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Kick those leydig cells back into action with cAMPHIBOLIC at synergymuscle.com!
FORSKOLIN AND TESTOSTERONE PRODUCTION
Testosterone is produced in testicular Leydig cells when LH binds to surface receptors and initiates a signaling cascade involving elevated levels of cAMP. This cascade leads ultimately to increased levels of an important Leydig cell cholesterol transfer protein (16) (testosterone is made from cholesterol) and activation of steroidogenic enzymes involved in testosterone production (17). So by elevating levels of cAMP, (with forskolin) an intermediate in the signaling cascade that ranges from LH binding to testosterone production, we should see an increase in testosterone output. This may be particularly important for those of us who are feeling the effects of aging. In a study by Chen et.al.,(18) the authors looked at cAMP levels in young and old rats, and found that testosterone production declined with age as a function of declining cAMP levels. So something is keeping LH from elevating cAMP and inducing steroidogenesis is aging rats. Notably, in the older rats, cAMP levels were restored to youthful levels upon administration of forskolin
FORSKOLIN INHIBITS CATABOLISM OF MUSCLE TISSUE
Thus far we have presented some possible mechanisms whereby forskolin, by elevating cAMP, promotes anabolism. Elevations in cAMP are also responsible for limiting catabolism of skeletal muscle as well. Muscle wasting is a characteristic of numerous disease states, as well as muscle disuse. AAS users are all too familiar with the latter effect, when hard-earned gains rapidly disappear post-cycle. Much of this atrophy is caused by the action of the so-called calpains. The calpains are a family of calcium dependent enzymes that degrade unused muscle tissue. Calpains in turn are inhibited by another endogenous compound called calpastatin. How is this related to forskolin? It turns out that calpastatin is upregulated by cAMP (19). Thus not only does forskolin promote anabolism, it slows muscle catabolism when muscle is not being used extensively. This would be expected to be important when a person is immobilized or unable to train due to injury, or is simply unable to maintain the rigorous training regimen off cycle that they adhered to while on AAS. So we have another potential mechanism whereby forskolin staves off post cycle muscle loss. It should be noted that even though reference (19) deals specifically with bovine calpains/calpastatin, the two are ubiquitous in all mammalian tissues, including human skeletal muscle, and calpastatin is cAMP dependent in all tissues thus far examined.
So we see that not only is forskolin safe and legal, it acts as both a mild anabolic compound as well as an anticatabolic agent in skeletal muscle tissue. This is in to the fat burning properties we discussed in detail. It may be the ideal compound for some wishing to avoid the illegalities of anabolic steroids, especially since prohormones are on the way out. It should appeal to women due to its relatively mild anabolic nature compared to harsher anabolics.
FORSKOLIN AND INFLAMMATION
Macrophages and monocytes are immune cells that secrete both pro inflammatory compounds (cytokines) as well as anti-inflammatory cytokines. Tumor Necrosis Alpha (TNF-alpha) is an example of the former, while Interleukin 10 (IL-10) exemplifies the latter. States of chronic inflammation are associated with high levels of TNF-alpha and low levels of IL-10. Both of these cytokines are dependent on cAMP for their control. Elevated cAMP suppresses TNF-alpha, while at the same time stimulating IL-10. (8) In animal models of rheumatoid arthritis, forskolin has been shown to dramatically shift the cytokine environment away from a pro-inflammatory one by suppressing TNF-alpha production. Of relevance to athletes and bodybuilders, overtraining leads to chronic inflammation associated with elevated TNF-alpha. Forskolin may help here as in arthritis.
TNF-alpha is believed to play a central role in the development and progression of insulin resistance and type II diabetes. Many athletes supplement with R-ALA to improve insulin sensitivity. Forskolin may help as well in improving glucose tolerance
Recent research has shown hypogonadism (low testosterone) to be an inflammatory condition associated with elevated levels of TNF-alpha (9). Testosterone administration normalizes the cytokine profile in these subjects. The elevated TNF-alpha in hypogonadism may be responsible for at least part of the diminished muscle mass in these patients, as well as their high incidence of inflammatory cardiovascular disease.
Finally, but far from being the least significant effect of TNF-alpha, is that it suppresses the local production of IGF-1 in skeletal muscle (10).
FORSKOLIN AND TESTOSTERONE PRODUCTION
Testosterone is produced in testicular Leydig cells when LH binds to surface receptors and initiates a signaling cascade involving elevated levels of cAMP. This cascade leads ultimately to increased levels of an important Leydig cell cholesterol transfer protein (16) (testosterone is made from cholesterol) and activation of steroidogenic enzymes involved in testosterone production (17). So by elevating levels of cAMP, (with forskolin) an intermediate in the signaling cascade that ranges from LH binding to testosterone production, we should see an increase in testosterone output. This may be particularly important for those of us who are feeling the effects of aging. In a study by Chen et.al.,(18) the authors looked at cAMP levels in young and old rats, and found that testosterone production declined with age as a function of declining cAMP levels. So something is keeping LH from elevating cAMP and inducing steroidogenesis is aging rats. Notably, in the older rats, cAMP levels were restored to youthful levels upon administration of forskolin
FORSKOLIN INHIBITS CATABOLISM OF MUSCLE TISSUE
Thus far we have presented some possible mechanisms whereby forskolin, by elevating cAMP, promotes anabolism. Elevations in cAMP are also responsible for limiting catabolism of skeletal muscle as well. Muscle wasting is a characteristic of numerous disease states, as well as muscle disuse. AAS users are all too familiar with the latter effect, when hard-earned gains rapidly disappear post-cycle. Much of this atrophy is caused by the action of the so-called calpains. The calpains are a family of calcium dependent enzymes that degrade unused muscle tissue. Calpains in turn are inhibited by another endogenous compound called calpastatin. How is this related to forskolin? It turns out that calpastatin is upregulated by cAMP (19). Thus not only does forskolin promote anabolism, it slows muscle catabolism when muscle is not being used extensively. This would be expected to be important when a person is immobilized or unable to train due to injury, or is simply unable to maintain the rigorous training regimen off cycle that they adhered to while on AAS. So we have another potential mechanism whereby forskolin staves off post cycle muscle loss. It should be noted that even though reference (19) deals specifically with bovine calpains/calpastatin, the two are ubiquitous in all mammalian tissues, including human skeletal muscle, and calpastatin is cAMP dependent in all tissues thus far examined.
So we see that not only is forskolin safe and legal, it acts as both a mild anabolic compound as well as an anticatabolic agent in skeletal muscle tissue. This is in to the fat burning properties we discussed in detail. It may be the ideal compound for some wishing to avoid the illegalities of anabolic steroids, especially since prohormones are on the way out. It should appeal to women due to its relatively mild anabolic nature compared to harsher anabolics.
FORSKOLIN AND INFLAMMATION
Macrophages and monocytes are immune cells that secrete both pro inflammatory compounds (cytokines) as well as anti-inflammatory cytokines. Tumor Necrosis Alpha (TNF-alpha) is an example of the former, while Interleukin 10 (IL-10) exemplifies the latter. States of chronic inflammation are associated with high levels of TNF-alpha and low levels of IL-10. Both of these cytokines are dependent on cAMP for their control. Elevated cAMP suppresses TNF-alpha, while at the same time stimulating IL-10. (8) In animal models of rheumatoid arthritis, forskolin has been shown to dramatically shift the cytokine environment away from a pro-inflammatory one by suppressing TNF-alpha production. Of relevance to athletes and bodybuilders, overtraining leads to chronic inflammation associated with elevated TNF-alpha. Forskolin may help here as in arthritis.
TNF-alpha is believed to play a central role in the development and progression of insulin resistance and type II diabetes. Many athletes supplement with R-ALA to improve insulin sensitivity. Forskolin may help as well in improving glucose tolerance
Recent research has shown hypogonadism (low testosterone) to be an inflammatory condition associated with elevated levels of TNF-alpha (9). Testosterone administration normalizes the cytokine profile in these subjects. The elevated TNF-alpha in hypogonadism may be responsible for at least part of the diminished muscle mass in these patients, as well as their high incidence of inflammatory cardiovascular disease.
Finally, but far from being the least significant effect of TNF-alpha, is that it suppresses the local production of IGF-1 in skeletal muscle (10).
