Written by Jose Antonio, PhD
06 April 2007

Growth of skeletal muscle is the result of both muscle fiber hypertrophy and hyperplasia (in some cases). The key to activating skeletal muscle growth is multifactorial. We know training, diet and genetics are all important.  And certainly, if we could choose our parents, genes might be the single most important factor. Take myostatin for example. Myostatin-deficient animals have extreme muscular development characterized by skeletal muscle fiber hypertrophy and hyperplasia.

If you see the myostatin-deficient bulls, they’re termed “double-muscled” because of their extreme size. So, myostatin is basically there to prevent excess growth. But on the other end, if you are losing muscle, myostatin kicks in to keep you from losing too much muscle. Or does it? In an investigation published in the American Journal of Physiology, researchers compared the effects of hindlimb suspension on muscle mass in wild-type mice (regular mice, or RM) and myostatin-deficient mice (MM).

If you’re wondering what hindlimb suspension is, it’s basically an experimental model that assesses the effects of unloading (think, polar opposite of weight lifting). What physiological situations would this mimic? You’re injured or bedridden, or if your limbs are in a cast, etc. All these conditions are similar to  “hindlimb suspension.” (OK, you science nerds out there, it’s not identical, but it’s close enough).  Before the hindlimb suspension, the MM had 28 percent greater body weights. After seven days of suspension, the MM was only eight percent greater than RM. In other words, the MM lost proportionately more body weight. This seems opposite of what you’d expect, right? Hmmm…
Also, the MM lost more muscle mass from the quads (17 vs. 11 percent) and lost more in the extensor digitorum longus (33 vs. 0 percent) compared to the RM. 
Contrary to what one would expect, the myostatin-mutant mice lost more muscle and body weight. So, even though under loading conditions, myostatin-mutant animals gain more muscle, apparently under conditions of unloading, they also lose more muscle. Scientists suggest that this may be due to a preferential loss of type IIB fibers (a fast type of muscle fiber). Future research needs to cofirm this. (Am J Physiol, 285:E82-E87, 2003)

Get Big, Old Man
They say you’re never too old to start lifting; nor are you ever too old to start taking supplements. In one of the very few long-term trials (nine months), 57 elderly men and women were plucked from their retirement homes in Lyon, France, and asked to participate (exercise plus protein supplementation). Or else they’d get shipped to Disneyworld and have overweight Americans throw French fries at them (kidding… no such thing was in the consent form; get a sense of humor). Muscle power improved by 57 percent at three months in the supplemented group, though it seemed to plateau after that. Also, body mass index increased more in the supplemented group, but decreased in the placebo group. These investigators felt that the data supported the use of exercise and supplementation in helping older individuals regain strength and mass. And with that, I agree!  (Br J Nutr, 89:731-9, 2003)

Creatine Comparison
Creatine monohydrate plus 18 grams dextrose, effervescent creatine, or how ‘bout just plain creatine monohydrate; which is best? One way to answer that is to see how well the creatine is absorbed. In a study done by Dr. Mike Greenwood of Baylor University, 16 men were given either five grams of creatine monohydrate (CM), five grams of CM plus 18 grams of dextrose, or an effervescent creatine product (five grams creatine, 18 grams dextrose, 320 milligrams sodium, 175 milligrams potassium) four times daily for three days (so it’s a short loading dose study). Creatine retention was determined by subtracting total urinary creatine excretion from total supplemental creatine intake over three days. 
What did they find? The average creatine retained was zero (placebo), 12.2 grams (CM only), 16.1 grams (CM plus dextrose) and 12.6 (effervescent).  In essence, they found no difference in retention rates between CM alone and effervescent creatine. This would suggest that both groups lost equal amounts in urine (and perhaps feces). On the other hand, plain old CM plus dextrose had the best effect. 
The effervescent drink is designed to maximize absorption; however, at least in this one investigation, no such advantage was found. Also, the effervescent group used creatine citrate rather than monohydrate. Perhaps, the citrate form is an inferior type of creatine. More research is needed to confirm the reality of these differences. (JEP online 6(2): May 2003)

Beta-Conglycinin Peptone: Weight Loss Agent?
In a very cool rat study, scientists infused B-Conglycinin, a major component of soy, into the small intestine of these furry little rodents. This small protein apparently has an appetite suppressant effect as well as slowing gastric emptying. It’s thought that CCK(cholecystokinin) is involved in the inhibition of gastric emptying. When you compared the numbers, infusing soy protein and wheat gluten inhibited food intake by roughly two to six percent. On the other hand, beta-conglycinin inhibited food intake by 17 percent. 
Certainly, with ephedra being pulled off the shelves (and let’s face it, there is no better fat-loss agent that caffeine plus ephedra), peptides like this may be one way of promoting weight loss vis a vis appetite reduction and gastric slowing. (J Nutr, 133:352-357, 2003.

I’ll Drink to That!
We know red wine is good for the heart, but maybe it’s also good for muscles. There are chemicals in red wine that act as aromatase inhibitors.  Remember, aromatase enzymes promote the conversion of testosterone to estrogens. By inhibiting this enzyme, theoretically, you could decrease levels of estrogen. Maybe? I’ll drink to that! (Ann NY Acad Sci, 963:239-46, 2002)