Improvement of muscle mass and force by certain hormones and endogen factors, contributing in muscle development

2007 ◽  
Vol 148 (10) ◽  
pp. 451-456
Author(s):  
Péter Apor ◽  
József Tihanyi ◽  
Andreas Costa
Keyword(s):  
Muscle Mass ◽  
Muscle Development

Az áttekintés az izomtömeg és az izomerő növelése célzatával alkalmazott hormonok (növekedési hormon, IGF-1, anabolikus-androgén szteroidok) és az izom fejlődésében szereplő, humán használatra kerülhető egyes faktorok fizikai aktivitással kapcsolatos élettanát és klinikai alkalmazásának lehetőségeit érinti. A hatásokat illetően mítoszok, a mellékhatásokat illetően alul- és túlértesültség egyaránt jellemzi e területet. A kórállapotok sorában, s nem csak a hiányállapotok szubsztitúciójában történnek terápiás próbálkozások, amelyekben figyelembe vehetők a sportolók, testépítők tapasztalatai is.

scholarly journals Forelimb unloading impairs glenohumeral muscle development in growing rats

2020 ◽  
Author(s):  
Sophia K. Tushak ◽  
Margaret K. Tamburro ◽  
Emily B. Fawcett ◽  
Lauren E. Merritt LE ◽  
Katherine R. Saul ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Muscle Development ◽  
Sarcomere Length ◽  
Glenohumeral Joint ◽  
Neuromuscular Disorders ◽  
Muscle Length ◽  
Hindlimb Unloading ◽  
Growing Rats ◽  
Musculoskeletal Development ◽  
Long Head

AbstractProper joint loading is essential for healthy musculoskeletal development. Many pediatric neuromuscular disorders cause irreversible muscle impairments resulting from both physiological changes and mechanical unloading of the joint. While previous studies have examined the effects of hindlimb unloading on musculoskeletal development in the lower limb, none have examined solely forelimb unloading. Thus, a large deficit in knowledge of the effect of upper limb unloading exists and must be addressed in order to better understand how the glenohumeral joint adapts during development. Two forelimb unloading models were developed to study the effects of varying degrees of unloading on the glenohumeral joint in growing rats: forelimb suspension (n=6, intervention 21 days post-natal) with complete unloading of both limbs via a novel suspension system and forearm amputation (n=8, intervention 3-6 days post-natal) with decreased loading and limb use in one limb after below-elbow amputation. After 8 weeks of unloading, changes in muscle architecture and composition were examined in ten muscles surrounding the shoulder. Results were compared to control rats from a previous study (n=8). Both methods of altered loading significantly affected muscle mass, sarcomere length, and optimal muscle length compared to control rats, with the biceps long head and triceps long head observing the most marked differences. Forearm amputation also significantly affected muscle mass, sarcomere length, and optimal muscle length in the affected limb relative to the contralateral limb. Muscle composition, assessed by collagen content, remained unchanged in all groups. This study demonstrated that forearm amputation, which was administered closer to birth, had greater effects on muscle than forelimb suspension, which was administered a few weeks later than amputation.

scholarly journals p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition

2021 ◽  
Vol 12 ◽  
Author(s):  
Caroline Barbé ◽  
Audrey Loumaye ◽  
Pascale Lause ◽  
Olli Ritvos ◽  
Jean-Paul Thissen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
The Body ◽  
Negative Regulator ◽  
Skeletal Muscle Hypertrophy ◽  
Myostatin Inhibition

Skeletal muscle, the most abundant tissue in the body, plays vital roles in locomotion and metabolism. Understanding the cellular processes that govern regulation of muscle mass and function represents an essential step in the development of therapeutic strategies for muscular disorders. Myostatin, a member of the TGF-β family, has been identified as a negative regulator of muscle development. Indeed, its inhibition induces an extensive skeletal muscle hypertrophy requiring the activation of Smad 1/5/8 and the Insulin/IGF-I signaling pathway, but whether other molecular mechanisms are involved in this process remains to be determined. Using transcriptomic data from various Myostatin inhibition models, we identified Pak1 as a potential mediator of Myostatin action on skeletal muscle mass. Our results show that muscle PAK1 levels are systematically increased in response to Myostatin inhibition, parallel to skeletal muscle mass, regardless of the Myostatin inhibition model. Using Pak1 knockout mice, we investigated the role of Pak1 in the skeletal muscle hypertrophy induced by different approaches of Myostatin inhibition. Our findings show that Pak1 deletion does not impede the skeletal muscle hypertrophy magnitude in response to Myostatin inhibition. Therefore, Pak1 is permissive for the skeletal muscle mass increase caused by Myostatin inhibition.

Sexual dimorphism is associated with decreased expression of processed myostatin in males

2003 ◽  
Vol 284 (2) ◽  
pp. E377-E381 ◽  
Author(s):  
Christopher D. McMahon ◽  
Ljiljana Popovic ◽  
Ferenc Jeanplong ◽  
Jenny M. Oldham ◽  
Sonnie P. Kirk ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Development ◽  
Biceps Femoris ◽  
Northern Analysis ◽  
Skeletal Muscle Development ◽  
Female Mice ◽  
Mrna And Protein Expression ◽  
Males And Females ◽  
Quadriceps Femoris Muscles

Myostatin inhibits skeletal muscle development. Therefore, we sought to determine whether larger body and muscle mass in male mice was associated with lower mRNA and protein expression of myostatin compared with females. Ten male and ten female mice of the C57 strain were killed at 16–18 wk of age, and their biceps femoris, gastrocnemius, and quadriceps femoris muscles were collected. Body and muscle masses were 40% heavier ( P < 0.001) in males than in females. Northern analysis showed no difference in mRNA between males and females. In contrast, Western analysis showed that processed myostatin (26 kDa) was 40–60% lower ( P < 0.001) in males compared with females. These data show first that decreased processed myostatin is a posttranscriptional and posttranslational event and, second, that decreased abundance of processed myostatin is associated with increased body mass and skeletal muscle mass in male compared with female mice.

Viral expression of insulin-like growth factor-I isoforms promotes different responses in skeletal muscle

2006 ◽  
Vol 100 (6) ◽  
pp. 1778-1784 ◽  
Author(s):  
Elisabeth R. Barton
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Muscle Mass ◽  
Muscle Hypertrophy ◽  
Muscle Development ◽  
Muscle Size ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Insulin-like growth factor I (IGF-I) is a critical protein for skeletal muscle development and regeneration. Its ability to promote skeletal muscle hypertrophy has been demonstrated by several methods. Alternative splicing of the Igf-1 gene does not affect the mature IGF-I protein but does produce different E peptide extensions, which have been reported to modify the potency of IGF-I. Viral-mediated delivery of murine IGF-IA and IGF-IB into skeletal muscle of 2-wk-old and 6-mo-old mice was utilized to compare the effects of the isoforms on muscle mass. In young mice, tissue content of IGF-I protein was significantly higher in rAAV-treated muscles than control muscles at 1, 2, and 4 mo postinjection. Viral injection of IGF-IB produced two- to sevenfold more IGF-I than rAAVIGF-IA. Hypertrophy was observed 2 and 4 mo postinjection, where both rAAVIGF-IA and rAAVIGF-IB were equally effective in increasing muscle mass. These results suggest that there is a threshold of IGF-I production necessary to promote muscle hypertrophy in young growing animals regardless of isoform. In 6-mo-old animals, only rAAVIGF-IA produced significant increases in muscle size, even though increased IGF-I content was observed after injection of both isoforms. Therefore, the ability for IGF-IB to promote muscle hypertrophy is only effective in growing animals, suggesting that the bioavailability of this isoform or its receptor affinity diminishes with age.

scholarly journals Epigenetic regulation of muscle phenotype and adaptation: a potential role in COPD muscle dysfunction

2013 ◽  
Vol 114 (9) ◽  
pp. 1263-1272 ◽  
Author(s):  
Esther Barreiro ◽  
Jacob I. Sznajder
Keyword(s):  
Environmental Factors ◽  
Muscle Mass ◽  
Muscle Development ◽  
Quadriceps Muscle ◽  
Future Research ◽  
Chronic Obstructive ◽  
Muscle Dysfunction ◽  
Epigenetic Mechanisms ◽  
Contributing Factors ◽  
Obstructive Pulmonary Disease

Quadriceps muscle dysfunction occurs in one-third of patients with chronic obstructive pulmonary disease (COPD) in very early stages of their condition, even prior to the development of airway obstruction. Among several factors, deconditioning and muscle mass loss are the most relevant contributing factors leading to this dysfunction. Moreover, epigenetics, defined as the process whereby gene expression is regulated by heritable mechanisms that do not affect DNA sequence, could be involved in the susceptibility to muscle dysfunction, pathogenesis, and progression. Herein, we review the role of epigenetic mechanisms in muscle development and adaptation to environmental factors such as immobilization and exercise, and their implications in the pathophysiology and susceptibility to muscle dysfunction in COPD. The epigenetic modifications identified so far include DNA methylation, histone acetylation and methylation, and non-coding RNAs such as microRNAs (miRNAs). In the present review, we describe the specific contribution of epigenetic mechanisms to the regulation of embryonic myogenesis, muscle structure and metabolism, immobilization, and exercise, and in muscles of COPD patients. Events related to muscle development and regeneration and the response to exercise and immobilization are tightly regulated by epigenetic mechanisms. These environmental factors play a key role in the outcome of muscle mass and function as well as in the susceptibility to muscle dysfunction in COPD. Future research remains to be done to shed light on the specific target pathways of miRNA function and other epigenetic mechanisms in the susceptibility, pathogenesis, and progression of COPD muscle dysfunction.

scholarly journals NFκB Regulates Muscle Development and Mitochondrial Function

2018 ◽  
Vol 75 (4) ◽  
pp. 647-653 ◽  
Author(s):  
Joseph M Valentine ◽  
Mengyao E Li ◽  
Steven E Shoelson ◽  
Ning Zhang ◽  
Robert L Reddick ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Life Span ◽  
Muscle Mass ◽  
Mitochondrial Function ◽  
Muscle Development ◽  
Tissue Mass ◽  
Lower Oxygen ◽  
Consumption Rates ◽  
Nfκb Pathway ◽  
Gastrocnemius Muscles

Abstract Nuclear factor (NF)κB is a transcription factor that controls immune and inflammatory signaling pathways. In skeletal muscle, NFκB has been implicated in the regulation of metabolic processes and tissue mass, yet its affects on mitochondrial function in this tissue are unclear. To investigate the role of NFκB on mitochondrial function and its relationship with muscle mass across the life span, we study a mouse model with muscle-specific NFκB suppression (muscle-specific IκBα super-repressor [MISR] mice). In wild-type mice, there was a natural decline in muscle mass with aging that was accompanied by decreased mitochondrial function and mRNA expression of electron transport chain subunits. NFκB inactivation downregulated expression of PPARGC1A, and upregulated TFEB and PPARGC1B. NFκB inactivation also decreased gastrocnemius (but not soleus) muscle mass in early life (1–6 months old). Lower oxygen consumption rates occurred in gastrocnemius and soleus muscles from young MISR mice, whereas soleus (but not gastrocnemius) muscles from old MISR mice displayed increased oxygen consumption compared to age-matched controls. We conclude that the NFκB pathway plays an important role in muscle development and growth. The extent to which NFκB suppression alters mitochondrial function is age dependent and muscle specific. Finally, mitochondrial function and muscle mass are tightly associated in both genotypes and across the life span.

scholarly journals ACTN3 genotype influences skeletal muscle mass regulation and response to dexamethasone

2020 ◽  
Author(s):  
J.T. Seto ◽  
K.N. Roeszler ◽  
L.R. Meehan ◽  
H.D. Wood ◽  
C. Tiong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Development ◽  
Muscle Wasting ◽  
The Elderly ◽  
Power Performance ◽  
Increased Risk ◽  
Disease Modifier ◽  
The Common ◽  
Anti Inflammatory

AbstractHomozygosity for the common ACTN3 null polymorphism (ACTN3 577X) results in α-actinin-3 deficiency in ~20% of humans worldwide and is linked to reduced sprint and power performance in both elite athletes and the general population. α-Actinin-3 deficiency is also associated with reduced muscle mass and strength, increased risk of sarcopenia in the elderly, and altered response to muscle wasting induced by denervation and immobilisation. ACTN3 genotype is also a disease modifier for Duchenne muscular dystrophy (DMD), with α-actinin-3 deficiency associated with slower disease progression. Here we show that α-actinin-3 plays a key role in the regulation of protein synthesis and breakdown signalling in skeletal muscle, and its influence on muscle mass begins during early postnatal muscle development. Actn3 genotype also influences the skeletal muscle response to the glucocorticoid dexamethasone. Following acute dexamethasone exposure, transcriptomic analyses by RT-qPCR and RNA-sequencing show reduced atrophy signalling (Mstn, Tmem100, mRas, Fbxo32, Trim63) and anti-inflammatory response in α-actinin-3 deficient mice compared to wild-type. α-Actinin-3 deficiency also protects against muscle wasting following prolonged daily treatment with dexamethasone in female, but not male mice. In combination, these data suggest that ACTN3 R577X is a pharmacogenetic variant influencing the anti-inflammatory and muscle wasting response to glucocorticoid therapy.

scholarly journals Localization, Distribution and Structure of Muscle Fibres Using Specific Antibody Markers in the zebrafish, Danio rerio (Hamilton, 1822)

2021 ◽  
Vol 34 (1) ◽  
pp. school
Author(s):  
Hussein A. Saud ◽  
Ilham J.J. Alshami ◽  
Ruth Cooper
Keyword(s):  
Muscle Mass ◽  
Danio Rerio ◽  
Early Life ◽  
Muscle Development ◽  
Life Stage ◽  
The Body ◽  
Muscle Fibres ◽  
High Fecundity ◽  
Whole Mount ◽  
Fluorescent Immunohistochemistry

The zebrafish Danio rerio is a popular model species  for genetic and early development studies. It is relatively easy to maintain in laboratory, has a high fecundity rate and produces transparent embryos. Here, we characterise muscle development in early life stage zebrafish using paraffin sections of embryos and larvae treated with haematoxylin and eosin staining, and whole mount fluorescent immunohistochemistry. We found variations in the distribution of muscle mass throughout the body, with the greatest proportion of muscle mass found in the tail. Our data also showed for the first time the reaction of antibodies (protein expression) in muscle at early life stages of development. Whole mount fluorescent immunohistochemistry staining with three markers (PAX7, MF20 and F59) suggests that muscle development starts even earlier than previously suggested at the embryonic stage (1 dpf).

scholarly journals Regulation of microRNAs in Satellite Cell Renewal, Muscle Function, Sarcopenia and the Role of Exercise

2020 ◽  
Vol 21 (18) ◽  
pp. 6732 ◽  
Author(s):  
Stefania Fochi ◽  
Gaia Giuriato ◽  
Tonia De Simone ◽  
Macarena Gomez-Lira ◽  
Stefano Tamburin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
The Elderly ◽  
Cell Renewal ◽  
Muscle Adaptation ◽  
Muscle Plasticity ◽  
Skeletal Mass ◽  
General Aspects

Sarcopenia refers to a condition of progressive loss of skeletal muscle mass and function associated with a higher risk of falls and fractures in older adults. Musculoskeletal aging leads to reduced muscle mass and strength, affecting the quality of life in elderly people. In recent years, several studies contributed to improve the knowledge of the pathophysiological alterations that lead to skeletal muscle dysfunction; however, the molecular mechanisms underlying sarcopenia are still not fully understood. Muscle development and homeostasis require a fine gene expression modulation by mechanisms in which microRNAs (miRNAs) play a crucial role. miRNAs modulate key steps of skeletal myogenesis including satellite cells renewal, skeletal muscle plasticity, and regeneration. Here, we provide an overview of the general aspects of muscle regeneration and miRNAs role in skeletal mass homeostasis and plasticity with a special interest in their expression in sarcopenia and skeletal muscle adaptation to exercise in the elderly.

8 weeks of 2S-Hesperidin supplementation improves muscle mass and reduces fat in amateur competitive cyclists: randomized controlled trial

2021 ◽  
Author(s):  
Francisco Javier Martínez Noguera ◽  
Pedro E. Alcaraz Ramón ◽  
Jorge Carlos Vivas ◽  
Linda H. Chung ◽  
Elena Marín Cascales ◽  
...  
Keyword(s):  
Randomized Controlled Trial ◽  
Muscle Mass ◽  
Citrus Sinensis ◽  
Muscle Development ◽  
Controlled Trial ◽  
Fat Accumulation ◽  
Randomized Controlled ◽  
Competitive Cyclists

2S-Hesperidin is the main flavonoid of orange (Citrus sinensis). Previous researches have pointed its effects in muscle development and fat accumulation reduction, although most of these results have not been...

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