Beta agonists and the diet : losing fat AND gaining muscle
Some interesting article for the summer cutting
The main regulator of the system is insulin, which has the exact opposite effect as noradrenaline. So obviously we will have to keep insulin under control as much as possible. That will allow us to use the beta-adrenergic system to its maximum potential. Now noradrenaline has been touted as anti-catabolic, but this effect is observed because it causes protein synthesis and thus less protein is released from the cell to be burned. The effect is in other words anabolic. Which is why it may serve us as far as increasing lean muscle mass, especially since we have demonstrated effectively that testosterone and most likely boldenone will upregulate beta-adrenoreceptors. By using beta stimulators later in the cycle and post-cycle (provided adequate calories in diet) we can insure maximum muscle gain and muscle maintenance post-cycle, while keeping the fat off.
Because we need to eat a certain amount of calories to grow it is unrealistic to expect a great deal of fat loss capacity from the use of these products. But it should go a long distance in preventing the addition of further fat mass, which, combined with a significant increase in lean body mass, will decrease body-fat percentage. However, some fat loss is not unthinkable, since we are eating a high protein diet and the body will prefer the available free fatty acids, especially if we can bring them into circulation.
Our first goal in this endeavour should be to have a product that stimulates noradrenaline. Now some may think it is wiser to opt for other methods of fat loss, but DNP, T3 and corticosteroids will make it increasingly difficult to preserve lean mass. Other still may profer that the use of stronger specific beta-2 or beta-3 agonists like clenbuterol, salbutamol, albuterol or octopamine should be used, but because of their potency they will quickly render the beta-adrenrgic system useless, and only make use of part of the available systems to us (either beta-2 or beta-3 instead of both). The beta-2 receptor is most certainly the prime mobilizer here, where the beta-3 only has minimal if any activity, but has been deemed crucial to continuation of cathecholamine responses under sustained sympathetic activity (21). Most likely it maintains a certain amount of beta-adrenergic stimulation, but without increasing metabolism, so as to spare calories but continue the use of fatty acids for survival. As much as 40% of the activity of ephedrine has been attributed to the beta-3 stimulatory effects (22).
Since ephedrine acts by increasing natural noradrenaline release, it serves our purpose the best. It is also the more natural approach and less taxing on our system than some other fat loss preparations (T3 causes rebound by TSH shutdown, clenbuterol is very strong in increasing heart rate, and the list goes on). As opposed to more specific beta-2 agonists such as the likes of clenbuterol, ephedrine actually seems to have improved effects on thermogenisis after continual use (23). Ephedrine Hcl is our best choice here, although some will no doubt opt for standardized preparations using ma huang. This herb, depending on preparation will contain more or less than the actual 8% ephedra from dose to dose and is hence unreliable. If this is the only thing available to you, it is better than nothing however, but pure ephedrine Hcl should be preferred.
Yohimbine is quite critical in the equation. It acts as a potent alpha-adrenoreceptor blocker (strong on alpha2, mild on alpha1). The alpha receptors inhibit adenylate cyclase activity in the cell, increase its breakdown and thus prohibit fat loss. In normal people with normal diets, there is a certain level of adrenergic action. But noradrenaline seems to have greater affinity for alpha receptors, so not enough beta receptors get filled to cause fat loss / protein synthesis. By increasing the noradrenaline release we have already filled all alpha receptors and a greater number of beta-receptors. But if we could block the alpha receptors, then that would lead not only to more potency from the existing noradrenaline / beta-latches, but it would create MORE noradrenaline / beta-latches since less NA is taken up by the alpha receptors. Thus a major strike in the right direction.
A second factor we need to consider is the alpha-2 receptor concentration on our nerve as well, which, when activated, will increase the re-uptake of noradrenaline into the nerve. By blocking this receptor we prevent re-uptake and again, more NA is available to us. So yohimbine interferes with the NA’s auto-regulated negative feedback loop by acting as an alpha receptor antagonist, pre-synaptic and post-synaptic.
This is also very crucial in fat loss or prevention of fat gain in predisposed areas (abdomen and obliques in men, gluteo-femoral region in women), because these area’s have adipocytes that are extremely rich in alpha receptors, but rather poor in beta receptors (ever tried getting rid of those love handles ?).
Apart from the well-documented findings that the combination of ephedrine and caffeine far outperformed either alone (24) in terms of lipolysis, caffeine acts very distinctly as a phospho-diesterase inhibitor. PDE’s are released in the cell as a response to continual beta-adrenergic stimulation and commences the breakdown of cAMP and creates adenosine from it. Adenosine travels outside the cell and has its own receptor, that acts very similarly to the alpha-receptor to block adenylate cyclase activity and stop fat loss. Caffeine has also been shown to prevent this process by blocking the adenosine receptor and seems to offer some benefit in preventing noradrenaline reuptake (25), like yohimbine does. Possibly via the same mechanism (adenosine receptor blockade).
Caffeine also decreases insulin sensitivity, further helping to assure maximal aid in preserving and enhancing the beta-adrenergic system, and possibly helping to prevent wrong doing from eventual lapses in our diet.
Lastly caffeine is a potent diuretic and will reduce water retention in the body, offering us a leaner and more striated appearance.
Forskolin is product derived from the coleus forskohlii plant that has been shown to upregulate the activity of the enzyme adenylate cyclase, which we have previously shown to be important as it creates cAMP accumulation needed for the second messenger response to beta-adrenergic stimulation. While forskolin by itself may have a null effect (it was previously used to lower blood pressure where beta-adrenergic stimulation should increase blood pressure), it should have various useful effects to us. In combination with these other products cAMP accumulation will further decrease any effect from prostaglandins and adenosine receptor stimulation, or alpha2-regulated inhibition. This allows a stable environment for second messenger transport.
Guggul sterones are an age-old ayurvedic medicine touted to increase thyroid activity. This has nothing to do with the beta-adrenergic system, and at first may seem rather obsolete. Continual fat loss and lower calorie diets have been known to cause a starvation response whereby T4 to T3 conversion is lowered and the opposite conversion increased to lower thyroid activity and thus slow metabolic rate. This occurs so that we do not use our entire fat supply in just a few days and can stay alive longer under starvation conditions. Now ephedrine has been shown to actually upgrade T4 to T3 conversion or at the very least lower the opposite reaction (23).
But this latter occurrence has been attributed to the continual alpha-receptor stimulation that ephedrine would display under normal conditions, but since we use an alpha-receptor blocker it is unlikely we will be able to make as much use of this benefit, and so the addition of Guggul is advisory, as it has been shown to increase T4 to T3 conversion (26).
Most likely, to avoid early beta-2 phosphorylation we will add yohimbine at a later stage, and should add guggul at the same time.
After HSL-P has released fatty acids they just sit there basically. They require protein transport to get them into circulation where they can be used as fuel. If not, and under the high caloric diet we have outlined this is most likely, they will simply be re-esterified again. This is why we do not expect any fat loss. But just to give nature a helping hand we might add some Acetyl-L-Carnitine (ALC), one of the proteins used to transport fatty acids. Adding too much has no use as supraphysiological amounts have shown little to no benefit, but adding some may increase any possible downregulation of the transport systems and increase the likelihood that some actual fat is used.
Putting it all together
So what sort of doses and what sort of dosing pattern do we need ? Well I won’t bore you with the details, but this particular mix has been most effective :
You can opt to take 1 dose 6 times per day, roughly every 2.5 hours, or 2 doses 3 times per day, roughly every 5 hours. This is preferably taken between meals when it is most likely there is least insulin interference and most chance of any additional calories being burned that are not from food. For people who have a tendency to get jittery on ephedrine and are bothered by this, I suggest the first dosing pattern which has lower peak doses. For most people I would recommend the 3 a day dosing pattern however.
Use the Ephedrine/Caffeine/Forskolin/ALC combo for the full outlined twelve weeks, then add the yohimbine and guggul the last 6 weeks. For those wishing to do so, the last two weeks clenbuterol can be added to emphasize the fat loss effect.