients. A reduction of Notch1 and Hes1 mRNA in tibialis anterior muscles of dko mice and quadriceps muscles of DMD patients and a reduction of Hes1 mRNA in the diaphragm of the mdx mice were observed, with other targets being inconsistent across species. Activation and inhibition of Notch signalling, followed by measures of muscle regeneration and function, were performed in the mouse models of DMD. Notch activation had no effect on functional regeneration in C57BL/10, mdx or dko mice. Notch inhibition significantly depressed the frequency-force relationship in regenerating muscles of C57BL/10 and mdx mice after injury, indicating reduced force at each stimulation frequency, but enhanced the frequency-force relationship in muscles from dko mice. We conclude that while Notch inhibition produces slight functional defects in dystrophic muscle, Notch activation does not significantly improve muscle regeneration in murine models of muscular dystrophy. Furthermore, the inconsistent expression of Notch targets between murine models and DMD patients suggests caution when making interspecies comparisons.

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Hypoxia is an important modulator of endurance exercise-induced oxidative adaptations in skeletal muscle. However, whether hypoxia affects resistance exercise-induced muscle adaptations remains unknown. Here, we determined the effect of resistance exercise training under systemic hypoxia on muscular adaptations known to occur following both resistance and endurance exercise training, including muscle cross-sectional area (CSA), one-repetition maximum (1RM), muscular endurance, and makers of mitochondrial biogenesis and angiogenesis, such as peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), citrate synthase (CS) activity, nitric oxide synthase (NOS), vascular endothelial growth factor (VEGF), hypoxia-inducible factor-1 (HIF-1), and capillary-to-fiber ratio. Sixteen healthy male subjects were randomly assigned to either a normoxic resistance training group (NRT, n = 7) or a hypoxic (14.4% oxygen) resistance training group (HRT, n = 9) and performed 8 weeks of resistance training. Blood and muscle biopsy samples were obtained before and after training. After training muscle CSA of the femoral region, 1RM for bench-press and leg-press, muscular endurance, and skeletal muscle VEGF protein levels significantly increased in both groups. The increase in muscular endurance was significantly higher in the HRT group. Plasma VEGF concentration and skeletal muscle capillary-to-fiber ratio were significantly higher in the HRT group than the NRT group following training. Our results suggest that, in addition to increases in muscle size and strength, HRT may also lead to increased muscular endurance and the promotion of angiogenesis in skeletal muscle.

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Classic physiology studies dating to the 1930s demonstrate that moderate or transient glucocorticoid (GC) exposure improves muscle performance. The ergogenic properties of GCs are further evidenced by their surreptitious use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle-wasting disease. A defined molecular basis underlying these performance-enhancing properties of GCs in skeletal muscle remains obscure. Here, we demonstrate that ergogenic effects of GCs are mediated by direct induction of the metabolic transcription factor KLF15, defining a downstream pathway distinct from that resulting in GC-related muscle atrophy. Furthermore, we establish that KLF15 deficiency exacerbates dystrophic severity and muscle GC-KLF15 signaling mediates salutary therapeutic effects in the mdx mouse model of DMD. Thus, although glucocorticoid receptor (GR)-mediated transactivation is often associated with muscle atrophy and other adverse effects of pharmacologic GC administration, our data define a distinct GR-induced gene regulatory pathway that contributes to therapeutic effects of GCs in DMD through proergogenic metabolic programming.

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There is a paucity of evidence-based support for the allocation of rest interval duration between incremental loads in the assessment of the load-power profile. We examined the effect of rest interval duration on muscular power production in the load-power profile and sought to determine if greater rest is required with increasing load (i.e., variable rest interval). Ten physically trained men completed 4 experimental conditions in a crossover balanced design. Participants performed jump squats across incremental loads (0-60 kg) on 4 occasions, with an allocated recovery interval of 1, 2, 3, or 4 minutes. The mean log-transformed power output at each load was used for comparison between conditions (rest intervals). Unloaded jump squats (0 kg) maximized power output at each condition. The maximal mechanical power output was 66.6 ± 6.5 W·kg (1 minute), 66.2 ± 5.2 W·kg (2 minutes), 67.1 ± 5.9 W·kg (3 minutes), and 66.2 ± 6.5 W·kg (4 minutes). Trivial or unclear differences in power output were observed between rest intervals at each incremental load. As expected, power declined per 10 kg increment in load, the magnitude of decrease was 13.9-14.5% (confidence limits [CL]: ±1.3-2.0%) and 13.4-14.6% (CL: ±2.4-3.9%) for relative peak and mean power, respectively, yet differences in power output between conditions were likely insubstantial. The prescription of rest intervals between loads that are longer than 1 minute have a likely negligible effect on muscular power production in the jump squat incremental load-power profile. Practitioners should select either a 1- to 4-minute rest interval to best accommodate the logistical constraints of their monitoring sessions.

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1. Skeletal muscle is a complex and heterogenous tissue capable of remarkable adaptation in response to exercise training. The role of gene transcription, as an initial target to control protein synthesis, is poorly understood.
2. Mature myofibres contain several hundred nuclei, all of which maintain transcriptional competency, although the localized responsiveness of nuclei is not well known. Myofibres are capable of hypertrophy. These processes require the activation and myogenic differentiation of mononuclear satellite cells that fuse with the enlarging or repairing myofibre.
3. A single bout of exercise in human subjects is capable of activating the expression of many diverse groups of genes.
4. The impact of repeated exercise bouts, typical of exercise training, on gene expression has yet to receive systematic investigation.
5. The molecular programme elicited by resistance exercise and endurance exercise differs markedly. Muscular hypertrophy following resistance exercise is dependent on the activation of satellite cells and their subsequent myogenic maturation. Endurance exercise requires the simultaneous activation of mitochondrial and nuclear genes to enable mitochondrial biogenesis.
6. Future analysis of the regulation of genes by exercise may combine high-throughput technologies, such as gene-chips, enabling the rapid detection and analysis of changes in the expression of many thousands of genes.

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Previous research has indicated that both boys and girls strive for a slim body, with boys having an additional focus on a muscular body build. The current study was designed to evaluate the utility of a biopsychosocial model to explain body image and body change strategies among children. The study evaluated changes over time in body image and strategies to lose weight and increase muscles among 132 normal weight and 67 overweight boys (mean age=9.23 years) and 158 normal weight and 55 overweight girls (mean age=9.33 years). The predictive role of BMI, positive and negative affect, self-esteem and perceived sociocultural pressures to lose weight or increase muscle on body image and body change strategies over a 16 month period was evaluated. All participants completed the questionnaire on both occasions. The results demonstrated that both overweight boys and girls were more likely to be dissatisfied with their weight, place more importance on their weight, engage in more strategies to lose weight as well as perceive more pressure to lose weight. Overweight boys and girls were also more likely to report lower levels of self-esteem and positive affect, and higher levels of negative affect, and reported a reduction in their self-esteem over time. Regression analyses demonstrated that among overweight boys, low self-esteem and high levels of perceived pressure to lose weight predicted weight dissatisfaction; for overweight girls, weight dissatisfaction was also predicted by low levels of self-esteem. The implication of these findings in terms of factors contributing to the adoption of health risk behaviors among children is discussed.

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Society provides messages about how people should ideally look and previous research has indicated these messages, both the actual messages provided and the perception of the message, influence body image. Research into male body image has shown males are concerned with having a lean and muscular body and as such, may want to decrease fat and increase their muscles. This paper explored the influence of a range of messages from parents, peers, and the media on a number of different measures of 362 adolescent boys’ body image and body change strategies. Specifically, messages about shape, food, exercise, losing weight and increasing muscles were explored in relation to satisfaction with weight and muscles, and the use of strategies to decrease weight and increase muscles. The findings indicated that parental messages were the strongest influence on body image and that parents, the media, and to a lesser extent messages from male friends were the strongest predictors of body change strategies.

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According to the unrevised Reinforcement Sensitivity Theory two motivational systems shape personality: a behavioural approach system (BAS) that determines sensitivity to rewards, and a behavioural inhibition system (BIS) that determines sensitivity to punishments. The role of reinforcement sensitivity in body change behaviour in males was explored with a non-clinical sample of 120 men aged 18–40 years. Self-reported symptoms of unhealthy weight loss (weight preoccupation, fasting, bingeing/purging) and body development (muscle/size preoccupation, obligatory exercise, use of chemical supplements) were regressed on measures of BAS and BIS sensitivity. Significant relationships were observed between BAS sensitivity and body development, and between BIS sensitivity and weight loss. These relationships were mediated by internalization of the athletic/muscular ideal, body comparisons, the importance of achieving one’s ideal or ‘best possible’ body (in the case of BAS but not BIS), and body dissatisfaction (in the case of BIS but not BAS). These results support the proposition that body development in males is influenced by sensitivity to rewards associated with achieving a certain body shape, and that weight loss is influenced by sensitivity to punishments associated with possessing an unsatisfactory body shape.

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OBJECTIVE -- To examine the effect of high-intensity progressive resistance training combined with moderate weight loss on glycemic control and body composition in older patients with type 2 diabetes.

RESEARCH DESIGN AND METHODS -- Sedentary, overweight men and women with type 2 diabetes, aged 60-80 years (n = 36), were randomized to high-intensity progressive resistance training plus moderate weight loss (RT & WL group) or moderate weight loss plus a control program (WL group). Clinical and laboratory measurements were assessed at 0, 3, and 6 months.

RESULTS -- HbA.1c fell significantly more in RT & WL than WL at 3 months (0.6 ± or -] 0.7 vs. 0.07 ± 0.8%, P < 0.05) and 6 months (1.2 ±1.0 vs. 0.4 ±0.8, P < 0.05). Similar reductions in body weight (RT & WL 2.5 ±2.9 vs. WL 3.1±2.1 kg) and fat mass (RT & WL 2.4 ± 2.7 vs. WL 2.7±2.5 kg) were observed after 6 months. In contrast, lean body mass (LBM) increased in the RT & WL group (0.5 ±1.1 kg) and decreased in the WL group (0.4±1.0) after 6 months (P < 0.05). There were no between-group differences for fasting glucose, insulin, serum lipids and lipoproteins, or resting blood pressure.

CONCLUSIONS -- High-intensity progressive resistance training, in combination with moderate weight loss, was effective in improving glycemic control in older patients with type 2 diabetes. Additional benefits of improved muscular strength and LBM identify high-intensity resistance training as a feasible and effective component in the management program for older patients with type 2 diabetes.

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Objective: We explored the extent to which changes in emotional states following exposure to images of idealized bodies predict unhealthy body change attitudes and behaviors in women and men, and whether particular psychological traits mediate these effects. Method: One hundred thirty-three women and 93 men were assessed for unhealthy attitudes and behaviors related to body weight and muscles using the Eating Disorder Inventory-2 (EDI-2), the Obligatory Exercise Questionnaire, and the strategies to increase muscles subscale of the Body Change Inventory. Psychological traits assessed included body dissatisfaction (EDI-2), internalization of the thin/athletic ideal (Sociocultural Attitudes Towards Appearance Questionnaire-3), body comparison (Body Comparison Scale), self-esteem (Rosenberg Self-Esteem Inventory), depression (Beck Depression Inventory-II), and identity confusion (Self-Concept Clarity Scale). Participants were then exposed to photographs of thin female models and muscular male models, and visual analogue scales were used to measure changes in postexposure state body dissatisfaction, anger, anxiety, and depression.
Results: Postexposure increases in state anger, anxiety, depression, and body dissatisfaction correlated with drive for thinness and disordered eating symptomatology in women, while postexposure increases in state body dissatisfaction correlated with muscle development in men. Analyses revealed that internalization and body comparison mediated these relationships, with trait body dissatisfaction, trait depression, self-esteem, and self-concept/identity confusion serving as mediators for women only. Conclusion: These results are indicative of gender differences in: (a) reactions to idealized bodies; (b) psychological traits that predispose individuals to experience these reactions; and (c) types of body change behavior that are associated with these reactions.