Information courtesy of Par Deus
One of the major contributors to body weight homeostasis in the human body is the sympathetic nervous system, the principal components of which are the catecholamines (epinephrine and norepinephrine) and the andrenergic receptors. There are two types of adrenergic receptors, alpha and beta, as well as subtypes of each -- and depending on which are activated, lipolysis (breakdown of fat) can be either stimulated or inhibited.
The most well-known adrenoreceptors to bodybuilders are the beta receptors. These can be divided into subtypes 1, 2, and 3 -- and it is through these receptors that drugs such as the ephedrine/caffeine stack and Clenbuterol exert their effects. While Clenbuterol acts directly on beta 2 receptors, ephedrine exerts its effects indirectly by stimulating the release of norepinephrine (NE), the body's primary endogenous thermogenic hormone. Unlike Clenbuterol, NE is not selective in its binding. In addition to binding to the beta 2 receptor, it also binds to both alpha receptors, as well as the beta 1 and 3 receptors. It is in regards to its binding to the alpha 2 receptor that yohimbine comes into play.
Norepinephrine and Yohimbine
Ativation of the alpha 2 receptor inhibits the release of NE. Thus, by binding to this receptor, NE functions as its own negative feedback signal. In other words, it shuts off its own release. Obviously, this is not a good thing for fat loss. This is particularly true at rest (which, unless you are a marathon runner is 95% of your day) -- this is because alpha 2 receptors are activated at lower catecholamine levels than are the beta receptors (1). Thus, thermogenesis is basically always turned off. It is the differences in regional distribution of alpha 2 and the beta receptors that is responsible for the gender differences in bodyfat storage (2). Basically, females have a large number of alpha 2 receptors and few beta receptors in the gluteofemoral area (hips, thighs, and butt), while men have the same problem in the midsection. With exercise or the use of compounds such as the ephedrine/caffeine stack, catecholamine levels can be increased to a point where the alpha 2 induced inhibition of lipolysis is partially overcome (1). However, even then, the alpha 2 receptors ARE still acting to reduce lipolysis. Yohimbine is a selective alpha 2 antagonist (3) and can thus short circuit this feedback loop, maximizing NE levels, thus maximizing fat loss, particularly in these problem areas.
A second, more indirect, mechanism by which Yohimbine can aid lipolysis via the adrenergic system is by increasing peripheral blood flow (4, 5). Adipose tissue is known to have rather poor vascularity. When triglycerides are broken down into free fatty acids and glycerol during lipolysis, they must also be transported away from the fat cell or they risk being reincorporated into adipose tissue. Beta receptor activation causes vasodilation, thus increasing blood flow, however, it does not increase enough to remove all of the free fatty acids released during lipolysis (6). Alpha 1 and 2 receptor activation, on the other hand, causes a decrease in blood flow (2, 7). Thus, antagonism of the alpha 2 receptor with yohimbine would be expected to increase blood flow, and thus increase the mobilization and disposal of these FFA's, further aiding fat loss.
Yohimbine vs. yohimbe
Quite a bit of confusion seems to exist about the difference between Yohimbine and yohimbe. Yohimbine is the principal alkaloid from the herb P. yohimbe. However, there are 31 other yohimbane alkaloids that can be present in herbal yohimbe preparations. Some of these have different and unknown selectivities and potencies (and thus, effects) at the adrenergic receptors (8, 9) -- in addition, these preparations vary greatly from brand to brand and even from batch to batch, as no standardization for extraction exists. In fact, a recent investigation found that most over the counter preparations have little to no actual yohimbine (10). And, even in the more potent preparations, most people find a higher degree of undesirable effects with the herb vs. pure Yohimbine (due to the afore mentioned 31 other yohimbane alkaloids that can be present).
Studies have concluded that the ideal dosing for Yohimbine is .2mg/kg (11) -- this would be 20mg for a 220lb person (0.09 mg/lb of body weight). Studies using smaller dosages have produced less favorable results. At this level, little to no side effects have been reported (Keep in mind, this is with Yohimbine HCl, not the yohimbe herb). Another thing to be considered when using yohimbine is that insulin completely blunts its lipolytic effects, thus it should ideally be used on a low-carb/ketogenic diet, or at the very least, first thing in the morning on an empty stomach, followed by moderate aerobic activity for an extended period.