guardianactual
MuscleChemistry Registered Member
GA notes: The reason for this is a spike in interest on black labs Follidrone the "myostatin inhibitor" this stuff is allegedly the "real deal" so here's the write up. There are other companies producing this w/o the ' propriety blend' and charging less. I would only test this if it were $30 or under bc I hate wasting money & I hardly believe the feedback I've read bc the forum that originated this hype isn't really know for great accuracy.
</br>
</br> This revolution in performance enhancement is not a new discovery but was found in only smaller dosages in green tea until recent studies tested the pharmacology of this gem and found that it was far more than just a potent antioxidant but it elicited a plethora of positive effects that were perfectly suited for athletes and bodybuilders alike.* Epicatechin is found in nature as a racemic (balanced) mixture of both the (-) and (+) stereoisomers but the (-) isomer is what packs a serious punch.* Studies have shown that epicatechin can interfere with one of the biggest genomic inhibitor of muscle growth known, myostatin.* Myostatin prevents your body from breaking through its genetic limit by sending signals to your body to stop muscle growth, known as myogenesis4.
</br>
</br> The fun does not stop there, epicatechin has also been shown to increase vascularity and use of nitric oxide (NO) by the body3, increase mitochondrial density which can improve energy utilization by creating more of the bodies energy-making organelles5,6, and act as a potent antioxidant by scavenging free radicals7
</br>
</br> Clinicals. Alternative approaches to reduce congenital muscle dysfunction are needed in cases where the ability to exercise is limited. (-)-Epicatechin is found in cocoa and may stimulate capillarity and mitochondrial proliferation in skeletal muscle. A total of 21 male rats bred for LCR (low running capacity) from generation 28 were randomized into three groups: vehicle for 30 days (control); (-)-epicatechin for 30 days; and (-)-epicatechin for 30 days followed by 15 days without (-)-epicatechin. Groups 2 and 3 received 1.0 mg of (-)-epicatechin/kg of body mass twice daily, whereas water was given to the control group. The plantaris muscle was harvested for protein and morphometric analyses. In addition, in vitro experiments were conducted to examine the role of (-)-epicatechin on mitochondrial respiratory kinetics at different incubation periods. Treatment for 30 days with (-)-epicatechin increased capillarity (P<0.001) and was associated with increases in protein expression of VEGF (vascular endothelial growth factor)-A with a concomitant decrease in TSP-1 (thrombospondin-1) and its receptor, which remained after 15 days of (-)-epicatechin cessation. Analyses of the p38 MAPK (mitogen-activated protein kinase) signalling pathway indicated an associated increase in phosphorylation of MKK3/6 (MAPK kinase 3/6) and p38 and increased protein expression of MEF2A (myocyte enhancer factor 2A). In addition, we observed significant increases in protein expression of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator 1α), PGC-1β, Tfam and cristae abundance. Interestingly, these increases associated with (-)-epicatechin treatment remained after 15 days of cessation. Lastly, in vitro experiments indicated that acute exposure of LCR muscle to (-)-epicatechin incubation was not sufficient to increase mitochondrial respiration. The results suggest that increases in skeletal muscle capillarity and mitochondrial biogenesis are associated with 30 days of (-)-epicatechin treatment and sustained for 15 days following cessation
</br>
</br> This revolution in performance enhancement is not a new discovery but was found in only smaller dosages in green tea until recent studies tested the pharmacology of this gem and found that it was far more than just a potent antioxidant but it elicited a plethora of positive effects that were perfectly suited for athletes and bodybuilders alike.* Epicatechin is found in nature as a racemic (balanced) mixture of both the (-) and (+) stereoisomers but the (-) isomer is what packs a serious punch.* Studies have shown that epicatechin can interfere with one of the biggest genomic inhibitor of muscle growth known, myostatin.* Myostatin prevents your body from breaking through its genetic limit by sending signals to your body to stop muscle growth, known as myogenesis4.
</br>
</br> The fun does not stop there, epicatechin has also been shown to increase vascularity and use of nitric oxide (NO) by the body3, increase mitochondrial density which can improve energy utilization by creating more of the bodies energy-making organelles5,6, and act as a potent antioxidant by scavenging free radicals7
</br>
</br> Clinicals. Alternative approaches to reduce congenital muscle dysfunction are needed in cases where the ability to exercise is limited. (-)-Epicatechin is found in cocoa and may stimulate capillarity and mitochondrial proliferation in skeletal muscle. A total of 21 male rats bred for LCR (low running capacity) from generation 28 were randomized into three groups: vehicle for 30 days (control); (-)-epicatechin for 30 days; and (-)-epicatechin for 30 days followed by 15 days without (-)-epicatechin. Groups 2 and 3 received 1.0 mg of (-)-epicatechin/kg of body mass twice daily, whereas water was given to the control group. The plantaris muscle was harvested for protein and morphometric analyses. In addition, in vitro experiments were conducted to examine the role of (-)-epicatechin on mitochondrial respiratory kinetics at different incubation periods. Treatment for 30 days with (-)-epicatechin increased capillarity (P<0.001) and was associated with increases in protein expression of VEGF (vascular endothelial growth factor)-A with a concomitant decrease in TSP-1 (thrombospondin-1) and its receptor, which remained after 15 days of (-)-epicatechin cessation. Analyses of the p38 MAPK (mitogen-activated protein kinase) signalling pathway indicated an associated increase in phosphorylation of MKK3/6 (MAPK kinase 3/6) and p38 and increased protein expression of MEF2A (myocyte enhancer factor 2A). In addition, we observed significant increases in protein expression of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator 1α), PGC-1β, Tfam and cristae abundance. Interestingly, these increases associated with (-)-epicatechin treatment remained after 15 days of cessation. Lastly, in vitro experiments indicated that acute exposure of LCR muscle to (-)-epicatechin incubation was not sufficient to increase mitochondrial respiration. The results suggest that increases in skeletal muscle capillarity and mitochondrial biogenesis are associated with 30 days of (-)-epicatechin treatment and sustained for 15 days following cessation
