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Milos Sarvec ... de contest prep goeroe
- Topic starter Driven1010
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OP
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- 16 nov 2004
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Dat zou ik nu ook weer niet durven zeggen, qua training en oefeningen kennis is er mijn inziens niemand beter. Contest prep en voeding houd hij zich volgens mij niet mee bezig. Dus als Gunter op een bepaalde wedstrijd een vettige vochtbal is, dan ligt dat niet aan Charles Glass. Als Gunter achterliggende spiergroepen had dan lag dat wel aan Glass...
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ik heb dat vaker gehoord inderdaad dat hoe hoger je in% van je max komt hoe meer myostatine word aangemaakt, maar heb geen idee hoe groot dat verschil is heb jij hier meer info over?
OP
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- #25
Myostatin info/studies:
INFO:
Myostatin (a.k.a. GDF-8) ia a member of the TGF-beta family and is specific to skeletal muscles (not found in smooth or cardiac muscles). It is secreted in the inactive (propeptide) form and circulates in the blood. At some point the protein is activated via an as yet unknown mechanism. In vitro studies have pointed to tissue specific (skeletal muscle) metalloproteinases (just an enzyme that cleaves proteins) in the activation but in vivo mechs have not yet been demonstrated. In circulation it has been found to be bound by FLRG and GASP-1; which inhibit its action (Two possible mechs for future control of myostatin activity). Post activation myostatin can then bind to specific receptors on skeletal muscle and activate a signaling cascade which activates factors to regulate transcription of the myostatin target genes. It helps to regulate differentiation, proliferation, and fiber size.
MYOSTATIN REVIEW
Myostatin, or GDF-8 (growth and differentiation factor-8), was first identified through sequence identity with members of the BMP (bone morphogenetic protein)/TGF-β (transforming growth factor-β) superfamily. The skeletal-muscle-specific expression pattern of myostatin suggested a role in muscle development. Mice with a targeted deletion of the myostatin gene exhibit a hypermuscular phenotype. In addition, inactivating mutations in the myostatin gene have been identified in ‘double muscled’ cattle breeds, such as the Belgian Blue and Piedmontese, as well as in a hypermuscular child. These findings define myostatin as a negative regulator of skeletal-muscle developmentt. Myostatin binds with high affinity to the receptor serine threonine kinase ActRIIB (activin type IIB receptor), which initiates signalling through a smad2/3-dependent pathway. In an effort to validate myostatin as a therapeutic target in a post-embryonic setting, a neutralizing antibody was developed by screening for inhibition of myostatin binding to ActRIIB. Administration of this antimyostatin antibody to adult mice resulted in a significant increase in both muscle mass and functional strength. Importantly, similar results were obtained in a murine model of muscular dystrophy, the mdx mouse. Unlike the myostatin-deficient animals, which exhibit both muscle hypertrophy and hyperplasia, the antibody-treated mice demonstrate increased musculature through a hypertrophic mechanism. These results validate myostatin inhibition as a therapeutic approach to muscle wasting diseases such as muscular rdystrophy, sarcopenic frailty of the elderly and amylotrophic lateral sclerosis.
MYOSTATIN IN MUSCLE REGENERATION
Purpose of review
Myostatin is an endogenous, negative regulator of muscle growth. Selective inhibition of myostatin may have broad clinical utility by improving regeneration in diverse and burdensome muscle disorders. An understanding of this potential is relevant because inhibitors of myostatin have recently entered clinical trials.
Recent findings: This article reviews the structure and function of myostatin, the effect of inhibiting myostatin in models of disease, and potential therapeutic approaches to blocking myostatin pharmacologically. The possibility that a myostatin inhibitor will promote muscle regeneration in human disease, as seen in animal models, is suggested by the observation that loss of myostatin results in muscle hypertrophy in a human subject.
Summary: Multiple approaches to inhibiting myostatin are suggested by the recent elucidation of its signaling pathway. An inhibitor of myostatin may be the first drug specifically designed to enhance muscle growth and regeneration.
MYOSTATIN AND OTHER DOPING
Advances in recombinant DNA technology have created one of the most powerful weapons in the current doping arsenal: recombinant proteins [Sweeney HL. Gene doping. Sci Am 2004;291:62–9; Unal M, Ozer Unal D. Gene doping in sports. Sports Med 2004;34:357–62]. Recombinant erythropoietin (EPO) and human growth hormone (hGH) are currently being abused but are fortunately detectable either directly by employing isoelectric focusing and immunoassays or indirectly by assessing changes in selected hematopoietic parameters. The detection is technically demanding due to the extent of similarity between the recombinant proteins and their endogenous counterparts.
Another issue facing detection efforts is the speed and conditions at which blood samples are collected and analyzed in a sports setting. Recently, gene doping, which stemmed out of legitimate gene therapy trials, has emerged as the next level of doping. Erythropoietin (EPO), human growth hormone (hGH), insulin-like growth factor-1 (IGF-1), peroxisome proliferator-activated receptor-delta (PPAR δ), and myostatin inhibitor genes have been identified as primary targets for doping. Sports clinical scientists today are racing against the clock because assuring the continued integrity of sports competition depends on their ability to outpace the efforts of dopers by developing new detection strategies.
MEER over het verband tussen het aantal herhalingen en het myostatin gehalte in het bloed.
-> In deze studie deed men 6-8 herhalingen met een load van 85%-90% van de 1-RM. In deze studie was het myostatin gehalte gestegen door deze training.
Als je er vanuit gaat dat deze studies correct zijn dan kan je zeggen dat meer herhalingen het myostatin gehalte verminderen waardoor je meer spiermassa gaat aanzetten. Klinkt wel logisch als je weet dat de gemiddelde bodybuilder traint met veel herhalingen en minder gewicht en toch veel spiermassa heeft. Terwijl een powerlifter het tegenovergestelde doet en dus krachtiger is maar minder spiermassa heeft.
INFO:
Myostatin (a.k.a. GDF-8) ia a member of the TGF-beta family and is specific to skeletal muscles (not found in smooth or cardiac muscles). It is secreted in the inactive (propeptide) form and circulates in the blood. At some point the protein is activated via an as yet unknown mechanism. In vitro studies have pointed to tissue specific (skeletal muscle) metalloproteinases (just an enzyme that cleaves proteins) in the activation but in vivo mechs have not yet been demonstrated. In circulation it has been found to be bound by FLRG and GASP-1; which inhibit its action (Two possible mechs for future control of myostatin activity). Post activation myostatin can then bind to specific receptors on skeletal muscle and activate a signaling cascade which activates factors to regulate transcription of the myostatin target genes. It helps to regulate differentiation, proliferation, and fiber size.
MYOSTATIN REVIEW
Myostatin, or GDF-8 (growth and differentiation factor-8), was first identified through sequence identity with members of the BMP (bone morphogenetic protein)/TGF-β (transforming growth factor-β) superfamily. The skeletal-muscle-specific expression pattern of myostatin suggested a role in muscle development. Mice with a targeted deletion of the myostatin gene exhibit a hypermuscular phenotype. In addition, inactivating mutations in the myostatin gene have been identified in ‘double muscled’ cattle breeds, such as the Belgian Blue and Piedmontese, as well as in a hypermuscular child. These findings define myostatin as a negative regulator of skeletal-muscle developmentt. Myostatin binds with high affinity to the receptor serine threonine kinase ActRIIB (activin type IIB receptor), which initiates signalling through a smad2/3-dependent pathway. In an effort to validate myostatin as a therapeutic target in a post-embryonic setting, a neutralizing antibody was developed by screening for inhibition of myostatin binding to ActRIIB. Administration of this antimyostatin antibody to adult mice resulted in a significant increase in both muscle mass and functional strength. Importantly, similar results were obtained in a murine model of muscular dystrophy, the mdx mouse. Unlike the myostatin-deficient animals, which exhibit both muscle hypertrophy and hyperplasia, the antibody-treated mice demonstrate increased musculature through a hypertrophic mechanism. These results validate myostatin inhibition as a therapeutic approach to muscle wasting diseases such as muscular rdystrophy, sarcopenic frailty of the elderly and amylotrophic lateral sclerosis.
MYOSTATIN IN MUSCLE REGENERATION
Purpose of review
Myostatin is an endogenous, negative regulator of muscle growth. Selective inhibition of myostatin may have broad clinical utility by improving regeneration in diverse and burdensome muscle disorders. An understanding of this potential is relevant because inhibitors of myostatin have recently entered clinical trials.
Recent findings: This article reviews the structure and function of myostatin, the effect of inhibiting myostatin in models of disease, and potential therapeutic approaches to blocking myostatin pharmacologically. The possibility that a myostatin inhibitor will promote muscle regeneration in human disease, as seen in animal models, is suggested by the observation that loss of myostatin results in muscle hypertrophy in a human subject.
Summary: Multiple approaches to inhibiting myostatin are suggested by the recent elucidation of its signaling pathway. An inhibitor of myostatin may be the first drug specifically designed to enhance muscle growth and regeneration.
MYOSTATIN AND OTHER DOPING
Advances in recombinant DNA technology have created one of the most powerful weapons in the current doping arsenal: recombinant proteins [Sweeney HL. Gene doping. Sci Am 2004;291:62–9; Unal M, Ozer Unal D. Gene doping in sports. Sports Med 2004;34:357–62]. Recombinant erythropoietin (EPO) and human growth hormone (hGH) are currently being abused but are fortunately detectable either directly by employing isoelectric focusing and immunoassays or indirectly by assessing changes in selected hematopoietic parameters. The detection is technically demanding due to the extent of similarity between the recombinant proteins and their endogenous counterparts.
Another issue facing detection efforts is the speed and conditions at which blood samples are collected and analyzed in a sports setting. Recently, gene doping, which stemmed out of legitimate gene therapy trials, has emerged as the next level of doping. Erythropoietin (EPO), human growth hormone (hGH), insulin-like growth factor-1 (IGF-1), peroxisome proliferator-activated receptor-delta (PPAR δ), and myostatin inhibitor genes have been identified as primary targets for doping. Sports clinical scientists today are racing against the clock because assuring the continued integrity of sports competition depends on their ability to outpace the efforts of dopers by developing new detection strategies.
MEER over het verband tussen het aantal herhalingen en het myostatin gehalte in het bloed.
-> In deze studie deed men 6-8 herhalingen met een load van 85%-90% van de 1-RM. In deze studie was het myostatin gehalte gestegen door deze training.
-> In deze studie deed men 8-12 herhalingen en hier daalde het myostatin gehalte in het bloed.
Als je er vanuit gaat dat deze studies correct zijn dan kan je zeggen dat meer herhalingen het myostatin gehalte verminderen waardoor je meer spiermassa gaat aanzetten. Klinkt wel logisch als je weet dat de gemiddelde bodybuilder traint met veel herhalingen en minder gewicht en toch veel spiermassa heeft. Terwijl een powerlifter het tegenovergestelde doet en dus krachtiger is maar minder spiermassa heeft.
Laatst bewerkt:
- Lid geworden
- 31 jan 2003
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- Lid geworden
- 21 nov 2004
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- 5.748
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- 2.279
- Lengte
- 2m30
- Massa
- 40kg
- Vetpercentage
- > 50%
Hij zag er duidelijk beter uit en nu hij niet meer met Milos werkt scoort hij hoger, strange
je naam en je begeleider zijn belangrijker dan je shape
dat moet je nu ondertussen al weten he
- Lid geworden
- 16 okt 2005
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- 4.227
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- 1m83
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- 8%
waarom kakken ze op Milos? Omdat ze jaloers zijn omdat ze niet begeleid worden door hem. Ik zou meteen tekenen moest hij mij komen vragen om nog maar een maand mij te begeleiden.
