You Can’t Flex Fat : Does bodyfat affect muscle gains? by Jerry Brainum

  Does having excess bodyfat adversely affect muscular gains? That was the focus of a recent study featuring 140 normal-weight and 81 overweight men and women who hadn’t trained in more than a year.1 They began training twice a week for 12 weeks, doing one-arm biceps curls. The researchers adjusted the training responses for bodyweight and initial values and found that the normal-weight group had made better gains than the overweight group. That led them to conclude that there’s something about being fat that hinders muscular gains. The question is: what is it about having excess bodyfat that would hinder muscle gains?
    The answer is inflammation. Fat,far from being just inactive tissue, releases over 100 chemicals, collectively known as "adopikines." Most of these substances, which are proteins, promote inflammation. This is the great danger of having too much bodyfat, since excess inflammation is the cornerstone of most serious diseases, such as cardiovascular disease and cancer. But excess inflammation also interferes with amino acid uptake into muscle, and promotes muscle breakdown (catabolism).Most obese people are also insulin insensitive,which adds to the problem, since insulin provides anti-catabolic effects in muscle, as well as aids in muscle uptake of amino acids necessary for muscle protein synthesis.
     From a practical standpoint, this means that those with higher levels of bodyfat should initially focus on losing that excess fat through diet and exercise, then switch to a more "anabolic" style of training designed to build extra lean mass.


1 Kelsey, B., et al. (2004). Adiposity alters muscle strength and size responses to resistance training in healthy men and women. Med Sci Sports Exerc. 36:S352.

©,2011 Jerry Brainum.Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

BODYBUILDING PHARMACOLOGY : Diet pill danger? By Jerry Brainum

Phenylpropanolamine (PPA), also known as “norephedrine,” is usually found in several types of over-the-counter medications, including nasal decongestants, cough and cold suppressants, and appetite suppressants. Some have suggested that is superior to ephedrine, the active component of the herb, Ma Huang, as a thermogenic aid to burning fat. Both ephedrine and norephedrine work by promoting the release of norepinephrine. Norepinephrine is a catecholamine, and works by increasing thermogenic activity in the body. Thermogenic activity refers to the conversion of fat calories into heat, sometimes also called a “futile energy cycle,” because calories are burned with no work performed.

PPA has a long history of relative safety. Few adverse effects are reported about this chemical, despite an estimated 16 billion doses taken annually. Yet, if you look at how PPA works, the danger potential is clearly evident. PPA directly stimulates alpha-adrenergic receptors, as well as the beta-adrenergic receptors linked to the thermogenic effect. The stimulation of alpha-adrenergic receptors promotes vasoconstriction, or a tightening of blood vessels in the respiratory lining, which in turn results in a shrinkage of swollen tissue. This explains its use in nasal decongestants. Unfortunately, this blood vessel constriction effect isn’t just limited to the respiratory area, but affects the entire body.

As such, it’s possible that the increased blood vessel “tightness” induced by PPA or norephedrine may increase blood pressure. The increased blood pressure, in turn, can increase the risk of strokes and heart attacks. To be fair, such untoward effects of PPA are rare. Most often they occur only when too large a dose is used, or if it is taken too often. Still, most doctors suggest that people with pre-existing heart disease, diabetes, or high blood pressure avoid using either PPA or ephedrine.

What about people free of any evidence of cardiovascular disease? Is using PPA safe for this population? The existing medical literature shows that it is safe, but as the adage says “Only the dose determines the poison.” This is evident in a recently published medical report about a 34-year-old woman who increased the dose of a PPA-based nasal decongestant. The particular formula that she used contained 75 milligrams of PPA with 400 milligrams of guifenesin (an ingredient used to thin mucus secretions, often also found in ephedrine formulations). She had no prior history of any type of cardiovascular problems, didn’t smoke or use any drugs, and had no signs of high blood pressure, elevated blood cholesterol levels, or diabetes.

The prescribed dose of the nasal decongestant she used was one tablet every 12 hours. However, this woman reasoned that taking the drug more often would likely maximize symptom relief, so she took another dose just 2 hours after ingesting the initial dose. Her unexpected symptoms began 30 minutes after the second dose. She felt a squeezing pain radiating across her chest and down both arms, along with excessive sweating, heart palpitations, light-headedness, and shortness of breath. These are all classic symptoms of a myocardial infarction or heart attack.

While this woman’s normal systolic blood pressure reading was 100, it now shot up to 198! Her heart rate, recorded as soon as she showed up at a local emergency room, was 52 beats a minute. Blood tests for various drugs, such as cocaine and amphetamines (both of which are capable of causing similar effects) was negative. She was given an aspirin tablet and transdermal nitroglycerin paste. The aspirin may prevent heart muscle damage if provided as soon as symptoms become apparent, while the nitroglycerin dilates coronary arteries, also helping to prevent excessive heart damage.

This treatment worked, since she was free of her previous frightening symptoms in 30 minutes. Her blood pressure also was normal within an hour. Blood chemistry tests revealed that she had suffered a small heart attack, what physicians call a “microinfarct.” She was discharged from the hospital 2 days later. Tests done 15 months later showed no recurring cardiac symptoms or disease.

As noted, side effects from PPA are rare, but when they do occur they usually are caused by a rapid increase in blood pressure. In the heart, however, PPA overdose leads to a potent blood vessel constriction effect that may deprive the heart of blood--which is precisely what occurs during a typical heart attack. While catecholamines, such as epinephrine, are also capable of constricting coronary arteries, the usual medical treatment for that effect, beta-blocking drugs, is dangerous for those who’ve taken an overdose of PPA. The proper treatment involves giving specific alpha-adrenergic blocking drugs, such as phentolamine. This type of treatment, however, should only be administered by a qualified medical professional.

The point of all this isn’t that PPA or norephedrine is inherently toxic or dangerous to normal people free of cardiovascular disease, but as illustrated by the case described here, could be highly dangerous if abused. If you opt to use any supplement containing PPA for fat-loss purposes, heed the dosing instructions, and don’t be tempted to increase the dose for faster results. Don’t be fooled into thinking that just because something is available without a prescription means that it’s innocuous.



Growth hormone and testosterone

Looking at competitive bodybuilders today compared to 20 years, it’s apparent that today’s competitors appear to have a lot more muscle than their earlier counterparts. Some ascribe these noticeable size and muscularity differences to improved dietary techniques and training equipment. Others just write it off to more athletes with better genetics. While all of these factors do play a role in the appearance of current top professional bodybuilders, jaded skeptics often point to newer combinations of anabolic drugs.

Perhaps the foremost combination of anabolic drugs to explain the rash of monstrous physiques that rule the posing platforms of today is that of testosterone, growth hormone, and insulin. The interesting thing about this particular combination is their synergistic effect. None of them alone provides the massive anabolic boost that many seek, yet when they are combined, the effect is dramatic for some people. The flip side of this incredible muscle size increase is side effects, some of which are more apparent than others.

For example, many competitors show bloated midsections. This is not from any accumulation of visceral fat deep in the gut (the usual cause of “beer bellies”), but may result from a combination of internal organ growth and increased thickness of the abdominal wall. The net effect is an abdominal area that protrudes like a pot belly at rest, yet transforms into a sculpted “six pack” when flexed. The suggested cause of this abdominal anomaly is thought to be the same anabolic combination of drugs; that is, growth hormone, testosterone, and insulin. My feeling is that the main offenders are growth hormone and insulin.

The active product of growth hormone is insulinlike growth factor-1 (IGF-1). The name derives from the structural similarity between IGF-1 and proinsulin, which is a storage form of insulin. The point here is that both insulin and IGF-1 are capable of interacting to a certain extent with their respective cellular receptors. These receptors induce cellular growth changes, and are located in abundance in the gastrointestinal area of the body. Thus, under the stimulation of exogenous insulin and growth hormone (by way of IGF-1), these hormones induce the growth of internal organs--hence the bloated abdominal appearance.

One question often asked concerns the relationship between growth hormone (GH) and testosterone. This is relevant because hormones tend to have interactions, and lowering one type of hormone may increase the release of another and vice-versa. For example, GH is known to blunt levels of cortisol in the body. GH does this by inhibiting cortisol production, most likely at the level of the adrenal glands. This would have an anticatabolic effect, since cortisol is the chief catabolic hormone in humans. On the other hand, cortisol is also a steroid hormone, albeit a catabolic one. If GH blocks cortisol synthesis, could it also adversely affect testosterone production?

Testosterone, similarly to cortisol is also a steroid, although an anabolic steroid. The same researchers who established the cortisol-blocking effects of GH tested the effects of GH on testosterone synthesis. This study involved 7 healthy men, ages 23-34 who were injected with 4 units daily of GH for a week. The test results showed that GH has no effect on testosterone production rates, either good or bad.
But how does testosterone affect GH release? This effect was examined in a study of the both testosterone and its byproduct, dihydrotestosterone (DHT) in a group of 12 boys with apparent GH deficiency. The study showed that giving the boys testosterone injections for 3 months increased GH secretion from the pituitary gland, while DHT did not. The explanation for this is that testosterone is converted into estrogen by way of the enzyme aromatase, and estrogen promotes the release of growth hormone-releasing hormone in the brain. DHT, because it cannot be converted into estrogen, has no effect on GH release.

One lesson to be learned from this study is that any drugs that inhibit the conversion of testosterone into estrogen will also blunt GH release in the body. This is, of course, a moot point if you’re already using exogenous growth hormone. Many athletes will prefer this route of taking direct GH injections and will use another drug to block testosterone conversion into estrogen. The latter effect produces side effects such as gynecomastia or excessive male breast tissue. Judging by the apparent preponderance of gyno seen in many competitors today, the estrogen-blocking drugs aren’t potent enough to completely block the aromatization process.

What about taking GH alone, without other anabolic drugs--will this promote increased muscle size and strength? A recent review of past studies involving the use of GH for anabolic effects in healthy athletes examined this subject. The study noted that in animals, providing GH increases muscle size, but not strength. The same holds true for people with acromegaly, a disease characterized by excess GH release caused by a tumor on the anterior pituitary gland of the brain. Such people often show large, but weak muscles. In one case, the man still listed in the Guinness Book of World Records as being the tallest man ever, 8-foot-11 inch Robert Wadlow, suffered from myopathy or weakness of his legs to such an extent that he had to wear leg braces. He eventually acquired an infection from those braces that killed him at age 23.

Studies with athletes who’ve used only GH show that these people do not seem to get any stronger or bigger than they would from weight-training alone. Any fat-free mass that does result from using GH usually turns out to be either an increase in connective tissue or fluid retention. While both insulin and testosterone favor the incorporation of amino acids into muscle (promoting muscle protein synthesis), GH does not. Nor does GH alone show any anticatabolic effects in muscle, despite the fact that it does inhibit cortisol synthesis. The muscle contractile proteins, actin and myosin, aren’t affected by GH administration. This is significant because an increase in contractile muscle proteins produces strength increases.

On the other hand, testosterone inhibits bodyfat synthesis by blocking the activity of a fat-synthesizing hormone called lipoprotein lipase. This effect is dramatically increased when GH is combined with testosterone. Thus, in this respect, GH is clearly synergistic with testosterone in blunting bodyfat accretion. Evidence shows that these hormones also boost each other’s activity in an anabolic sense. Add it all up and you have massive muscularity--and often, bloated bellies.

For more information see www.appliedmetabolics.com

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
 

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

7-keto DHEA: is it safe? By Jerry Brainum

As regular readers of this publication know, 7-keto DHEA wasdeveloped and marketed to provide a form of DHEA that would bedevoid of certain side effects linked to regular DHEA usage.While such side effects are rare, most of them are associatedwith the fact that DHEA is a precursor for the primary sexhormones in the body, estrogen and testosterone. Thus, Dr. Henry Lardy, of the University of Wisconsin, searched for a DHEA analog that would provide the recognized health benefits of DHEA minus the major side effects. He found this in 3-acetyl-7-oxo-DHEA, better known as "7-keto DHEA."

Since then, several studies indicate that 7-keto DHEA has a powerful immune system enhancing effect; can increase the efficiency of cognitive function, i.e., memory and intelligence; and provide a thermogenic effect that may aid body fat loss. The latter effect, thermogenesis, induced by 7-keto DHEA may be superior to that of DHEA itself. While DHEA has consistently provided fat-loss benefits in animal studies, the studies with humans are far less conclusive.For example, in one human study with DHEA, men provided with 1,600 milligrams of oral DHEA daily showed some beneficial body
composition changes. However, a follow-up study later released, using the same dose of DHEA, failed to show any fat loss at all in another group of men. Older people provided with DHEA in far smaller doses--averaging 50-100 milligrams daily--show beneficial effects in lean mass (attributed to DHEA promotion of IGF-1 secretion), but virtually no changes in bodyfat levels.Those studies with older people also showed that while the effects of DHEA were beneficial, the fact that DHEA readily
converted into other hormones led to some possible problems. In women, DHEA usually converts into testosterone. Some older women showed increases in basal testosterone levels 9-fold over normal.
While many bodybuilders would rejoice over a comparable testosterone increase, in the older women this level of testosterone often led to a drop in protective high density lipoprotein cholesterol levels (HDL). When HDL levels decline (as they always do when using oral anabolic steroids), the risk of
cardiovascular disease onset increases.

In older and younger men, the fate of DHEA varied depending
of the existing hormonal milieu of the individual. Most often,
the DHEA converted into androstenedione, which is commercially
available as a so-called "pro-hormone." Androstenedione, while
being a direct precursor to testosterone, can also be converted
into either dihydrotestosterone (DHT) or estrogen, depending on
whether it encounters either the 5-alpha reductase enzyme that
converts it into DHT, or the aromatase enzyme that changes it
into estrogen. These conversions can lead to such side effects as
male pattern baldness (if genetically predisposed), acne, or
gynecomastia (male breasts).

The main benefit of 7-keto DHEA is that, because of its
structure, it isn't prone to conversion to either testosterone or
estrogen, thus eliminating any side effects associated with those
hormonal conversions. But while 7-keto appears to retain most of
the beneficial effects of straight DHEA, the question remains--just
how safe is 7-keto DHEA itself?

The toxicology and endocrine effects of 7-keto DHEA were
examined in studies presented at the Experimental Biology 98
meeting. In one study, the safety of 7-keto was examined in rats
and monkeys. In the rat study, 5 groups of rats were given 0,
250, 500, 1,000, or 2,000 milligrams per kilogram of 7-keto in a
single dose. After 15 days, the animals were killed and then
examined. The results showed that even a 2,000 milligram dose of
7-keto didn't produce any observable side effects in the rodents.
The researchers then examined the effects of 7-keto DHEA on
rhesus monkeys, a species closer to humans than rats (at least,
closer in some people). The monkeys were given 7-keto doses of
250, 500, and 1,000 milligrams per kilogram/BW on days 1,3, and
5. On days 7-11, the monkeys got 1,000 milligrams per kilogram of
7-keto. On the 12th day, the monkeys were killed. Once again,
autopsy of the monkeys showed "no adverse clinical or anatomical
pathology results." Other than the fact that they were killed, of
course!

While these animal studies do appear to show a high safety
factor associated with 7-keto DHEA, it still doesn't completely
apply to human usage. So another study presented at the same
scientific conference looked at the hormonal and safety effects
of 7-keto DHEA in human subjects. The study consisted of men
between the ages of 18 and 49, 18 of whom took 7-keto DHEA, while
another 6 took a placebo or inactive substance for 8 weeks.
The dose of 7-keto were gradually increased to 100 milligrams,
twice daily during the final 4 weeks of the study.
The levels of hormones in the men before using 7-keto or the
placebo didn't differ either before or during treatment. However,
at the end of the study, the men taking genuine 7-keto DHEA
showed a small reduction in total testosterone levels in addition
to a clinically insignificant increase in free or active
testosterone levels. Since no significant changes occurred in any
hormone levels in those taking the real 7-keto DHEA, the study
authors concluded that,"This study shows that 7-keto DHEA is
well-tolerated at doses up to 200 milligrams a day, and does not
produce clinically important sex hormone changes in healthy men."

In another rat study presented at the conference, the
effects of 7-keto DHEA on memory was examined. The rats were
given a drug called scopolamine that interferes with the activity
of acetylcholine, a vital brain neurotransmitter required for
memory processes. In rats given 7-keto DHEA at a dose of just 20
milligrams per kilogram of bodyweight, the memory-interference
effects of scopolamine were nullified.


The same study also compared the effects of DHEA to 7-keto
DHEA for memory enhancement in rats trained to locate a foot
pedal. Control rats (not taking either DHEA or 7-keto) found the
pedestal in 34 seconds. Those taking DHEA found the pedestal in
22 seconds. In the 7-keto group, the rats located the pedestal in
7.6 seconds. This indicates that 7-keto shows memory-enhancing
effects that are clearly superior to that of regular DHEA.

Do soy isoflavones affect testosterone in men?

Soy isoflavones, such as genistein and others, have been
touted as having many important preventive health effects. These
include cardiovascular disease prevention through antioxidant
effects, and cancer prevention by interfering with the activity
of hormones such as estrogen that are associated with several
types of cancer in women.
These same isoflavones are linked to a lower prevalence of
prostate cancer in men. But since these isoflavones have a
chemical structure similar to estrogen, and since high levels of
estrogen may interfere with testosterone activity in men, the
question is: do soy isoflavones adversely affect androgen levels
in men?
This question is examined in two studies published in the
American Journal of Clinical Nutrition 1998;68(suppl):1531S-1533S.
In the first study, the effects of phytoestrogens or plant
estrogens (such as the isoflavones) were investigated in 13 older
women and 12 middle-aged men. The subjects were given 40 grams a
day of linseed oil containing a natural precursor to lignan, a
fiber known to have effects on hormones in the body, and 60 grams
a day of textured soy protein containing 45 milligrams of
isoflavones. The study subjects took the linseed for 4-6 weeks
and the soy protein for 4 weeks, both incorporated into bread
rolls.
The results showed that serum gonadotropin levels (FSH and
LH) were suppressed by both the linseed and soy protein. The
concentrations of luteinizing hormone (LH), a gonadotropin that
controls testosterone synthesis in the body, dropped by 10-13%
with both the linseed and soy diets. While consuming the linseed,
the serum androgen levels dropped in 6 of the male subjects,
although there was no changes in urinary androgen levels. Both
total and low density lipoprotein cholesterol decreased with the
linseed intake, with a significant drop showing up in the female
subjects.
Note that serum androgen levels i.e., testosterone levels,
were affected only by the linseed ingestion, although both the
linseed and soy did slightly lower gonadotropin output--which
dictates androgen levels in the body. Lignan, found in the
linseed, is a form of fiber, and this accounts for the beneficial
effects shown in lowering plasma lipids, such as total
cholesterol and LDL cholesterol. This would have a preventive
effect on cardiovascular disease onset.

Linseed also locks on to sex hormones in the body, promoting
the excretion of such hormones. This effect may have been more
potent with estrogens in this study, since the male subjects
showed lower serum androgen levels, but no greater excretion of
androgens through the urine. The drop in serum androgens in the
men was probably the result of both the linseed and soy slightly
interfering with gonadotropin release (LH). This may be due to
the estrogen-like structure of isoflavones, since estrogen is
known to be a potent inhibitor of gonadotropin release. In fact,
this is the main mechanism behind oral contraceptives, which
contain synthetic estrogens.
The decrease in gonadatropins shown in the study is
problematic, even though the men didn't appear to be adversely
affected as judged by the lack of change in androgen excretion.
Another study looked closer at this issue of how soy intake
affects hormone levels in the body. Unlike the previous study,
this study was more specific since it only focused on soy
products.
Again, the study involved older women and younger men, who
ingested 12 ounces a day of soy milk with each meal for one
month. The isoflavone intake each day averaged 100 milligrams of
genistein and 100 milligrams of daidzein, considered the most
active and biologically important isoflavones found in soy. In
the women levels of estrogen, progesterone, and DHEA-S (a
circulating, nonactive bound-form of DHEA in the blood) declined
by 60%, 35%, and 30% after one month of consuming the soy.
The men showed no changes in serum testosterone levels. They
did, however, show decreased levels of a metabolite of
dihydrotestosterone (DHT) by 13% after 4 weeks of soy ingestion.
This is a beneficial effect, since DHT, a metabolite of
testosterone, is considered to be responsible for promoting male
pattern baldness, acne, and prostate enlargement. Thus, soy may
provide a DHT reduction effect without adversely affecting normal
testosterone synthesis or release.
In another study, this time involving rats, Chinese
researchers focused on the effects of the soy isoflavone,
daidzein on muscle growth and hormone levels in the rodents. The
daidzein was given to both male and female rats in a dose of 3
milligrams per each 100 grams of bodyweight. The daidzein was
injected subcutaneously into the animals for 16 days. Compared to
a control group not getting the daidzein, male rats showed a
bodyweight gain of 14.7 percent, most of which was muscle.
The rats on daidzein also showed lower nitrogen excretion
(an indication of greater protein retention in the body), and
increased levels of testosterone, estrogen, beta-endorphin, and
growth hormone. In castrated rats, no muscle increase occurred,
despite higher levels of both testosterone and growth hormone
after being injected with daidzein, most likely due to the still
low levels of testosterone, averaging only 8% of the levels shown
by "intact" rats. The study authors concluded that the muscle
growth effects of daidzein appear to be linked to normal
testosterone production.

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©,2015 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited

Have you been ripped off  by supplement makers whose products don’t work as advertised? Want to know the truth about them? Check out Jerry Brainum's book Natural Anabolics, available at JerryBrainum.com.

 

The Applied Ergogenics blog is a collection of articles written and published by Jerry Brainum over the past 20 years. These articles have appeared in Muscle and Fitness, Ironman, and other magazines. Many of the posts on the blog are original articles, having appeared here for the first time. For Jerry’s most recent articles, which are far more in depth than anything that appears on this blog site, please subscribe to his Applied Metabolics Newsletter, at www.appliedmetabolics.com. This newsletter, which is more correctly referred to as a monthly e-book, since its average length is 35 to 40 pages, contains the latest findings about nutrition, exercise science, fat-loss, anti-aging, ergogenic aids, food supplements, and other topics. For 33 cents a day you get the benefit of Jerry’s 53 years of writing and intense study of all matters pertaining to fitness,health, bodybuilding, and disease prevention.

 

See Jerry's book at  http://www.jerrybrainum.com

 

Want more evidence-based information on exercise science, nutrition and food supplements, ergogenic aids, and anti-aging research? Check out Applied Metabolics Newsletter at www.appliedmetabolics.com

 

                            Please share this article on facebook