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Anabolic skeletal therapy for osteoporosis
Girotra, Monica;Rubin, Mishaela R.;Bilezikian, John P.;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2006, DOI: 10.1590/S0004-27302006000400019
Abstract: antiresorptive agents for osteoporosis are a cornerstone of therapy, but anabolic drugs have recently widened our therapeutic options. by directly stimulating bone formation, anabolic agents reduce fracture incidence by improving bone qualities besides increasing bone mass. in this article, we review the role of anabolic treatment for osteoporosis. the only anabolic agent currently approved in the united states for osteoporosis, teriparatide [recombinant human parathyroid hormone(1-34)], has clearly emerged as a major approach to selected patients with osteoporosis. teriparatide increases bone density and bone turnover, improves microarchitecture, and changes bone size. the incidence of vertebral and nonvertebral fractures is reduced. teriparatide is approved for both postmenopausal women and men with osteoporosis who are at high risk for fracture. other potential anabolic therapies for osteoporosis, including other forms of parathyroid hormone, strontium ranelate, growth hormone, and insulin-like growth factor-1, are also reviewed in this article.
Exercise and Amino Acid Anabolic Cell Signaling and the Regulation of Skeletal Muscle Mass  [PDF]
Stefan M. Pasiakos
Nutrients , 2012, DOI: 10.3390/nu4070740
Abstract: A series of complex intracellular networks influence the regulation of skeletal muscle protein turnover. In recent years, studies have examined how cellular regulators of muscle protein turnover modulate metabolic mechanisms contributing to the loss, gain, or conservation of skeletal muscle mass. Exercise and amino acids both stimulate anabolic signaling potentially through several intracellular pathways including the mammalian target of rapamycin complex 1 and the mitogen activated protein kinase cell signaling cascades. As novel molecular regulators of muscle integrity continue to be explored, a contemporary analysis of the literature is required to understand the metabolic mechanisms by which contractile forces and amino acids affect cellular process that contribute to long-term adaptations and preservation of muscle mass. This article reviews the literature related to how exercise and amino acid availability affect cellular regulators of skeletal muscle mass, especially highlighting recent investigations that have identified mechanisms by which contractile forces and amino acids modulate muscle health. Furthermore, this review will explore integrated exercise and nutrition strategies that promote the maintenance of muscle health by optimizing exercise, and amino acid-induced cell signaling in aging adults susceptible to muscle loss.
Effects of anabolic hormones on structural, metabolic and functional aspects of skeletal muscle
Flávio de Oliveira Pires,Adriano Eduardo Lima Silva,Valmor Tricoli
Revista Brasileira de Cineantropometria e Desempenho Humano , 2009,
Abstract: This study reviewed information regarding the effects of anabolic hormones on strength gain and muscle hypertrophy, emphasizing the physiological mechanisms that may increase muscle strength. Structural, metabolic and functional aspects were analyzed and special attention was paid to the dose-response relationship. The Pubmed database was searched and studies were selected according to relevance and date of publication (last 15 years). The administration of high testosterone doses (~600 mg/week) potentiates the effects of strength training, increasing lean body mass, muscle fiber type IIA and IIB cross-sectional area, and the number of myonuclei. There is no evidence of conversion between MHC isoforms. The interaction between testosterone administration and strength training seems to modify some metabolic pathways, increasing protein synthesis, glycogen and ATP-CP muscle stores and improving fat mobilization. Changes in 17 -estradiol concentration or in the ACTH-cortisol and insulin-glucagon ratios seem to be associated with these metabolic alterations. Regarding performance, testosterone administration may improve muscle strength by 5-20% depending on the dose used. On the other hand, the effects of growth hormone on the structural and functional aspects of skeletal muscle are not evident, with this hormone more affecting metabolic aspects. However, strictly controlled human studies are necessary to establish the extent of the effects of anabolic hormones on structural, metabolic and functional aspects.
MicroRNAs in skeletal muscle and their regulation with exercise, ageing, and disease  [PDF]
Evelyn Zacharewicz,Séverine Lamon,Aaron P. Russell
Frontiers in Physiology , 2013, DOI: 10.3389/fphys.2013.00266
Abstract: Skeletal muscle makes up approximately 40% of the total body mass, providing structural support and enabling the body to maintain posture, to control motor movements and to store energy. It therefore plays a vital role in whole body metabolism. Skeletal muscle displays remarkable plasticity and is able to alter its size, structure and function in response to various stimuli; an essential quality for healthy living across the lifespan. Exercise is an important stimulator of extracellular and intracellular stress signals that promote positive adaptations in skeletal muscle. These adaptations are controlled by changes in gene transcription and protein translation, with many of these molecules identified as potential therapeutic targets to pharmacologically improve muscle quality in patient groups too ill to exercise. MicroRNAs (miRNAs) are recently identified regulators of numerous gene networks and pathways and mainly exert their effect by binding to their target messenger RNAs (mRNAs), resulting in mRNA degradation or preventing protein translation. The role of exercise as a regulatory stimulus of skeletal muscle miRNAs is now starting to be investigated. This review highlights our current understanding of the regulation of skeletal muscle miRNAs with exercise and disease as well as how they may control skeletal muscle health.
Lack of anabolic response to skeletal loading in mice with targeted disruption of the pleiotrophin gene
Chandrasekhar Kesavan, Subburaman Mohan
BMC Research Notes , 2008, DOI: 10.1186/1756-0500-1-124
Abstract: Four-point bending caused an acute increase in PTN expression (2-fold) within 2 days of loading and further increased (3–6 fold) with continued loading. This increase was also seen in 16 and 36-week old mice. Based on these findings, we next used PTN knockout (KO) mice to evaluate the cause and effect relationship. Quantitative analysis showed that two weeks of ML induced changes in vBMD and bone size in the PTN KO mice (8% and 6% vs. non-loaded bones) were not significantly different from control mice (11% and 8% in vBMD and bone size vs. non-loaded bones).Our results imply that PTN is not a key upstream mediator of the anabolic effects of ML on the skeleton.Mechanical loading is now recognized as an important stimulator of bone formation. Numerous studies in animal and humans, using various loading models have demonstrated that loading increases bone mass while unloading decreases bone mass [1-6]. To date, reports have shown that several growth factors and signaling pathways are known to be activated by ML [7-11]. However, the relative contribution of each of these pathways to ML induced bone formation is not known. We previously, using genome-wide microarray approach have reported that mechanical loading by four-point bending caused a 4-fold increase in Heparin binding growth factor, otherwise known as PTN, in a good responder B6 mouse [7]. PTN, a 36 amino acid bone growth factor rich in lysine and cysteine residues, is also known as Osteoblast Specific Factor 1. PTN is involved in diverse functions, which includes: cell recruitment, cell attachment and proliferation, differentiation, angiogensis, and neurogenesis [12-14]. In vitro studies have demonstrated that PTN has the ability to promote adhesion, migration, expansion and differentiation of human osteoprogenitor and MC3T3-E1 cells [15-17]. In vivo studies using transgenic approach have shown that ovariectomy induced bone loss, due to estrogen deficiency, were protected by an increase in the expression of the
Effects of Anabolic Steroids and High-Intensity Aerobic Exercise on Skeletal Muscle of Transgenic Mice  [PDF]
Karina Fontana, Gerson E. R. Campos, Robert S. Staron, Maria Alice da Cruz-H?fling
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0080909
Abstract: In an attempt to shorten recovery time and improve performance, strength and endurance athletes occasionally turn to the illicit use of anabolic-androgenic steroids (AAS). This study evaluated the effects of AAS treatment on the muscle mass and phenotypic characteristics of transgenic mice subjected to a high-intensity, aerobic training program (5d/wk for 6 weeks). The transgenic mice (CETP+/-LDLr-/+) were engineered to exhibit a lipid profile closer to humans. Animals were divided into groups of sedentary (Sed) and/or training (Ex) mice (each treated orally with AAS or gum arabic/vehicle: Sed-C, Sed-M, ex-C, ex-M). The effects of AAS (mesterolone: M) on specific phenotypic adaptations (muscle wet weight, cross-sectional area, and fiber type composition) in three hindlimb muscles (soleus:SOL, tibialis anterior:TA and gastrocnemius:GAS) were assessed. In order to detect subtle changes in fiber type profile, the entire range of fiber types (I, IC, IIAC, IIA, IIAD, IID, IIDB, IIB) was delineated using mATPase histochemistry. Body weight gain occurred throughout the study for all groups. However, the body weight gain was significantly minimized with exercise. This effect was blunted with mesterolone treatment. Both AAS treatment (Sed-M) and high-intensity, aerobic training (ex-C) increased the wet weights of all three muscles and induced differential hypertrophy of pure and hybrid fibers. Combination of AAS and training (ex-M) resulted in enhanced hypertrophy. In the SOL, mesterolone treatment (Sed-M and ex-M) caused dramatic increases in the percentages of fiber types IC, IIAC, IIAD, IID, with concomitant decrease in IIA, but had minimal impact on fiber type percentages in the predominantly fast muscles. Overall, the AAS-induced differential adaptive changes amounted to significant fiber type transformations in the fast-to-slow direction in SOL. AAS treatment had a significant effect on muscle weights and fiber type composition in SOL, TA and GAS which was even maximized in animals subjected to metabolically high-intensity aerobic exercise.
Ageing prolongs inflammatory marker expression in regenerating rat skeletal muscles after injury
Chris van der Poel, Luc E Gosselin, Jonathan D Schertzer, James G Ryall, Kristy Swiderski, Meron Wondemaghen, Gordon S Lynch
Journal of Inflammation , 2011, DOI: 10.1186/1476-9255-8-41
Abstract: Right extensor digitorum longus (EDL) muscles from young (3 month), adult (12 month) and old (24 month) male F344 rats were injected with bupivacaine hydrochloride to cause complete muscle fibre degeneration, then excised 12, 24, 36, and 72 hours later (n = 5/age group/time point). We used qRT-PCR to quantify the mRNA expression levels of the inflammatory markers TNFα, IFNγ, IL1, IL18, IL6, and CD18 as well as regenerative markers MyoD and myogenin.Inflammatory markers were all increased significantly in all age groups after myotoxic injury. There was a trend for expression of inflammatory markers to be higher in uninjured muscles of old rats, especially at 72 hours post injury where the expression levels of several markers was significantly higher in old compared with young and adult rats. There was also a decrease in the expression of regenerative markers in old rats at 72 hours post injury.Our findings identify a prolonged inflammatory signature in injured muscles from old compared with young and adult rats together with a blunted expression of key markers of regeneration in muscles of old rats. Importantly, our findings identify potential targets for future therapeutic strategies for improving the regenerative capacity of skeletal muscle during ageing.Skeletal muscle regeneration is a complex process composed of three stages: (1) myofibre degeneration; (2) inflammation; and (3) myofibre regeneration and involves the activation of quiescent satellite cells which, through the processes of proliferation and differentiation, participate in the reconstitution of damaged tissues [1,2]. Successful skeletal muscle regeneration after injury requires a carefully regulated inflammatory response to remove cell debris and initiate the activation of the normally quiescent satellite cells [3]. It is widely accepted that inflammation is a natural response to acute skeletal muscle injury as blocking inflammatory cell function by various methods has been demonstrated to result in
Influence of Amino Acids, Dietary Protein, and Physical Activity on Muscle Mass Development in Humans  [PDF]
Kasper Dideriksen,S?ren Reitelseder,Lars Holm
Nutrients , 2013, DOI: 10.3390/nu5030852
Abstract: Ingestion of protein is crucial for maintenance of a variety of body functions and within the scope of this review we will specifically focus on the regulation of skeletal muscle mass. A quantitative limitation exists as to how much muscle protein the body can synthesize in response to protein intake. Ingestion of excess protein exerts an unwanted load to the body and therefore, it is important to find the least amount of protein that provides the maximal hypertrophic stimulus. Hence, research has focused on revealing the relationship between protein intake (dose) and its resulting stimulation of muscle protein synthesis (response). In addition to the protein amount, the protein digestibility and, hence, the availability of its constituent amino acids is decisive for the response. In this regard, recent studies have provided in-depth knowledge about the time-course of the muscle protein synthetic response dependent on the characteristics of the protein ingested. The effect of protein intake on muscle protein accretion can further be stimulated by prior exercise training. In the ageing population, physical training may counteract the development of “anabolic resistance” and restore the beneficial effect of protein feeding. Presently, our knowledge is based on measures obtained in standardized experimental settings or during long-term intervention periods. However, to improve coherence between these types of data and to further improve our knowledge of the effects of protein ingestion, other investigative approaches than those presently used are requested.
ANABOLIC ANDROGENIC STEROIDS AND DEPENDENCE  [PDF]
IHSAN SARI
Citius Altius Fortius , 2010,
Abstract: Anabolic androgenic steroids are used for sportive, cosmetic, therapeutic and occupational reasons and there are many side effects reported (George, 2005; Nieminen et al., 1996; O'Sullivan et al., 2000). Prevalence of anabolic steroids’ use also indicates the importance of this topic. Moreover, it is now known that use of anabolic steroids could lead to dependence which could be psychological or/and physiological (Copeland et al., 2000). It isimportant to know about all aspects of anabolic steroids including dependence. Therefore, this study has attempted to give an insight into use of anabolic steroids and dependence. The discussion will focus on prevalence, reasons, and side effects of use and physiological and psychological dependence
Enfoque terapéutico global de la sarcopenia
Burgos Peláez,R.;
Nutrición Hospitalaria , 2006,
Abstract: sarcopenia is the loss of skeletal muscle mass that occurs with ageing, and is a major contributing factor to disability and loss of independence in the elderly. the etiopathogenesis involves a number of underlying mechanisms including intrinsic changes in the muscle and central nervous system, and hormonal and lifestyle factors. many hormones and cytokines affect muscle mass and function. reductions in testosterone and estrogens that accompany ageing appear to accelerate loss of muscle mass. growth hormone has been hypothesised to contribute to loss of lean body mass. although sarcopenia is not completely reversed with exercise, physical inactivity leads to accelerated muscle loss. the diagnosis of sarcopenia is difficult because the most reliable methods to measure muscle mass are not easily available. various treatment strategies have been tested for combating the loss of muscle mass: testosterone replacement and other anabolic androgens for men, estrogen replacement in women, growth hormone replacement, nutritional treatment and physical training. only high resistance exercise training has been effective in increasing muscle mass, with or without nutritional supplementation.
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