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Showing posts with label Researchers Article. Show all posts
Showing posts with label Researchers Article. Show all posts

Thursday, May 17, 2007

Muscle Growth Without Working Out!

Title: Bodybuilding Without Power Training: Endogenously Regulated Pectoral Muscle Hypertrophy in Confined Shorebirds.

Researchers: Dietz MW, Piersma T, Dekinga A.

Institution: Centre for Ecological and Evolutionary Studies, Zoological Laboratory, University of Groningen. The Netherlands and Netherlands Institute for Sea Research (NIOZ)

Reference: Journal of Experimental Biology. 1999 Oct; 202 (Pt 20):2831-7.

Summary: Shorebirds such as Red Knots (Calidris canutus) routinely make migratory flights of 3000 km or more. Previous studies on this species, based on compositional analyses, suggest extensive pectoral muscle hypertrophy in addition to fat storage before take-off. Such hypertrophy could be due to power training and/or be effected by an endogenous circannual rhythm.

Methods: Red Knots of two subspecies with contrasting migration patterns were placed in a climate-controlled aviary (12 h:12 h L:D photoperiod) where exercise was limited. Using ultrasonography, we measured pectoral muscle size as the birds stored fat in preparation for migration.

Results: At capture, there were no differences in body mass and pectoral muscle mass between the two subspecies. As they prepared for southward and northward migration, respectively, the tropically wintering subspecies (C. c. canutus) gained 31g and the temperate wintering subspecies (C. c. islandica) gained 41g. During this time, pectoral mass increased by 43-44 % of initial mass, representing 39% (C. c. canutus) and 29% (C. c. islandica) of the increase in body mass. The gizzard showed atrophy in conjunction with a diet change from molluscs to food pellets.

Conclusion: Although we cannot exclude the possibility that the birds' limited movement may still be a prerequisite for pectoral muscle hypertrophy, extensive power training is certainly not a requirement. Muscle hypertrophy in the absence of photoperiod cues suggests the involvement of an endogenous circannual process.

Discussion: Some of you may be thinking, "What do we care about shore birds?" Well, admittedly, if you are not a bird watcher, which I am not, we don't really care about shore birds. But these shore birds are no ordinary shore birds! The pecs on these guys actually grow once a year without any kind of exercise. Now that is interesting...

Essentially what these researchers found was that these birds have a circadian rhythm of sorts that acts on a yearly cycle, causing significant muscle growth every year, right on schedule. This is just one more amazing physiological adaptation involving muscle growth we find in nature, but not in humans. Another nifty adaptation we find is in bears that hibernate. They are able to go a few months without food and yet not lose any muscle mass. Their bodies, with the help of willing kidneys, are able to recycle amino acids so that no muscle mass is lost despite not eating any food at all.

Of course these two examples have little to do with what I or you are going to do in the gym today, but it does expand the mind to the possibilities of the future...a little genetic tinkering and presto! Muscles that grow on their own just in time for summer, and at the same time are entirely immune from the ravages of dieting. Not a bad future wouldn't you say?

Reference: http://www.hypertrophy-specific.com/HSreport/iss07

Ribose Fails to Perform

Title: Effects of Ribose Supplementation on Repeated Sprint Performance in Men

Researchers: JOHN M. BERARDI and TIM N. ZIEGENFUSS

Institution: Applied Physiology Laboratory, Eastern Michigan University, Ypsilanti, Michigan 48197

Reference: The Journal of Strength and Conditioning Research: (2003) Vol. 17, No. 1, pp. 47Ð52.

Summary: This study used a randomized, placebo-controlled, crossover design to evaluate the effects of oral ribose supplementation on short-term anaerobic performance.

Methods: After familiarization, subjects performed 2 bouts of repeated cycle sprint exercise (six 10-second sprints with 60-second rest periods between sprints) in a single day. After the second exercise bout, subjects ingested 32 g of ribose or cellulose (4 _ 8-g doses) during the next 36 hours. After supplementation, subjects returned to the laboratory to perform a single bout of cycle sprinting (as described above). After a 5-day washout period, subjects repeated the protocol, receiving the opposite supplement treatment.

Results: Ribose supplementation lead to statistically significant increases in mean power and peak power only in sprint 2 (10.9 and 6.6%, respectively) and higher (although not significant) absolute values in sprints 1, 3, and 4.

Conclusion: In conclusion, ribose supplementation did not show reproducible increases in performance across all 6 sprints. Therefore, within the framework of this investigation, it appears that ribose supplementation does not have a consistent or substantial effect on anaerobic cycle sprinting.

Discussion: Before we touch on this study, lets review what exactly ribose is for a second.

Ribose is a naturally occurring 5-carbon sugar called a "pentose". It is found in several foods we eat, but our body makes most of the ribose it needs from scratch. It is active in many of our body's systems, usually in its D-form (the L- form is it's mirror opposite). D-Ribose plays an important role as a structural component of high-energy phosphates such as adenosine triphosphate (ATP) as well as nucleic acids like DNA. As you can guess, ribose is an important substrate for every system and tissue in your body. When we consider taking ribose as a dietary supplement we are mainly focusing on its role as a substrate in ATP production, theoretically to improve exercise performance.

This is exactly the kind of research that we need on ALL supplements we spend our money on. Imagine if prescription drugs didn't have to be effective to be sold by doctors. It's a ludicrous thought! So why do we continue to spend our money on supps that haven't really been tested to see if they in fact do anything beneficial? If you're like me, its because we are desperate to make gains, desperate to see changes in our body, and desperate to find a way to ensure that all our hard work in the gym is going to pay off.

That brings us to our present study. The recommended dose for Ribose when you buy it as a supplement is 3 grams per day. Lest there be any doubt, they use 32 grams per day in this study, eliminating any doubt that they might not have used enough to see an effect.
Using over 10 times the recommended dose, these investigators were unable to produce a statistically significant and consistent effect. There own conclusions tell it all, "This investigation has not revealed any clear performance increases with oral ribose supplementation using doses even higher than those commonly ingested. Therefore, with the current high-price tag of oral ribose supplements, ribose does not appear to be a cost-effective supplement for athletes." Might I ad that it clearly is not a cost effective supplement for bodybuilders either.

Before wrapping this up I wanted to mention one other thing about attempts to prevent ATP levels from dropping. There are some beneficial adaptations to exercise that actually require a temporary reduction in ATP levels. This drop in ATP levels serves as the stimulus for metabolic adaptations. One of the most important ones is the increase in insulin sensitivity and/or glucose uptake into muscle cells after training. Studies have shown that if you artificially maintain ATP levels during the initiation of a high intensity exercise program, you don't get the up regulation of glucose transport into muscle cells. 1

Let me qualify these statements by saying that these studies were done on animals, and that ATP levels were maintained by means other than ribose supplementation. Nevertheless, these studies should tell the discerning supplement consumer that trying to reduce the metabolic consequences of training might be good for short-term performance, but in the long run, it also reduces the potency of the training stimulus.

Reference: http://www.hypertrophy-specific.com/HSreport/iss07

Blaming Creatine for Injuries?

Title: Creatine Supplementation and Its Effect on Musculotendinous Stiffness and Performance.

Researchers: MARK L. WATSFORD, ARON J. MURPHY, and WARWICK L. SPINKS, ANDREW D. WALSHE*

Institution: Human Movement Department, School of Leisure, Sport, and Tourism, University of Technology, Sydney, Australia 2070

Reference: The Journal of Strength and Conditioning Research: (2003) Vol. 17, No. 1, pp. 26Ð33.

Summary: Anecdotal reports suggesting that creatine (Cr) supplementation may cause side effects, such as an increased incidence of muscle strains or tears, require scientific examination. In this study, it was hypothesized that the rapid fluid retention and lean tissue accretion evident after Cr supplementation may cause an increase in musculotendinous stiffness.

Methods: Twenty men were randomly allocated to a control or an experimental group and were examined for musculotendinous stiffness of the triceps surae and for numerous performance indices before and after Cr ingestion.

Results: The Cr group achieved a significant increase in body mass (79.7 ± 10.8 kg vs. 80.9 ± 10.7 kg), counter movement jump height (40.2 ± 4.8 cm vs. 42.7 ± 5.9 cm), and 20-cm drop jump height (32.3 ± 3.3 cm vs. 35.1 ± 4.8 cm) after supplementation. No increase was found for musculotendinous stiffness at any assessment load. There were no significant changes in any variables within the control group.

Conclusion: These findings have both performance- and injury-related implications. Primarily, anecdotal evidence suggesting that Cr supplementation causes muscular strain injuries is not supported by this study. In addition, the increase in jump performance is indicative of performance enhancement in activities requiring maximal power output.

Discussion: Probably the most common misconception I hear from coaches, parents, and even uninformed athletes, is that creatine causes injuries. Before gently debunking their concerns I ask why they think creatine would cause injuries. Nine out of ten times the answer is dehydration. Dehydration? What?! Ok, ok, rather than get sarcastic I'll simply explain that the osmotic effect of creatine doesn't affect your body's hydration state. On the contrary, creatine supplementation increases total body water. (1,2)

Another injury related misconception about creatine is that it causes cramps. Recent research indicates that in fact, creatine may produce the opposite affect by increasing the muscle's ability to relax. (3,4) To further corroborate this, recent research found that creatine supplementation actually decreased the incidence of muscle cramping in haemodialysis patients. (5) Muscle cramping is a common and frustrating complication of haemodialysis treatment.

This study is only one more in a growing line of research done to explore and confirm the safety of creatine supplementation. Nevertheless, as with any supplement, there will be uninformed skepticism, and as long as there is a lack of information or worse, misinformation, we will continue to share research to establish the truth for the benefit of all, whether you chose to use supplements or not.

Reference: http://www.hypertrophy-specific.com/HSreport/iss07

Wednesday, May 16, 2007

Long Term Creatine Use

Title: Effects of Long-term Creatine Supplementation on Liver and Kidney Functions in American College Football Players.

Researchers: Mayhew DL, Mayhew JL, Ware JS

Institution: Exercise Science Program at Truman State University, Kirksville, MO 63501 and the Athletic Department at Truman State University, Kirksville, MO.

Summary: The purpose of this study was to determine the effect of long-term Cr supplementation on blood parameters reflecting liver and kidney function.
Methods: Twenty-three members of an NCAA Division II American football team (ages = 19-24 years) with at least 2 years of strength training experience were divided into a Cr monohydrate group (CrM, n = 10) in which they voluntarily and spontaneously ingested creatine, and a control group (n = 13) in which they took no supplements. Individuals in the CrM group averaged regular daily consumption of 5 to 20g for 0.25 to 5.6 years. Venous blood analysis for serum albumin, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, bilirubin, urea, and creatinine produced no significant differences between groups.

Results: Creatinine clearance was estimated from serum creatinine and was not significantly different between groups. Within the CrM group, correlations between all blood parameters and either daily dosage or duration of supplementation were nonsignificant.

Conclusion: Oral supplementation with CrM has no long-term detrimental effects on kidney or liver functions in highly trained college athletes in the absence of other nutritional supplements.

Discussion: Questions about creatine's safety are probably the most frequently brought up by people who don't like (and usually don't understand) supplements. This study by Mayhew and colleagues is a welcome addition to the already growing body of creatine safety research. (1,2,3,4,5,6,7)

Most questions revolve around the effects of creatine supplementation on the liver and kidney. These are the two organs are involved in "processing" creatine once it is ingested. The Liver breaks it down and the kidneys excrete it. From this study, and others before it, we see that long term supplementation with creatine in doses usually taken by bodybuilders (5-20 grams) for extended periods of time do not lead to dysfunction of either organ, nor does it cause abnormalities in the indicators of liver and kidney function.

Considering that fact that creatine supplementation has been shown to enhance anaerobic exercise performance by increasing power output (8), muscular strength and work (9,10,11), and muscle fiber size (12), and to top it off, completely safe even with long term supplementation, its no wonder this is one of my first tier recommendation for effective and safe supplements for putting on muscle size.

Reference: http://www.hypertrophy-specific.com/HSreport/iss06/

Creatine: More than just boosting strength

Title: Dietary creatine monohydrate supplementation increases satellite cell mitotic activity during compensatory hypertrophy.

Researchers: Dangott B, Schultz E, Mozdziak PE.
Institution: Department of Anatomy, University of Wisconsin-Medical School, Madison, USA.

Source: International Journal of Sports Medicine 2000 Jan;21(1):13-6.

Summary: Nutritional status influences muscle growth and athletic performance, but little is known about the effect of nutritional supplements, such as creatine, on satellite cell mitotic activity. The purpose of this study was to examine the effect of oral creatine supplementation on muscle growth, compensatory hypertrophy, and satellite cell mitotic activity.

Methods: Compensatory hypertrophy was induced in the rat plantaris muscle by removing the soleus and gastrocnemius muscles. Immediately following surgery, a group of six rats was provided with elevated levels of creatine monohydrate in their diet. Another group of six rats was maintained as a non-supplemented control group. Twelve days following surgery, all rats were implanted with mini-osmotic pumps containing the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) to label mitotically active satellite cells. Four weeks after the initial surgery the rats were killed, plantaris muscles were removed and weighed. Subsequently, BrdU-labeled and non-BrdU-labeled nuclei were identified on enzymatically isolated myofiber segments.

Results: Muscle mass and myofiber diameters were larger in the muscles that underwent compensatory hypertrophy compared to the control muscles, but there were no differences between muscles from creatine-supplemented and non-creatine-supplemented rats. Similarly, compensatory hypertrophy resulted in an increased number of BrdU-labeled myofiber nuclei, but creatine supplementation in combination with compensatory hypertrophy resulted in a higher number of BrdU-labeled myofiber nuclei compared to compensatory hypertrophy without creatine supplementation.

Conclusion: Creatine supplementation in combination with an increased functional load results in increased satellite cell mitotic activity compared to increased functional load alone.

Discussion: People seem to want to pigeonhole creatine into some sort of hit-or-miss water-retention supplement. Creatine is so much more than that. Creatine is truly one of the greatest supplements there is for building muscle and strength. Study after study attest to this fact. This is only one of many studies exploring the exciting anabolic properties of creatine monohydrate which we will consider in upcoming issues.

In short, creatine is a naturally occurring compound made within our own bodies. It is also found in many foods we eat, especially meat. Creatine monohydrate has been used as a dietary supplement for at least a decade now, though it was first discovered nearly 170 years ago.
Now in the study we're considering today, the examined the effect of dietary creatine monohydrate on satellite cell activity and subsequent muscle hypertrophy. I won't lie to you and tell you that I have no interest in educating Hypertrophy-Specific readers about creatine. On the contrary, I believe so highly in the effectiveness of creatine that I introduced it into the HSN line of products. Not because people demanded it, but instead because I believe in it. And taking a look at the available research on creatine will make you a believer too. The writing is on the wall with this one folks.

This study looked at the activity of satellite cells. Satellite cells are myogenic stem cells that make hypertrophy of adult skeletal muscle possible. These stem cells are simply generic or non-specific cells that have the ability to transform themselves into new muscle cells when they are instructed to.

Following proliferation (reproduction) and subsequent differentiation (to become a specific type of cell), these satellite cells will fuse with one another or with the adjacent damaged muscle fiber, thereby increasing myonuclei numbers necessary for fiber growth and repair.

In order to better understand what is physically happening between satellite cells and muscle cells, try to picture 2 oil droplets floating on water. The two droplets represent a muscle cell and a satellite cell. Because the lipid bilayer of cells are hydrophobic just like common oil droplets, when brought into proximity to one another in an aqueous environment, they will come into contact for a moment and then fuse together to form one larger oil droplet. Now whatever (i.e. nuclei) was within one droplet will then mix with the contents of the other droplet. This is a simplified model of how satellite cells donate nuclei to existing muscle cells.

The reason this finding about creatine is so exciting is that the process of satellite cells adding nuclei to regenerating muscle cells appears to be critical for hypertrophy. There appears to be a finite limit placed on the cytoplasmic/nuclear ratio (Rosenblatt,1994). This is the ratio of the volume of the muscle cell to the number of nuclei. Whenever a muscle grows in response to functional overload there is a positive correlation between the increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating their nuclei, overloaded muscle simply will not grow (Rosenblatt,1992; Phelan,1997).

This study was able to show that creatine supplementation increased the number of myonuclei donated from satellite cells. This increases the potential for growth of those fibers due to the aforementioned cytoplasmic/nuclear ratio. This isncrease in myonuclei probably stems from creatine's ability to increase levels of the myogenic transcription factor MRF4 (Hespel, 2001).
So when it comes to answering the question, "what works and what doesn't" stick to those supplements that have real research behind them. Creatine, proteins, and essential fatty acids top the list of highly researched, highly effective supplements.

Reference: http://www.hypertrophy-specific.com/HSreport/iss03/

Tuesday, May 15, 2007

How Soon Can I Train Again?

Title: Effects of a 7-day eccentric training period on muscle damage and inflammation.

Researchers: Chen TC, Hsieh SS.

Institution: Department of Ball-Related Sports Science, Taipei Physical Education College, Taipei City, Taiwan.

Source: Medicine and Science Sports & Exercise 2001 Oct;33(10):1732-8

Purpose: This study examined the effects of a 7-day repeated maximal isokinetic eccentric training period on the indicators of muscle damage and inflammatory response.

Methods: Twenty-two college-age males were randomly assigned to eccentric training (ET) and control groups (CON). The initial exercise was 30 repetitions of maximal voluntary isokinetic eccentric contraction (ECC1) on non-dominant elbow flexors with Cybex 6000 at 60 degrees.s-1 angular velocity. The ET group performed the same exercise for the following 6 consecutive days (referred to as ECC2 to ECC7) after ECC1. Upper arm circumference (CIR), range of motion (ROM), and maximal isometric force (MIF) were measured before, immediately after, and every 24 h for 7 consecutive days after ECC1. Plasma creatine kinase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetate transaminase (GOT), leukocyte counts, and serum interleukin-1beta and -6 (IL-1beta, IL-6) levels were assessed before; at 2 h; and at 1, 3, 4, 6, and 7 d after ECC1. Muscle soreness was measured before and for 7 consecutive days after ECC1.

Results: The ECC1 produced significant changes in most of the measures for both groups, with the exception of leukocyte counts. No indicators of increased damage were found from the second consecutive day of eccentric training to the 7th day for the eccentric training group.

Conclusion: Continuous intensive isokinetic eccentric training performed with damaged muscles did not exacerbate muscle damage and inflammation after ECC1. In addition, a muscular "adaptation effect" may occur as early as 24 h after ECC1, as shown by the ET group's performance for 6 consecutive days after ECC1.

Discussion: One of the most controversial aspects of HST is the suggestion that people train in a predominantly eccentric fashion for two weeks straight. Heresy! they shout. Then when you ask them why it's so bad to train a muscle more frequently or, heaven forbid, do negatives two workouts in a row, they say because your muscle can't "recover" that fast. This study calls into question the belief that muscles can't recover if trained again soon or even the next day.

They looked at a wide variety of markers for muscle damage including plasma creatine kinase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetate transaminase (GOT), leukocyte counts, and serum interleukin-1beta and -6 (IL-1beta, IL-6). Although both groups experienced a significant change in all these indicators (accept leukocyte count), no indicators of increased damage were found from ECC2 to ECC7 for the ET group.

What about soreness? For both the group who only did one training session as well as those who did seven in a row, muscle soreness developed 1 day after the first eccentric training bout, and remained through the 3rd day, then gradually diminished regardless of which group they were in. The group that did the eccentric sets every day experienced the same progression and subsidence of soreness as the group that did only one set at the beginning of the week. The soreness level was almost back to baseline on 7 day for both groups.

The results of this investigation indicated that repeated bouts of the eccentric exercise performed on each of the following 6 days after the first bout did not affect recovery from the first training bout. This is in agreement with a substantial amount of other studies indicating that muscle adapts effectively to physical load even when the loading is frequent or even continuous. Keep in mind that we are only talking about the physical recovery of the muscle. We are not talking about performance. After all, HST is "Hypertrophy-Specific" by design.

So once again, HST turns out not to be so outlandish, but instead, simply a derivative of the research. The results and the science, speak for themselves.

Reference: http://www.hypertrophy-specific.com/HSreport/iss02/

Make Your Protein Drink More Anabolic

Title: Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise.

Researchers: Tipton KD, Rasmussen BB, Miller SL, Wolf SE, Owens-Stovall SK, Petrini BE, & Wolfe RR.

Source: American Journal of Physiology Endocrinology & Metabolism. 2001 Aug;281(2):E197-206.

Summary: This study was designed to determine whether drinking an essential amino acid-carbohydrate supplement (6gEAA+35g carbs) before exercise results in a greater anabolic response than supplementation after resistance exercise.

Methods: Six healthy human subjects participated in two trials in random order, PRE (6g EAA+35g carbs consumed immediately before exercise), and POST (6g EAA+35g carbs consumed immediately after exercise). A primed, continuous infusion of L-[ring-(2)H(5)]phenylalanine, femoral arteriovenous catheterization, and muscle biopsies from the vastus lateralis were used to determine phenylalanine concentrations, enrichments, and net uptake across the leg.

Results: Blood and muscle phenylalanine concentrations were increased by approximately 130% after drink consumption in both trials. Amino acid delivery to the leg was increased during exercise and remained elevated for the 2 h after exercise in both trials. Delivery of amino acids (amino acid concentration times blood flow) was significantly greater in PRE than in POST during the exercise bout and in the 1st h after exercise. Total net phenylalanine uptake across the leg was greater during PRE (209 +/- 42 mg) than during POST (81 +/- 19). Phenylalanine disappearance rate, an indicator of muscle protein synthesis from blood amino acids, increased after EAC consumption in both trials.

Conclusion: These results indicate that the response of net muscle protein synthesis to consumption of an EAC solution immediately before resistance exercise is greater than that when the solution is consumed after exercise, primarily because of an increase in muscle protein synthesis as a result of increased delivery of amino acids to the leg.

Discussion: First let's talk about what's right with this study. Then we'll tackle what's wrong with it to keep things in perspective.

Here's what they did right. These researchers measured systemic levels of amino acids after the drink, the amount of amino acids delivered to muscle tissue, as well as the uptake of amino acids into the muscle for protein synthesis. This way they were able to follow the effects of the protein drink from the time it entered the blood stream to its eventual incorporation into muscle protein.

What they found was that systemic (amino acids in the blood stream) levels of amino acids were the same whether you took the drink before or after training. Amino acid delivery to the leg increased during exercise, and remained elevated for at least 2 hours after training. This is the result of increased blood flow to the working muscle. This increase in blood flow peaks during exercise then returns to normal over the next 2 hours.

Here is where it gets interesting. Delivery of amino acids, meaning the quantity of amino acids delivered to the muscle, was significantly greater when they gave the protein drink before training and remained significantly higher for at least an hour after the workout, compared to drinking it immediately after training. The increased delivery of amino acids from drinking the protein drink before training increased amino acid uptake into muscle by over 250%!

The superiority of taking protein before training is obvious when comparing the percentage of amino acids taken up by the leg from the protein drink. When the protein drink was taken before training, ~42% of the amino acids in the drink were taken up into the muscle. The proportion was much lower when the protein was drank after training, only about 16% of the drink was taken up into the muscle. That's over twice as much of the amino acids being taken up by muscle when it is consumed before training. It was estimated that ~86% of total uptake was incorporated into proteins whereas only ~48% of total uptake during the post workout trail was incorporated into proteins. That's a huge difference.

As for the bad, this study only used 6 grams of amino acids! I can blow my nose and produce more than 6 grams of protein. These researchers had previously (1) used higher amounts of protein (40 grams) without carbs, so in this study they wanted to see if they could elicit a similar anabolic response with less protein and more carbs. Of course, anybody who's serious about putting on muscle weight is going to need more than 6 grams of amino acids before their workout. I would suggest at least 20 grams before and another 20 grams after. Although they used only essential amino acids in this study, using a whole protein source is equally effective as long as it contains all the essential amino acids.

If you want the most muscle growth from your protein supplements, you must take one right before training, and the another right after. Although I alone have been recommending this for some time, you will surely see others making these recommendations in the near future. At least you'll know you knew about it way before the rest of the world did.

Reference: http://www.hypertrophy-specific.com/HSreport/iss02/

Saturday, April 7, 2007

Creatine Builds Muscle

Title: Performance and muscle fiber adaptations to creatine supplementation and heavy resistance training.

Researchers: Volek JS, Duncan ND, Mazzetti SA, Staron RS, Putukian M, Gomez AL, Pearson DR, Fink WJ, Kraemer WJ.

Institution: Department of Kinesiology/Center for Sports Medicine, The Pennsylvania State University, University Park 16802, USA. Source: Med Sci Sports Exerc 1999 Aug;31(8):1147-56 Related Articles, Books, LinkOut

Summary: The purpose of this study was to examine the effect of creatine supplementation in conjunction with resistance training on muscle fiber hypertrophy and muscle creatine accumulation.

Methods: Nineteen healthy resistance-trained men were matched and then randomly assigned in a double-blind fashion to either a creatine or placebo group. Periodized heavy resistance training was performed for 12 wk. Creatine or placebo capsules were consumed (25 g x d(-1)) for 1 wk followed by a maintenance dose (5 g x d(-1)) for the remainder of the training period.

Results: After 12 wk, significant increases in body mass and fat-free mass were greater in creatine (6.3% and 6.3%, respectively) than placebo (3.6% and 3.1%, respectively) subjects. After 12 wk, increases in bench press and squat were greater in creatine (24% and 32%, respectively) than placebo (16% and 24%, respectively) subjects. Compared with placebo subjects, creatine subjects demonstrated significantly greater increases in Type I (35% vs 11%), IIA (36% vs 15%), and IIAB (35% vs 6%) muscle fiber cross-sectional areas. Muscle total creatine concentrations were unchanged in placebo subjects. Muscle creatine was significantly elevated after 1 wk in creatine subjects (22%), and values remained significantly greater than placebo subjects after 12 wk. Average volume lifted in the bench press during training was significantly greater in creatine subjects during weeks 5-8. No negative side effects to the supplementation were reported.

Conclusion: Creatine supplementation enhanced fat-free mass, physical performance, and muscle morphology in response to heavy resistance training.

Discussion: Creatine is a naturally occurring compound made within our own bodies. It is also found in many foods we eat, especially meat. Creatine monohydrate has been used as a dietary supplement for at least a decade now, though it was first discovered nearly 170 years ago.

People seem to want to pigeonhole creatine into some sort of hit-or-miss water-retention supplement. Creatine is so much more than that. Creatine is truly one of the greatest supplements there is for building muscle and strength.

There was significant weight gain in this study. The creatine group "loaded" creatine the first 7 days. This was followed by 5 grams per day thereafter. One would expect a significantly greater weight gain the first week over placebo simply because of the well known effect of creatine loading on acute intracellular water retention (cell volumizing). But if this was the only way creatine lead to weight gain, this accelerated weight gain should have tapered off by the end of the first week, then stayed parallel to the placebo group through week 12. Instead, the acceleration of weight gain continued throughout the entire study period reaching nearly 10 pounds of lean mass by week 12! The placebo group gained only 4—in the same period. The creatine group literally doubled their muscle growth by using creatine. This means that creatine continued to effect lean mass gains long after its initial effect on water levels. This increase in body weight was then demonstrated to be true hypertrophy of muscle fibers.

In this study they were able to show, that in trained subjects, creatine supplementation increased muscle mass by nearly twice as much as placebo. Type I muscle fibers increased 35% with creatine but only 11% without it. Likewise, type IIA increased 36% compared to 15%. And finally, Type IIAB fibers increased 35% with creatine supplementation compared to only 6% without it. So on average, creatine supplementation produced 3 times the percentage of muscle fiber growth as placebo. You'd have to be a fool to ignore that!

There's no time to go into the many of other beneficial effects of creatine monohydrate. Suffice it to say, we will be taking a closer look at a lot of research on creatine in the issues to come. Stay tuned!

Reference: http://www.hypertrophy-specific.com/HSreport/iss01/

Thursday, March 15, 2007

Testosterone, IGF-1, and Training

Title: Mechanical load increases muscle IGF-I and androgen receptor mRNA concentrations in humans.

Researchers: Bamman MM, Shipp JR, Jiang J, Gower BA, Hunter GR, Goodman A, McLafferty CL Jr, Urban RJ.

Institution: Department of Surgery, University of Texas Medical Branch, and 2 Metabolism Unit, Shriners Hospitals for Children, Galveston, Texas 77550 Source: American Journal of Physiology Endocrinology & Metabolism. 2001 Mar;280(3):E383-90.

Summary: These investigators looked at the effects of concentric (CON) reps vs. eccentric (ECC) reps on muscle insulin-like growth factor-1 (IGF-I) mRNA concentration. They hypothesized a greater IGF-I response after ECC compared with CON.

Methods: Ten healthy subjects (Average age 24.4 yrs) completed eight sets of eight CON or ECC squats separated by 6-10 days. IGF-I, IGF binding protein-4 (IGFBP-4), and androgen receptor (AR) mRNA concentrations were determined in vastus lateralis from muscle biopsy before and 48 h after ECC and CON. Serum total testosterone (TT) and IGF-I were measured serially across 48 h, and serum creatine kinase activity (CK), isometric maximum voluntary contraction (MVC), and soreness were determined at 48 h.

Results: IGF-I mRNA concentration increased 62% and IGFBP-4 mRNA concentration decreased 57% after ECC. The direction of these changes after CON were similar but not statistically significant. AR mRNA concentration increased after ECC (63%) and CON (102%). Serum levels of total testosterone and IGF-I showed little change. MVC fell 10% and CK rose 183% after ECC squats. Perceived soreness was higher after ECC compared with CON.

Conclusion: Results indicate that a single bout of mechanical loading in humans alters activity of the muscle IGF-I system, and the enhanced response to ECC suggests that IGF-I may somehow modulate tissue regeneration after mechanical damage.

Discussion: Nothing in this study should really surprise us. But it does shed light on how lifting weights selectively regulates anabolic activity to specific tissues of the body. Training increased both androgen receptors as well as muscle specific IGF-1.

Training causes an increase in androgen receptors (testosterone receptors) on muscle cells, which increases the sensitivity of your muscle to your natural testosterone levels. This effect of training on androgen receptors is specific to muscle tissue. In other words, you are not going to see an increase in the effects of testosterone in other tissues such as your hair or your skin. So unlike using steroids, training only increases the effects of testosterone in muscle tissue.

IGF-1 is another critical player in muscle growth. Muscle growth from weight training is the result of IGF-1 being produced by the muscle cells themselves, not the liver. In fact, IGF-1 from the liver is genetically different from IGF-1 produced in your muscles. This is the reason why using IGF-1 systemically (from the blood stream) has been a hit and miss proposition.

IGF-1 formation in muscle tissue is absolutely critical if significant muscle hypertrophy is to occur. IGF-1 produced inside muscle cells that have been damaged by heavy training, oozes out of the cell and activates satellite cells. These satellite cells then donate nuclei to the damaged muscle cell, thereby allowing it to grow larger than before. There is a limit to the size of a muscle cell, and it depends largely on the number of nuclei it has. If you prevent a muscle cell from getting more nuclei from satellite cells, it simply will not grow, no matter how heavy things get. (1,2,3) The reduction in IGF binding protein-4 (IGFBP-4) leads to increased IGF-1 activity.(4) [Note: IGFBP-"3" also binds IGF-1 but in a good way. IGFBP-3 is the main carrier of IGF-1 and prolongs the half-life of IGF-1]

I would like to voice my strongly held opinion that the ever so slight changes in systemic hormone levels as a result of exercise are not responsible for the muscle growth observed with resistance exercise. Instead, as this study illustrates, it is the changes that occur within the muscle cells themselves that account for any hormonal contributions to hypertrophy. Both an increase the muscle's sensitivity to existing androgen levels, increases in intracellular IGF-1 levels, with concomitant decreases in inhibitory IGF binding proteins are the primary "hormonal" mechanisms for muscle growth as a result of training (excluding the use of exogenous hormones).

Reference: http://www.hypertrophy-specific.com/HSreport/iss01/