Showing posts with label supplements. Show all posts
Showing posts with label supplements. Show all posts

Tuesday, January 20, 2009

Does Fish Oil Make You Smart? Neurodevelopmental Outcomes of Preterm Infants Fed High-Dose Docosahexaenoic Acid


Very interesting study below that is hot off the presses from JAMA. It once again shows the benefits of fish oils, especially DHA (EPA is the other fish oil). Expect to see fish oils in all sorts of products in the future! Maybe eating fish does make you smart? Hmmmm.

From an interview on Medscape (below), there was not a response in boys. Very odd.

"The lack of responsiveness of boys to the intervention is puzzling," the researchers write, "and the reasons are unclear."

"We can only speculate that there are differences in the metabolism of boys and girls that we do not yet understand," Dr. Makrides said during an interview. "The higher metabolic rate in boys may mean that they utilize much of the DHA they receive into energy. Also, boys may have a higher requirement for DHA. Clearly, this is an area of important research for the future."

The abstract is below and you can click on the title for the full study to read it for yourself

Neurodevelopmental outcomes of preterm infants fed high-dose docosahexaenoic acid: a randomized controlled trial.

JAMA. 2009 Jan 14;301(2):175-82

Makrides M, Gibson RA, McPhee AJ, Collins CT, Davis PG, Doyle LW, Simmer K, Colditz PB, Morris S, Smithers LG, Willson K, Ryan P.

Child Nutrition Research Centre, Women's and Children's Health Research Institute, Women's and Children's Hospital, 72 King William Rd, North Adelaide SA 5006, Australia. maria.makrides@cywhs.sa.gov.au

CONTEXT: Uncertainty exists about the benefit of dietary docosahexaenoic acid (DHA) on the neurodevelopment of preterm infants.

OBJECTIVE: To determine the effect of meeting the estimated DHA requirement of preterm infants on neurodevelopment at 18 months' corrected age.

DESIGN, SETTING, AND PARTICIPANTS: Randomized, double-blind controlled trial enrolling infants born at less than 33 weeks' gestation from April 2001 to October 2005 at 5 Australian tertiary hospitals, with follow-up to 18 months.

INTERVENTION: High-DHA (approximately 1% total fatty acids) enteral feeds compared with standard DHA (approximately 0.3% total fatty acids) from day 2 to 4 of life until term corrected age. MAIN

OUTCOME MEASURES: Bayley Mental Development Index (MDI) at 18 months' corrected age. A priori subgroup analyses were conducted based on randomization strata (sex and birth weight < 1250 g vs > or = 1250 g).

RESULTS: Of the 657 infants enrolled, 93.5% completed the 18-month follow-up. Bayley MDI scores did not differ between the high- and standard-DHA groups (mean difference, 1.9; 95% confidence interval [CI], -1.0 to 4.7). The MDI among girls fed the high-DHA diet was higher than girls fed standard DHA in unadjusted and adjusted analyses (unadjusted mean difference, 4.7; 95% CI, 0.5-8.8; adjusted mean difference, 4.5; 95% CI, 0.5-8.5). The MDI among boys did not differ between groups. For infants born weighing less than 1250 g, the MDI in the high-DHA group was higher than with standard DHA in the unadjusted comparison (mean difference, 4.7; 95% CI, 0.2-9.2) but did not reach statistical significance following adjustment for gestational age, sex, maternal education, and birth order (mean difference, 3.8; 95% CI, -0.5 to 8.0). The MDI among infants born weighing at least 1250 g did not differ between groups.

CONCLUSION: A DHA dose of approximately 1% total fatty acids in early life did not increase MDI scores of preterm infants overall born earlier than 33 weeks but did improve the MDI scores of girls.

Saturday, December 20, 2008

Reserach Update Dec: BCAAs and Athletic Performance


A newer study for all of ya. While BCAAs (branched chain amino acids) did not direct enhance athletic performance they may reduce muscle soreness. I was not able to get a full copy of the study, so I don't have any details to share and just more questions about the study.

Whey protein is a great source of BCAAs, so be sure to include some around your training time. Check out the other posts on below:

International society of sports nutrition position stand: nutrient timing

Performance Research for August: Protein Synthesis

Charles Saley Seminar: Dave Barr and Supplements


If you are interested in the effects of the immune system and inflammation, be sure to check out the guest blog post from Dr. Lonnie Lowery HERE.


Branched-chain amino acid supplementation does not enhance athletic performance but affects muscle recovery and the immune system.

Negro M, Giardina S, Marzani B, Marzatico F.
J Sports Med Phys Fitness. 2008 Sep;48(3):347-51.Links


Since the 1980's there has been high interest in branched-chain amino acids (BCAA) by sports nutrition scientists. The metabolism of BCAA is involved in some specific biochemical muscle processes and many studies have been carried out to understand whether sports performance can be enhanced by a BCAA supplementation. However, many of these researches have failed to confirm this hypothesis. Thus, in recent years investigators have changed their research target and focused on the effects of BCAA on the muscle protein matrix and the immune system. Data show that BCAA supplementation before and after exercise has beneficial effects for decreasing exercise-induced muscle damage and promoting muscle-protein synthesis. Muscle damage develops delayed onset muscle soreness: a syndrome that occurs 24-48 h after intensive physical activity that can inhibit athletic performance. Other recent works indicate that BCAA supplementation recovers peripheral blood mononuclear cell proliferation in response to mitogens after a long distance intense exercise, as well as plasma glutamine concentration. The BCAA also modifies the pattern of exercise-related cytokine production, leading to a diversion of the lymphocyte immune response towards a Th1 type.

According to these findings, it is possible to consider the BCAA as a useful supplement for muscle recovery and immune regulation for sports events.

Tuesday, December 16, 2008

Performance Research for Decemeber: Fat Loss--Supplements and Social Support

Greetings! The current temp this AM in snowy and cold Minnesota was -11F--friggin cold that is what!

Jodie and I had an awesome time skiing and snowboarding (she was the two planker) this past weekend up at Indianhead in da UP of MI. We took the bus with a bunch of other craziest (Ski Hawks--whooo ha) and got there in time Friday night for a tasty adult style beverage (Bells White Ale) and some live music and dancing.

Saturday we were up early and skied and boarded all day in great snow! Sat night after a group dinner we did some more dancing again and then more boarding and skiing on Sunday before the bus ride home.

It was a great time and I already have 2 days logged this winter on my snowboard which is more than all of last year. Back to reality now and tons to get done this week as always.

That Time Again!
It is that time again, New Year's Eve is about 2 weeks away! Are you going to avoid the Happy Holiday Weight Gain? What is your plan? You do have a plan, right? Here are some tips to help you out based on some brand new research.

Telephone-based diet and exercise coaching and a weight-loss supplement result in weight and fat loss in 120 men and women.


Tucker LA, Cook AJ, Nokes NR, Adams TB.

College of Health and Human Performance, Brigham Young University, Provo, Utah 84602, USA. tucker@byu.edu PURPOSE: Determine the effects of telephone-based coaching and a weight-loss supplement on the weight and body fat (BF) of overweight adults.

DESIGN: Randomized, placebo-controlled experiment with assessments at baseline, 2 months, and 4 months.

SETTING: Community. SUBJECTS: Sixty overweight or obese men and 60 overweight or obese women, 25 to 60 years INTERVENTION: Eleven 30-minute telephone coaching sessions were spaced throughout the study; the initial conversation lasted 60 to 90 minutes. Supplement or placebo capsules were taken daily over the 17 weeks.


MEASURES: Weight was measured using an electronic scale, and BF was assessed using dual energy x-ray absorptiometry.

RESULTS: Subjects taking the placebo lost 1.8 +/- 3.3 kg of weight and 0.7 +/- 2.2 kg of BF, whereas supplement users lost more: 3.1 +/- 3.7 kg of weight (F = 4.1, P = .045) and 1.7 +/- 2.6 kg of BF (F = 4.4, p = .039). Participants receiving no coaching lost 1.8 +/- 3.3 kg of weight and 0.7 +/- 2.2 kg of BF, whereas adults receiving coaching lost more: 3.2 +/- 3.6 kg of weight (F = 4.8, p = .032) and 1.6 +/- 2.5 kg of BF (F = 4.2, p = .044). Adults receiving both the supplement and coaching had the greatest losses of weight and BF, suggesting an additive effect (F = 3.2, p = .026; F = 2.9, p = .039, respectively).


CONCLUSIONS: Both treatments, coaching and the supplement, viewed separately and in combination, worked to help subjects lose weight and body fat. Adults can be educated and motivated via telephone to change behaviors leading to weight loss, and a weight-loss supplement can be included to increase success.

My Notes:
It shows that having someone check up on you and provide social support makes a difference! Another reason why most (not all) do not succeed on their own--get some professional help and at min enroll support from your family and friends.

I found it interesting that they did not mention what supplement was used in the abstract. Here it is from the research study:


Each capsule contained 700 mg of
supplement, and the fotir capsules
together inclttded the following: vitamin
B| (15 mg), vitamin Bg (10 mg),
niacinamide (SO mg), vitamin B5
(50 mg), \'itamin Bf, (2 mg), xntamin
B|¡; (1 mg), biodn (2 mg), vitamin C
(22.5 mg), vitamin D (1000 IU), dimethylglycine
(100 mg), chromium
(0.05 mg), copper (0.5 mg), magnesitim
(200 mg), vanadyl sulphate
(1 mg), manganese citrate (1 mg),
zinc glticonate (10 mg), indium sulphate
(25 mg), Cardnia cambogia
(250 mg), Gymnema sylvestre (10:1;
100 mg), bitter melon (10:1; 70 mg),
cinnamon bark (500 mg), Poria cocos
(5:1; 100 mg), Rhizoma zingiberis (4:1;
50 mg), green tea (10:1; 100 mg),
Korean ginseng (100 mg), L-theanine
(50 mg), gamma-aminobtityric acid
(50 mg), alpha lipoic acid (110 mg).
Calcárea carbónica (12X; 10 mg), natrum
stilphuricum (12X; 10 mg), graphites
(30C1; 10 mg), nux vómica
(30C; 10 mg), lycopodium (30C;
10 mg), and glucomannan (700 mg).


My Notes (continued):
It should be noted that the supplement only accounted for an additional fat loss of 1.2 kg over the course of the study in over 17 weeks of use---so not much at all. I am also not a fan of "kitchen sink" supplements like this one. Let's put everything in one supplement and hope that SOMETHING in there will work! Pleeeeeeze.

The study was quite weak on what the subjects actually DID, and comparing weight loss to fat loss, most loss almost the same amount of lean body mass as they did fat! That is NOT good as long term you may depress your metabolic rate.


Summary
Social support can make a difference, especially if combined with an intelligent strength training and nutrition plan. Most fat loss supplements have zero to a very small effect, spend your money on professional help instead of supplements! At least this company ran an actual trial and conducted some science, as most supplement companies do NOT do this. Just call and ask them.

Saturday, December 6, 2008

Supplement Usage: Protein Powder, Creatine, Beta Alanine, etc

(note: There were a few typos in the earlier version since I may have published an earlier rev. All fixed now--thanks Brad).

Question: So given the extensive information below (see this post HERE), what daily supplements do you take?
Charles


Answer:

Thanks for the good question!

Yep, the whole area of supplements can be incredibly confusing. Add in that some companies spend millions on advertising with normally little to zero scientific backing and the consumer is many times left confused.

Supplements are just that SUPPLEMENTS to a healthy lifestyle. I think it was Paul Chek that said something like (paraphrasing here), "supplement are like gold nails and food is like the wood. If you use gold nails to put together crappy wood (poor nutrition), it will not work very well."

I don't get too concerned over supplements until athletes can hit 90% compliance on their nutrition plan. There are times when I may add a supplement(s) sooner, but that depends on the time line I have and the issues that are going on. The following are ones I think most can use.

The list
1) Protein supplement: This is mostly just a convenience item since I like to have athletes get some protein at every meal. There are some data showing that the addition of a whey protein around training time is a big benefit (nutrient timing). Plus it is very convenient.

2) Fish oil/Essential Fatty Acids (EFAs): Most just don't get enough fish oils (EPA and DHA) or enough Omega 3 fatty acids (an EFA) in their diet, period. These oils are used EVERYWHERE in the body and are literally incorporated into almost EVERY CELL. No, these will not make you fat, and many times are the reason you are NOT deflating that spare tire. Are they "magical?"--no, but they are essential and most don't get enough.

3) Greens/fruit veggies supplement: Again for convenience. Just like EFAs, most don't eat enough fruit/veggies. They also lie their butts off and say they get "enough" as shown by studies where most OVER estimate how many servings of fruits/veggies they eat. There are some limited data that a more basic diet (think more fruits/veggies) is better for muscle growth too and general health.

4) Multi Vitamin: Don't go overboard on this, just cheap insurance.

Others to add:
5) Creatine monohydrate: Don't waste your money on any other form as there are virtually zero studies showing any additional benefit. Plus this form is by far the cheapest. There are some newer data showing possible cool neuro protective effects too. Side effects in almost every study have been extremely minor.

Optional depending on goals:
6) Beta Alanine: If you are doing some very high intensity work (e.g. repeated sprints, sports, intervals, etc) this may be one to try out. The current data looks promising, but it is far from conclusive. Personally, I notice a difference as beta alanine helps to buffer those pesky H ions (the ones that cause that burning feeling).
Be sure to check out this link to other beta alanine studies HERE.

7) L-Carnitine: Dave Barr is a big fan of this one. Check out his info HERE. There was one study showing that L Carnitine may need high levels of insulin in order to "push" it in.

8) Anti oxidants: Vit C and Vit E are the big ones. Remember that any antioxidant can be a PRO oxidant at a high enough dose so don't go crazy. Notice a moderation theme yet?

9) Vit D: Esp is you live in a northern climate in the winter (uh, like Minnesota). I personally promote more vacations to warm climates, but that is not always possible. See this link for a cool study I put up the other day on Vit D and muscle growth/strength.

10) Probiotic: These work to help restore the healthy bacteria in your gut. If you have had antibiotics within the past 1-2 years and any digestion issues, this would be worth a try in most cases.

11) Proteolytic Enzymes: These can work to push down inflammation and promote healing. Most need higher doses between meals though, but they seem to work great for acute/chronic injuries/pain. Mobility work like Z Health is HUGE for those issues too.

For me personally, I typically use
Protein powder, Udo's oil (EFAs), creatine, L carnitine (with pro/cho drink around training time), beta alanine (when doing more intervals and trying to increase CRF), Vit C (500 mg), Vit E (400 IUs).

If I travel, I may use a bit more since my access to fruits/veggies/food is more limited.

I take 2 hours on Sundays to prepare all my food for the week so I am good to go come Monday AM. I use Dr. John Berardi's Precision Nutrition system---it rocks!

Summary
I know that seems like a lot, but most are not using all of these at the same time and not right away. Get your nutrition in order first. There are some many compounds in food that we have no idea about yet. I think broccoli alone has something like 300 different polyphenols in it.

Your mom was right, eat your fruits and veggies.

Thoughts? What do you current use? Results?

Monday, November 10, 2008

Charles Staley Seminar: Dave Barr and Supplements


Alright! I am finally getting to type up some notes for all of you from Staley’s Seminar in AZ. I really appreciate your patience as I had some work on my study that I had to get done. The notes will be a bit cryptic so be sure to ask questions about anything.

Dave Barr
I got to crash in a room with Dave Barr while I was there (thanks again buddy!). I literally got off the super shuttle in front of the hotel room on Friday night and him and Dr. Lonnie Lowery were headed off to dinner; so I joined in. If you are in the area in AZ, be sure to check out the Tilted Kilt—great place! It was so good we ended up there 2 times that night as we hit it up again when Rob “Fortress” Fortney got into town. We had a blast and more to come on that soon.

Dave Barr—supplements and stuff

Leucine is amazing stuff and can directly stimulate anabolic (build things up like muscle tissue) processes in the body

How much?
Current thoughts are 20 gm of leucine per day, divided in 4 doses for about 3 weeks.
Pre lifting and 1 hr before meals are best
If you want to be in an anabolic state, you need more calories than you are spending!!

Elephant in the room is the nervous system (NS).
What the hell is going on with it?

How to optimize the NS
Fish oils/ Omega 3s
Load fish oils for 3 weeks
About 20 gram of Carlsons fish oil
Mike’s note
I did the math and that is about 3 TABLEspoons of Carlsons a day

Cassandra mentioned that there is a cold distillation fish oil out now—mimahi?

Vit E
Go with about 400 IU per day

Fat Loss
NS is key here again! (I am nodding my head)
Control insulin
Calories—yes, control them but not all calories are the same
Add more fiber like powdered glucomnnan to yogurt
Flax fiber is great
Mike’s note---I put flax seeds in my coffee grinder and it works great and saves me some coin!
Green tea is great for anti oxidants
Need more anti oxidants as metabolic rate increases
“If you are not happy with your results, then fix it!”

I got there a bit late from lunch, so I missed the first part of his talk where he was talking about protein pulse feeding. In short, protein should be "pulsed" during the day and not held at a steady constant--it should go up and down a bit. Layne Norton (PhD candidiate) and Dr. Donald Layman have done some really cool work on this lately showing that even if protein levels are held high for up to 6 hours, anabolic processes (protein synthesis) start to go back down around 3 hours or so in INSPITE of high protein (amino acid) levels.

Take away--5 to 6 meals a day may be the max for number of meals to elicit the most anabolic processess. This is all cutting edge and still highly debateable.

Be sure to check out Dave's books on "The Anabolic Index" HERE. In the interest of full disclosure, I do highly recommend the books and I get ZERO money so far to plug his stuff. Heck, I even bought both copies with my own hard earned cash.

Any questions, post them below!
Rock on
Mike N

Tuesday, November 4, 2008

Glutamine and Weight Training: Worth Your Money?


Greetings!

Just a quick new study today and more info soon on the Z Health/ Dragon Door event that I was helping with this past Sat and Sun. A quick hello to all that I met there and please drop me an email and keep in touch.

Staley Seminar info soon, I just need to carve out time to get the notes typed up.

Here is a new abstract showing that glutamine once again is not worth your money. While the chance that it MAY help gut health is more of an open question, I would personally not spend money on it.

Get the rest of your nutrition, movement and training in order first. I use Precision Nutrition, Z Health, and Kettlebells along with some basic lifts wtih my clients/athletes.

Once you have everything else dialed in and you can hit 90% compliance for 4 weeks, then try to add ONE thing and monitor the results. I would put BCAAs and creatine at the top of the list for extra supplements to try well before glutamine (protein powder and fish oil/EFAs I count more as a food than a supplement).

Here is the abstract and judge for yourself.

Dosing and efficacy of glutamine supplementation in human exercise and sport training.
Gleeson M.

J Nutr. 2008 Oct;138(10):2045S-2049S
School of Sport and Exercise Sciences, Loughborough University, Loughborough LE11 3TU England.

Some athletes can have high intakes of l-glutamine because of their high energy and protein intakes and also because they consume protein supplements, protein hydrolysates, and free amino acids. Prolonged exercise and periods of heavy training are associated with a decrease in the plasma glutamine concentration and this has been suggested to be a potential cause of the exercise-induced immune impairment and increased susceptibility to infection in athletes. However, several recent glutamine feeding intervention studies indicate that although the plasma glutamine concentration can be kept constant during and after prolonged strenuous exercise, the glutamine supplementation does not prevent the postexercise changes in several aspects of immune function. Although glutamine is essential for lymphocyte proliferation, the plasma glutamine concentration does not fall sufficiently low after exercise to compromise the rate of proliferation. Acute intakes of glutamine of approximately 20-30 g seem to be without ill effect in healthy adult humans and no harm was reported in 1 study in which athletes consumed 28 g glutamine every day for 14 d. Doses of up to 0.65 g/kg body mass of glutamine (in solution or as a suspension) have been reported to be tolerated by patients and did not result in abnormal plasma ammonia levels.

However, the suggested reasons for taking glutamine supplements (support for immune system, increased glycogen synthesis, anticatabolic effect) have received little support from well-controlled scientific studies in healthy, well-nourished humans.

Thursday, October 23, 2008

Charles Staley Seminar Update and Exericse in a Pill?

Staley Seminar Wrap Up

The Staley Seminar in AZ this past weekend was AWESOME! I will have a full update starting next week and I learned tons of new stuff. It was great to see old friends like Dr. Lonnie Lowery and Dave Barr--I got off the shuttle to the hotel and ran into them walking out the door for dinner on Friday night, so perfect timing. The Tilted Kilt in Scottdale is a great place for dinner! It was so good we went back there twice in one night (longer story).

It was great to meet new people also such as Cassandra Forsythe-New Last Name (I owe you some studies and follow up yet, great to meet ya in person), Rob "Fortress" Fortney who has the most hilarious stories ever and is a huge metal music fan, Anthony Almada, all the presenters on both days, Nick Nillson (nice to chat business and thanks for the rides around), Phil Stevens (last time I saw Phil was Test Fest in DC), Matt and Vick from CT (nice to chat and thanks for the coffee Vick), and everyone else there I met and special thanks to Charles and friends of course for putting it all together and Velocity sports for the use of their venue. Great times!

Exercise in a Pill?
Below is a great short article just published the other day in the New England Journal of Medicine about exercise in a pill. Great stuff.

NEJM Vol 359:1842-1844 October 23, 2008 Number 17

The Exercise Pill — Too Good to Be True?

Laurie J. Goodyear, Ph.D.

PubMed Citation Regular physical exercise has undisputed health benefits in the prevention — and in some cases, the treatment — of many diseases. The problem is that for the great majority of Americans, probably as much as 70% of the population, there is an inability or unwillingness to meet the minimum physical activity guidelines established by the American College of Sports Medicine. The idea of taking a pill to gain the benefits of exercise is extremely attractive for the millions of "couch potatoes." A recent study by Narkar et al.1 suggests that a couple of molecules could mimic some effects of exercise training. Skeletal muscle is an extraordinary tissue that is critical not only in locomotion but also in controlling an organism's metabolic homeostasis. Skeletal muscles are composed of different types of elongated, multinucleated cells called myofibers. Type I myofibers have a slow-twitch speed of contraction, are exceedingly oxidative, and have a reddish appearance. Type II myofibers have a faster-twitch speed of contraction, can have both oxidative and glycolytic metabolic properties, and are fairly white in appearance. Skeletal muscle is highly adaptable, or plastic, in that exercise training effects a change in metabolic and contractile properties of the myofibers. For aerobic exercise training, such as running and swimming, myofibers take on a slow-twitch phenotype, with an increase in the levels of oxidative enzymes, glycogen, and glucose transporter 4 (GLUT4), the protein that transports glucose into the muscle. These changes are accompanied by an increase in insulin sensitivity of the muscle and an overall improvement in glucose homeostasis in the body. When a rodent or human becomes inactive, a number of myofibers may convert to the fast-twitch phenotype, making them less able to perform sustained aerobic work and contributing to an insulin-resistant state.

See the rest of the article by clicking HERE

Tuesday, October 21, 2008

Supplements to Naturally Increase Testosterone?

I had some questions recently if there are any compounds around that may help to increase testosterone "naturally" and if there are any data to support it.

In short, there are few but the 2 most popular appear to be 6-OXO and Novedex (product name). Both are in a class called aromatase inhibitors and they work to prevent the formation of estradiol, a female hormone, by interfering with an aromatase enzyme. Aromatase inhibitors work by inhibiting the action of the enzyme aromatase, which converts androgens into estrogens by a process called aromatization.

Clinically, there are drugs that do this and they are used as a potential treatment for breast cancer since breast tissue is stimulated by estrogens, thus decreasing their production is a way of suppressing recurrence of the breast tumor tissue.

So as we just learned in this short and FREE organic chemistry lesson, aromatase is responsible for the conversion of testosterone to estrogen. Blocking aromatase causes the body to decrease its levels of estrogen (primarily estradiol for those uber geeks out there), this results in increase of LH and finally testosterone. And the people rejoice!

This is all find and dandy, but are there any over the counter (currently) supplements that can do this? Here are 2 studies on two of them (below)

Another class of compounds that are supposed to have similar effects are methoxyisoflavone, ecdysterone, and sulfo-polysaccharide supplementation. There is a study and my notes on those at the end also.

On to the science!

Effects of eight weeks of an alleged aromatase inhibiting nutritional supplement 6-OXO (androst-4-ene-3,6,17-trione) on serum hormone profiles and clinical safety markers in resistance-trained, eugonadal males.


Rohle D, Wilborn C, Taylor L, Mulligan C, Kreider R, Willoughby D. Department of Health, Human Performance, and Recreation, Baylor University, Box 97313, Waco, TX 76798, USA. darryn_willoughby@baylor.edu.


ABSTRACT: The purpose of this study was to determine the effects of 6-OXO, a purported nutritional aromatase inhibitor, in a dose dependent manner on body composition, serum hormone levels, and clinical safety markers in resistance trained males. Sixteen males were supplemented with either 300 mg or 600 mg of 6-OXO in a double-blind manner for eight weeks. Blood and urine samples were obtained at weeks 0, 1, 3, 8, and 11 (after a 3-week washout period). Blood samples were analyzed for total testosterone (TT), free testosterone (FT), dihydrotestosterone (DHT), estradiol, estriol, estrone, SHBG, leutinizing hormone (LH), follicle stimulating hormone (FSH), growth hormone (GH), cortisol, FT/estradiol (T/E).


Blood and urine were also analyzed for clinical chemistry markers. Data were analyzed with two-way MANOVA. For all of the serum hormones, there were no significant differences between groups (p > 0.05). Compared to baseline, free testosterone underwent overall increases of 90% for 300 mg 6-OXO and 84% for 600 mg, respectively (p < style="font-weight: bold;">


Conclusion: Body composition did not change with supplementation (p > 0.05) and clinical safety markers were not adversely affected with ingestion of either supplement dose (p > 0.05). While neither of the 6-OXO dosages appears to have any negative effects on clinical chemistry markers, supplementation at a daily dosage of 300 mg and 600 mg for eight weeks did not completely inhibit aromatase activity, yet significantly increased free testosterone, dihydrotestosterone, and free testosterone /estradiol.



My notes:
So this small study shows that this supplement does cause some increase in testosterone and its anabolic friends although I hate it when only percentages from BASELINE are reported since it can be completely misleading.

BUT there were no body composition changes. Hmmmm. If it was increasing muscle and/or decreasing fat there would have been some body composition change. It did appear to be safe in those doses for a short length of time.



Eight weeks of aromatase inhibition using the nutritional supplement Novedex XT: effects in young, eugonadal men.

Willoughby DS, Wilborn C, Taylor L, Campbell W.

Department of Health, Human Performance, and Recreation, Baylor University, Waco, TX 76798-7313, USA.

This study examined the effects of an aromatase-inhibiting nutritional supplement on serum steroid hormones, body composition, and clinical safety markers. Sixteen eugonadal young men ingested either Novedex XT or a placebo daily for 8 wk, followed by a 3-wk washout period. Body composition was assessed and blood and urine samples obtained at weeks 0, 4, 8, and 11.


Data were analyzed by 2-way repeated-measures ANOVA. Novedex XT resulted in average increases of 283%, 625%, 566%, and 438% for total testosterone (P=0.001), free testosterone (P=0.001), dihydrotestosterone (P=0.001), and the testosterone:estrogen ratio (P=0.001), respectively, whereas fat mass decreased 3.5% (P=0.026) during supplementation. No significant differences were observed in blood and urinary clinical safety markers or for any of the other serum hormones (P>0.05).

Conclusion: This study indicates that Novedex XT significantly increases serum androgen levels and decreases fat mass.

My Notes:
See my thoughts above about percentages. Although this one did show some body comp changes which is good. Hormones are completely non linear and while more (in general) is good of our anabolic friends, this does have a limit where the optimal amount should be is up for debate. Remember, the body has all sorts of feedback systems in place for good reason and what goes up must come down at some point.

I do like that this study was a double blind, placebo controlled flavor. Body fat was done by DEXA (gold standard), although it was statistically significant--it was still very small. I pulled the full study and it is only about 1-2 lbs total change (effect size of 0.6 for the stats geeks out there). The variation also on the changes in hormones was huge, although there did appear to be a statistical/significant change, we are still stuck that lean body mass did NOT change.

Interestingly enough, while marketed to change estrogen levels (which should therefore change testosterone levels), it was shown to NO decrease on estrogen and a non significant INCREASE in E1, E2 and E3.

So, some hormones may change but it did NOT appear to alter body composition in this study. The study was funded by Gaspari Nutrition and I do applaud them for doing a randomized, double blind study. This is WELL beyond what most supplement companies do.

Effects of methoxyisoflavone, ecdysterone, and sulfo-polysaccharide supplementation on training adaptations in resistance-trained males.

Wilborn CD, Taylor LW, Campbell BI, Kerksick C, Rasmussen CJ, Greenwood M, Kreider RB. Human Performance Lab, University of Mary Hardin Baylor, Belton, TX.

PURPOSE : Methoxyisoflavone (M), 20-hydroxyecdysone (E), and sulfo-polysaccharide (CSP3) have been marketed to athletes as dietary supplements that can increase strength and muscle mass during resistance-training. However, little is known about their potential ergogenic value. The purpose of this study was to determine whether these supplements affect training adaptations and/or markers of muscle anabolism/catabolism in resistance-trained athletes.

METHODS : Forty-five resistance-trained males (20.5 +/- 3 yrs; 179 +/- 7 cm, 84 +/- 16 kg, 17.3 +/- 9% body fat) were matched according to FFM and randomly assigned to ingest in a double blind manner supplements containing either a placebo (P); 800 mg/day of M; 200 mg of E; or, 1,000 mg/day of CSP3 for 8-weeks during training. At 0, 4, and 8-weeks, subjects donated fasting blood samples and completed comprehensive muscular strength, muscular endurance, anaerobic capacity, and body composition analysis. Data were analyzed by repeated measures ANOVA.

RESULTS : No significant differences (p > 0.05) were observed in training adaptations among groups in the variables FFM, percent body fat, bench press 1 RM, leg press 1 RM or sprint peak power. Anabolic/catabolic analysis revealed no significant differences among groups in active testosterone (AT), free testosterone (FT), cortisol, the AT to cortisol ratio, urea nitrogen, creatinine, the blood urea nitrogen to creatinine ratio. In addition, no significant differences were seen from pre to post supplementation and/or training in AT, FT, or cortisol.

CONCLUSION : Results indicate that Methoxyisoflavone, 20-hydroxyecdysone, and sulfo-polysaccharide supplementation do not affect body composition or training adaptations nor do they influence the anabolic/catabolic hormone status or general markers of catabolism in resistance-trained males.

My notes:
Don't even bother wasting ANY of your money on these. Historically this class of supplements has a horrible track record. The only thing they are good for is dropping some weight from your wallet. If anyone has any peer reviewed research that otherwise, please post it in the comments.

Thursday, August 7, 2008

Fish Oil and Stroke? More Fishy Stuff from Japan

I am on a fish oil kick lately with all the new research coming out. Here is another one! I put my thoughts at the end.

Reduction in the recurrence of stroke by eicosapentaenoic acid for hypercholesterolemic patient: subanalysis of the JELIS trial [Stroke. 2008]

Stroke. 2008 Jul;39(7):2052-8. Epub 2008 May 1.

Reduction in the recurrence of stroke by eicosapentaenoic acid for hypercholesterolemic patients: subanalysis of the JELIS trial. Tanaka K, Ishikawa Y, Yokoyama M, Origasa H, Matsuzaki M, Saito Y, Matsuzawa Y, Sasaki J, Oikawa S, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K; JELIS Investigators, Japan.

BACKGROUND AND PURPOSE: The JELIS trial examined the preventive effect of eicosapentaenoic acid (EPA) against coronary artery diseases. Hypercholesterolemic patients received statin only (no EPA group: n=9319) or statin with EPA (EPA group: n=9326) for around 5 years. EPA significantly suppressed the incidence of coronary events in previous analysis. Herein, we investigated the effects of EPA on the primary and secondary prevention of stroke.

METHODS: We conducted a subanalysis of JELIS with respect to stroke incidence in the primary and secondary prevention subgroups defined as those without and with a prior history of stroke using Cox proportional hazard ratios, adjusted for baseline risk factor levels.

RESULTS: As for primary prevention of stroke, this occurred in 114 (1.3%) of 8862 no EPA group and in 133 (1.5%) of 8841 EPA group. No statistically significant difference in total stroke incidence (Hazard Ratio, 1.08; 95% confidence interval, 0.95 to 1.22) was observed between the no EPA and the EPA groups. In the secondary prevention subgroup, stroke occurred in 48 (10.5%) of 457 no EPA group and in 33 (6.8%) of 485 EPA group, showing a 20% relative reduction in recurrent stroke in the EPA group (Hazard Ratio, 0.80; 95% confidence interval, 0.64 to 0.997).

CONCLUSIONS: Administration of highly purified EPA appeared to reduce the risk of recurrent stroke in a Japanese population of hypercholesterolemic patients receiving low-dose statin therapy. Further research is needed to determine whether similar benefits are found in other populations with lower levels of fish intake.

My Notes: In general I am not a huge fan of subanalysis since statistically speaking you can end up with some weaker conclusions, but still evidence that the fish oil EPA (the other fish oil is DHA) are healthy. It should also be noted that these patients were on a statin drug (to lower cholesterol), so it is unclear if you are NOT on a statin if the results would be similar.

Wednesday, August 6, 2008

Something Fishy in Japan--Fish Oil and Heart Health

Marine-Derived n-3 Fatty Acids and Atherosclerosis in Japanese, Japanese-American, and White Men: A Cross-Sectional Study -- Sekikawa et al. 52 (6): 417 -- Journal of the American College of Cardiology

Objectives: We sought to examine whether marine-derived n-3 fatty acids are associated with less atherosclerosis in Japanese versus white populations in the U.S.

Background: Marine-derived n-3 fatty acids at low levels are cardioprotective through their antiarrhythmic effect.

Methods: A population-based cross-sectional study in 281 Japanese (defined as born and living in Japan), 306 white (defined as white men born and living in the U.S.), and 281 Japanese-American men (defined as Japanese men born and living in the U.S.) ages 40 to 49 years was conducted to assess intima-media thickness (IMT) of the carotid artery, coronary artery calcification (CAC), and serum fatty acids.

Results: Japanese men had the lowest levels of atherosclerosis, whereas whites and Japanese Americans had similar levels. Japanese had 2-fold higher levels of marine-derived n-3 fatty acids than whites and Japanese Americans in the U.S. Japanese had significant and nonsignificant inverse associations of marine-derived n-3 fatty acids with IMT and CAC prevalence, respectively. The significant inverse association with IMT remained after adjusting for traditional cardiovascular risk factors. Neither whites nor Japanese Americans had such associations. Significant differences between Japanese and whites in multivariable-adjusted IMT (mean difference 39 µm, 95% confidence interval [CI]: 21 to 57µm, p <> 2.9% to 18.4%, p = 0.007) became nonsignificant after we adjusted further for marine-derived n-3 fatty acids (22 µm, 95% CI: –1 to 46 µm, p = 0.065 and 5.0%, 95% CI: –5.3% to 15.4%, p = 0.341, respectively).

Conclusions: Very high levels of marine-derived n-3 fatty acids have antiatherogenic properties that are independent of traditional cardiovascular risk factors and may contribute to lower the burden of atherosclerosis in Japanese, a lower burden that is unlikely the result of genetic factors.

My notes: While there is data on both sides of the fence in patients that have an implanted ICD (an internal defibrilator to shock the heart back to normal), this study shows that fish oil is heart healthy. Yet another study to take fish oil!


SOURCE Heartwire

The low rate of atherosclerosis and heart disease in Japanese people may be related to their very high levels of marine-derived omega-3 fatty acids rather than genetic factors, a new study suggests [1].

The study, published in the August 5, 2008 issue of the Journal of the American College of Cardiology (available online July 28), was conducted by a group led by Dr Akira Sekikawa (University of Pittsburgh, PA, and Shiga University of Medical Science, Japan).

They found that compared with white or Japanese American men living in the US, Japanese men living in Japan had twice the blood levels of omega-3 fatty acids a finding that was independently linked to low levels of atherosclerosis.

"The death rate from coronary heart disease in Japan has always been puzzlingly low. Our study suggests that the very low rates of coronary heart disease among Japanese living in Japan may be due to their lifelong high consumption of fish," Sekikawa said.

The researchers note that coronary heart disease (CHD) mortality in Japan has been decreasing since the 1970s, despite the changes in lifestyle toward Westernization that have brought a continuous increase in dietary fat intake and serum cholesterol. They point out that recent studies in Japan, where fish intake is one of the highest in the world, showed that additional supplementation or intake of marine-derived omega-3 fatty acids is significantly associated with a reduced risk of nonfatal coronary events. They thus conducted the current study to investigate whether greater levels of serum marine-derived omega-3 fatty acids in Japanese men vs white men are associated with lower levels of atherosclerosis.

The study, known as Electron-Beam Tomography, Risk Factor Assessment Among Japanese and US Men in the Post-World War II Birth Cohort (ERA JUMP) included 868 randomly selected men aged 40 to 49. Of these, 281 were Japanese men living in Japan; 306 were white men living in the US, and 281 were third- or fourth-generation Japanese American men from Hawaii. All study participants had a physical examination, completed a lifestyle questionnaire, and had blood tests to measure cholesterol levels and levels of omega-3 fatty acids. Atherosclerosis was assessed by measuring carotid intima-medial thickness (IMT) and coronary artery calcification (CAC).

Results showed that the Japanese men had the lowest levels of atherosclerosis, whereas whites and Japanese Americans had similar higher levels. The Japanese men also had twofold higher levels of marine-derived omega-3 fatty acids than white and Japanese Americans.

In addition, the significant differences between Japanese and American men in multivariable-adjusted IMT and CAC prevalence became nonsignificant after adjustment further for marine-derived omega-3 fatty acids.

The researchers say: "Our results suggest that marine-derived omega-3 fatty acids have antiatherogenic effects, especially at the high levels observed in Japanese men," a hypothesis they note is supported by two recent Japanese studies. The Japan Eicosapentaenoic Acid Lipid Interventions Study (JELIS) randomized trial showed a reduced CHD rate with eicosapentaenoic acid (EPA), and the Japan Public Health Center-Based (JPHC) study, a 10-year prospective cohort study of 41,578 middle-aged Japanese subjects, showed significant inverse associations between dietary intake of marine-derived omega-3 fatty acids and nonfatal coronary events.

They point out that in the current study, Japanese American men had similar or greater levels of atherosclerosis compared with US white men, a finding that they say was unexpected and was still apparent after they excluded those with diabetes, those with hypertension, and those taking lipid-lowering medications, indicating that the low atherosclerosis in Japanese men is unlikely to be primarily a result of genetic factors.

"Our findings indicate that the antiatherogenic effect of marine-derived omega-3 fatty acids is likely to be present only in populations with fish intake well above those of most Western populations. It thus appears unlikely that short-term supplementation in a low-fish-intake population would show such a relationship," Sekikawa et al comment.

They conclude: "If the high intake of marine-derived omega-3 fatty acids in Japanese men is the primary reason for their extremely low CHD mortality in the face of high traditional cardiovascular risk factors, dietary interventions to increase marine-derived omega-3 fatty acids in the US and other countries where fish intake is not as high as in Japan could have a very substantial impact on CHD."

The Japanese factor
In an accompanying editorial [2], Dr William Harris (Sanford Research/University of South Dakota [USD], Metabolism and Nutrition Research Center, Sioux Falls, South Dakota) notes that with the adoption of a more Western lifestyle, Japanese men have been found to have similar lifetime cholesterol and blood-pressure levels as white men in the US, along with a greater rate of smoking and prevalence of diabetes, but CHD rates in Japan remain less than one-half of those in the US. "This unexpected finding has stimulated the search for a factor or factors in the Japanese diet or lifestyle that have the power to withstand the onslaught of advancing risk factors," Harris comments, adding that the results of the current study add weight to the idea that omega-3 fatty acids could be that factor.

Harris reports that the Japanese consume between eight and 15 times more EPA and docosahexaenoic acid (DHA) than typical Westerners, but omega-3 intakes in Japan are only one-quarter of those in Eskimos, the population that birthed the omega-3 hypothesis, with studies conducted 30 years ago showing unusually low cholesterol and triglyceride levels and MI [myocardial infarction] rates in Greenland Inuit despite a diet very low in fruits, vegetables, and complex carbohydrates and high in fat.

But no match for Western saturated fat levels?
But he points out that more recent evidence from the Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) study indicates that carotid atherosclerosis is not only unrelated to omega-3 fatty-acid intakes in this cohort, but its prevalence is now greater than that in US white populations. At least part of the problem in Alaska appears to be not a lack of omega-3 but the introduction of massive amounts of saturated fats into their Westernizing diet, Harris suggests, noting that a similar situation is also being seen in Norway. "The Japanese experience, when contrasted to that of the Inuit and the Norwegians, suggests that the cardioprotective punch of the long-chain omega-3 fatty acids may be no match for diets high in fat, particularly saturated fat," he comments.

Harris notes that while relatively short-term studies of high-dose omega-3 fatty acids have shown no effect on atherosclerosis progression, observational studies have shown slower progression of coronary artery disease in individuals with higher levels of DHA. "These findings suggest the not-unreasonable hypothesis that decades of a moderately high omega-3 dietary intake may be the best way to slow atherosclerosis. The observations of Sekikawa et al harmonize with this view and strongly suggest that the 'Japanese factor' is likely to be omega-3 fatty acids," he concludes.

The National Institutes of Health and the Japanese Ministry of Education, Culture, Sports, Science and Technology supported this study. Dr. Harris is a scientific advisor and speaker for GlaxoSmithKline (which now markets Lovaza, the prescription omega-3), and he is an advisor to and receives grants from Monsanto, which is developing a soybean-based omega-3-enriched oil.

Sources

  1. Sekikawa A, Curb JD, Ueshima H, et al. Marine-derived n-3 fatty acids and atherosclerosis in Japanese, Japanese-American, and white men. A cross-sectional study. J Am Coll Cardiol. 2008;52:417-424.
  2. Harris W. Omega-3 fatty acids: The "Japanese" factor? J Am Coll Cardiol. 2008;52:425-427.


Thursday, July 31, 2008

Research Review--HMB, A New Review Published


Up now is a great review of the sports supplement HMB. I met Jacob briefly at ACSM and he hinted at some new data on HMB and it is released now.

You may remember HMB as being popular about 10 years ago (or maybe not). There were some great studies (not sure I agree with that) on it, but in reality it just never seemed to pan out. It did not help that the patent on it was held by Dr. Nissen--Hmmm. This is not inherently bad, but makes you want to dig a little deeper. See the patent HERE for yourself. Although HMB has sort of stood the test of time as it is still around and from a research stand point, we could learn some cool stuff.

Background
HMB, or "beta-hydroxy beta-methylbutyrate", is a second downstream metabolite of the amino acid Leucine and is produced naturally by the human body. HMB is produced from a metabolite of leucine, called ketoisocaproate (KIC), by the enzyme KIC-dioxygenase. If you have been around for a bit like myself, you will remember KIC as a supplement too. Personally, it did not do squat for me and tasted absolutely horrible and was stupid expensive. I worked at a supplement store while I was going to college the first 8 years and got it for dirt cheap when it did not sell it. It was back when they sold things in actual glass containers! I am feeling old now.

I will hold any future thought for now since the review is very comprehensive and all the others did their homework on it. Writing a review is a MUCH bigger pain in the butt than most realized, so kudos to them for all the outstanding work on it. It allows people like myself (and you) to sit back with a good cup of dark coffee and read the most recent work without spending hours and hours combing through 100+ papers.

Here is a link to the FULL study

Effects of beta-hydroxy-beta-methylbutyrate (HMB) on exercise performance and body composition across varying levels of age, sex, and training experience: A review.

Wilson GJ
, Wilson JM, Manninen AH.

Division of Nutritional Sciences, University of Illinois, Urbana, Illinois, USA. gwilson@abcbodybuilding.com.

ABSTRACT: The leucine metabolite beta-hydroxy-beta-methylbutyrate (HMB) has been extensively used as an ergogenic aid; particularly among bodybuilders and strength/power athletes, who use it to promote exercise performance and skeletal muscle hypertrophy. While numerous studies have supported the efficacy of HMB in exercise and clinical conditions, there have been a number of conflicting results. Therefore, the first purpose of this paper will be to provide an in depth and objective analysis of HMB research. Special care is taken to present critical details of each study in an attempt to both examine the effectiveness of HMB as well as explain possible reasons for conflicting results seen in the literature. Within this analysis, moderator variables such as age, training experience, various states of muscle catabolism, and optimal dosages of HMB are discussed. The validity of dependent measurements, clustering of data, and a conflict of interest bias will also be analyzed. A second purpose of this paper is to provide a comprehensive discussion on possible mechanisms, which HMB may operate through. Currently, the most readily discussed mechanism has been attributed to HMB as a precursor to the rate limiting enzyme to cholesterol synthesis HMG-coenzyme A reductase.

However, an increase in research has been directed towards possible proteolytic pathways HMB may operate through. Evidence from cachectic cancer studies suggests that HMB may inhibit the ubiquitin-proteasome proteolytic pathway responsible for the specific degradation of intracellular proteins. HMB may also directly stimulate protein synthesis, through an mTOR dependent mechanism. Finally, special care has been taken to provide future research implications.

Any comments, let me know.
Rock on
Mike N

Tuesday, July 29, 2008

Performance Research for June: Protein Synthesis--How to Use Research to Get Hyooooge


So I am a few months behind on research updates, but have no fear as more good stuff is coming. For June some great studies on pre and post protein and carbohydrate beverages, NSAIDs (like Advil) and their effects on muscle growth, and some molecular mechanisms in action.

Be sure to check out my previous post HERE on protein synthesis (adding muscle) and what you can do to maximize it based on bleeding edge research.

If all this crazy research makes your head spin back like a Pez dispenser and just want to get the plan and get started today, check out Jimmy Smith's Physique Formula.

Let's get to it

Differential effects of resistance and endurance exercise in the fed state on signaling molecule phosphorylation and protein synthesis in human muscle.

Wilkinson SB, Phillips SM, Atherton PJ, Patel R, Yarasheski KE, Tarnopolsky MA, Rennie MJ. McMaster University.

Resistance (RE) and endurance (EE) exercise stimulate mixed skeletal muscle protein synthesis. The phenotypes induced by RE (myofibrillar protein accretion) and EE (mitochondrial expansion) training must result from differential stimulation of myofibrillar and mitochondrial protein synthesis. We measured the synthetic rates of myofibrillar and mitochondrial proteins and the activation of signaling proteins (Akt-mTOR-p70S6K) at rest and after an acute bout of RE or EE in the untrained state and after 10 wk of RE or EE training in young healthy men. While untrained, RE stimulated both myofibrillar and mitochondrial protein synthesis, 67% and 69% (P<0.02), p=" 0.05)." style="font-weight: bold;">

Conclusion: Chronic resistance exercise (wt training) or endurance exercise training modifies the protein synthetic response of functional protein fractions, with a shift toward exercise phenotype-specific responses, without an obvious explanatory change in the phosphorylation of regulatory signaling pathway proteins.

My notes: sounds like the SAID principle in action! The body is adapting specifically to the stimulus (exercise)

Essential amino acid and carbohydrate ingestion prior to resistance exercise does not enhance post-exercise muscle protein synthesis.

Fujita S, Dreyer HC, Drummond MJ, Glynn EL, Volpi E, Rasmussen BB.University of Tokyo. Ingestion of an essential amino acid-carbohydrate (EAA+CHO) solution following resistance exercise enhances muscle protein synthesis during post-exercise recovery. It is unclear whether EAA+CHO ingestion prior to resistance exercise can improve direct measures of post-exercise muscle protein synthesis (FSR; fractional synthetic rate). We hypothesized that EAA+CHO ingestion prior to a bout of resistance exercise would prevent the exercise-induced decrease in muscle FSR and would result in an enhanced rate of muscle FSR during post-exercise recovery. We studied 22 young healthy subjects before, during, and for 2 hr following a bout of high-intensity leg resistance exercise. The Fasting control group (N=11) did not ingest nutrients and the EAA+CHO group (N=11) ingested a solution of EAA+CHO 1 hr prior to beginning the exercise bout. Stable isotopic methods were used in combination with muscle biopsies to determine FSR. Immunoblotting procedures were utilized to assess cell signaling proteins associated with the regulation of FSR. We found that muscle FSR increased in the EAA+CHO group immediately following EAA+CHO ingestion (P<0.05),>0.05). Eukaryotic elongation factor 2 phosphorylation was reduced in both groups at 2 hr post-exercise (EAA+CHO: 39+/-7%; Fasting: 47+/-9%; P<0.05). style="font-weight: bold;">

Conclusion: We conclude that essential amino acids and carbs (EAA+CHO) ingestion prior to resistance exercise does not enhance post-exercise fractional synthesis rate (FSR--Fractional Synthetic Rate--aka rate of adding protein to muscles) as compared to exercise without nutrients.

My note--while this interesting, I would not dump your protein carb drink before lifting just yet. Based on info from Dave Barr (source, AI and personal conversation) moving it to 15 minutes before training may be more ideal. Stay tuned!

Gene expression profiling in human skeletal muscle during recovery from eccentric exercise.

Mahoney DJ, Safdar A, Parise G, Melov S, Fu M, MacNeil L, Kaczor J, Payne ET, Tarnopolsky MA. Department of Medical Sciences, McMaster University Medical Center, 1200 Main Street W., Hamilton, Ontario, Canada. We used cDNA microarrays to screen for differentially expressed genes during recovery from exercise-induced muscle damage in humans. Male subjects (n = 4) performed 300 maximal eccentric contractions, and skeletal muscle biopsy samples were analyzed at 3 h and 48 h after exercise. In total, 113 genes increased 3 h postexercise, and 34 decreased. At 48 h postexercise, 59 genes increased and 29 decreased. On the basis of these data, we chose 19 gene changes and conducted secondary analyses using real-time RT-PCR from muscle biopsy samples taken from 11 additional subjects who performed an identical bout of exercise.
Real-time RT-PCR analyses confirmed that exercise-induced muscle damage led to a rapid (3 h) increase in sterol response element binding protein 2 (SREBP-2), followed by a delayed (48 h) increase in the SREBP-2 gene targets Acyl CoA:cholesterol acyltransferase (ACAT)-2 and insulin-induced gene 1 (insig-1). The expression of the IL-1 receptor, a known regulator of SREBP-2, was also elevated after exercise. Taken together, these expression changes suggest a transcriptional program for increasing cholesterol and lipid synthesis and/or modification. Additionally, damaging exercise induced the expression of protein kinase H11, capping protein Z alpha (capZalpha), and modulatory calcineurin-interacting protein 1 (MCIP1), as well as cardiac ankryin repeat protein 1 (CARP1), DNAJB2, c-myc, and junD, each of which are likely involved in skeletal muscle growth, remodeling, and stress management.

Conclusion: In summary, using DNA microarrays and RT-PCR, we have identified novel genes that respond to skeletal muscle damage, which, given the known biological functions, are likely involved in recovery from and/or adaptation to damaging exercise.

My notes: I wonder why all this muscle physiology stuff is so elusive, to quote the authors "In total, 113 genes increased 3 h postexercise, and 34 decreased." That is a lot of stuff going on! Still wondering if you need to damage the muscle for it to increase in size?

Post exercise carbohydrate-protein supplementation: phosphorylation of muscle proteins involved in glycogen synthesis and protein translation.

Ivy JL, Ding Z, Hwang H, Cialdella-Kam LC, Morrison PJ.Exercise Physiology and Metabolism Laboratory, Department of Kinesiology and Health Education, The University of Texas, Austin, Texas 78712-0360, USA. johnivy@mail.utexas.edu The enzymes Akt, mTOR, p70(S6K), rpS6, GSK3, and glycogen synthase interact in the control of protein and/or glycogen synthesis in skeletal muscle, and each has been found to respond to exercise and nutrient supplementation. In the present study, we tested the hypothesis that nutrient supplementation post exercise, in the form of a carbohydrate-protein (CHO-PRO) supplement, would alter the phosphorylation state of these enzymes in a manner that should increase muscle protein and glycogen synthesis above that produced by exercise alone. After a 45 min cycling session followed by sprints and again 15 min later, the subjects (n = 8) ingested 400 ml of a CHO-PRO drink (7.8% dextrose and 1.8% protein-electrolyte) or a placebo drink, as assigned using a randomized, counter-balanced design with repeated measures. Biopsies of the vastus lateralis were taken before exercise and at 45 min of recovery.
At 45 min after supplementation, CHO-PRO treatment yielded greater phosphorylation of Akt (65%), mTOR (86%), rpS6 (85-fold), and GSK3alpha/beta (57%) than pre-exercise levels (p < style="font-weight: bold;">

Conclusion: These results suggest that a post exercise carb and protein (CHO-PRO) supplement alters the phosporylation levels of the enzymes tested in a manner that should accelerate muscle glycogen synthesis and protein initiation during recovery from cycling exercise.

My notes: cool info, but I would like to see this carried out in the future to any performance changes. This would say that it should help. I am sure that is in the pipeline and there is some data already out in that area

The effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance training.

Krentz JR, Quest B, Farthing JP, Quest DW, Chilibeck PD. High doses of ibuprofen have been shown to inhibit muscle protein synthesis after a bout of resistance exercise. We determined the effect of a moderate dose of ibuprofen (400 mg.d-1) consumed on a daily basis after resistance training on muscle hypertrophy and strength. Twelve males and 6 females (~24 years of age) trained their right and left biceps on alternate days (6 sets of 4-10 repetitions), 5 d.week-1, for 6 weeks.
In a counter-balanced, double-blind design, they were randomized to receive 400 mg.d-1 ibuprofen immediately after training their left or right arm, and a placebo after training the opposite arm the following day. Before- and after-training muscle thickness of both biceps was measured using ultrasound and 1 repetition maximum (1 RM) arm curl strength was determined on both arms.
Subjects rated their muscle soreness daily. There were time main effects for muscle thickness and strength (p < style="font-weight: bold;">

Conclusion: We conclude that a moderate dose of ibuprofen ingested after repeated resistance training sessions does not impair muscle hypertrophy or strength and does not affect ratings of muscle soreness.

My Notes: If you would have asked me even a few months ago, I would have said that the use of NSAIDs (like Advil) is not a good idea as it may limit muscle growth (hypertrophy). After talking to some at ACSM, looking at some newer litature, I am thinking it will probably be ok. It may even be beneficial after an acute injury to keep your movement quality better and limit pain, thus reducing the chance on longer term chronic pain ala the neuromatrix of pain. See the following posts on that below

Pain Perception and the Neuromatrix--Guest Blog by Katelin Bigelow

Pre-emptive Analgescis--what is he talking about now?


Cellular and molecular events controlling skeletal muscle mass in response to altered use.

Favier FB, Benoit H, Freyssenet D.Unité Physiologie et Physiopathologie de l’Exercice et Handicap, IFR143, Université Jean Monnet, 15 rue Ambroise Paré, 42023, Saint Etienne, cedex 2, France.
Gain or loss of skeletal muscle mass occurs in situations of altered use such as strength training, aging, denervation, or immobilization. This review examines our current understanding of the cellular and molecular events involved in the control of muscle mass under conditions of muscle use and disuse, with particular attention to the effects of resistance exercise/training. The DNA content, which is a critical determinant of protein synthesis by providing the amount of DNA necessary to sustain gene transcription, can be either increased (activation of satellite cells) or decreased (apoptosis) depending on muscle activity and ongoing physiological processes. In addition, several transcription factors are sensitive to functional demand and may control muscle-specific protein expression to promote or repress myofiber enlargement. The control of skeletal muscle mass is also markedly mediated by the regulation of transduction pathways that promote the synthesis and/or the degradation of proteins. Insulin-like growth factor-I plays a key role in this balance by activating the Akt/tuberous sclerosis complex 2/mammalian target of rapamycin pathway.

Conclusion: Stimulation of this pathway leads to the concomitant activation of initiation and elongation factors resulting in the elevation of protein translation and the downregulation of ubiquitin proteasome components through Forkhead-box O transcription factors.

My Notes: Good review (with lots of big words), but the take away is still the same--USE IT OR LOSE IT!

Rock on
Mike N

Friday, June 6, 2008

Research Review: Protein Synthesis Part I

Here are some cool, cutting edge studies below on protein synthesis for you!


A few key points to remember

  • Ideally, a study would measure protein increases (fractional synthesis rate, increase in lean body mass, etc) or what is referred to as an anabolic process (which means "building stuff" and this stuff can be muscle, fat, bone, etc) AND protein break down referred to as a catabolic process ("breaking down stuff"). The balance will hopefully be positive (if we are talking protein, bone, but not fat!)
  • Similar to your checking account. If you only look at the money coming in you are only seeing half of it!

In a perfect world, we would know how much muscle/strength was added (performance effect)

  • Creatine kinase (CK) and other items are used to look at muscle breakdown/injury. Some injury is needed for growth (how much, when, for how long, no one really knows) but we really want to look at body composition and performance changes. Incidentally, even though CK is measured is lots of studies, is it very poorly correlated to performance changes.

Protein/carbohydrate timing is a whole book on to its self. A few key points to look for are:

  • Fasting or in a fed state? Most athletes will be in a fed state prior to training
  • Training stimulus? Aerobic (running), or Anaerobic (weight training) or something in-between?
  • How long did they look? 30 min? 48 hrs? Some literature suggests that a response from weight training may last at least 48 hours or even longer!

Here you go! Part II will be out tomorrow with some conclusions. ACSM updates will be coming soon
Any questions, thoughts let me know
Mike N


The effects of the 5-HT2C agonist m-chlorophenylpiperazine on elite athletes suffering from unexplained underperformance syndrome (overtraining)

Conclusion: “The study suggests that this adaptation may be lost in athletes with UUPS (unexplained, underperformance syndrome): this might explain some of their observed symptoms.”

Effect of a Pre-Exercise Energy Supplement on the Acute Hormonal Response to Resistance Exercise

Conclusion: “The enhanced exercise performance resulted in a significantly greater increase in both growth hormone and insulin concentrations, indicating an augmented anabolic hormone response to this pre-exercise S.”

Co-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men

Conclusion: “Co-ingestion of leucine with carbohydrate and protein following physical activity does not further elevate muscle protein fractional synthetic rate in elderly men when ample protein is ingested.”

Leucine-enriched essential amino acid and carbohydrate ingestion following resistance exercise enhances mTOR signaling and protein synthesis in human muscle

Conclusion: “The data suggest that enhanced activation of the mTOR (mammalian target of rapamycin) signaling pathway is playing a role in the greater synthesis of muscle proteins when resistance exercise is followed by EAA+CHO (Essential Amino Acids + Carbohydrates) ingestion.”

Amino acid metabolism and regulatory effects in aging.

Conclusion: “Muscle loss with aging is associated with significant changes in amino acid metabolism, which can be acutely reversed using nutritional manipulations and exercise. Long-term, large clinical trials are, however, needed to determine the clinical significance of these findings in the elderly population, and to establish if nutritional and exercise interventions can help prevent and treat sarcopenia.”

Branched-chain amino acid supplementation and indicators of muscle damage after endurance exercise.

Conclusion: “The data suggest that BCAA (branched-chain amino acid) supplementation attenuates muscle damage during prolonged endurance exercise in untrained college-age men. CHO (Carbohydrates) ingestion attenuates CK (Creatine kinase) activities at 24 and 48 h postexercise as compared with a placebo beverage.”

Exercise- and nutrient-controlled mechanisms involved in maintenance of the musculoskeletal mass.

Conclusion: “Exercise not only stimulates protein synthesis in muscle, but also in tendon; and disuse atrophy is accompanied by marked decreases of both muscle and tendon collagen protein synthesis. Bone collagen synthesis appears to be nutritionally regulated by the availability of amino acids, but not lipid or glucose.”

Saturday, May 31, 2008

ACSM Random Updates

Greetings from ACSM! Just waiting to fly back home soon and wanted to drop some random notes. I will have more updates coming in the next few weeks as I get threw over 40 pages of notes. Excellent information presented!

Here they are random, rapid fire style. More details soon
Inspiration Muscle Training
  • May work really really well. Poster from highly competitive cross country runners showed a shaving of 40 seconds off 5km times!! That is insane!
Central Pattern Generation
  • May be located in the spinal cord! The basic program for gait appears to be there too. Huge implications for spinal cord injury patients.
  • Gait has a normal variability to it on each step, we need to replicate this to obtain a normal gait again in rehab areas
  • Injuries will alter your gait (I see that all the time)
  • Interlimb coordination more important than INTRAlimb coordination
  • Rats with full spinal cord cut at around the top of the lumbar area can walk sideways and backwards on a treadmill on 2 legs with body weight support. No input from the brain--must be a FEED FORWARD mechanism on some level
Central vs Peripheral Fatigue
  • Studies, posters point to some of each
  • BCAAs don't seems to decrease central fatigue (although tyrosine seems to work)
Brain and Cognition and Exercise
  • Brain will adapt by increasing neurons
  • Brain actually increases in size and weight!! (Up to a limit)
  • Enriched environment is important, not just exercise---new movements, use of visual system
  • Exercise has an anti-depressant activity
Creatine
  • New mechanisms--potential cognition and ergogenic benefits
  • Full details soon
Random Tidbits
  • Vit D RDA most likely to increase dramatically soon
  • Women athletes should probably have ferritin iron test and Vit D test done
  • Talk by top protein researchers on protein and exercise--more info soon
  • Beta Alanine seems to work great in elite wrestlers (source--conversation on unpublished work)
  • NSAIDS and training may NOT interfere with each other

More soon!
Any questions in the meantime, post them here
Mike