Black Lion Research introduces a supplement that changes the way we look at performance enhancing supplements.
-Serious increases in strength and serious potential for muscle mass gain.
-Follidrone will not test positive on any test for natural competitors or competitive athletes.
-Follidrone causes changes that are associated with a healthier and longer lifespan, including improved skeletal muscle stress output, reduced systematic inflammation markers and serum LDL cholesterol.
-Follidrone increases angiogenesis 30-50% which in turn increases blood flow as well as oxygen and nutrient transport into muscle tissues.
-Follidrone imitates the effects of endurance training as well as making endurance training more effective. Use of Follidrone can lead to significant increases in treadmill performance (∼50%) and enhanced in situ muscle fatigue resistance (∼30%).
-Follidrone increases follistatin levels. Follistatin is an antagonist to myostatin which inhibits excessive muscle growth. A study has also shown that increased levels of follistatin leads to increased muscle mass. Follistatin is part of the inhibin-activin-follistatin axis. Follistatin is an Activin binding protein. In the tissues activin has a strong role in cellular proliferation, thereby making follistatin the safeguard against uncontrolled cellular proliferation and also allowing it to function as an instrument of cellular differentiation. Both of these roles are vital in tissue rebuilding and repair.
In addition, increased follistatin levels combined with a lack of myostatin DOUBLED MUSCLE GROWTH.
Study results regarding Follidrone ingredients
Animals with reduced myostatin
Follodrone decreases Myostatin levels 49%+ as well as increasing markers of muscle growth. Myostatin is a secreted growth differentiation factor that is a member of the TGF beta protein family that inhibits muscle differentiation and growth in the process known as myogenesis. Myostatin is produced primarily in skeletal muscle cells, circulates in the blood and acts on muscle tissue, by binding a cell-bound receptor called the activin type II receptor. Reductions in myostatin = increased muscle mass and strength.
Follidrone Increases strength dramatically and quickly.
Treatment for 7 days yielded a bilateral increase in hand strength of 7%, which was accompanied by a significant decrease (-49%) in myostatin.
In addition our internal testers reported serious strength gains including-
-100lb increase in Deadlift in 4 days
-20lbs per arm on DB incline press in 10 days.
-6 inch gain on vert jump to 53 inches.
-one user compared the strength increase to halotestin.
Increases in mass were also reported by our internal testers including 10lbs weight gain in 10 days with what appears to be 0 BF% increase.
Users have also been reporting significant physique changes. Harder, leaner, and overall larger.
Effects of (-)-epicatechin on molecular modulators of skeletal muscle growth and differentiation.
Gutierrez-Salmean G1, Ciaraldi TP, Nogueira L, Barboza J, Taub PR, Hogan MC, Henry RR, Meaney E, Villarreal F, Ceballos G, Ramirez-Sanchez I.
Sarcopenia is a notable and debilitating age-associated condition. Flavonoids are known for their healthy effects and limited toxicity. The flavanol (-)-epicatechin (Epi) enhances exercise capacity in mice, and Epi-rich cocoa improves skeletal muscle structure in heart failure patients. (-)-Epicatechin may thus hold promise as treatment for sarcopenia. We examined changes in protein levels of molecular modulators of growth and differentiation in young vs. old, human and mouse skeletal muscle. We report the effects of Epi in mice and the results of an initial proof-of-concept trial in humans, where muscle strength and levels of modulators of muscle growth were measured. In mice, myostatin and senescence-associated β-galactosidase levels increase with aging, while those of follistatin and Myf5 decrease. (-)-Epicatechin decreases myostatin and β-galactosidase and increases levels of markers of muscle growth. In humans, myostatin and β-galactosidase increase with aging while follistatin, MyoD and myogenin decrease. Treatment for 7 days with (-)-epicatechin increases hand grip strength and the ratio of plasma follistatin/myostatin. In conclusion, aging has deleterious effects on modulators of muscle growth/differentiation, and the consumption of modest amounts of the flavanol (-)-epicatechin can partially reverse these changes. This flavanol warrants its comprehensive evaluation for the treatment of sarcopenia.
Epicatechin imitates the effects of endurance training as well as making endurance training more effective.
In a 2012 research study one group of mice ran daily on a tread mill for five weeks where as the control group did nothing.
At the end of five weeks all animals did nothing for 14 days.
Half the trained mice were given epicatechin twice a day and the other half were given water. At the end of the 14-day detraining period, the mice that had been given (-)-epicatechin had retained much of the condition they had built up previously. When the researchers got the animals to run to the point of exhaustion, the mice that had been given (-)-epicatechin were faster, were able to keep running for longer and therefore also covered a greater distance.
When the mice's muscles were examined researchers saw that epicatechin supplementation had prevented training induced changes in muscle fibers from disappearing during inactivity.
Epicatechin enhances fatigue resistance and oxidative capacity in muscle
Twenty-five male mice (C57BL/6N) were randomized into four groups: (1) water, (2) water-exercise (W-Ex), (3) (-)-epicatechin ((-)-Epi), and (4) (-)-epicatechin-exercise ((-)-Epi-Ex). Animals received 1 mg kg(-1) of (-)-epicatechin or water (vehicle) via oral gavage (twice daily). Exercise groups underwent 15 days of treadmill exercise. Significant increases in treadmill performance (∼50%) and enhanced in situ muscle fatigue resistance (∼30%) were observed with (-)-epicatechin. Components of oxidative phosphorylation complexes, mitofilin, porin, nNOS, p-nNOS, and Tfam as well as mitochondrial volume and cristae abundance were significantly higher with (-)-epicatechin treatment for hindlimb and cardiac muscles than exercise alone. In addition, there were significant increases in skeletal muscle capillarity. The combination of (-)-epicatechin and exercise resulted in further increases in oxidative phosphorylation-complex proteins, mitofilin, porin and capillarity than (-)-epicatechin alone. These findings indicate that (-)-epicatechin alone or in combination with exercise induces an integrated response that includes structural and metabolic changes in skeletal and cardiac muscles resulting in greater endurance capacity.
Dietary epicatechin promotes survival of obese diabetic mice and Drosophila melanogaster.
Si H1, Fu Z, Babu PV, Zhen W, Leroith T, Meaney MP, Voelker KA, Jia Z, Grange RW, Liu D.
The lifespan of diabetic patients is 7-8 y shorter than that of the general population because of hyperglycemia-induced vascular complications and damage to other organs such as the liver and skeletal muscle. Here, we investigated the effects of epicatechin, one of the major flavonoids in cocoa, on health-promoting effects in obese diabetic (db/db) mice (0.25% in drinking water for 15 wk) and Drosophila melanogaster (0.01-8 mmol/L in diet). Dietary intake of epicatechin promoted survival in the diabetic mice (50% mortality in diabetic control group vs. 8.4% in epicatechin group after 15 wk of treatment), whereas blood pressure, blood glucose, food intake, and body weight gain were not significantly altered. Pathological analysis showed that epicatechin administration reduced the degeneration of aortic vessels and blunted fat deposition and hydropic degeneration in the liver caused by diabetes. Epicatechin treatment caused changes in diabetic mice that are associated with a healthier and longer lifespan, including improved skeletal muscle stress output, reduced systematic inflammation markers and serum LDL cholesterol, increased hepatic antioxidant glutathione concentration and total superoxide dismutase activity, decreased circulating insulin-like growth factor-1 (from 303 ± 21 mg/L in the diabetic control group to 189 ± 21 mg/L in the epicatechin-treated group), and improved AMP-activated protein kinase-α activity in the liver and skeletal muscle. Consistently, epicatechin (0.1-8 mmol/L) also promoted survival and increased mean lifespan of Drosophila. Therefore, epicatechin may be a novel food-derived, antiaging compound.
Stimulatory effects of the flavanol (-)-epicatechin on cardiac angiogenesis: additive effects with exercise.
Ramirez-Sanchez I1, Nogueira L, Moreno A, Murphy A, Taub P, Perkins G, Ceballos GM, Hogan M, Malek M, Villarreal F.
The consumption of moderate amounts of cocoa products has been associated with reductions in the incidence of cardiovascular diseases. In animal studies, the flavanol (-)-epicatechin (Epi) yields cardioprotection. The effects may be partly due to its capacity to stimulate endothelial nitric oxide synthase (eNOS). The sustained activation of eNOS, as observed with exercise, can serve as a trigger of muscle angiogenesis via the activation of vascular endothelial growth factor (VEGF)-related events. Experiments were pursued to examine the potential of Epi to stimulate myocardial angiogenesis and determine the effects that its combined use with exercise (Ex) may trigger. Hearts obtained from a previous study were used for this purpose. Animals received 1 mg/kg of Epi or water (vehicle) via oral gavage (twice daily). Epi and/or Ex (by treadmill) was provided for 15 days. Results indicate that Ex or Epi significantly stimulate myocardial angiogenesis by ~30% above control levels. The use of Epi-Ex lead to further significant increases (to ~50%). Effects were associated with increases in protein levels and/or activation of canonical angiogenesis pathway associated events (HIF1a, VEGF, VEGFR2, PI3K, PDK, AKT, eNOS, NO, cGMP, MMP-2/-9, Src-1, and CD31). Thus, the use of Epi may represent a safe and novel means to stimulate myocardial angiogenesis.
(-)-Epicatechin maintains endurance training adaptation in mice after 14 days of detraining.
Hüttemann M1, Lee I, Malek MH.
The purpose of this study was to determine whether (-)-epicatechin (mainly found in cocoa) could attenuate detraining effects in the hindlimb muscles of mice. Thirty-two male mice were randomized into 4 groups: control, trained, trained with 14 d of detraining and vehicle (DT-14-W), and trained with 14 d of detraining and (-)-epicatechin [DT-14-(-)-Epi]. DT-14-(-)-Epi received (-)-epicatechin (1.0 mg/kg 2 ×/d), whereas water was given to the DT-14-W group. The latter 3 groups performed 5 wk of endurance training 5 ×/wk. Hindlimb muscles were harvested, and Western blots, as well as enzyme analyses, were performed. Training significantly increased capillary-to-fiber ratio (≈ 78.8%), cytochrome-c oxidase (≈ 35%), and activity (≈ 144%) compared to controls. These adaptations returned to control levels for the DT-14-W group, whereas the DT-14-(-)-Epi group was able to maintain capillary-to-fiber ratio (≈ 44%), CcO protein expression (≈ 45%), and activity (≈ 108%) above control levels. In addition, the increase in capillarity was related to decreased protein expression of thrombospondin-1, an antiangiogenic regulator. Furthermore, there were no significant differences in endurance capacity between the trained and DT-14-(-)-Epi groups. Our data suggest that (-)-epicatechin may be a suitable compound to maintain exercise-induced improved capillarity and mitochondrial capacity, even when exercise regimens are discontinued.
Follistatin improves skeletal muscle healing after injury and disease through an interaction with muscle regeneration, angiogenesis, and fibrosis.
Zhu J1, Li Y, Lu A, Gharaibeh B, Ma J, Kobayashi T, Quintero AJ, Huard J.
Recovery from skeletal muscle injury is often incomplete because of the formation of fibrosis and inadequate myofiber regeneration; therefore, injured muscle could benefit significantly from therapies that both stimulate muscle regeneration and inhibit fibrosis. To this end, we focused on blocking myostatin, a member of the transforming growth factor-β superfamily and a negative regulator of muscle regeneration, with the myostatin antagonist follistatin. In vivo, follistatin-overexpressing transgenic mice underwent significantly greater myofiber regeneration and had less fibrosis formation compared with wild-type mice after skeletal muscle injury. Follistatin's mode of action is likely due to its ability to block myostatin and enhance neovacularization. Furthermore, muscle progenitor cells isolated from follistatin-overexpressing mice were significantly superior to muscle progenitors isolated from wild-type mice at regenerating dystrophin-positive myofibers when transplanted into the skeletal muscle of dystrophic mdx/severe combined immunodeficiency mice. In vitro, follistatin stimulated myoblasts to express MyoD, Myf5, and myogenin, which are myogenic transcription factors that promote myogenic differentiation. Moreover, follistatin's ability to enhance muscle differentiation is at least partially due to its ability to block myostatin, activin A, and transforming growth factor-β1, all of which are negative regulators of muscle cell differentiation. The findings of this study suggest that follistatin is a promising agent for improving skeletal muscle healing after injury and muscle diseases, such as the muscular dystrophies.