Morphological Hypertrophic Muscle Adaptations (aka “I Wanna Get Hyoooge!!”)

Morphological Hypertrophic Muscle Adaptations (aka, Mechanisms Behind “I Wanna Get Hyoooge!!”)

Pop your head into just about any gym in America, and observe the male population (especially the younger ones) train. While the training methods are interesting in themselves, the common battle cry of the young Arnold wannabes is usually the same “I Wanna Get Hyoooge.” In an effort to explore the mechanisms behind the scenes in the body to help out these “bros” it is time to board the magical muscle mystery tour. Tour stops include a drive by of the nervous system, muscle fiber types, and how muscles adapt to exercise to get bigger and badder (as in a Michael Jackson “bad” is now good way).

Before we dive in head first into this, we need to do a short little anatomy tour. They say a picture is worth a thousand words, so check out figure below.

This time around I will spare you all the details on the exact names of each, but notice how a single fiber at the end goes into another group of fibers and then THAT group goes into another group until we are all the way up to the muscle itself. Muscle fibers can be broadly defined as type2 fast twitch or type 1 slow twitch (8). Fast twitch (type 2) fibers can produce more force, but they don’t last as long (26). Think of an NFL lineman. He can produce a ton of force to knock you into next week, but it is unlikely he will be chasing your around the block or very far at all. Type 2 (slow twitch) muscle fibers are like the slower cousin to the type 2, think energizer bunny. They can’t produce as much force, but they keep going and going and going and going………..

Remember that the nervous system is the head cheese, numero uno, el presidente, the commander in charge that controls all muscle movements. The nervous system also controls which fibers are type 1 or 2! Buller et al. (9) in 1960, carefully did the ole “switcheroo” on cats and switched nerves and a type 2 muscle fiber with a new type 1 NERVE now took on the properties of a type 1 muscle fiber! Think of this as “what the commander says goes.”
Another key point is that “living systems are build up through use and atrophy (get smaller) with disuse.” So when you are in the gym blasting away, you are actually making your muscle SMALLER! Yikes! The good part is that your body responds by BUILDING up those damaged fibers during the recovery period (33). So next time you do a similar exercise, the body has “new and improved” muscle tissue to better handle the damage. Pretty sweet!

Muscle Growth Time
Skeletal muscle is a very dynamic tissue capable of adapting to the stress placed on it. The process of exercise-induced adaptation in skeletal muscle involves a multitude of signaling mechanisms all the way down to the genetic level, ultimately putting together strings of amino acids to form new proteins in the form of more muscle tissue (10). Whooo ha, and the gym “bros” rejoice!

As mentioned, muscle growth is commonly referred to as “hypertrophy” (34) or more accurately as an increase in muscle fiber SIZE. How does this happen? While a complete answer to that question is beyond this short article, what do you think are some key processes? “TESTOSTERONE!” Good guess and there is a fair amount of data to support this (16, 17, 29, 30), there is also data (although less) to show that in castrated (denutted—youch!!!) animals (yeah I know it was not done in humans but do you want to volunteer for those studies?) are still able to increase muscle size despite having testosterone levels at very low levels (22, 24). “NUTRITION!” Yes, there is no denying that nutrition especially extra calories and protein are needed for muscle hypertrophy (11, 13, 19) but even in caloric restriction muscles can still get bigger (12). “INSULIN!” While insulin is the most anabolic (building) hormone in the body, it is not required either (7). (Side note, I am using the term “anabolic” in the physiologic sense where it is taking small things and making bigger things with them. This can be proteins into new muscle or fatty acids into new fat storage around your waist. And yes, too much insulin can make you a fat bastard). So the muscle building process is a complicated one.

How Do These Genes Look
Further down the hole, we have a whole slew of molecular signaling guys, some newly discovered like Mighty that can dramatically influence muscle growth. Mighty is a downstream metabolite of myostatin. Most have probably heard of myostatin now or seen the huge picture of the Belgium Bull.

Belgian Blue Bulls (say that fast three times in a row) have a mutation in the myostatin gene that produces a truncated, ineffective form of the protein (20), so in English there is almost no myostatin hanging around. The absence of myostatin allows unchecked muscle growth and interferes with fat deposition; the result is a lean, “double-muscled” bull. Yikes! Remember that LESS myostatin = MORE muscle.

The new kid on the block now is Mighty. Mighty is expressed in a variety of different tissues but appears to be specifically regulated by myostatin in skeletal muscle. Overexpression of Mighty in certain cells (ok, C2C12 cells if you really want to know) results in enhanced and accelerated differentiation and hypertrophy of myotubes (this is good for muscle growth, trust me) and leads to increased and earlier expression of MyoD and insulin like growth factor II (IGF-II) (both are good for muscle growth) (23).

Enough Biochem Yacking already
So I spared you from a detailed talk on Interleukin-4 (IL-4) and interleukin-13 (IL-13) that are involved in getting hyoooge (27), so be thankful! Watch out—Geek alert! Serrano et al. (28) recently showed a role for IL-6 in hypertrophic muscle growth and provide mechanistic evidence for the contribution of satellite cells to this process, in our fury friends the mouse.

So back to our irregularly scheduled program. So far we know 1) nutrition is key-calories and protein are needed to build muscle 2) we need a stimulus—weight training works well here (31) 3) certain hormonal and biochemical changes need to take place—from hormonal changes down to even the molecular level.
Shut Up Already and Tell Me HOW to Get Hyoooooooooge!
During short term studies of less than 10 weeks, it was shown that type 2 fibers hypertrophy (get bigger) much faster from training than their slow cousins the Energizer bunny type 1 fibers (1). MacDougall et al.(21) however investigated a longer time period of 5–6 months of heavy resistance training (weight lifting) in seven males and demonstrated a significant cross sectional increase in type 2 AND type 1 fibers; so long term it appears that BOTH fiber types can increase in size. Take home message, use a wide variety of reps.

Damage Plan
The goal of some dedicated Arnold wannabes is to destroy tissue! No pain no gain! Go hard or go home! Is there any research to support this method if we can get hyoooooooooge? There is actually some evidence to support this notion. Goldspink about 30 years ago proposed that if you literally tear the muscle fiber in half (these would be very small tears of course), that this may promote splitting of the muscle fibers once the body goes to work repairing those fibers; thus resulting in more fibers over time. More fibers= more size. The fancy word associated with increasing muscle fiber NUMBER is hyperplasia. The downside is that this phenomena is highly debatable with virtually the studies being conducted on animals (primarily cats and birds), so how it applies to humans is not currently known (2-6, 15, 18, 32).

We know that eccentric (lowering a heavy weight) can scramble the muscle fibers (induce lots of damage) and it appears that fiber disruption induced by habitual weightlifting exercise is essentially repaired after 5 days of inactivity in trained men (14) and oxidative stress indices changed significantly with most peaking at 48 hours (25).

What does any of this mean?
Although data is somewhat limited on the “destroy tissue” approach in relation to hypertrophy there is enough to support the idea for muscle hypertrophy, but keep in mind that your recovery time may be longer with this approach. Your muscles get bigger OUTSIDE the gym when they are repairing!

Conclusion
Thus ends our very brief ride on the magically, muscle mystery tour! I hoped you have enjoyed the tour and kept your hands inside the bus at all times. We got to spend some time in the land of the nervous system, fiber types, stimulus for adaptation (aka weight training), and the adaptation process itself. The take away is that muscle hypertrophy is a complicated process and our best bet in the quest for huge-dom is 1) excellent nutrition with a surplus of calories and proteins and 2) consistent weight training with adequate time for recovery; especially if eccentric movements are used to induce muscle damage.
Time to get to the gym!

Mike T. Nelson has a BA in Natural Science, a MS in Mechanical Engineering (Biomechanics) and is currently a PhD student in Kinesiology (Exercise Physiology) at the University of Minnesota. His research interests are on the effects of energy drinks on metabolic health and the nervous system.

References
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4. Antonio J, WJ Gonyea. Role of muscle fiber hypertrophy and hyperplasia in intermittently stretched avian muscle. J Appl Physiol. . 1993; 74(4):1893-8.
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7. Bolster DR, LS Jefferson, SR Kimball. Regulation of protein synthesis associated with skeletal muscle hypertrophy by insulin-, amino acid- and exercise-induced signalling. Proc Nutr Soc. . 2004; 63(2):351-6.
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13. Dreyer HC, MJ Drummond, B Pennings, et al. Leucine-enriched essential amino acid and carbohydrate ingestion following resistance exercise enhances mTOR signaling and protein synthesis in human muscle. Am J Physiol Endocrinol Metab. . 2008; 294(2):E392-400.
14. Gibala MJ, SA Interisano, MA Tarnopolsky, et al. Myofibrillar disruption following acute concentric and eccentric resistance exercise in strength-trained men. Can J Physiol Pharmacol. . 2000; 78(8):656-61.
15. Giddings CJ, WJ Gonyea. Morphological observations supporting muscle fiber hyperplasia following weight-lifting exercise in cats. Anat Rec. . 1992; 233(2):178-95.
16. Herbst KL, S Bhasin. Testosterone action on skeletal muscle. Curr Opin Clin Nutr Metab Care. . 2004; 7(3):271-7.
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18. Kelley G. Mechanical overload and skeletal muscle fiber hyperplasia: a meta-analysis. J Appl Physiol. . 1996; 81(4):1584-8.
19. Kerksick CM, B Leutholtz. Nutrient administration and resistance training. J Int Soc Sports Nutr. . 2005; 2:50-67.
20. Li ZB, HD Kollias, KR Wagner. Myostatin directly regulates skeletal muscle fibrosis. J Biol Chem. . 2008; 283(28):19371-8.
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22. Mackova EV, P Hnik. Some hormonal factors (hypophysectomy, castration and testosterone administration) modifying the course of "compensatory" muscle hypertrophy in the rat. Physiol Bohemoslov. . 1976; 25(4):325-32.
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24. Max SR, NE Rance. No effect of sex steroids on compensatory muscle hypertrophy. J Appl Physiol. . 1984; 56(6):1589-93.
25. Paschalis V, MG Nikolaidis, IG Fatouros, et al. Uniform and prolonged changes in blood oxidative stress after muscle-damaging exercise. In Vivo. . 2007; 21(5):877-83.
26. Powers SK, ET Howley. Exercise Physiology : Theory and Application to Fitness and Performance. McGraw-Hill Humanities/Social Sciences/Languages; 2006. p. 624.
27. Prokopchuk O, Y Liu, L Wang, K Wirth, D Schmidtbleicher, JM Steinacker. Skeletal muscle IL-4, IL-4Ralpha, IL-13 and IL-13Ralpha1 expression and response to strength training. Exerc Immunol Rev. . 2007; 13:67-75.
28. Serrano AL, B Baeza-Raja, E Perdiguero, M Jardi, P Munoz-Canoves. Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy. Cell Metab. . 2008; 7(1):33-44.
29. Singh R, JN Artaza, WE Taylor, NF Gonzalez-Cadavid, S Bhasin. Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway. Endocrinology. . 2003; 144(11):5081-8.
30. Sinha-Hikim I, SM Roth, MI Lee, S Bhasin. Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men. Am J Physiol Endocrinol Metab. . 2003; 285(1):E197-205.
31. Spiering BA, WJ Kraemer, JM Anderson, et al. Resistance exercise biology : manipulation of resistance exercise programme variables determines the responses of cellular and molecular signalling pathways. Sports Med. . 2008; 38(7):527-40.
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33. Wernig A. Regeneration capacity of skeletal muscle. Ther Umsch. . 2003; 60(7):383-9.
34. Wilmore JH, DL Costill. Physiology of Sport and Exercise, Fourth Edition. Human Kinetics Publishers; 2007. p. 574.

Happy Halloween and Updates

Updates
To all those that celebrate Halloween--Happy Halloween!

Fitcast Interview
Kevin Larabee gave me an opportunity to yack about Z Health and other training items over at the Fitcast and answer some questions. Special thanks to Kevin and check out the interview HERE. Be sure to listen to the podcast version of the Fitcast each week too at the same link or look for it on iTunes. Kevin does a great job and I listen in every week.

Staley Updates
Staley Seminar updates will start next week. I had to push them out a bit since I need to finish up my IRB questions for my upcoming research study.

New Article Up
Brand new original article is up in another blog entry for this date on muscle growth

Z Health Seminar Friday to Sunday with Dragon Door
If you happen to read this and are in town for the seminar, I will be there helping out on Sat and Sun; so please say hi! It will be a great time.

Rock on
Mike N

International society of sports nutrition position stand: nutrient timing

Below is a great abstract/review of the latest science around nutrient timing. You can access the full version there too by clicking on the link. Highly recommended.

International society of sports nutrition position stand: nutrient timing

Chad Kerksick , Jeff Stout , Bill Campbell , Colin Wilborn , Richard Kreider , Doug Kalman , Tim Ziegenfuss , Hector Lopez , Jamie Landis , John Ivy and Jose Antonio

Journal of the International Society of Sports Nutrition 2008, 5:17doi:10.1186/1550-2783-5-17

Published:	3 October 2008

Abstract (provisional)

Position Statement: The position of the Society regarding nutrient timing and the intake of carbohydrates, proteins, and fats in reference to healthy, exercising individuals is summarized by the following eight points: 1.) Maximal endogenous glycogen stores are best promoted by following a high-glycemic, high-carbohydrate (CHO) diet (600 - 1000 grams CHO or ~ 8 - 10 g CHO/kg/d), and ingestion of free amino acids and protein (PRO) alone or in combination with CHO before resistance exercise can maximally stimulate protein synthesis. 2.) During exercise, CHO should be consumed at a rate of 30 - 60 grams of CHO/hour in a 6 - 8 % CHO solution (8 - 16 fluid ounces) every 10 - 15 minutes. Adding PRO to create a CHO:PRO ratio of 3 - 4:1 may increase endurance performance and maximally promotes glycogen re-synthesis during acute and subsequent bouts of endurance exercise. 3.) Ingesting CHO alone or in combination with PRO during resistance exercise increases muscle glycogen, offsets muscle damage, and facilitates greater training adaptations after either acute or prolonged periods of supplementation with resistance training. 4.) Post-exercise (within 30 minutes) consumption of CHO at high dosages (8 - 10 g CHO/kg/day) have been shown to stimulate muscle glycogen re-synthesis, while adding PRO (0.2 g - 0.5 g PRO/kg/day) to CHO at a ratio of 3 - 4:1 (CHO: PRO) may further enhance glycogen re-synthesis. 5.) Post-exercise ingestion (immediately to 3 h post) of amino acids, primarily essential amino acids, has been shown to stimulate robust increases in muscle protein synthesis, while the addition of CHO may stimulate even greater levels of protein synthesis. Additionally, pre-exercise consumption of a CHO + PRO supplement may result in peak levels of protein synthesis. 6.) During consistent, prolonged resistance training, post-exercise consumption of varying doses of CHO + PRO supplements in varying dosages have been shown to stimulate improvements in strength and body composition when compared to control or placebo conditions. 7.) The addition of creatine (Cr) (0.1 g Cr/kg/day) to a CHO + PRO supplement may facilitate even greater adaptations to resistance training. 8.) Nutrient timing incorporates the use of methodical planning and eating of whole foods, nutrients extracted from food, and other sources. The timing of the energy intake and the ratio of certain ingested macronutrients are likely the attributes which allow for enhanced recovery and tissue repair following high-volume exercise, augmented muscle protein synthesis, and improved mood states when compared with unplanned or traditional strategies of nutrient intake.

Exercise and Neurogenesis in the Mouse Brain

More information once again that exercise may help your brain function better! I know it is a fury critter study, but there are not many that are going to sign up for brain damage as part of a study (unless they already have brain damage).

Be sure to check the other blog entries such as
Be smart exercise your heart:exercise and cognition
and
Movement and brain deterioration-new study

The abstract:
Voluntary running rescues adult hippocampal neurogenesis after irradiation of the young mouse brain

Andrew S. Naylor*,†,‡, Cecilia Bull*,‡, Marie K. L. Nilsson§, Changlian Zhu*, Thomas Björk-Eriksson¶,‖, Peter S. Eriksson*, Klas Blomgren*,**,††, and H. Georg Kuhn*,

Cranial radiation therapy is commonly used in the treatment of childhood cancers. It is associated with cognitive impairments tentatively linked to the hippocampus, a neurogenic region of the brain important in memory function and learning. Hippocampal neurogenesis is positively regulated by voluntary exercise, which is also known to improve hippocampal-dependent cognitive functions. In this work, we irradiated the brains of C57/BL6 mice on postnatal day 9 and evaluated both the acute effects of irradiation and the effects of voluntary running on hippocampal neurogenesis and behavior 3 months after irradiation. Voluntary running significantly restored precursor cell and neurogenesis levels after a clinically relevant, moderate dose of irradiation. We also found that irradiation perturbed the structural integration of immature neurons in the hippocampus and that this was reversed by voluntary exercise. Furthermore, irradiation-induced behavior alterations observed in the open-field test were ameliorated. Together, these results clearly demonstrate the usefulness of physical exercise for functional and structural recovery from radiation-induced injury to the juvenile brain, and they suggest that exercise should be evaluated in rehabilitation therapy of childhood cancer survivors.

Fear, Turkey Time, and Weight Gain

Hard to believe that Thanksgiving day (for all of those in the USA) is only about 4 weeks away! Halloween is right around the corner!

Yes, it is that time of year when everyone seems to "magically" gain 5 pounds around the ole mid section until they decide Jan 1 to go on a diet.

How about this? Maybe, just maybe, this year you can do a pre-emptive strike and work to MAINTAIN your weight over the holidays. I recommend kettlebells and Z Health of course! Even if your weight is the same, you are already way ahead!

If fear is stopping you, check out this quote

Fear is the mind-killer.
Fear is the little-death that brings total obliteration.
I will face my fear.
I will permit it to pass over me and through me.
And when it has gone past I will turn the inner eye to see its path.
Where the fear has gone there will be nothing.
Only I will remain.
-Frank Herbert

Is only fear stopping you?

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

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.

Neuroscience Research Updates for October

Some fascinating brand new studies in the land of neuroscience recently. Check out the 3 studies and write ups below from our friends at PhysOrg.com

Any thoughts?
Mike N

Scientists restore movement to paralyzed limbs through artificial brain-muscle connections

Researchers in a study funded by the National Institutes of Health have demonstrated for the first time that a direct artificial connection from the brain to muscles can restore voluntary movement in monkeys whose arms have been temporarily anesthetized. The results may have promising implications for the quarter of a million Americans affected by spinal cord injuries and thousands of others with paralyzing neurological diseases, although clinical applications are years away.

"This study demonstrates a novel approach to restoring movement through neuroprosthetic devices, one that would link a person's brain to the activation of individual muscles in a paralyzed limb to produce natural control and movements," said Joseph Pancrazio, Ph.D., a program director at the National Institute of Neurological Disorders and Stroke (NINDS).

The research was conducted by Eberhard E. Fetz, Ph.D., professor of physiology and biophysics at the University of Washington in Seattle and an NINDS Javits awardee; Chet T. Moritz, Ph.D., a post-doctoral fellow funded by NINDS; and Steve I. Perlmutter, Ph.D., research associate professor. The results appear in the online Oct. 15 issue of Nature. The study was performed at the Washington National Primate Research Center, which is funded by NIH's National Center for Research Resources.

In the study, the researchers trained monkeys to control the activity of single nerve cells in the motor cortex, an area of the brain that controls voluntary movements. Neuronal activity was detected using a type of brain-computer interface. In this case, electrodes implanted in the motor cortex were connected via external circuitry to a computer. The neural activity led to movements of a cursor, as monkeys played a target practice game.

After each monkey mastered control of the cursor, the researchers temporarily paralyzed the monkey's wrist muscles using a local anesthetic to block nerve conduction. Next, the researchers converted the activity in the monkey's brain to electrical stimulation delivered to the paralyzed wrist muscles. The monkeys continued to play the target practice game—only now cursor movements were driven by actual wrist movements—demonstrating that they had regained the ability to control the otherwise paralyzed wrist.

The group's approach is one of several lines of current neuroprosthetic research. Some investigators are using brain-computer interfaces to record signals from multiple neurons and convert those signals to control a robotic limb. Other researchers have delivered artificial stimulation directly to paralyzed arm muscles in order to drive arm movement—a technique called functional electrical stimulation (FES). The Fetz study is the first to combine a brain-computer interface with real-time control of FES.

"A robotic arm would be better for someone whose physical arm has been lost or if the muscles have atrophied, but if you have an arm whose muscles can be stimulated, a person can learn to reactivate them with this technology," says Dr. Fetz.

Until now, brain-computer interfaces were designed to decode the activity of neurons known to be associated with movement of specific body parts. Here, the researchers discovered that any motor cortex cell, regardless of whether it had been previously associated with wrist movement, was capable of stimulating muscle activity. This finding greatly expands the potential number of neurons that could control signals for brain-computer interfaces and also illustrates the flexibility of the motor cortex.

"The cells don't have to have a preordained role in the movement. We can create a direct link between the cell and the motor output that the user can learn to control and optimize over time," says Dr. Fetz.

Dr. Fetz and his colleagues found that the monkeys' control over neuronal activity—and the resulting control over stimulation of their wrist muscles—improved significantly with practice. Practice time was limited by the duration of the nerve block. Comparing the monkeys' performance during an initial two-minute practice and a two-minute peak performance period, the scientists found the monkeys successfully hit the target three times more frequently and with less error during the peak performance. In the future, greater control could be gained by using implanted circuits to create long-lasting artificial connections, allowing more time for learning and optimizing control, Dr. Fetz says.

The researchers also found that the monkeys could achieve independent control of both the wrist flexor and extensor muscles.

"An important next step will be to increase the number of direct connections between cortical cells and muscles to control coordinated activation of muscles," says Dr. Fetz.

If researchers are able to establish a connection between the motor cortex and sites in the spinal cord below the injury, people with spinal injuries may be able to achieve coordinated movements.

Clinical applications are still probably at least a decade away, according to Dr. Fetz. Better methods for recording cortical neurons and for controlling multiple muscles must be developed, along with implantable circuitry that could be used reliably and safely, he says.

Source: National Institute of Neurological Disorders and Stroke

Mike says
If you liked this article, check out this one Army Funds "Synthetic Telepathy" Research from Wired Magazine

Experiments support alternative theory of information processing in the cortex

Neurons in the sound-processing part of the brain's cortex are experts at timing. With remarkable precision, they fire electrochemical pulses or "spikes" in sync with the cues they receive from other neurons, even when these cues are separated by very small time intervals.

A team of neuroscientists at Cold Spring Harbor Laboratory (CSHL), studying this phenomenon in rats, has demonstrated that "spike timing" in cortical neurons can influence behavior even at minuscule time intervals, more precise than previously imagined. Experiments focusing on the auditory cortex revealed that animals in the midst of decision-making have the ability to distinguish incoming signals separated by as little as three milliseconds.

Probing the relation of neuronal firing rates and behavior

The finding, published ahead of print October 12 in the online edition of Nature Neuroscience, adds to the current understanding of how neuronal activity in the brain's cortex modulates behavior. According to the standard model of cortical activity, behavior is thought to be determined by the rate of spiking -- the number of spikes occurring within a given interval. The CSHL team, led by Professor Anthony Zador, Ph.D., wanted to determine whether spike timing had any impact on decision-making and measure the shortest decision-driving interval between spikes.

Zador's group designed an experiment in which rats were trained to behaviorally distinguish between two sounds. When placed in a cage with two water outlets, the rats were trained to turn either to the left or to the right waterspout depending on the sound. The sounds were then replaced by electrical impulses delivered directly to two spatially separated groups of neurons in the auditory cortex. The animals were then re-trained so that simultaneous stimulation of both groups of neurons spurred the animal toward the left waterspout, whereas sequential stimulation of the neuron bundles led the animal to the right waterspout. The rats consistently homed to the right waterspout until the timing between the two sequential stimuli narrowed to below 3 milliseconds. "This suggests that the cortex is capable of 'reading out' very precise nuances in spike timing to drive behavior," says Zador.

Deciphering the "Neural Code"

The group's discovery helps make the case for an alternate theory of how the brain processes information. Neuroscientists have made vast leaps in understanding how neurons communicate with each other in the brain. But they are still in the dark about what the neuron-to-neuron message actually consists of and how it's processed. Known as the "neural code," this blueprint for the brain's information-processing language has proved to be much more elusive than language that is encoded in our genome, which was deciphered decades ago.

The prevailing theory behind the neural code is based on the observation that neurons spike faster when they are transmitting information. This supports a "rate" code model, which stipulates that information is contained within the spiking rate of the neuron. But the CSHL team's new data suggest that the neural code might actually be a "timing" code, where information is encoded within the precise pattern of spiking – something that can be deduced by examining how the spikes are distributed over time.

Zador explains the difference between the two possibilities by likening the brain to an office and neurons to the people working in the office. "If lots of people are talking within each department in a company, you might get a good idea of what's going on in the company by just measuring how loudly people are talking within a given department, which is what the classical 'rate' model predicts," he says.

But as Zador also observes, conversation is not just about loudness; it's also about the identity of the speakers, their speech patterns, etc. "Our results demonstrate directly that there is more to this 'office' than just how loudly people are talking, and motivate us to try to figure out what that extra dimension is," he says. He and his CSHL team will continue to probe for the answers as their work on this and related mysteries about neural communication continues.

Citation: "Millisecond-scale differences in neural activity in auditory cortex can drive decisions" appeared October 12, 2008 as an advance online publication in Nature Neuroscience. The complete citation is: Yang Yang, Michael R DeWeese, Gonzalo Otazu, Anthony M Zador. The paper is available online at http://www.nature.com/neuro/journal/vaop/ncurrent/scriptbs/nn.2211.html

Source: Cold Spring Harbor Laboratory

Emotion and scent create lasting memories -- even in a sleeping brain

When French memoirist Marcel Proust dipped a pastry into his tea, the distinctive scent it produced suddenly opened the flood gates of his memory.

In a series of experiments with sleeping mice, researchers at the Duke University Medical Center have shown that the part of the brain that processes scents is indeed a key part of forming long-term memories, especially involving other individuals.

"We can all relate to the experience of walking into a room and smelling something that sparks a vivid, emotional memory about a family member from years or even decades ago," says Stephen Shea, Ph.D., the lead author of the study published in The Journal of Neuroscience. "This research sought to understand that phenomenon on a cellular level."

The researchers examined how strong memories are formed by creating new memories in the minds of mice while under sedation and monitoring their response to a memory-inducing stimulus afterwards, when they were awake.

"Our work is unique because it allows us to examine the cellular make-up of a memory, evaluate how the neurons change when a memory is formed and learn how that memory affects behavior," Shea adds.

The researchers created memories by stimulating the release of noradrenaline, a chemical present in the body during strong emotional events ranging from excitement to fear.

Previous studies have established a link between noradrenaline and the formation of enduring memories, especially during intense social events such as mating and childbirth. In mice and humans, the presence of noradrenaline also creates changes in the odor processing center of the brain, called the olfactory bulb.

"When an animal forms a strong memory about another, it is reliant on odor cues and noradrenaline. Both need to be present at the same time in order for the memory to be formed," Shea says. "Long-term memories created under these conditions often result in a permanent change in behavior."

The Duke team administered anesthesia to a mouse and stimulated the release of noradrenaline with an electrode while wafting the scent of either food or the urine of another mouse under the nose.

"We wanted to see if these two elements – noradrenaline and odor – present at the same time were the key ingredients needed in the recipe for creation of memory – this is a concept that had not been directly tested before this study," Shea says. "In essence, we recreated the chemical reaction that would occur when the mouse experiences a social event, such as giving birth," Shea says.

Researchers knew they could observe brain activity in more detail when the mouse was under anesthesia. If awake, the mouse would be forming memories from the surrounding environment. "When the animal is asleep, you can watch neurons in the brain rewire to store a memory and once awake see what the mouse learned even though it was asleep when the memory was created."

What they saw was an approximate 40 percent reduction in neuron activation after triggering the noradrenaline release – suggesting that a memory of the odor had been formed.

A day later, after the mouse was awake, the team observed changes in behavior in response to the scents, showing that they remembered the smells from when they were asleep.

"This work may have implications for furthering our understanding of how long-lasting memories are formed that are important to social bonding," says Richard Mooney, Ph.D., co-author and associate professor of neurobiology.

Source: Duke University

Mobility Work Is the Missing Link for Fat Loss

I've been on the mobility soapbox as of late (see the posts Mobility and Mood, and also Dopamine, Mood, Movement and Exercise)

Mobility has a huge role I believe in long term fat loss, but probably not in the way you were thinking.

Behavior issues are full entwined into the reason for maintenance of fat loss, since nobody is putting food into your mouth other than yourself (in a vast majority of cases).

One thing that I think plays a HUGE role, although I don't see it talked about anywhere is how YOU (and your brain ) perceives your body.

Say I am overweight, I get my nutrition in order, hire a coach/trainer and drop 30 lbs of fat. Whoo ha!! Awesome work! Seriously that is an amazing job!!

The trick now is to no regain the fat! The issue I think is that most of the time, you still have a "fat person's maps." The brain integrates "movement maps" as I learned in Z Health R/I Phase taking inputs from the joints (proprioception), eyes (visual) and vestibular (inner ear/balance) to form my overall body map.

Now if I drop 30 lbs and I don't do any work (primarily mobility and some times visual/vestibular) to update my maps---at a base level my body is much thinner physically, but my brain still thinks I am 30 lb overweight! Uh oh. Guess what happens next----I will tend to slip back to behaviors that match what my brain perceives. This concept is taken from the book "The body has a mind of its own"

Physiology is messy, completely non linear and has lots of "bad" engineering words (anisotropic, etc). See the post You Body as a Black Box for more info.

It is my biased belief that for most people following a good nutrition system (I use Precision Nutrition) and intelligent training that work to update your body maps is the best direction to go for 95% of people. Plus most want to move and be treated like athletes So if you were to stop in at my place, you will only see the basics--a power rack, bars, kettlebells, sandbags, big tires, sledge hammers, etc. No fancy shining equipment but it gets results and is "fun" in a weird, twisted way. I think trainers should spent their money on top of the line BASIC equipment and then keep spending on education.

Speaking of education, I am off to Charles Staley's Training Sumitt in AZ now. See Wed's post for info and hope to see some of you there in AZ.

Exercise and Testosterone, A Quote and Charles Staley's Seminar

New Exercise Study, Cool Quote and in AZ this Weekend!

Very interesting study below from Dr. Kraemer and friends. Once again, it shows that animal studies tend to not match human studies, but those little critters are so much easier to study than humans!

While this study shows that testosterone did NOT change, this only applies to the specific exercise they used and was an acute study, so it did NOT look at any changes in protein synthesis (building muscle). We know from many other studies that lifting weights helps build muscle and strength, but the exact mechanism is pretty complicated.

Effect of Resistance Exercise on Muscle Steroidogenesis.

Vingren JL, Kraemer WJ, Hatfield DL, Anderson JM, Volek JS, Ratamess NA, Thomas GA, Ho JY, Fragala MS, Maresh CM.

J Appl Physiol. 2008 Oct 2. [Epub ahead of print]

University of Connecticut. Circulating testosterone is elevated acutely following resistance exercise (RE) and is an important anabolic hormone for muscle adaptations to resistance training. The purpose of this study was to examine the acute effect of heavy RE on intracrine muscle testosterone production in young resistance trained men and women. 15 young highly resistance trained men (n=8; 21+/-1 years, 175.3+/-6.7 cm, 90.8+/-11.6 kg) and women (n=7; 24+/-5 years, 164.6+/-6.7 cm, 76.4+/-15.6 kg) completed 6 sets of 10 repetitions of Smith's machine squats with 80% of their 1-repetition maximum. Before RE, and 10 min and 70 min after RE, muscle biopsies were obtained from the vastus lateralis.

Before RE, after 3 and 6 sets of squats, and 5, 15, 30 and 70 min into recovery from RE blood samples were obtained using venipuncture from an anticubital vein. Muscle samples were analyzed for testosterone, 17beta-hydroxysteroid dehydrogenase (HSD) type 3, and 3beta-HSD type 1-2 content. Blood samples were analyzed for the glucose and lactate concentrations. No changes were found for muscle testosterone, 3beta-HSD1-2, and 17beta-HSD3 concentrations. However, a change in protein migration in the Bis-Tris gel was observed for 17beta-HSD3 post-exercise; this change in migration indicated ~2.8 kd increase in molecular weight.

Conclusion: These findings indicate that species differences in muscle testosterone production may exist between rats and humans.

In humans, muscle testosterone concentrations do not appear to be affected by Resistance Exercise. This study expands on the current knowledge obtained from animal studies by examining resting and post-exercise concentrations of muscle testosterone and steroidogenic enzymes in humans.

Cool Quote
"Only in the absence of certainty can we have open-mindedness, mental flexibility and willingness to contemplate alternative ideas."

---Robert Burton from "The Certainty Bias"


Charles Staley's Training Summit
I am off to Charles Staley's Training Summit this weekend. It will be a short trip as I fly out Friday evening and then back on Monday. I am excited about seeing some people that I have not seen in a long time. I will be crashing in a room with Dave Barr, so that will be a trip! Be sure to check out his products the Anabolic Index books HERE (I get no money for any sales of his books and I do recommend them as I have both).

Charles Staley's Training Summit
Sunday, October 18 &19th, 2008
Scottsdale, AZ

If you are going to be there, please come up and say hi to me! I still need to find a place to crash on Sunday night, but I am sure something will work out.

The agenda (which may change at our discretion) is as follows:

Day 1 Oct 18th

8:00 AM Charles Staley
10:30 AM Phil Stevens
11:45 AM Lunch
1:00 PM Cassandra Forsythe
2:15 PM Robert Fortney
3:30 PM David Barr
4:45 PM Christopher Drummond
6:00 PM Optional Dinner

Day 2 Oct 19th

7:00 AM Dr. Lonnie Lowery
8:15 AM Tim Larkin
9:30 AM Luiz Da Silva
10:45 AM Lunch
12:00 PM Joe Micela
1:15 PM Anthony Almada
2:15 PM Joe Marsit
3:30 PM Q and A Roundtable

It will be a blast and I am looking forward to it. I will provide updates most likely once I return, so stay tuned!

Dopamine, Mood, Movement and Exercise

Good ole dopamine! Watch out, major geek alert ahead and it involves some biochemistry. I think everyone just clicked off, but hold that mouse as this will be a short crash course some cool stuff.

Dopamine is neurotransmitter with five flavors of dopamine receptors — D1, D2, D3, D4 and D5, and their variants. It works on the sympathetic nervous system (think "fight, flight or freeze"), producing effects such as increased heart rate and blood pressure. It canNOT cross the blood-brain barrier, so dopamine given as a DRUG (via injection etc) does not directly affect the central nervous system. To get around this, patients that need it (such as in Parkinson's disease) may take L-DOPA which is a precursor to dopamine.

Dopamine is also a precursor of norepinephrine (noradrenaline) and epinephrine (adrenaline) which qualifies it as a card carrying member of the catecolamine family. .

How does the body make it?
It is made in the body via hydroxylation (think oxidizing) the amino acid L-tyrosine to L-DOPA and then on to dopamine, which can then in turn go on to norepinephrine (noradrenaline) and epinephrine (adrenaline).


Can I increase dopamine without drugs?
Some have used L-tyrosine to possible increase dopamine levels, although more research is needed in this area. There are very few studies done on it and most seem to be split in terms of L-tyrosine enhancing exercise performance. One researcher I spoke to at ACSM this past year was quite convinced that L-tyrosine would enhance exercise performance based on his review of the literature (source: personal conversation).

Functions in the brain
Dopamine does tons of stuff in the brain. Everything from motor activity, motivation/reward, sleep, mood, learning and on down the list--yep, it is important!

Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment. Drugs like cocaine and amphetamines inhibit the RE- UPTAKE of dopamine; so there is more floating around in the brain to do its job. Cocaine is a dopamine transporter blocker that competitively inhibits dopamine uptake to increase the lifetime of dopamine and augments an overabundance of dopamine (an increase of up to 150 percent) within the parameters of the dopamine neurotransmitters; aka it cranks up the dopamine in your brain by a crap load!

Amphetamines are similar in structure to dopamine and sort "mimic it" They can actually enter presynaptic neuron and then shove the poor dopamine molecules out of their storage vesicles! Think of them as a drill sargent shoving you out of bed in the AM to get to work.

Obviously both of these drugs have consequences (like what goes up must come down) and are illegal. Although I remember asking my neuroscience prof a few years back that if Parkinson's patients have an issue with dopamine, what happens if you give them cocaine? I was actually serious!

We know that the body and mind are highly integrated. Below are some new abstracts showing the connection between exercise (movement) and dopamine. Be sure to check out a previous blog I did recently on Mood and Mobility.

Thoughts?

Neuroplasticity of dopamine circuits after exercise: implications for central fatigue.

Foley TE, Fleshner M. Department Integrative Physiology, Center for Neuroscience, Clare Small Building, University of Colorado-Boulder, Boulder, CO 80309-0354, USA.

Habitual exercise increases plasticity in a variety of neurotransmitter systems. The current review focuses on the effects of habitual physical activity on monoamine dopamine (DA) neurotransmission and the potential implication of these changes to exercise-induced fatigue. Although it is clear that peripheral adaptations in muscle and energy substrate utilization contribute to this effect, more recently it has been suggested that central nervous system pathways "upstream" of the motor cortex, which initiate activation of skeletal muscles, are also important. The contribution of the brain to exercise-induced fatigue has been termed "central fatigue." Given the well-defined role of DA in the initiation of movement, it is likely that adaptations in DA systems influence exercise capacity. A reduction in DA neurotransmission in the substantia nigra pars compacta (SNpc), for example, could impair activation of the basal ganglia and reduce stimulation of the motor cortex leading to central fatigue. Here we present evidence that habitual wheel running produces changes in DA systems. Using in situ hybridization techniques, we report that 6 weeks of wheel running was sufficient to increase tyrosine hydroxylase mRNA expression and reduce D2 autoreceptor mRNA in the SNpc. Additionally, 6 weeks of wheel running increased D2 postsynaptic receptor mRNA in the caudate putamen, a major projection site of the SNpc.

These results are consistent with prior data suggesting that habitually physically active animals may have an enhanced ability to increase DA synthesis and reduce D2 autoreceptor-mediated inhibition of DA neurons in the SNpc compared to sedentary animals. Furthermore, habitually physically active animals, compared to sedentary controls, may be better able to increase D2 receptor-mediated inhibition of the indirect pathway of the basal ganglia.

Conclusion: Results from these studies are discussed in light of our understanding of the role of DA (monoamine dopamine) in the neurobiological mechanisms of central fatigue.

Elevated central monoamine receptor mRNA in rats bred for high endurance capacity: implications for central fatigue.

Foley TE, Greenwood BN, Day HE, Koch LG, Britton SL, Fleshner M. Department of Integrative Physiology, University of Colorado, Boulder, CO 80309 0354, USA. teresa.foley@colorado.edu

Although alteration to peripheral systems at the skeletal muscle level can contribute to one's ability to sustain endurance capacity, neural circuits regulating fatigue may also play a critical role. Previous studies demonstrated that increasing brain serotonin (5-HT) release is sufficient to hasten the onset of exercise-induced fatigue, while manipulations that increase brain dopamine (DA) release can delay the onset of fatigue. These results suggest that individual differences in endurance capacity could be due to factors capable of influencing the activity of 5-HT and DA systems.

We evaluated possible differences in central fatigue pathways between two contrasting rat groups selectively bred for high (HCR) or low (LCR) capacity running. Using quantitative in situ hybridization, we measured messenger RNA (mRNA) levels of tryptophan hydroxylase (TPH), 5-HT transporter (5-HTT), 5-HT1A and 5-HT1B autoreceptors, dopamine receptor-D2 (DR-D2) autoreceptors and postsynaptic receptors, and dopamine receptor-D1 (DR-D1) postsynaptic receptors, in discrete brain regions of HCR and LCR. HCR expressed higher levels of 5-HT1B autoreceptor mRNA in the raphe nuclei relative to LCR, but similar levels of TPH, 5-HTT, and 5-HT1A mRNA in these areas. Surprisingly, HCR expressed higher levels of DR-D2 autoreceptor mRNA in the midbrain, while simultaneously expressing greater DR-D2 postsynaptic mRNA in the striatum compared to LCR. There were no differences in DR-D1 mRNA levels in the striatum or cortex between groups.

Conclusion: These data suggest that central serotonergic and dopaminergic systems may be involved in the mechanisms by which HCR (high capacity running) have delayed onset of exercise-induced fatigue compared to LCR (low capacity running).

Running wheel exercise enhances recovery from nigrostriatal dopamine injury without inducing neuroprotection.

O'Dell SJ, Gross NB, Fricks AN, Casiano BD, Nguyen TB, Marshall JF. Department of Neurobiology and Behavior, 1452 McGaugh Hall, University of California, Irvine, Irvine, CA 92697, USA. sjodell@uci.edu

Forced use of the forelimb contralateral to a unilateral injection of the dopaminergic neurotoxin 6-hydroxydopamine can promote recovery of motor function in that limb and can significantly decrease damage to dopamine terminals. The present study was conducted to determine (1) whether a form of voluntary exercise, wheel running, would improve motor performance in rats with such lesions, and (2) whether any beneficial effects of wheel running are attributable to ameliorating the dopaminergic damage. In experiment 1, rats were allowed to run in exercise wheels or kept in home cages for 2 1/2 weeks, then given stereotaxic infusions of 6-hydroxydopamine into the left striatum. The rats were replaced into their original environments (wheels or home cages) for four additional weeks, and asymmetries in forelimb use were quantified at 3, 10, 17, and 24 days postoperatively. After killing, dopaminergic damage was assessed by both quantifying 3 beta-(4-iodophenyl)tropan-2 beta-carboxylic acid methyl ester ([(125)I]RTI-55) binding to striatal dopamine transporters and counting tyrosine hydroxylase-positive cells in the substantia nigra.

Exercised 6-hydroxydopamine-infused rats showed improved motor outcomes relative to sedentary lesioned controls, effects that were most apparent at postoperative days 17 and 24. Despite this behavioral improvement, 6-hydroxydopamine-induced loss of striatal dopamine transporters and tyrosine hydroxylase-positive nigral cells in exercised and sedentary groups did not differ. Since prior studies suggested that forced limb use improves motor performance by sparing nigrostriatal dopaminergic neurons from 6-hydroxydopamine damage, experiment 2 used a combined regimen of forced plus voluntary wheel running. Again, we found that the motor performance of exercised rats improved more rapidly than that of sedentary controls, but that there were no differences between these groups in the damage produced by 6-hydroxydopamine.

Conclusion: It appears that voluntary exercise can facilitate recovery from partial nigrostriatal injury, but it does so without evident sparing of dopamine nerve terminals.

Testimonial and Bone Rhythm-Lift More Weight!

Shout out for Mike T Nelson and Z-Health Bone Rhythm
Recipe for some impressed fighters:
Step one:
Take an extremely fast kid and add years of stand up martial arts training.
Step two:
Take said fast kid as a busted up older guy, put him on PN (Precision Nutrition) as a moderator and have him read a post by Mike T Nelson about a Z-Health principle about levering your bones.
Step three:
Have busted up older guy mess with the idea with his jab and cross, but since he is busted up, he does it slowly and often over a couple of months.
Step four:
Have busted up older guy go for dinner with a bunch of fighters and explain the idea without showing the result. Then have bunch of fighters with blank looks on their faces say show me.
Step five:
Show the punch they have seen for years, then show the same punch with the added focus on levering the bones involved.
Step six:
Jaws drop as the speed was noticeably faster... way faster.

You likely are out of your tree most of the time, but no one in the tree ever made big changes, so Rock On!

I bet it's exciting to see the end of the tunnel with education. Exciting times ahead.

If I lived closer to you I'd camp out in your gym and on your couch. I think you're likely one of the most underrated people in this game.

Thanks Mike!!
Roland Fisher, CFT Canada

---Special thanks to Roland for all the super kind words. Be sure to check out Precision Nutrition where Roland and many other really bright people hang out and exchange great ideas. Thanks again!

Here is the information about Bone Rhythm from an older blog post I did. Eric Franklin talks about it also in his book Dynamic Alignment Through Imagery.

The Z Health Bone Rhythm method will revolutionize lifting as we know it today. Is that a bold statement--yes, and I stand behind it even though it sounds like I went swimming in the Z Kool Aid pool. It is the most radical change to lifting I have ever seen and my guess (I have no evidence of this yet) is that most elite lifters are already doing it and they probably don't realize it.

What is it? Basically you think about levering the bones in your skeleton to lift the weight. Wow, on a surface level that seems so darn simple. Let's take the squat as an example. For the squat you think about levering the femur (thigh bone) to move up the weight or bring it down. In a tall (neutral spine, that includes the head so no looking at the ceiling due to the extensor reflex--a whole different topic that I will cover soon), as you lower the weight you think about moving the top part of the femur near the hip back as you move the bottom part of the femur forward. Think of a teeter totter, as one end goes down, the other end MUST go up (assuming it is rigid and some fat ass did not break it). For optimal efficiency, BOTH ends MUST move at the same rate. This takes some practice and cueing for a coach to get it down, but it feels awesome.

Why is this so cool? You can lift more INSTANTLY and there is LESS stress on your joints! Read that again. Sounds like a win win to me if I have ever heard one. You can also increase your neural drive to the motion since your brain is only thinking of two things 1) neutral spine, 2) bone rhythm of the femur (in this case)! This allows you to use more of your brain (increased neural drive) to move the femur, thus moving the weight! You are much stronger than what you think you are.

Chad Watebury (1) pointed this out when he took athletes and had them do a set of squats normally, and then one other group that had to count backwards WHILE doing squats. Guess which one had their performance go into the hopper--yep, the ones counting backwards which makes perfect sense.

In this post is some more details and a before and after video HERE

Any questions?
Rock on!
Mike N

Z Health Seminar, New Sailing Speed Record, Five Finger Death Punch

Random Updates: Kiteboarding at 58 mph, Five Finger Death Punch and Z Health Seminar

As most readers of this blog know, I am a huge kiteboarding fan and have had many times when I just wanted to get on a plane and end up at the ocean and kiteboard for days on end.
It is now official (well, as of Oct 2) that the speed record has been broken! Rob Douglas went 49.84 knots (57.35 mph for those of you who are nautically challenged). That is stupid fast! Congrats to Rob and Cabrinha kites (my personal favs for kites too--love them).

If you are interested in what kettlebells and Z Health can do for your kiteboarding, check out this older post HERE.

Oct 2, 2008

from Cabrinhakites.com/news

Its official. Kitesurfing is the fastest sailing craft on the planet! Rob Douglas, from Martha's Vineyard (USA) has just broken the world speed sailing record in Luderitz, Namibia on a Cabrinha Crossbow kite. The record, previously held by Antoine Albeau on a Neil Pryde windsurfing rig was just shattered by Douglas with an official posting of 49.84 knots.

With his record breaking run, Rob had this to say. "The 7 meter Crossbow IDS is the perfect engine...... every run...... a Ferrari for sure!" Rob worked together with Cabrinha designer, Pat Goodman to outfit a production Crossbow canopy with a specially tuned bridle and control system for top end speed. The result of this collaboration speaks for itself.

Rob's incredible rise to the top of the speed chain did not come by accident. Rob is one of the most professionally equipped and methodical kitesurfing athletes we've seen in a long time..... perhaps ever. He is joined in Luderitz by Olympic silver medalist Mike Gebhart who has acted as coach, trainer and equipment assistant during the campaign. At 5'11 inches and yielding a solid 225 lbs of muscle, Rob is the perfect candidate for speed sailing.

The celebration period will be short lived for Rob as he now gets back to business and sets his sights squarely on the coveted 50 knot benchmark. According to Rob, the 50 knot ceiling will fall by the end of this event.


Five Finger Death Punch-New Video and live show!
The boys in Five Finger Death Punch will be here in Minnesota this Sat Oct 11 with Bury Your Dead and In This Moment at First Avenue. Below is their new video (may not be kid or work friendly if you are easily offended). Any "knuckleheads" that are going to be at the show, drop me a line.
In related music news, the new In This Moment CD is really really good also. Other CDs as of late I am enjoying are: Scar Symmetry, Slipknot, Poisonblack, Opiate for the Masses, Kataklysm, and Paradise Lost (new live double CD/DVD).

Five Finger Death Punch "Never Enough"



Upcoming Z Health 3 Day Training in Minnesota
Note: If you are in town for the Z Health Training at the end of this month, I have a few open slots for Z Health assessments (improve performance, reduce pain, learn the movements in detail), so drop me a line. First come first serve. I will be there all day Sat and Sun helping instruct, so please say hi.

Why Top Z-Health Trainers are flocking to "The Essential Secrets of Elite Performance" Workshop

One of the most frequently asked questions by Z trainers is, "How do I incorporate Z into my current training and that of my clients?"

This workshop will answer that question and give you a new approach to utilizing your complete Z-Health toolbox. You see how easy it is to incorporate R, I, and S Phase techniques into EVERY training session. And learn why simply applying this to your client practice can dramatically impact not only the results you get... but quickly bump up the cash you take in.

Since we're cramming 14 days of certification material into three days, we are truly creating a "best of" approach for learning the practical application of Z-Health. And you'll find all of this presented in "layman's terms" that will provide you fresh ideas for introducing, utilizing and integrating Z-Health in both personal and client training sessions.

Here is a chance to GET YOUR REPS IN and hear and see material presented in a new way. And, at an incredible discount! As a current Z-Health trainer, you can attend this workshop at a full 50% off.

Some of what you can expect:

New takes on old lecture topics:

• Body movement map
• Arthrokinetic reflex
• Startle reflex
• SAID
• Neural hierarchy (visual, vestibular, proprioceptive)
• Visual muscles vs visual acuity vs field vision

Programming:

• Movement template
• Demos
• Practical programming tip
• Simple self assessments
• Personal practice

Don’t miss out on this exciting opportunity to experience Z-Health in a new way. And with a full 50% discount for current Z-Health certified trainers, this is a very cost effective introduction and/or review of your R, I, and S-Phase Z-Health training.

Tuition: $797

50% Z-Health Certified Trainer Tuition: Only $398.50

To register, contact Dragon Door at www.dragondoor.com/zhealth or call 1-800-899-5111. You MUST reference discount code ZHDD08 to receive the discount.

Nalgene Bottles--Good or Evil?

Q and A time!
Mike, I hear that Nalgene bottles are now causing cancer and as a health concious person, I am thinking of ditching all my Nalgene plastic bottles. Is there any evidence behind this or is it another media scare tactic?

Answer
Excellent question. While I am far from a toxicologist, there is some newer evidence to show that there may be an issue. A study based on the NHANES databased from 2003-2004 (think a huge health database that collects lots of information) was just published in the Journal of American Medical Association (JAMA) a few weeks back.

"....(this) is the first-ever large-scale study on BPA in a human population," according to the authors, led by Dr Ian A Lang (Peninsula Medical School, Exeter, UK), in a statement they prepared for the media. "This is also the first time that evidence has emerged of higher BPA levels being associated with disease in adults."

What is it?
Bisphenol A (BPA), is an additive in plastic and other materials used in food packaging and consumer products and one of the world's most widely used industrial chemicals. BPA is thought to bind to estrogen receptors and mimic some of the hormone's physiologic activities. Of course if you are a guy, having higher estrogen levels should not be at the top of your list. If you are subject to the "chick flick" movie night be sure to pass on the Nalgene bottle.

While the data is not completely overwhelming by any stretch of the imagination, I personally have switched over to a bottle from Sigg that is metal and has a special liner. They are about 30 clams each with shipping, but they should last a lifetime. I notice that water stays cooler and tastes better as my Nalgene bottles tended to get that "ick factor" despite my best attempts at cleaning them and the water had funky taste to it.

The studies' authors concluded

"Using data representative of the adult US population, we found that higher urinary concentrations of BPA were associated with an increased prevalence of cardiovascular disease, diabetes, and liver-enzyme abnormalities. These findings add to the evidence suggesting adverse effects of low-dose BPA in animals. Independent replication and follow-up studies are needed to confirm these findings and to provide evidence on whether the associations are causal."

Again, association does not mean that BPA will have a DIRECT effect on you, but for about 30 clams I decided to switch.

Reference
Association of Urinary Bisphenol A Concentration With Medical Disorders and Laboratory Abnormalities in Adults

Iain A. Lang, PhD; Tamara S. Galloway, PhD; Alan Scarlett, PhD; William E. Henley, PhD; Michael Depledge, PhD, DSc; Robert B. Wallace, MD; David Melzer, MB, PhD

JAMA. 2008;300(11):1303-1310. Published online September 16, 2008