Simple Truths About Muscle Growth (part 4)

Last post, I explained how certain studies have suggested that creatine supplementation stimulates muscle cells to express the Insulin-like Growth Factors Type 1, IGF-1s. This is potentially a very important effect, clinically as well as athletically, as these essential anabolic factors are responsible for the development of muscle, bones, heart, and blood vessels. In reality, the growth of most of our body mass is under the control of the IGF-1s. These findings give creatine supplementation an entirely new dimension.

Go here for more information about the Insulin-Like Growth Factors Type 1: http://www.creatinemonohydrate.net/creatine_newsletter_33.html

In reality, several different versions of IGF-1 (isoforms) are produced from the same strand of DNA (gene) depending on the needs of the organism; one IGF-1 isoform awakens the muscle stem cell pool (phase 1), whereas another isoform facilitates the transformation of these now activated stem cells into contractile (force generating) muscle fibers (phase 2).

Intriguingly, one particularly rare isoform of IGF-1 appears to be specifically activated by physical activity; that is, by exercise. This isoform has become known as Mechano-Growth Factor, or MGF, as it is recruited by the “mechanical” stimulation that is exercise. On the mechanistic level, MGF awakens the muscle stem cell pool (phase 1). On the other hand, a more commonly expressed isoform of IGF-1 is the one reputed to promote the maturation of muscle stem cells (phase 2), yet is relatively insensitive to mechanical stimulation. It remains to be shown which IFG-1 isoform(s) is(are) put into play by creatine.

Read about all the latest creatine research here: http://www.creatinemonohydrate.net/creatineguide

The implication is that when one is unable to exercise, because of old age, disease, injury, etc., MGF levels would drop and muscle regeneration would be inhibited at the very onset of the process, phase 1, the activation of the muscle stem cell pool. This is one reason we lose so much muscle mass when a limb is immobilized with a cast, for example. This condition is known as immobilization atrophy.

Most intriguingly, as creatine was shown to exert this positive effect over IGF-1s expression (MGF?) in isolated muscle cells in tissue culture (not within an animal), that is, in muscle cells that were not subjected to movement, the possibility exists that creatine supplementation might be able to mimic the molecular response of exercise (MGF expression) in individuals that are unable to exercise. That is, creatine supplementation might partially bypass the need for exercise (to maintain muscle mass) in persons with restricted mobility, for whatever reason…

This would truly be an exciting result. Obviously, the clinical implications of this potential benefit of creatine supplementation would be huge!

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In subsequent posts, I will explain how to optimize your creatine use to extract this potential anabolic benefit; that is, how to best combine creatine use with exercise to enhance the expression of the IGF-1s.

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23 Comments

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    We and other groups have previously showed that IGF-1 and VEGF were specific growth factors that were elevated in the culture media and could therefore be associated with increased cardiomyocyte survival in co-culture conditions [20] , [40] . Lai et al. (2009) demonstrated that BMDC possess potent myocardial protective properties and IGF-1R is required for this protection [41] . However, IGF-1 and IGF-2 supplementation did not affect creatine kinase release and cell death caused by ischemia/reoxygenation of human myocardial slices [41] . These findings would suggest that other factors are acting through the IGF-1R to produce the protective effects or that the role of IGF-1 and IGF-2 is necessary but not sufficient to achieve the benefit by BMDC and requires the concomitant effect of additional factor(s) [41] . In the present findings, it is also possible that as well as IGF-1, other factor(s) produced through the cCSC/cardiomyocyte co-culture conditions work through IGF-1/IGF-1R/Akt signaling pathway to improve cardiomyocyte survival.

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