Extreme Muscle: The Thinking Bodybuilder

Neuro-hormonal modulation for extreme muscle growth Part II: The serotonergic and dopaminergic promoters
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To recap for those who missed last month’s Part 1 of my article on the serotonergic and dopaminergic systems, I introduced these physiologic systems and what they mean to the bodybuilder.
 In particular, I described in detail the neuro-hormonal modulatory interplay between serotonin and dopamine and how they orchestrate our psychological outlook, daily conduct, and physiologic function. Given the fact that maximum lean muscle is utterly 100% dependent on the fortitude and continuity of these functions, an understanding of how to naturally support and promote these levels is critical for maximizing your bodybuilding success.

As discussed last month, serotonin is a neurotransmitter that when deficient can produce side effects. These include psychological symptoms ranging from headaches and sleep disorders to anxiety and depression. Non-psychological physical manifestations may include digestive problems, poor nutrient absorption, and fat gain. In simple bodybuilding terms, the aforementioned psychological symptoms of having 
too low serotonin clearly precludes routinely reaching the needed training intensity and focus in the gym to force the muscles to perform the resistive exercises needed to achieve lean muscle gain. In
 other words, with no serotonin, you’ll 
be a candy-ass in the gym! Furthering the point, no matter how many protein shakes, vitamins, and minerals you gulp down, if you’re not properly digesting and absorbing these nutrients, you won’t gain much muscle. In simplified terms, as you bloat, the only fat you’ll trim is from your wallet!

Although ample amounts of vegetables and fiber-based roughage may provide enough incidental carbohydrates to adequately support serotonergic system in a bodybuilder with a low-sugar intake, sometimes this support just isn’t enough.

Sometimes it’s as simple as sunlight. Studies have shown that seasonal exposure (not overexposure) to sunlight helps support serotonin levels.(1) Tryptophan can also help. It’s an essential amino acid (a building block of protein) that the body has 
a natural requirement to ingest. This particular amino acid functions as a biochemical precursor to serotonin. Specifically, serotonin is synthesized in the body from tryptophan via an enzyme called tryptophan hydroxylase, which converts tryptophan to the serotonin precursor L-5-hydroxytryptophan.(2)

The efficacy of supplementing with tryptophan to naturally promote serotonin levels in the right subject cannot be understated. In fact, one study even attributed a reduction in national suicide rates to increasing dietary tryptophan levels.(3) Rhodiola rosea (also known as golden root, roseroot, or Aaron’s rod) is another way of promoting serotonin levels. It’s a plant that grows in the cold regions of the world including the Arctic, Rocky Mountains, and Alps, to name a few. Supplementing with this herb has been shown to have a positive effect on mood and even curb depressive symptoms.(4,5) Hypericum perforatum (also known more commonly as St. John’s wort) is also a helpful promoter of serotonin levels in the right person. Some clinical studies found it useful in cases of mild depression; others used it effectively in milder mood disorders like dysthymia.(6) Of course at the extreme there’s also medication. Selective serotonin reuptake inhibitors (SSRIs) fall into the category of antidepressant medications. They work by causing serotonin to remain the neurologic synapse for a longer period, thus allowing it to exert a more sustained effect. It works in the right subjects, but don’t expect immediate results, because clinical improvement is generally observed after several weeks of treatment.(7) Of course finding the stuff on the black market and then taking it without a prescription and a true medical need as determined by a licensed medical doctor is beyond stupid. If you are trying to boost serotonin to superhuman levels, trouble is coming. Medications have side effects and those effects are only enhanced when the medication is administered to the wrong person. SSRI drugs are no exception. Side effects of serotonin overkill in the body include agitation, sweats, confusion, and muscle jerks. Scarier scenarios include hardening of the heart muscle lining. Other medications available for increasing serotonin levels include some antimigraine medications and various antinausea drugs. But again, the same caveats apply.

In contrast to the serotonergic system, the dopaminergic system governs physiologic responses resulting in a contrasting outcome. As discussed in my last month’s column, dopamine is a brain neurotransmitter that regulates behavior, attention, and learning. Dopamine controls physical movement, emotional response, and our perception of pleasure and pain. More severe dopamine deficiency is commonly linked to movement disorders like Parkinson’s disease. Less known is that even slight sustained dopamine deficiencies can have
a profound effect on motivation and mood, manifesting in sadness and depression. Good motor control and proper mood are not only critical to bodybuilding success, but so is a healthy growth hormone level, which dopamine also stimulates. Often overlooked is the role
of dopamine as an aid in maintaining a healthy body weight and actually losing body fat. Dopamine is the precursor to catecholamines like epinephrine and norepinephrine and thus has a role in speeding up metabolism, satiety, and appetite suppression.(8) In fact, dysregulation of dopamine as a cause for overeating and resultant obesity has been well documented.(9) Dopamine dysregulation has even been documented in individuals with eating disorders.(10)

Higher amounts of the essential fatty acids like those in raw almonds, avocados, and pumpkin and sesame seeds naturally supports basal dopamine levels. Foods rich in the essential amino acid tyrosine—like bananas and some types of beans—can help. There’s also supplemental tyrosine available in capsule form. Tyrosine exerts its benefit by providing the precursor molecule that is converted into the molecule “L-3,4-dihydroxy- phenylalanine” (also known as L-DOPA). In turn, L-DOPA is the precursor molecule that can be converted in the central nervous system into dopamine.(11) Dopamine cannot pass
through the blood-brain
barrier. Only a smaller
 precursor molecule can
 make it through. The
seeds of the herb Mucuna
pruriens (also known as
velvet bean) were the
first earthly substance
in which the precursor
molecule L-DOPA was detected and isolated as early as 1937.(12) In fact some more modern studies even suggest a superiority of the herb over the synthetic “levodopa” equivalents.(13) There are several other naturally occurring substances purported to have dopamine-promoting value including but in no way limited to substances like caffeine, phenylalanine, vinpocetine, and theobromine, along with a host of necessary vitamin and elemental cofactors.

In the world of pharmacological therapeutics, there are several approaches in our arsenal. Although amphetamines and some antidepressants have been shown to be dopaminergic, the most common approach is the use of levodopa, the synthetic version of L-DOPA.(14) But in my medical practice, as with any doctor who knows what they are doing, levodopa is almost never given as
a mono-therapy because when it is taken orally, it doesn’t just stream across the blood-brain barrier and into the brain to be converted to dopamine. Rather, it tends to be rapidly broken down in the periphery. As a result, early prescribers had to give massive doses of the drug just to boost dopamine concentrations to adequate levels. Now levodopa is prescribed to patients along with another synergistic drug known as “carbidopa.” Carbidopa is added to prevent the breakdown of levodopa before it crosses over into the brain. This critical addition of carbidopa allows for lesser dosing of levodopa, resulting in a much lower risk of drug desensitization as well as side effects.(15)

Of course there are also the so-called “dopamine reuptake inhibitors” (also known as DRIs). This is a classification of drug that blocks the synaptic reuptake of dopamine in the same way the SSRIs block the reuptake of serotonin.(16) The result is a more sustained dopaminergic signal. DRIs are frequently used in the patients I see simply because of the relatively widespread prevalence of depression, mood disorders, and ADHD. But the less known off-label value of these drugs centers on a psychostimulant effect that results in appetite suppression. For this reason, many so-called “medical weight-loss centers” utilize DRIs. Although weight-loss success is undeniable, the problem with this pharmaceutical approach is the heavy propensity for abuse. Another way to understand the inherent dangers of DRIs used off-label is to simply recognize that popular street drugs like cocaine and methylphenidate are technically DRIs.

That said, the lure on the street of excessively ramping-up one’s dopamine levels has opened up a wellspring of abuse. In fact, a substance as seemingly innocuous as cold medicine can provide the dopaminergic euphoria junkies crave. Pseudoephedrine, commonly found in many over-the-counter nasal decongestants, releases more dopamine than nearly every common synthetic releasing agent, and nearly four-fold that
 of ephedrine.(17) Perhaps the current most wide-spread party drug MDMA (also known as ecstasy) functions on the basis of flooding the receptors with a massive release of dopamine with the frightful long-term effects of a proverbial brain frying.(18)

The take-home message is be cognizant not only of how neurohormonal modulation effects muscle growth, but also how to support levels of serotonin and dopamine so you can make extreme improvement.


REFERENCES: 1. G.W. Lambert et. al., Lancet, 2002, 360:1840–2; 2. A. Ichiyama et. a1, J Biol Chem., 1970, 245(7):1699–1709; 3. M. Voracek and U.S. Tran,
J Affect Disord., 2007; 98:259–62; 4. V.A. Shevtsov et al., Phytomed., 2003, 10 (2–3):95–105; 5. V. Darbinyan et al., 2000, Phytomed., 2000, 7(5):365–71; 6. C. Randløv et. al., Phytomed., 2006, 13(4):215–21; 7. S.W. Kim et. al., Mol Pharmacol. 2002 Apr; 61(4):778–85; 8. I.P. Stolerman, editor, Encyclopedia of Psychopharmacology, Vol. 2., Springer Publishing, 2010; 9. W.F. Mathes et. al., Behav. Brain Res., 210(2010), 155–163; 10. C. Davis et. al., Prog Neuropsychopharmacol Biol Psych., 2008;32:620–8; 11. D. Merims and N. Giladi, Parkinsonism Relat Disord., 14(4):(2008), 273–280; 12. M. Damodaran and R. Ramaswamy, Biochem J., 1937;31:2149–451; 13. B.V. Manyan, et. al., Phytother Res., 2004 Sept; 18(9):706–12; 14. Dopamine Vs. Serotonin, eHow.com; 15. medicinenet.com /levodopa-carbidopa/article.htm; 16. S.M. Stahl et. al., Prim Care Companion, J Clin Psychiatry, 2004; 6(4):159–66; 17. L. L. Brunton, ed. (2006). Goodman & Gilman’s The Pharmacological Basis of Therapeutics (11th ed.) N.Y.; McGraw-Hill Medical Publishing Division; 18. M.I. Colado et al., J Psychopharm; 2004 May; 173(3–4):249–63 (E-pub 2004 Apr 9).


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