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Mgf
- Topic starter BassD
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duidelijk stuk, ben erg benieuwd wanneer dit hier te verkrijgen is!
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http://forums.steroid.com/showthread.php?t=230134&highlight=mgf
Logje van een gebruiker...link van Klaas
Logje van een gebruiker...link van Klaas
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- 8 dec 2004
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nog eentje..
[Link niet meer beschikbaar]
edit: nog meer info over MGF ....
[Link niet meer beschikbaar]
http://anabolicminds.com/forum/igf-1-gh-slin/42716-mechano-growth-factor-mgf-insulin-like.html
[Link niet meer beschikbaar]
edit: nog meer info over MGF ....
[Link niet meer beschikbaar]
http://anabolicminds.com/forum/igf-1-gh-slin/42716-mechano-growth-factor-mgf-insulin-like.html
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Kon het niet laten net 4 MG besteld
Wel de kort werkende versie..stond wel nieuws bij dat de lange onderweg was.
Geef wel seintje als het binnen is.
Van de site waar die amerikanen het ook halen.
Wel de kort werkende versie..stond wel nieuws bij dat de lange onderweg was.
Geef wel seintje als het binnen is.
Van de site waar die amerikanen het ook halen.
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OP
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- 13 jan 2004
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- Lengte
- 1m93
- Massa
- 119kg
- Vetpercentage
- 13%
- Topic Starter
- #26
Shit je bent me net voor! 
Ik wacht nog even op de langwerkende versie. Zag dat ze wel de prijs flink naar beneden hadden gegooid van de kortwerkende versie, nu de langwerkende eraan komt.
kortwerkende versie meot ook goed te doen zijn. alleen moet je toch flink wat mcg's erin knallen wil het effectief zijn heb ik begrepen. Toch minimaal 80 mcg per spiergroep. Heb je al een schema voor jezelf in gedachten?
Ik zag ook dat je nu bezig bent met een lekker kuurtje..... man o man met die mgf erbij dan moet je echt uit je voegen groeien
Ik wacht nog even op de langwerkende versie. Zag dat ze wel de prijs flink naar beneden hadden gegooid van de kortwerkende versie, nu de langwerkende eraan komt.
kortwerkende versie meot ook goed te doen zijn. alleen moet je toch flink wat mcg's erin knallen wil het effectief zijn heb ik begrepen. Toch minimaal 80 mcg per spiergroep. Heb je al een schema voor jezelf in gedachten?
Ik zag ook dat je nu bezig bent met een lekker kuurtje..... man o man met die mgf erbij dan moet je echt uit je voegen groeien
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Vond een voorbeeld schema voor een eerste keer MGF
MGF + LR3 IGF-1 Dosage Scheme (following intense loading of lagging muscle group)
Day 1
Pre Workout (~1.5 hours)- 75-200mcg total MGF (half dosage in each side)
Post Workout- 50-100mcg x 2 MGF (left and right sides of lagging muscle) following workout
Day 2
Morning- 20mcg LR3 IGF-1
50-100mcg x 2 in lagging muscle group MGF
Afternoon-50-100mcg x 2 in lagging muscle group MGF
Late afternoon (at least 10 hours after first injection optimally)- 20mcg LR3 IGF-1
Day 3
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
Day 4
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
Day 5
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
Day 6+7 (optional)
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
MGF + LR3 IGF-1 Dosage Scheme (following intense loading of lagging muscle group)
Day 1
Pre Workout (~1.5 hours)- 75-200mcg total MGF (half dosage in each side)
Post Workout- 50-100mcg x 2 MGF (left and right sides of lagging muscle) following workout
Day 2
Morning- 20mcg LR3 IGF-1
50-100mcg x 2 in lagging muscle group MGF
Afternoon-50-100mcg x 2 in lagging muscle group MGF
Late afternoon (at least 10 hours after first injection optimally)- 20mcg LR3 IGF-1
Day 3
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
Day 4
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
Day 5
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
Day 6+7 (optional)
Morning- 10-20mcg LR3 IGF-1
Late Afternoon- 10-20mcg LR3 IGF-1
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- 13 jan 2003
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http://anabolicminds.com/forum/igf-1-gh-slin/42836-newest-development-you-mgf-users.html?highlight=mechano-growth-factor
intressant stuk
Conclusie (grof)
Dag 1 Berg MGF
Dag 6-7 IGF-1
intressant stuk
Conclusie (grof)
Dag 1 Berg MGF
Dag 6-7 IGF-1
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The main thing is that you use the MGF in the trained bodypart for no longer than 36 hours after training it. This is due to the fact that MGF, although it proliferates satellite cells needed for growth, it cannot differentiate them (meaning change their identity to that of a muscle cell), IGF-1 is the only thing that can do this. Not only that, though, MGF actually inhibits myotube formation. I am attaching a graph to show what I mean by this. Your body's natural reaction to a stimulus is a peak in MGF levels for the first day or so followed by a sharp decline of MGF and a raise of IGF-1. I would also split IGF into two separate injections. LR3 has an ~10 hour active life so you can best utilize it by twice daily injections unless you are dead set on once per day. They don't have to be full 60mcg injections either, I would split them so that if you want to get 60mcg for that day, just do two 30 mcg injections. Definitely let me know how it goes.
I also suggest you read the other thread that Rex and I were talking about in this same forum. It explains the reason i feel LR3 loses effectiveness after 3-4 weeks and I don't believe its fully because of down-regulation, in fact I feel that is more a small piece of the pie.
plaatje zegt wel genoeg denk ik
Dus achterliggende spier:
NA trainen MGF eerste dag. Daarna IGF-1
I also suggest you read the other thread that Rex and I were talking about in this same forum. It explains the reason i feel LR3 loses effectiveness after 3-4 weeks and I don't believe its fully because of down-regulation, in fact I feel that is more a small piece of the pie.
plaatje zegt wel genoeg denk ik
Dus achterliggende spier:
NA trainen MGF eerste dag. Daarna IGF-1
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how to use igf + mgf together:
To optimize the effects of both compounds they should be taken together but not on the same days. Here is why: MGF increases the number of myoblast, which are basically the building blocks for adult muscle cells, myotubules. IGF also has this effect but not to the degree MGF does. The other effect of IGF is to actually utilize the myoblast into fusing with the myotubules so that More muscle is created and the potential for further growth increased. B/c of this we can use MGF to increase the myoblast, b/c it is the best at doing this, and IGF to actually use the high levels of myoblast created by the IGF. IGF can not do both things at once. So by using MGF before hand we are maximizing the effects we want out of the IGF.
If you can't tell from the above. If you are going to take any of these peptides alone. IGF is the better choice. It can do both increase/use the myoblast. Where as MGF will just increase the myoblast, but this does not mean you will use them for new muscle. Many people report a pump for a few days while on MGF and then it subsides. This is liekly do to increased myoblast, but they are not all fusing and are just dying off when the MGF is discontinued so not as much muscle is gained compared to using MGF and IGF.
These two compounds however should not be taken the same day b/c MGF actually inhibits the effect of IGF as far as using the myoblast. Ideally a person would take MGF the day before a workout, and the IGF post workout.
To optimize the effects of both compounds they should be taken together but not on the same days. Here is why: MGF increases the number of myoblast, which are basically the building blocks for adult muscle cells, myotubules. IGF also has this effect but not to the degree MGF does. The other effect of IGF is to actually utilize the myoblast into fusing with the myotubules so that More muscle is created and the potential for further growth increased. B/c of this we can use MGF to increase the myoblast, b/c it is the best at doing this, and IGF to actually use the high levels of myoblast created by the IGF. IGF can not do both things at once. So by using MGF before hand we are maximizing the effects we want out of the IGF.
If you can't tell from the above. If you are going to take any of these peptides alone. IGF is the better choice. It can do both increase/use the myoblast. Where as MGF will just increase the myoblast, but this does not mean you will use them for new muscle. Many people report a pump for a few days while on MGF and then it subsides. This is liekly do to increased myoblast, but they are not all fusing and are just dying off when the MGF is discontinued so not as much muscle is gained compared to using MGF and IGF.
These two compounds however should not be taken the same day b/c MGF actually inhibits the effect of IGF as far as using the myoblast. Ideally a person would take MGF the day before a workout, and the IGF post workout.
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klaas zei:
http://forums.steroid.com/attachment.php?attachmentid=65658&d=1144046102
Komt inderdaad overeen met dit grafiekje
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Changes in muscle mass and phenotype and the expression of autocrine and systemic growth factors by muscle in response to stretch and overload. Goldspink G. J Anat. ;194 ( Pt 3):323-34 (1999).
The study of the underlying mechanisms by which cells respond to mechanical stimuli, i.e. the link between the mechanical stimulus and gene expression, represents a new and important area in the morphological sciences. Several cell types ('mechanocytes'), e.g. osteoblasts and fibroblasts as well as smooth, cardiac and skeletal muscle cells are activated by mechanical strain and there is now mounting evidence that this involves the cytoskeleton. Muscle offers one of the best opportunities for studying this type of mechanotransduction as the mechanical activity generated by and imposed upon muscle tissue can be accurately controlled and measured in both in vitro and in vivo systems. Muscle is highly responsive to changes in functional demands. Overload leads to hypertrophy, whilst decreased load force generation and immobilisation with the muscle in the shortened position leads to atrophy. For instance it has been shown that stretch is an important mechanical signal for the production of more actin and myosin filaments and the addition of new sarcomeres in series and in parallel. This is preceded by upregulation of transcription of the appropriate genes some of which such as the myosin isoforms markedly change the muscle phenotype. Indeed, the switch in the expression induced by mechanical activity of myosin heavy chain genes which encode different molecular motors is a means via which the tissue adapts to a given type of physical activity. As far as increase in mass is concerned, our group have cloned the cDNA of a splice variant of IGF-1 that is produced by active muscle that appears to be the factor that controls local tissue repair, maintenance and remodelling. From its sequence it can be seen that it is derived from the IGF-1 gene by alternative splicing but it has different exons to the liver isoforms. It has a 52 base insert in the E domain which alters the reading frame of the 3' end. Therefore, this splice variant of IGF-1 is likely to bind to a different binding protein which exists in the interstitial tissue spaces of muscle, neuronal tissue and bone. This would be expected to localise its action as it would be unstable in the unbound form which is important as its production would not disturb the glucose homeostasis unduly. This new growth factor has been called mechano growth factor (MGF) to distinguish it from the liver IGFs which have a systemic mode of action. Although the liver is usually thought of as the source of circulating IGF-1, it has recently been shown that during exercise skeletal muscle not only produces much of the circulating IGF-1 but active musculature also utilises most of the IGF-I produced. We have cloned both an autocrine and endocrine IGF-1, both of which are upregulated in cardiac as well as skeletal muscle when subjected to overload. It has been shown that, in contrast to normal muscle, MGF is not detectable in dystrophic mdx muscles even when subjected to stretch and stretch combined with electrical stimulation. This is true for muscular dystrophies that are due to the lack of dystrophin (X-linked) and due to a laminin deficiency (autosomal), thus indicating that the dystrophin cytoskeletal complex may be involved in the mechanotransduction mechanism. When this complex is defective the necessary systemic as well as autocrine IGF-1 growth factors required for local repair are not produced and the ensuing cell death results in progressive loss of muscle mass. The discovery of the locally produced IGF-1 appears to provide the link between the mechanical stimulus and the activation of gene expression.
Muscle satellite (stem) cell activation during local tissue injury and repair.Hill M, Wernig A, Goldspink G. J Anat. 2003 Jul;203(1):89-99
In post-mitotic tissues, damaged cells are not replaced by new cells and hence effective local tissue repair mechanisms are required. In skeletal muscle, which is a syncytium, additional nuclei are obtained from muscle satellite (stem) cells that multiply and then fuse with the damaged fibres. Although insulin-like growth factor-I (IGF-l) had been previously implicated, it is now clear that muscle expresses at least two splice variants of the IGF-I gene: a mechanosensitive, autocrine, growth factor (MGF) and one that is similar to the liver type (IGF-IEa). To investigate this activation mechanism, local damage was induced by stretch combined with electrical stimulation or injection of bupivacaine in the rat anterior tibialis muscle and the time course of regeneration followed morphologically. Satellite cell activation was studied by the distribution and levels of expression of M-cadherin (M-cad) and related to the expression of the two forms of IGF-I. It was found that the following local damage MGF expression preceded that of M-cad whereas IGF-IEa peaked later than M-cad. The evidence suggests therefore that an initial pulse of MGF expression following damage is what activates the satellite cells and that this is followed by the later expression of IGF-IEa to maintain protein synthesis to complete the repair.
The study of the underlying mechanisms by which cells respond to mechanical stimuli, i.e. the link between the mechanical stimulus and gene expression, represents a new and important area in the morphological sciences. Several cell types ('mechanocytes'), e.g. osteoblasts and fibroblasts as well as smooth, cardiac and skeletal muscle cells are activated by mechanical strain and there is now mounting evidence that this involves the cytoskeleton. Muscle offers one of the best opportunities for studying this type of mechanotransduction as the mechanical activity generated by and imposed upon muscle tissue can be accurately controlled and measured in both in vitro and in vivo systems. Muscle is highly responsive to changes in functional demands. Overload leads to hypertrophy, whilst decreased load force generation and immobilisation with the muscle in the shortened position leads to atrophy. For instance it has been shown that stretch is an important mechanical signal for the production of more actin and myosin filaments and the addition of new sarcomeres in series and in parallel. This is preceded by upregulation of transcription of the appropriate genes some of which such as the myosin isoforms markedly change the muscle phenotype. Indeed, the switch in the expression induced by mechanical activity of myosin heavy chain genes which encode different molecular motors is a means via which the tissue adapts to a given type of physical activity. As far as increase in mass is concerned, our group have cloned the cDNA of a splice variant of IGF-1 that is produced by active muscle that appears to be the factor that controls local tissue repair, maintenance and remodelling. From its sequence it can be seen that it is derived from the IGF-1 gene by alternative splicing but it has different exons to the liver isoforms. It has a 52 base insert in the E domain which alters the reading frame of the 3' end. Therefore, this splice variant of IGF-1 is likely to bind to a different binding protein which exists in the interstitial tissue spaces of muscle, neuronal tissue and bone. This would be expected to localise its action as it would be unstable in the unbound form which is important as its production would not disturb the glucose homeostasis unduly. This new growth factor has been called mechano growth factor (MGF) to distinguish it from the liver IGFs which have a systemic mode of action. Although the liver is usually thought of as the source of circulating IGF-1, it has recently been shown that during exercise skeletal muscle not only produces much of the circulating IGF-1 but active musculature also utilises most of the IGF-I produced. We have cloned both an autocrine and endocrine IGF-1, both of which are upregulated in cardiac as well as skeletal muscle when subjected to overload. It has been shown that, in contrast to normal muscle, MGF is not detectable in dystrophic mdx muscles even when subjected to stretch and stretch combined with electrical stimulation. This is true for muscular dystrophies that are due to the lack of dystrophin (X-linked) and due to a laminin deficiency (autosomal), thus indicating that the dystrophin cytoskeletal complex may be involved in the mechanotransduction mechanism. When this complex is defective the necessary systemic as well as autocrine IGF-1 growth factors required for local repair are not produced and the ensuing cell death results in progressive loss of muscle mass. The discovery of the locally produced IGF-1 appears to provide the link between the mechanical stimulus and the activation of gene expression.
Muscle satellite (stem) cell activation during local tissue injury and repair.Hill M, Wernig A, Goldspink G. J Anat. 2003 Jul;203(1):89-99
In post-mitotic tissues, damaged cells are not replaced by new cells and hence effective local tissue repair mechanisms are required. In skeletal muscle, which is a syncytium, additional nuclei are obtained from muscle satellite (stem) cells that multiply and then fuse with the damaged fibres. Although insulin-like growth factor-I (IGF-l) had been previously implicated, it is now clear that muscle expresses at least two splice variants of the IGF-I gene: a mechanosensitive, autocrine, growth factor (MGF) and one that is similar to the liver type (IGF-IEa). To investigate this activation mechanism, local damage was induced by stretch combined with electrical stimulation or injection of bupivacaine in the rat anterior tibialis muscle and the time course of regeneration followed morphologically. Satellite cell activation was studied by the distribution and levels of expression of M-cadherin (M-cad) and related to the expression of the two forms of IGF-I. It was found that the following local damage MGF expression preceded that of M-cad whereas IGF-IEa peaked later than M-cad. The evidence suggests therefore that an initial pulse of MGF expression following damage is what activates the satellite cells and that this is followed by the later expression of IGF-IEa to maintain protein synthesis to complete the repair.
