C2--The new frontier on weight loss
- 09-12-2005, 03:29 PM
C2--The new frontier on weight loss
C2 "The ThermoBolic Cognative Stimulant"
C2 is a uniquely designed blend of compounds designed to increase fat burning, improve athletic performance, enhance cognitive functioning, enhance recovery, adapt to stress, combats diet related depression, improve sex drive and promote anabolism of muscle tissue.
Our original fat burning/muscle-preserving product called cAMPHIBOLIC addresses the issue that many supplements companies failed to address. Which is muscle loss while dieting. Common Knowledge that Lean Body Mass (muscle) is our fat burning furnace. In the past dieting was a double edge sword. Which entailed sacrificing hard earned muscle for fat loss, feeling
miserable and depressed, and performance suffered. The dieting concept was a dreaded experience.
cAMPHIBOLC has proven successful in muscle preservation while accelerating fat loss while improving performance in the gym. cAMPHIBOLIC exerts an anti-depressant effects so the experience is enjoyable. How could we improve on cAMPHIBOLC? What if you could take a substance that allows the user to more work (exercise) while speeding the recovery process.That would be brilliant! A product that preserves muscle while it EFFECTIVELY execrates fat loss and increasing work capacity without the threat of over-training. Those well versed in dieting know that once over-training kicks in the body's ability to function halts drastically, and the dieting process comes to a crashing end. A miserable feeling of mental confusion and the depression of seeing your muscle waste before your eyes.
USPlab brings you C2, the ONLY product that increases fat burning, improves athletic performance, enhances cognitive function, combats diet related depression and helps the body adapt to stress. C2 is the ONLY product that increases work capacity without the threat of over-training. We are not preaching 4 hour a day workouts. Your workout will have an intensity as if
you where eating surplus calories. You will not dread tomorrow's workout and the experience becomes enjoyable and full of results!
Can we back it up with research? Read below!
The extract of the root of this plant possesses several scientifically proven properties of interest not only to athletes and bodybuilders, but anyone interested in improving their overall health. In a double blind placebo-controlled randomized study involving healthy young humans, it was shown that ingestion of 200 mg of Rhodiola extract prior to exercise resulted in a significant improvement in
increased ATP production in skeletal muscle. exercise performance (1). Animal experiments confirm this (2) and point to a mechanism:Exercise is a form of stress, and Rhodiola has been shown by researchers to
increase resistance to a number of different forms of biological, chemical, and physical stress. For this reason it is termed an "adaptogen", allowing the body to more successfully adapt to stressful situations. It is a popular plant in traditional medical systems in Eastern Europe and Asia, with a reputation for stimulating the nervous system, improving depression, enhancing work performance, improving cognitive functioning, improving sleep, eliminating fatigue, and preventing high altitude sickness (3).
Animal studies have demonstrated anticancer and hepatoprotective effects as well. The ability to protect the liver against toxins may be of particular interest to users of oral anabolic steroids (4).
In addition to Rhodiola's ability to enhance exercise performance by increasing ATP levels, other research has shed light on how Rhodiola may work in other stressful situations. The adaptogenic properties, cardiopulmonary protective effects, and central nervous system activities of Rhodiola rosea have been attributed primarily to its ability to influence levels and activity of biogenic monoamine neurotransmitters such as serotonin, dopamine, and norepinephrine in the cerebral cortex, brain stem, and hypothalamus. It is believed the changes in monoamine levels are due to inhibition of the activity of enzymes responsible for monoamine degradation and facilitation of neurotransmitter transport within the brain
In addition to these central effects, Rhodiola has been reported to prevent both catecholamine release and subsequent cyclic AMP elevation in the hear tissue, and the depletion of adrenal catecholamines induced by acute stress. Rhodiola's adaptogenic activity might also be secondary to induction of opioid peptide biosynthesis and through the activation of both central and peripheral opioid receptors (5).
The numerous beneficial properties of Forskolin have been documented in the description of USPLab's flagship product, cAMPhibolic. Here we will only list the actions of forskolin without detailed references. For those readers wishing greater detail, see the product description for cAMPhibolic at www.synergymuscle.com.
The scientifically documented properties of forskolin are as follows.
- Mobilizes fat for use as fuel by activating so-called Hormone Sensitive
- When added to thyroid tissue in culture, mimics the effect of TSH (Thyroid Stimulating Hormone) and stimulates the production of thyroid hormone. Thyroid hormone is well known to increase metabolic rate by way of several mechanisms, and this increased metabolic rate will lead to the use of the mobilized fatty acids for fuel. In addition to stimulating the secretion of primarily T4 from the thyroid, forskolin promotes the conversion of the relatively inactive T4 to its potent metabolite T3 via the action of type II deiodinase. Forskolin has been shown to induce the expression of type II deiodinase in peripheral tissue, especially skeletal
- Has the ability to relax cavernosal smooth muscles in the penis, allowing the organ to fill with blood. For those readers familiar with drugs like Viagra and Cialis, they would recognize that this is exactly how these drugs work, albeit in a somewhat different manner. These drugs are known as phosphodiesterase inhibitors, and prevent the breakdown of another second messenger, cGMP that is involved in signaling cascades similar to cAMP. In particular, in the penis the prevention of breakdown of cGMP leads to erections. So forskolin and Viagra (as well as Cialis) act via different pathways to stimulate erections. Researchers observed a synergistic effect on erection when forskolin was combined with Viagra. So both agents alone promote erection, and when combined exhibit synergism, an effect greater than the sum of the two.
- Lowers levels of the proinflammatory cytokine TNF-alpha. 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. In animal models of rheumatoid arthritis, forskolin has been shown to dramatically 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. 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 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 in skeletal muscle
- Increases 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 (testosterone is made from cholesterol) and activation of steroidogenic enzymes involved in testosterone production. 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., 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
- Stimulates the production of Gonadatropin Releasing Hormone (GnRH) from the hypothalamus. GnRH acts on the pituitary gland to increase LH production, and LH in turn stimulates testicular testosterone production.
- Inhibits muscle catabolism. Elevations in cAMP are responsible for limiting catabolism of skeletal muscle. 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. 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.
Caffeine is perhaps the most widely used agent to mobilize fat for use as fuel, and one that actually helps burn that fat by elevating energy expenditure (basal metabolic rate). Several studies have shown that caffeine promotes lipolysis, the breakdown
of stored fats into fatty acids which can be used by working muscle and other tissues for fuel while sparing glycogen in the process (6). Other studies, while not questioning increased lipolysis, have expressed doubts about another widely held belief, namely the glycogen sparing effects of caffeine in skeletal muscle. This question appears to remain open (7).
The traditional theory on how caffeine promotes lipolysis rests on the fact that at relatively high concentrations caffeine acts as a phophodiesterase inhibitor, maintaining elevated levels of cAMP (cyclic AMP) and in the process amplifying the effects of the body's natural lipolytic hormones epinephrine and norepinephrine. Many experts still adhere to this view. During the lipolytic (fat mobilizing) signaling cascade, natural hormones like norepinephrine and epinephrine (or synthetic analogs like ephedrine or
clenbuterol) bind to so-called alpha-1 and beta-1 and beta-2 adrenergic receptors on the surface of fat cells, activating cyclic Adenosine Monophosphate, or cAMP (8,9). (The extent to which the third identified beta receptor, beta-3, contributes to lipolysis in humans is debated. It is important however in lipolysis in the brown fat of many animals.) cAMP ultimately acts to turn on the enzyme Hormone Sensitive Lipase (HSL). HSL breaks up stored fat so that it can be used for fuel. cAMP is deactivated
by an enzyme called phosphodiesterase. Caffeine inhibits the action of phospodiesterase thereby prolonging lipolysis.
Other research has shown that caffeine can inhibit lipoprotein lipase (LPL) expression both during adipose tissue differentiation and in mature adipocytes. LPL is one of the body's primary fat accumulating hormones. It allows for the removal of triglycerides from the blood and their entry into adipocyctes where they are stored as fat (10)
Besides acting as a cutting agent, we mentioned the ergogenic (sports performance enhancing) properties of caffeine. The fat burning/glycogen sparing effect discussed above may contribute to this.
Caffeine has been shown to stimulate the production of endorphins, the body's natural painkillers. This would certainly imply an increased tolerance for the pain associated with exercise. An increase in ß-endorphin is well known to enhance exercise performance through its ability to decrease pain perception and promote euphoria (11). The same study showed caffeine caused an increase in plasma cortisol, the long-distance cyclist's best friend (other than EPO)
Caffeine has also been demonstrated to increase the force of low frequency muscular contractions by potentiating the release of Ca++ from the muscle cell's sarcoplasmic reticulum (SR) (12) suggesting that caffeine has an ergogenic effect in and not high-intensity/power-type activities. However, the endorphin release and CNS stimulation caused by caffeine would likely help a bodybuilder or powerlifter as well as a distance runner. We should mention that the stimulatory effect of caffeine depends on its ability to reduce adenosine transmission in the brain (13)
For the reader unfamiliar with the role of calcium in muscle contraction,
provides a nice tutorial. In a nutshell, when a nerve impulse originating from the brain crosses the neuromuscular junction and travels along the membrane of the SR, the calcium "gates" that are closed when the muscle is at rest open and calcium diffuses rapidly out of the SR and into the sarcoplasm where the myofibrils & myofilaments are located.
The presence of Ca++ allows for the interaction of two major proteins in the muscle, actin and myosin. In the resting state, these proteins (which have a natural affinity for each other) are prevented from coming into contact. Two other proteins, troponin and tropomyosin, form a complex weave between the actin and myosin, and prevent contact. When Ca++ enters the picture, the shape of the troponin-tropomyosin complex changes, and now actin and myosin can come into contact with each other and contraction can occur.
For athletes considering the combined use of forskolin, an activator of cAMP, and caffeine, they may receive an added benefit in the form of slowed glycogen use, compared to forskolin alone, which strongly promotes glycogenolysis. We noted above that caffeine seems to promote the burning of fat for fuel while promoting the sparing of muscle glycogen, at least according to Costill, et.al. Recall however that several later studies have called into question caffeine's glycogen sparing ability.
Perhaps the feature of caffeine with which we are all most familiar is its ability to stimulate the central nervous system. It acts as a CNS stimulant by blocking adenosine receptors in the brain. Adenosine is an inhibitory neuromodulator that slows neuronal activity in the brain. It primarily inhibits the release from the CNS of excitatory neurotransmitters such as dopamine and norepinephrine. Caffeine, by blocking certain classes of the adenosine receptor, has the opposite effect, increasing the firing of
neurons (14). Caffeine also acts to increase the release of epinephrine from the adrenal glands perhaps by increasing nerve signaling from the brain to the adrenals (15).
Since Costill's original paper [which we cited as (6)], more emphasis has been placed on the adenosine blocking effects of caffeine than on caffeine's ability to act as a phosphodiesterase inhibitor and Ca++ releaser. This change in viewpoint is due to the observation that in some studies much larger doses of caffeine are required to promote lipolysis and release Ca++ than to block adenosine. However, the matter is considered far from settled. As a counterexample to the theory that adenosine blockade
accounts for the major fraction of caffeine's metabolic effects, we mentioned above that according to the adenosine blockade theory adenosine inhibits the release of norepinephrine, and that many of caffeine's effects such as lipolysis are attributable to the release of adenosine blocked norepinephrine and epinephrine. In one study that suggests a contrary mechanism of caffeine action, patients with spinal cord lesions who were unable to secrete epinephrine from the adrenal glands were administered
caffeine. Not unexpectedly, there was no increase in epinephrine. There was also no increase in plasma norepinephrine. Yet the patients showed a 2-fold increase in plasma free fatty acids and a concomitant increase in glycerol, showing that caffeine stimulates lipolysis with no increase in either epinephrine or adenosine sequestered norepinephrine (16). This suggests that the phosphodiesterase inhibitor theory of caffeine is not without merit.
Some recent research sheds yet more light on how caffeine burns calories to increase metabolic rate: futile cycling in adipocytes. Fats are stored as triacylglycerol, fatty acid chains attached to a glycerol backbone. Lipolysis is the process of breaking the fatty acid chains off the glycerol backbone. Reesterification represents the reattachment of the chains. Caffeine induces a futile cycle of energy requiring lipolysis and reesterification (17). Incidentally, leptin induces a similar futile cycling of fats to free fatty acids and back, and this is believed to account for a significant contribution to the increase in energy
expenditure when leptin is administered to normal (nonobese) humans and animals. Obese humans and animals seem to show resistance to the effects of leptin and fail to exhibit increased energy expenditure when given leptin. On the other hand obese individuals are quite sensitive to the effects of combined beta agonists, such as ephedrine and caffeine.
Interestingly, when coffee is substituted for caffeine in some
decaffeinated water, as compared to placebo. But still the increases in endurance with pure caffeine are greater than those employing coffee or decaffeinated water with added caffeine. studies caffeine improves endurance while coffee (containing an amount of caffeine leading to identical plasma caffeine levels as when caffeine itself was given) seems to have no effect (18). The mechanism behind this is not clear, but it has been suggested that coffee contains some other compound(s) that is detrimental to performance. Other studies (1) employing coffee show a positive effect on endurance when caffeine is added to
So in summary, we see that the mechanisms for increased lipolysis and energy expenditure due to caffeine are still debated. Studies differ as to the effectiveness of caffeine as a lipolytic as well as ergogenic agent. Perhaps one of the most puzzling aspects of the various studies is why in some individuals (all equally untrained) caffeine seems to exert a glycogen sparing effect during exercise while in others no such effect is seen (19).
Some of the apparent contradictions plaguing caffeine research, as well as some of the proposed mechanisms we have discussed are summarized in a paper by Greer et.al. :
"Many studies examining the mechanism behind the ergogenic effect of caffeine have focused on the methylxanthine-induced increase in circulating plasma epinephrine and the metabolic changes that occur with exercise. However, recent studies have provided evidence that the original hypothesis by Costill et al. may not be the critical mechanism behind the effects of
caffeine in all exercise conditions. For example, an ergogenic effect of caffeine has been demonstrated without an increase in plasma epinephrine. In addition, an increase in free fatty acid (FFA) mobilization without a corresponding catecholamine response has been demonstrated, indicating a direct effect of caffeine on fat cells. Carbohydrate metabolism has been
shown to be unaltered when epinephrine was infused to mimic the caffeine-induced epinephrine response. Glycogen sparing has not always been found during exercise after caffeine ingestion, and an increase in performance has been observed in exercise situations in which muscle glycogen is not the limiting factor and when no glycogen sparing was observed. A direct effect of caffeine on the central nervous system has also been postulated to explain the ergogenic effect of this methylxanthine; however, it has been demonstrated that this is not a critical mechanism"(20). In summary,
"Three possible mechanisms through which the methylxanthines may exert their metabolic effects include increased intracellular Ca2+ release, inhibition of cAMP phosphodiesterase, and antagonism of adenosine receptors. It is now [according to these authors] established that adenosine receptor antagonism is the most relevant mechanism in vivo because pharmacological doses of methylxanthines (mM) rather than physiological doses (µM) are needed to elicit a Ca2+ or phosphodiesterase
inhibition effect" (20)
So it would seem that according to the majority of researchers adenosine receptor antagonism is the most important effect elicited by caffeine, with the other mechanisms described above playing less significant roles in the action of caffeine. However, adenosine receptor antagonism is unable to explain all of the effects seen with caffeine consumption. For example, the
adenosine receptor rapidly develops tolerance to agonists and antagonists. However, in (7) no difference in muscle force generation was observed between groups of subjects habituated to caffeine, and caffeine naïve subjects. This argues against an adenosine receptor mediated effect in this instance.
In light of the above, another receptor, the so called ryanodine "receptor" (actually a calcium release channel and not a true receptor) has been proposed to mediate the effects of Ca++ release from muscle sarcoplasmic reticulum and generate muscle contraction (21). Ryanodine itself is an insecticidal alkaloid isolated from Ryania speciosa originally proposed as a myocardial depressant. It was later discovered that caffeine is a ligand for this receptor. Interestingly, the venom from certain species of
scorpions (e.g. Pandinus imperator) target the ryanodine receptor inducing a state of subconductance and paralysis. Caffeine potentiates this effect, so it is probably not a smart idea to drink large amounts of coffee when handling scorpions.
So ultimately there may very well be a number of mechanisms through which caffeine exerts its effects, and it is likely overly simplistic to attribute all of the effects of caffeine to adenosine receptor antagonism.
Synephrine acts primarily as an agonist at alpha 1 adrenergic receptors. On fat cells, when synephrine binds to these receptors it initiates lipolysis (22). Recall that forskolin and caffeine are also involved in the lipolytic process, but these act independently of alpha receptors.
Interestingly though, several studies have shown that the alpha receptor related lipolysis seen with synephrine is potentiated by caffeine, forskolin, and ephedrine. Hence the rationale for combining synephrine, forskolin, and caffeine together in NeuroHeat (23, 24, 25).
Bacopa monniera, also referred to as Bacopa monnieri, Herpestis monniera, water hyssop, and "Brahmi," has been used in the Ayurvedic system of medicine for centuries. Traditionally, it was used as a brain tonic to enhance memory development, learning, and concentration, and to provide relief to patients with anxiety or epileptic disorders. The plant has also been used in India and Pakistan as a cardiac tonic, digestive aid, and to improve respiratory function in cases of bronchoconstriction. Recent research has focused primarily on Bacopa's cognitive-enhancing effects, specifically memory, learning, and concentration, and results support the traditional Ayurvedic claims. Research on anxiety, epilepsy, bronchitis and asthma, irritable bowel
syndrome, and gastric ulcers also supports the Ayurvedic uses of Bacopa. Bacopa's antioxidant properties may offer protection from free radical damage in cardiovascular disease and certain types of cancer.
Here we will look only at the results of modern studies dealing with the ability of Bacopa to improve cognitive functioning, as well as its antioxidant properties that may provide health benefits.
In one placebo controlled, double-blinded experiment, Bacopa was able to significantly improve the speed of visual information processing, learning rate and memory consolidation, with maximal effects evident after 12 weeks (26). In another study (27) seventy-six adults aged between 40 and 65 years were tested and levels of anxiety measured. There were three testing
sessions: one prior to the trial, one after three months on the trial, and one six weeks after the completion of the trial. The results show a significant effect of the Bacopa on a test for the retention of new information. Follow-up tests showed that the rate of learning was unaffected, suggesting that Bacopa decreases the rate of forgetting of newly acquired information.
It has been proposed that the mechanism behind the action of Bacopa is due to an increase in certain enzymes that aid in the repair of neurons and neuronal synthesis, synaptic activity, and ultimately nerve impulse transmission (28). Other research points to a protective antioxidant effect that may be responsible for the improved neuronal functioning seen with Bacopa administration (29).
Bacopa's traditional use as an anti-anxiety remedy in Ayurvedic medicine is supported by both animal and clinical research. Research using a rat model of clinical anxiety demonstrated a Bacopa extract of 25-percent bacoside A exerted anxiolytic activity comparable to Lorazepam, a common benzodiazapene anxiolytic drug. Importantly, the Bacopa extract did not
induce amnesia, side effects associated with Lorazepam, but instead had a memory-enhancing effect (30).
Last but not least, in animal studies Bacopa has been shown to increase T(4) concentration by 41% without enhancing hepatic lipid peroxidation (LPO) suggesting that it can be used as a thyroid-stimulating drug (31). In fact, hepatic LPO was decreased and superoxide dismutase (SOD) and catalase (CAT) activities were increased by B. monnieri. LPO is a bad thing because
it creates a chain reaction of cell-damaging free radicals. SOD and catalase on the other hand quench harmful free radicals.
Chocolate can be healthful, believe it or not, at least certain constituents of chocolate, anyway. Chocamine is a cocoa extract that contains several compounds that exert fat burning, nootropic, and antioxidant actions.
Fat Burning and Appetite Suppressing Compounds:
Chocamine contains several compounds known as methylxanthines that are chemically similar to caffeine. In fact, caffeine is one of these agents. The others are theobromine, and minor amounts of theophylline. Each gram of chocamine contains about 120 mg theobromine and 80 mg caffeine. Theobromine exerts a somewhat weaker lipolytic action that caffeine, but is longer
lasting. Theophylline on the other hand is more potent than caffeine, but chocamine contains so little that it likely only contributes in a minor way, if at all, to the lipolytic properties of chocamine.
Tyramine is another lipolytic compound found in chocamine. It acts somewhat like ephedrine in that it promotes the release of norepinephrine from nerve endings. The norepinephrine binds to beta receptors on fat cells and stimulates lipolysis. Like ephedrine, tyramine suppresses appetite in addition to its lipolytic properties.
Chocamine contains minor amounts of the amino acid tryptophan, which is a precursor to the neurotransmitter serotonin. Serotonin is a well documented appetite suppressant. Another amino acid found in chocamine is tyrosine, which is a precursor to dopamine. Tyrosine ingestion elevates brain levels of both dopamine and norepinephrine, and this may also contribute to
appetite suppression. (On a side note, the elevated dopamine levels associated with chocolate consumption are thought by some to play a role in the addictive nature of chocolate.)
Nootropics are compounds that improve cognitive function. Besides the tyrosine found in chocamine which may elevate the stimulatory neurotransmitter dopamine, chocamine also contains phenylethylamine, a compound known to stimulate neuronal activity in the brain. Administered orally however, several studies have shown little if any effect of phenylethylamine on brain function. It has been suggested that some individuals are particularly sensitive to phenylethylamine and may experience stimulatory effects from oral doses.
Chocamine is rich in so called flavanoids, which act as antioxidants. They have been shown to have an anticarcinogeneic effect, as well as conferring cardiovascular benefits. One major theory about the development of atherogenic heart disease is that it originates from oxidized LDL particles. Dietary flavinoids may help prevent this LDL oxidation.
: Fat Burning and Muscle Building Day and Night
The question has often been posed whether thermogenics require exercise to work their fat burning magic. This often arises in the context of interpreting labels that say something like "Take two capsules before exercise". The answer is yes; it is possible to increase the rate of fat burning even during sleep by using the right combination of supplements. The combination that I believe is most effective at night without disrupting sleep (i.e. lacking stimulants like high concentrations of caffeine) and has data to support it is green tea/forskolin/
supporting data to see why.
Several studies have demonstrated that green tea extract increases metabolic rate and the rate of fat burning in humans. A study that is of particular interest to us looked at the rate of green tea fat burning over a 24 hour period, both during wake and sleep (32). In addition, this study examined the so-called respiratory quotient (RQ) in subjects using green tea. RQ measures the relative amounts of fat vs carbohydrate (glycogen) being used for energy at any given time. The lower the RQ, the more fat being burned compared to carbohydrate. This particular study showed that averaged over a 24 hour period supplementation with green tea extract increased energy expenditure by 3.5% and fat oxidation 10% compared to placebo. We see then that green tea increases the rate of use of both carbohydrate and fat. What about nighttime vs daytime rates of fat
burning and energy expenditure? This study showed that while there was only a small 1% increase (not statistically significant) in energy expenditure during sleep with green tea supplementation compared to placebo, there was a significant drop in the RQ, meaning that during sleep, green tea shifted fuel use away from stored glycogen towards fat burning! We should also note
that the authors looked at nitrogen excretion, a measure of protein use for fuel, to make sure that the green tea was not increasing protein breakdown for use as fuel. They saw no differences in rates of nitrogen excretion between the placebo and green tea groups. So we can be confident that green tea is not increasing the rate that protein is burned./Bacopa monniera. Let's look at this combination and the
The data from this study are summarized in the tables below:
TABLE 1. Energy expenditure (EE) during diurnal, nocturnal, and total 24-h periods1
PlaceboCaffeineGreen teaP2kJDiurnal EE6463 ± 3866547 ± 3836754 ± 3523<0.01Nocturnal EE3075 ± 1493053 ± 1483112 ± 140NSTotal 24-h EE9538 ± 5219599 ± 5189867 ± 4883,4<0.01
TABLE 2. Respiratory quotient (RQ) during diurnal, nocturnal and total 24-h periods1
PlaceboCaffeineGreen teaP2Diurnal RQ0.887 ± 0.00810.878 ± 0.00710.858 ± 0.0093<0.002Nocturnal RQ0.870 ± 0.0090.864 ± 0.0080.841 ± 0.013<0.01Total 24-h RQ0.881 ± 0.0080.873 ± 0.0070.852 ± 0.0093<0.001
TABLE 3. Substrate oxidation during 24 h in the respiratory chamber1
PlaceboCaffeineGreen teaP2Protein (g)65.6 ± 3.166.9 ± 4.768.3 ± 3.5NS(% of 24-h EE)13.2 ± 113.4 ± 0.9813.3 ± 0.98NSCarbohydrate (g)336 ± 16324 ± 16285 ± 173<0.001(% of 24-h EE)55.1 ± 2.452.7 ± 2.145.2 ± 2.74<0.001Fat (g)76.2 ± 10.681.9 ± 8.7103 ± 134<0.001(% of 24-h EE)31.6 ± 3.133.8 ± 2.441.5 ± 3.14<0.001
Green tea contains a small amount of caffeine, which we know is a stimulant. Might the caffeine in green tea be responsible for the increase in energy expenditure and fat utilization? To check this, the authors of the study also looked at rates of increase in both factors when the same amount of caffeine was given to the subjects as was contained in the green tea. They found that the green tea led to significantly more fat burning than did the caffeine alone. This is consistent with a number of other studies showing that compounds in green tea called catechins contribute to tea's fat burning effect. The authors concluded that Green tea has thermogenic properties and promotes fat oxidation beyond that explained by its caffeine content per se. The green tea extract may play a role in the control of body composition via sympathetic activation of thermogenesis,
fat oxidation, or both.
Green tea fights fat in other was besides increasing fat burning. Studies have shown that green tea acts as an appetite suppressant as well as an inhibitor of fat digestion, so less fat is absorbed after a meal. In addition, green tea extract inhibits the enzymes responsible for building fats from other foodstuffs.
Normally when the body requires the use of stored fat for fuel, hormones such as epinephrine or norepinephrine bind to receptors on fat cells and initiate a signaling cascade that eventually results in the activation of an enzyme within the fat cell called hormone sensitive lipase (HSL). Fat is stored in the form of triglycerides, composed of fatty acid chains bound to a glycerol backbone. HSL frees up the fatty acids so they can leave the fat cell, enter the bloodstream, and travel to wherever they are needed for fuel, primarily working muscle. The authors of the study discussed above speculate that green tea may be acting as an adrenergic agonist, activating HSL and freeing up fats for use as fuel.
After studying the above detailed product description, the reader should come away with several key impressions. Of primary importance is that C2 does not take a "shotgun approach" to fat burning and enhancement of athletic performance. Each ingredient was carefully chosen to work in concert, and even synergistically in some cases, with the other ingredients. Take fat burning as an example. Forskolin (and chocamine to some extent) as well as synephrine primarily liberates stored fat, with a
minor fat burning effect likely due to elevated conversion or T4 to its active metabolite T3 in the case of forskolin. But liberating fat is not sufficient to lose body fat: it will simply be redeposited. In order to burn the freed up fat, either resting metabolic rate (RMR) must be increased, or a shift of substrate use towards fat must be effected. Caffeine is a known elevator of RMR as we saw above, so this is one ingredient that will promote the burning of the fat stores liberated by forskolin. Green Tea Extract also increases RMR during the day, and as we saw above, shifts fuel use away from glycogen and protein to fat at night.
So we see another additive effect of the combination of ingredients. Continuing, Bacopa exerts a thyroid stimulating effect, again contributing to an increase in RMR. So by combining some ingredients that liberate fat and other ingredients that burn the liberated fat (and spare muscle and glycogen), we are assured of effective fat loss.
1) De Bock K, Eijnde BO, Ramaekers M, Hespel P. Acute Rhodiola rosea intake can improve endurance exercise performance. Int J Sport Nutr Exerc Metab. 2004 Jun;14(3):298-307.
2) Abidov M, Crendal F, Grachev S, Seifulla R, Ziegenfuss T. Effect of extracts from Rhodiola rosea and Rhodiola crenulata (Crassulaceae) roots on ATP content in mitochondria of skeletal muscles. Bull Exp Biol Med. 2003 Dec;136(6):585-7.
3) Petkov VD, Yonkov D, Mosharoff A, Kambourova T, Alova L, Petkov VV, Todorov I. Effects of alcohol aqueous extract from Rhodiola rosea L. roots on learning and memory. Acta Physiol Pharmacol Bulg. 1986;12(1):3-16.
4) Iaremii IN, Grigor'eva NF. Hepatoprotective properties of liquid extract of Rhodiola rosea. Eksp Klin Farmakol. 2002 -Dec;65(6):57-9.
5) Thorne Research Inc. Rhodiola rosea. Monograph. Altern Med Rev. 2002 Oct;7(5):421-3.
6) Costill, DL, Dalsky G, and Fink W. Effects of caffeine ingestion on metabolism and exercise performance. Med Sci Sports Exerc 10: 155-158, 1978
7) Hawley JA Effect of increased fat availability on metabolism and exercise capacity. Med Sci Sports Exerc. 2002 Sep;34(9):1485-91
8) Schiffelers SL, Saris WH, Boomsma F, van Baak MA. beta(1)- and beta(2)-Adrenoceptor-mediated thermogenesis and lipid utilization in obese and lean men. J Clin Endocrinol Metab. 2001 May;86(5):2191-9.
9) Flechtner-Mors M, Jenkinson CP, Alt A, Adler G, Ditschuneit HH. In vivo alpha(1)-adrenergic lipolytic activity in subcutaneous adipose tissue of obese subjects J Pharmacol Exp Ther 2002 Apr;301(1):229-33
10) Couturier C, Janvier B, Girlich D, Bereziat G, Andreani-Mangeney M. Effects of caffeine on lipoprotein lipase gene expression during the adipocyte differentiation process Lipids 1998 May;33(5):455-60.
11) Laurent D, Schneider KE, Prusaczyk WK, Franklin C, Vogel SM, Krssak M, Petersen KF, Goforth HW, Shulman GI. Effects of caffeine on muscle glycogen utilization and the neuroendocrine axis during exercise J Clin Endocrinol Metab 2000 Jun;85(6):2170-5
12) Tarnopolsky M, Cupido C Caffeine potentiates low frequency skeletal muscle force in habitual and nonhabitual caffeine consumers J Appl Physiol. 2000 Nov;89(5):1719
13) Fisone G, Borgkvist A, Usiello A Caffeine as a psychomotor stimulant: mechanism of action Cell Mol Life Sci 2004 Apr;61(7-8):857-72
14) Davis JM, Zhao Z, Stock HS, Mehl KA, Buggy J, Hand GA. Central nervous system effects of caffeine and adenosine on fatigue. Am J Physiol Regul Integr Comp Physiol 2003 Feb;284(2):R399-404
15) Telang RS, Tripathi HC, Mishra SK, Raviprakash V. Adenosine affects the calcium dynamics of rat portal vein. Auton Autacoid Pharmacol 2003 Jun;23(3):181-92
16) Van Soeren M, Mohr T, Kjaer M, Graham TE. Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses. J Appl Physiol 1996 Mar;80(3):999-1005
17) Acheson KJ, Gremaud G, Meirim I, Montigon F, Krebs Y, Fay LB, Gay LJ, Schneiter P, Schindler C, Tappy L. Metabolic effects of caffeine in humans: lipid oxidation or futile cycling? Am J Clin Nutr. 2004 Jan;79(1):40-6.
18) Graham TE, Hibbert E, Sathasivam P. Metabolic and exercise endurance effects of coffee and caffeine ingestion. J Appl Physiol. 1998 Sep;85(3):883-9
19) Chesley A, Howlett RA, Heigenhauser GJ, Hultman E, Spriet LL. Regulation of muscle glycogenolytic flux during intense aerobic exercise after caffeine ingestion. Am J Physiol 1998 Aug;275(2 Pt 2):R596-603
20) Greer F, Friars D, Graham TE. Comparison of caffeine and theophylline ingestion: exercise metabolism and endurance. J Appl Physiol 2000 Nov;89(5):1837-44
21) Penner R, Neher E, Takeshima H, Nishimura S, Numa S. Functional expression of the calcium release channel from skeletal muscle ryanodine receptor cDNA. FEBS Lett. 1989 Dec 18;259(1):217-21
22) Flechtner-Mors M, Jenkinson CP, Alt A, Adler G, Ditschuneit HH. In vivo alpha(1)-adrenergic lipolytic activity in subcutaneous adipose tissue of obese subjects. J Pharmacol Exp Ther 2002 Apr;301(1):229-33
23) Zhao J, Cannon B, Nedergaard J alpha1-Adrenergic stimulation potentiates the thermogenic action of beta3-adrenoreceptor-generated cAMP in brown fat cells. J Biol Chem. 1997 Dec 26;272(52):32847-56.
24) Schimmel RJ, Elliott ME, Dehmel VC Interactions between adenosine and alpha 1-adrenergic agonists in regulation of respiration in hamster brown adipocytes. Mol Pharmacol. 1987 Jul;32(1):26-33.
25) Raasmaja A, Larsen PR. Alpha 1- and beta-adrenergic agents cause synergistic stimulation of the iodothyronine deiodinase in rat brown adipocytes. Endocrinology. 1989 Nov;125(5):2502-9.
26) Stough C, Lloyd J, Clarke J, Downey LA, Hutchison CW, Rodgers T, Nathan PJ. The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects. Psychopharmacology (Berl). 2001 Aug;156(4):481-4.
27) Roodenrys S, Booth D, Bulzomi S, Phipps A, Micallef C, Smoker J. Chronic effects of Brahmi (Bacopa monnieri) on human memory. Neuropsychopharmacology. 2002 Aug;27(2):279-81.
28) Singh HK, Dhawan BN.Neuropsychopharmacological effects of the Ayurvedic nootropic Bacopa monniera Linn.(Brahmi). Indian J Pharmacol 1997;29:S359-S365.
29) Russo A, Izzo AA, Borrelli F, Renis M, Vanella A. Free radical scavenging capacity and protective effect of Bacopa monniera L. on DNA damage. Phytother Res. 2003 Sep;17(8):870-5.
30) Bhattacharya SK, Ghosal S. Anxiolytic activity of a standardized extract of Bacopa monniera in an experimental study. Phytomedicine 1998;5:77-82.
31) Kar A, Panda S, Bharti S. Relative efficacy of three medicinal plant extracts in the alteration of thyroid hormone concentrations in male mice. J Ethnopharmacol. 2002 Jul;81(2):281-5
32) Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, Vandermander J Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. Am J Clin Nutr. 2000 Nov;72(5):1232-4.
- Mobilizes fat for use as fuel by activating so-called Hormone Sensitive
- 09-12-2005, 03:33 PM
FREE SAMPLES with a PM.
We will gift 2 day cycle of C2 confident that you will love the Focus and long lasting energy. In return, we ask for your quick review on your 2 day use of C2.
- 09-12-2005, 03:55 PM
09-12-2005, 04:06 PM
USP how do you compare C2's fat burning capablities with the orginaly cAMPHIBOLIC. I for one enjoy the original version but I mainly take it for the fat burning effects.
09-12-2005, 05:50 PM
Man depends!Originally Posted by jminis
C2 is superior as fat loss agent as its stacked with adaptagens and attacks fat from many different angles and preserves muscles, allows recovery from stress and allows for more stress (dieting).
cAMPHIBOLIC used at night will preserve muscle and switch your energy source to fat while sleeping so C2/cAMP is a deadly combo.
C2 is awesome and to trully appreciate its effects use for over 30 days as its a supplement that keeps on working unlike anything else on the market.
09-12-2005, 06:44 PM
09-12-2005, 09:30 PM
09-13-2005, 08:09 AM
Sounds like a winner USP. That combo sounds perfect for someone like me who doesn't handle strong stims very well. Keep up the good work broOriginally Posted by USPLabs
09-13-2005, 03:06 PM
Pretty much the same blend I've been using for several months..sans the caffiene and synephrine. I love it. Works great for chasing away the blues. I add ALCAR to it. ALCAR + Coleus + Rhodiola is a very pleasant antidepressant combo and I burn some fat without even trying.
I figured CEOSM would home in on this combo..now I have more options. Good work man!
09-14-2005, 12:22 AM
Similar Forum Threads
- By boxer12 in forum SupplementsReplies: 0Last Post: 09-05-2011, 07:58 PM
- By kraftkid in forum SupplementsReplies: 1Last Post: 07-03-2007, 02:11 PM
- By freezito in forum Weight LossReplies: 1Last Post: 01-26-2007, 11:24 AM
- By mixedup in forum SupplementsReplies: 3Last Post: 07-31-2006, 10:25 PM