The neuroprotective effects of creatine appear to exist in regard to dopamine biosynthesis, and the suppression of dopamine synthesis seen with some neurological toxins appears to be partially attenuated with dietary intake of creatine. The protective effect is weak to moderate in animal research, but appears to be additive with anti-inflammatories.
Negative regulators of the creatine transporter (CrT) are those that, when activated, reduce the activity of the CrT and overall creatine uptake into cells. As noted above, CrT activity is positively regulated by mTOR. Consistent with the well-known role of AMPK as a suppressor mTOR signaling, CrT activity has also been shown to be inhibited in response to AMPK activation in kidney epithelial cells. Since AMPK suppresses mTOR via upstream TSC2 activation, the negative regulation of AMPK on CrT activity in these cells appears to occur through an indirect mechanism. Although indirect, activation of AMPK has been noted to reduce the Vmax of the CrT without altering creatine binding, and is involved in internalizing the receptors. This pathway seems to max out at around 30% suppression, with no combination of mTOR antagonists and AMPK inducers further suppressing creatine uptake.
One study demonstrated that daily supplementation with 5 g of creatine monohydrate increased the intracellular creatine and PCr content of quadriceps muscle in 17 human subjects. Those with the lowest initial total creatine content had the greatest increase. In addition, exercise enhanced creatine uptake in muscle. No adverse effects were reported .
Glutamine and beta-alanine are amino acids and HMB, beta-hydroxy-beta-methyl butyrate, is a byproduct of leucine, another amino acid. Promoting individual amino acids, the building blocks of protein, to enhance performance in the strength sports has been a particular focus of supplement manufacturers over the years. To date, the evidence for any advantage has been mixed and mostly unimpressive.
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It is known that intracellular energy depletion (assessed by a depletion of ATP) stimulates AMPK activity in order to normalize the AMP:ATP ratio, and when activated AMPK (active in states of low cellular energy and colocalizes with creatine kinase in muscle tissue) appears to inhibit creatine kinase via phosphorylation (preserving phosphocreatine stores but attenuating the rate that creatine buffers ATP). While phosphocreatine technically inhibits AMPK, this does not occur in the presence of creatine at a 2:1 ratio. It seems that if the ratio of phosphocreatine:creatine increases (indicative of excess cellular energy status) that AMPK activity is then attenuated, since when a cell is in a high energy status, there is less AMP to directly activate AMPK.