A Few Of My Favorite Things!

This is the continuation of a  serial style segment titled "a few of my favorite things".

The intended purpose of for this series is to both allow me to do "mini product reviews" as well as bring you market awareness of some of the industries more niche products and items I like that I feel you should be aware of!

 B.Chavez

MET-Rx High Protein Pancake Mix
Product Description
Flavor: Original Buttermilk
These pancakes are light and fluffy, with only 2.5 grams of fat per serving.
Each serving also provides several key vitamins and minerals needed for muscle metabolism.

An EvilGSP breakfast 3-5 days/week!


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Waxy Maize

Waxy Maize, a genetically drifted (mutated) variety of normal dent corn was first identified in China in 1909. The endosperm of waxy maize was found to contain only amylopectin and no amylose in opposition to normal dent maize varieties that contain both. The starch Amylopectin is heavily used in food products, in the textile, adhesive, corrugating and paper industry.

Commercially prepared Waxy Maize products are nothing more than corn starch from a distinct variety of maize that only bears amylopectin as its storage carbohydrate.

Amylopectin is a highly branched polymer of glucose found in plants. It is one of the two components of “normal” starch, the other being amylose. Amylopectin is soluble and highly stable in water. Starch is made of about 70% amylopectin by weight. Amylopectin is highly branched, being formed of 2,000 to 200,000 glucose units. Its counterpart in animals is glycogen which has the same composition and structure, but with more extensive branching that occurs every 8 to 12 glucose units.

With a relatively rapid transport and early digestion AP (amylopectin) becomes available as plasma blood sugar more quickly than most other “starch” sources. Despite its rapid onset and large molecular structure AP consistently shows a moderate to high glycemic index rating on most charts.

History of Waxy Maize

The first mentions of Waxy Maize were found in the archives of the U.S. Department of Agriculture. In 1908, the Rev. J. M. W. Farnham, a Presbyterian missionary in Shanghai, sent a sample of seeds to the U.S. Office of Foreign Seed and Plant Introduction. A note with the seeds called it: “A peculiar kind of corn. These seeds were planted on May 9, 1908, near Washington, D.C., by a botanist named G.N. Collins. He was able to grow 53 plants to maturity and made a thorough characterization of these plants, including photographs, which were published in a USDA bulletin issued in December 1909.

In 1922, another researcher, P. Weatherwax of Indiana University in Bloomington, reported that the starch in waxy maize was entirely of a “rare” form called “erythrodextrin”, known today as amylopectin. He found that this rare starch stained red with iodine, in contrast to normal starch which stained blue. Bates, French et al. and Sprague, Brimhall, et al. confirmed that endosperm starch of waxy maize consists nearly exclusively of amylopectin.

Biology

Experiments have shown that ten to twenty plants are required for adequate representation of genetic diversity in an open-pollinated maize variety. Since the number of ears saved for seed by ancient Asian maize cultivators with only small plots of land at their disposal was often smaller than this and, indeed, since new maize populations are sometimes established by growing the progeny of a single ear, it follows that there must often have been a high potential for genetic drift (changes in gene frequencies resulting from the creation of small breeding populations).

Genetics

A single recessive gene (wx), located on the short arm of chromosome 9, codes for the waxy endosperm of the kernel (Wx codes for endosperm with normal starch). This was first shown by Collins and Kempton.

Characterization with iodine

Amylose and amylopectin have different iodine binding-properties, with maize amylose and amylopectin giving iodine affinity (IA) values of about 19 to 20 and 1%, respectively, depending upon the source. The amount of apparent amylose can be determined either by measuring the absorbency of the starch-iodine complex (blue-value) and relating this value to that of pure amylose and amylopectin standards or by measuring the amount of iodine (mg) bound per 100 mg of starch in a potentiometric titration and relating the value to the amount bound by an amylose standard. Values used on the iodine binding, however, are only estimates of amylose content because of differences in the binding abilities (and structure) of amylose and amylopectin among starch types.

Biochemistry

Normal dent maize has two different pathways for starch formation: one leading to branched chain (amylopectin) and the other to straight-chain polysaccharides (amylose). The amylopectin consists of chain of α-D-(1-4) and α-D-(1-6)-glucosidic linkages that form a branched molecule. Amylose is primarily linear with α-D-(1-4)-linked glucose residues.

Agronomic features

Growing maize with pure amylopectin starch is not easy. The waxy gene being recessive, the waxy maize has to be isolated from any nearby normal maize field by at least 200 meters.

Amylopectin: industrial uses

Starch is the reserve carbohydrate in the plant kingdom. Although starch occurs throughout the plant world, there are only a few plants used to produce it commercially, and maize is the major source of starch produced world-wide. At the second range comes potato, then wheat and to a lesser extent rice. Maize starch was first produced in the U.S. in 1844 at the plant owned by William Colgate.

The amylopectin yield of the kernel ranges from 58.5 to 69% (of dry solid mass). Wet-milling waxy maize results in starch yields that are only 90% of those of dent maize. The wx starch is relatively easy to gelatinize and produces a clear viscous paste with a sticky or tacky surface, rather than one with sharp edges. This paste resembles pastes of root or tuber starches, such as potato or tapioca. Most starches in their native or unmodified form have limited use in various industries. Therefore, most starches including waxy maize starch are modified either to improve or repress their inherent properties as may be required for special use applications. Many types of modified waxy starches have a multitude of applications in the paper, textile, corrugating, and adhesive industries in addition to an enormous array of application in the food industry.

Food products

Modified waxy maize starches serve essential functions in foods, including the improvement of uniformity, stability, and texture in various food products. The clarity and stability of amylopectin starch make it especially suitable for thickening fruit pies. It improves smoothness and creaminess of canned food and dairy products as well as freeze-thaw stability of frozen foods. It gives a more desirable texture and appearance to dry foods and mixes. Waxy maize starch is also the preferred starting material for the production of maltodextrins because of improved water solubility after drying and greater solution stability and clarity. As of recent, the dietary supplement industry has seen an increase in the usage of Swedish Waxy Maize Starch. WM starch does have a moderate to slow Glycemic index; however, it is its unique osmolity that allows it to pass through the digestive system relatively quickly.

Livestock, dairy and poultry feeding

The feeding of waxy maize began in the 1940s. Beginning with a research report in 1944, waxy maize seemed to have the potential to increase feed conversion efficiencies. Manyother feeding trials involving swine, beef and dairy cattle, lambs and poultry were designed to compare the feeding value of waxy to normal dent grain. Generally, the trials indicated an advantage for feeding waxy grain. Seldom have the investigations shown any negative or adverse effects from feeding waxy grains. Increases of both milk production and butterfat content are not uncommon when waxy maize is fed to lactating dairy cattle. Increases of more than 20% in average daily weight gains in fattening lambs were observed when waxy grain was compared with normal dent. In addition, a 14% increase in feed efficiency was noted in favor of waxy grain. Likewise an increase in feed efficiency approaching 10% was obtained in trials where waxy grain was compared with the dent counterparts when fed to finishing beef cattle.

Conclusion

Waxy Maize is a great source of Amylopectin! What value a high molecular weight high GI starch is to body composition is a lot less certain! Sucrose and Dextrose have a dollar cost in the range of ten percent of commercial WM products and offer equal (or similar) Kcal/g and GI profiles. Amylopectin (WM) could have applications under extremely controlled conditions like pre-contest carb-up. Off season carb sources are vast and relatively low in cost making WM a hard sell in my view.

B.”EvilGenius”Chavez                                                                                                                                          EvilGenius Sports Performance
www.EvilGSP.com

Glucophobia

“The irrational fear of sugar”

Glucose / C6H12O6 
a monosaccharide (or simple sugar), is an important carbohydrate in mammalian biology. The living cell uses it as a source of energy and metabolic intermediate. Glucose is one of the main products of photosynthesis and starts cellular respiration in both prokaryotes and eukaryotes. The name comes from the Greek word glykys (γλυκύς), which means "sweet", plus the suffix "-ose" which denotes a carbohydrate.

Insulin
(from Latin insula, "island", as it is produced in the Islets of Langerhans in the pancreas) is an anabolic polypeptide hormone that regulates blood plasma glucose levels and the availability and entry of macro nutrients to the cellular mitochondria. Insulin is composed of 51 amino acid residues and has a molecular weight of 5808. Insulin's structure varies slightly between animal species. Apart from being the primary agent in carbohydrate homeostasis, it has effects on amino acid & fat metabolism as well as changes the liver's activity in storing or releasing glucose and in processing blood lipids. Insulin exerts a strong effect on other tissues such as fat and muscle. The amount of insulin in circulation has extremely widespread effects throughout the body.

The actions of insulin on cells include

translocation of Glut-4 transporter to the plasma membrane and influx of glucose, glycogen synthesis, glycolysis  and fatty acid synthesis
Control of cellular intake of substrates, most prominently glucose in muscle and adipose tissue.
Increase of DNA replication and protein synthesis via control of amino acid uptake.
Modification of the activity of numerous enzymes (allosteric effect).
Increased glycogen synthesis – insulin facilitates the entry of glucose to the liver (and muscle) cells; lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood.
Increased fatty acid synthesis – insulin facilitates the entry of blood lipids to adipose tissue which can then be converted to triglycerides; lack of insulin causes the reverse.
Decreased proteinolysis – forces reduction of protein degradation; lack of insulin increases protein degradation.
Decreased lipolysis – forces reduction in conversion of fat cell lipid stores into plasma fatty acids; lack of insulin causes the reverse.
Decreased gluconeogenesis – decreases production of glucose from various substrates in liver; lack of insulin causes glucose production from assorted substrates in the liver and elsewhere.
Increased amino acid uptake – facilitates the absorption of circulating amino acids; lack of insulin inhibits absorption.
Increased potassium uptake – forces cells to absorb serum potassium; lack of insulin inhibits absorption.
Arterial muscle tone – forces arterial wall muscle to relax, increasing blood flow, especially in micro arteries; lack of insulin reduces flow by allowing these muscles to contract.

The above excerpts are from various papers I’ve written and works by other authors I’ve reference in the past. I bring forth these items in response to the ever loudening clamor on the internet message boards in regard to what I can only term as ”glucaphobia”…….the irrational fear of sugar!

I’ve not written much on the subject of carbohydrate consumption and bodybuilding only because I felt it was a bit of a no brainer and to some degree an unworthy subject for an “EvilGenius”!

However for my own entertainment here is all you need to know to understand why you NEED sugar to achieve muscle building success!

Factual Statements
Athletes both professional and recreational are known to be taking exogenous insulin for its obvious and clinically documented ANABOLIC properties!

Sugars potentiate a potent insulin response

In child like simplicity!

INSULIN IS ANABOLIC
SUGAR STIMULATES INSULIN
THEREFORE
SUGAR IS ANABOLIC

In truth there is a bit more to the subject than just that, but not a whole lot more!

B.”EvilGenius”Chavez                                                                                                                                              EvilGenius Sports Performance
www.EvilGSP.com

Posted via Blogaway Pro

George Frenn

One Of  the very best strength athletes no one has heard of!

B."EvilGenius"Chavez
www.EvilGSP.com 

Conjugated Linoleic Acid

B."EvilGenius"Chavez 
www.EvilGSP.com

Volume Training

Big Alex N. finishing up his 10th set of 10 reps in the high-bar squat. EvilGSP athletes know the "POWER" of high volume training! Filmed on 5-18-13 during an EvilGSP Happy Hour" Squat & Deadlift Session!

Volume Training

To squat a lot you must squat a lot……as in shitloads of them! That’s what I was told in broken English when I visited the national training facility in the former czechoslovakia in the early 1990’s. The athletes that I met in Eastern Europe followed this dictum with deranged monk like dedication. I watched amazed as these men (and Women) did set after relentless set of high bar squats and front squats and cleans. The coaches and trainers later explained to me in graphic detail the failings of western thought on the subject of strength training and how there athletes would never “forget” to be strong!

In modern strength-coaching circles, this method is often called the "ten sets method." This methodology seemingly has its roots in German-speaking countries so; it is most often referred to as German Volume Training. I’ve seen dozens if not hundreds of variants on this theme, so for the sake of simplicity we will limit our discussion to the original as much as possible.

This training system originated in Germany in the mid-'50's and was popularized by Rolf Feser throughout the 1960’s & 70’s. Feser was the German National Weightlifting Coach and prototype for all modern thinkers in the field of strength and sports performance. A similar training protocol was being promoted by Vince Gironda on the west coast of the U.S. at or around the same time, but likely he gleaned it from one or more high profile ‘exchange” athletes he was famous for working with.

In Germany and the eastern bloc, this volume based method was used in the off-season to help athletes gain lean body mass and provide repetitive skill at the basic weightlifting movements. It was found to be so efficient at promoting lean body weight gains that lifters routinely moved up a full weight class within one off-season. Arnold Schwarzenegger himself mentioned squatting for 10 sets of 10 in some of his earliest interviews as the only thing that helped developed his legs.

The program works because it targets a group of motor units, and exposes them to an extensive volume of repeated efforts. The body adapts to this extraordinary and specific stress by hypertrophying the targeted fibers and developing a deep neurological connection (coordination) to the targeted motion.

Protocol
The goal of the German Volume Training method is to complete ten sets of ten reps with the same weight for each exercise. You want to begin with a weight you could lift for 20 reps to failure.

Rest Intervals
Rest 90 seconds between sets. Because of the importance of the rest intervals, you should use a stopwatch to keep the rest intervals constant.
Number of Exercises
One exercise should be performed, with little or no assistance work.
Training Frequency
One training session every seven days per body part is plenty.
Progressive Overload
Once you're able to do 10 sets of 10 with constant rest intervals, increase the weight on the bar by 5lbs and repeat the process.
Application
A simple 3 day split provides plenty of stimulation and adequate rest.
Day 1:
Squat 10x10
Leg curls 3x10 (Rotate the kind used ever 2-3 weeks)
Calf raise 3x10 (Rotate the kind used ever 2-3 weeks)
Day 2:
Bench Press 10x10
Overhead Press 3x10
Triceps Pushdowns 3x10 (Rotate the kind used ever 2-3 weeks)
Day 3:
Barbell Cleans 10x10
DB Row 3x10
Biceps Curls 3x10 (Rotate the kind used ever 2-3 weeks)

*Note:
 Day 3 utilizes cleans rather than deadlifts due to the similar neurological recruitment patterns and muscular/skeletal overlap between squats and deadlifts. If a trainee need to perform volume training for deadlifts insert deadlifts in place of cleans, drop squats in favor of machine hack squats and flip the position of days 1 & 3.

B.”EvilGenius”Chavez
www.EvilGSP.com

The 4-Hour Chef: The Simple Path to Cooking Like a Pro, Learning Anything, and Living the Good Life

[Hardcover]Timothy Ferriss (Author)

Book Description

Release date: November 20, 2012

“If you crossed Jason Bourne with Julia Child, you’d end up with Tim Ferriss.” – Marco Canora, Chef-Partner of Hearth & Terroir

“Wildly inventive.. [a] rangy, obsessive immersion in food and its many wonders. [T]he tools needed to learn to cook well can be deployed in every manner of endeavor, from skinning a deer to memorizing a deck of cards. The author distills them into minimal, learnable units and examines how to order the units so as to keep readers engaged in their endeavors. Ferriss is a beguiling guide to this process, at once charmingly smart aleck-y and deadly serious, and he aims to make readers knowledgeable and freethinking.” - Kirkus Reviews

"Tim Ferriss distills kitchen wisdom like a rotary evaporator on power surge. The results are potent, lucid, and delicious." - Nick Kokonas, Co-Owner, Alinea, Next, The Aviary

WHAT IF YOU COULD BECOME WORLD-CLASS IN ANYTHING IN 6 MONTHS OR LESS?

The 4-Hour Chef isn’t just a cookbook. It’s a choose-your-own-adventure guide to the world of rapid learning.

#1 New York Times bestselling author (and lifelong non-cook) Tim Ferriss takes you from Manhattan to Okinawa, and from Silicon Valley to Calcutta, unearthing the secrets of the world’s fastest learners and greatest chefs. Ferriss uses cooking to explain “meta-learning,” a step-by-step process that can be used to master anything, whether searing steak or shooting 3-pointers in basketball. That is the real “recipe” of The 4-Hour Chef.

You'll train inside the kitchen for everything outside the kitchen. Featuring tips and tricks from chess prodigies, world-renowned chefs, pro athletes, master sommeliers, super models, and everyone in between, this “cookbook for people who don’t buy cookbooks” is a guide to mastering cooking and life.

The 4-Hour Chef is a five-stop journey through the art and science of learning:

1. META-LEARNING. Before you learn to cook, you must learn to learn. META charts the path to doubling your learning potential.

2. THE DOMESTIC. DOM is where you learn the building blocks of cooking. These are the ABCs (techniques) that can take you from Dr, Seuss to Shakespeare.

3. THE WILD. Becoming a master student requires self-sufficiency in all things. WILD teaches you to hunt, forage, and survive.

4. THE SCIENTIST. SCI is the mad scientist and modernist painter wrapped into one. This is where you rediscover whimsy and wonder.

5. THE PROFESSIONAL. Swaraj, a term usually associated with Mahatma Gandhi, can be translated as “self-rule.” In PRO, we’ll look at how the best in the world become the best in the world, and how you can chart your own path far beyond this book.

EvilGSP Review

The 4 Hour Chef is my new favorite book! I love both the science & art of the culinary world and this book does them both major justices. This is the book I wish I had when I embarked on my food education!

Not only does Tim Ferriss do a wonderful job “teaching” basic cooking skill he does much more, he teaches you how to learn! With the mindset and lessons between the pages of this tome you could & should learn to feed yourself and ENOJY feeding yourself as well as almost any other aspect of life!

I cannot recommend this book enough! Buy the book, learn to feed yourself, learn to enjoy feeding yourself & loved ones and learn how to learn!

B.”EvilGenius”Chavez
www.EvilGSP.com

Musings On Strongman Training

A good friend of mine asked my opinion on the “best” method of training style & structure for competitive strongman events. Knowing that I’m (or at least think of myself) an EvilGenius and have been actively competitive in strongman events in the late 90’s & early 2000’s he felt I would have a ready-made answer for him. In truth I didn’t have much of a response prepped for that particular question and felt more than a little self-conscious about my intellectual inadequacy and did what any Genius (Evil or otherwise) would do……………..I bluffed!

The next morning I sat down in front of my laptop with the intention of penning him a valid strongman training program that would meet his needs and lives up to the EvilGenius standards.

That was 2 months ago!

I’ve boiled things down to 2 major schools of thoughts, what ive come to think of as “Integrated” and “segregated” training.

Segregated Training:
I define as a  program with a separation (or Segregation) between Traditional gym oriented weight training and the competitive strongman events. A workable example of this would be a scheme where an athlete did traditional weight training motions in the weight room Monday- Thursday and then did a full day of strongman events on Saturday, with Wednesday & Sunday off.

Integrated Training:
I define as a program with NO separation between; and in fact a smooth integration of competitive strongman events and traditional in weight room strength training. An example of this methodology would be dedicating a day to one (or perhaps two related) competitive events. The athlete would do for example Strong man log press then smoothly transition into “standard” weight room accessory movements that compliment shoulders and triceps.

After defining what I think are the two major “types” or “styles” of training available to a potential strongman competitor I put my friends needs and resources into the equation and found he really only had the option of a Segregated Training Scheme.

In truth I believe that an Integrated Training Scheme would in the long term be the better option, athletes are most often faced with the option of choosing the most practical over the most effective.

B.”EvilGenius”Chavez
www.EvilGSP.com

Glycemic Index

The glycemic index or GI is a measure of the effects of carbohydrates (laden foods) on blood sugar levels. Carbohydrates (laden foods) that break down quickly during digestion and release glucose rapidly into the bloodstream have by definition a high GI; carbohydrates (laden foods) that break down more slowly have by definition a low GI.

The concept was developed by Dr. David J. Jenkins and colleagues in 1980–1981 at the University of Toronto. The purpose of their research was to find out which foods were most suitable for subjects with Diabetes Miletus.

A lower glycemic index suggests slower rates of digestion and absorption of the foods' carbohydrates and may also indicate greater extraction of carbohydrate digestion. A lower glycemic response usually equates to a lower insulin demand but not always, and may improve long-term blood glucose control.

You can find additional info relating to the GI at http://www.glycemicindex.com The Official Website of the Glycemic Index and Database.

Glycemic Index Defined
The glycemic index of a food is defined as the area under the two hour blood glucose response curve (AUC) following the ingestion of a fixed portion of carbohydrate (usually 50 g). The AUC of the test food is divided by the AUC of the standard (glucose) and multiplied by 100. The average GI value is calculated from data collected in 10 human subjects. Both the standard and test food must contain an equal amount of available carbohydrate. The result gives a relative ranking for each tested food in comparison to 50g of pure glucose.

Glycemic Indexes Of Foods    

Classification	GI range	Examples
Low GI	55 or less	most fruits and vegetables, whole-grain breads, pasta, legumes/pulses, milk, yogurt, fructose
Medium GI	56–69	whole wheat products, basmati rice, sweet potato, table sugar
High GI	70 and above	corn flakes, puffed rice, baked potatoes, watermelon, croissants, white bread, white rice, glucose (100)

The glycemic effect of foods depends on a number of factors such as the type of starch (amylose vs. amylopectin), physical matrix of the food, fat and protein content of the food and organic acids or their salts content. Adding vinegar, for example, will lower the GI of a meal. The presence of fat or soluble dietary fiber can slow the gastric emptying rate, thus lowering the GI
The glycemic index can be applied only to only foods with reasonable carbohydrate content, as the test relies on subjects consuming enough of the test food to yield about 50 g of available carbohydrate. Many fruits and vegetables contain very little carbohydrate per serving, and the average person is not likely to eat 50 g of carbohydrate from these foods. Fruits and vegetables tend to have a low glycemic index and a low glycemic load.

Related Glycemic Indexes

Glycemic load
The glycemic load (GL) is a ranking system for carbohydrate baring food portions based on their glycemic index (GI) and the portion size. Glycemic load or GL combines both the quality and quantity of carbohydrate into one ‘number’. It is one of the better best ways to predict blood glucose values of different types and amounts of food.

The formula is: GL = (GI x the amount of carbohydrate) divided by 100.The usefulness of glycemic load is based on the idea that a high glycemic index food consumed in small quantities would give the same plasma glucose effect as larger quantities of a low glycemic index food. By way of example white rice has a somewhat high GI, so eating 50g of white rice at one sitting would give a particular glucose curve in the blood, while 25g would give the same curve but half the height. Since the peak height is considered by many experts the most important parameter for diabetes control, multiplying the amount of carbohydrates in a food serving by the glycemic index gives an idea of how much effect an actual portion of food has on blood sugar level.

Many have questioned the value of using glycemic load as a basis for weight loss programs; however, glycemic load is generally a useful concept in dietary designs targeting health maintenance. Studies have shown that elevation in blood sugar and insulin levels may lead to increased diabetes risk. Studies concluded (repeatedly) that women whose diets had the highest glycemic index were 21 percent more likely to develop type 2 diabetes than women whose diets had the lowest glycemic index.

Insulin index
The Insulin Index is a measure used to quantify the typical insulin response to various foods. The index is similar to the Glycemic Index and Glycemic Load, but rather than relying on blood glucose levels, the Insulin Index is based upon blood insulin levels. This measure can be more useful than either the Glycemic Index or the Glycemic Load because certain foods (e.g., lean meats and proteins) cause an insulin response despite there being no carbohydrates present, and some foods cause a disproportionate insulin response relative to their carbohydrate load.

Holt et al. have noted that the glucose and insulin scores of most foods are highly correlated, but high-protein foods and bakery products that are rich in fat and refined carbohydrates "elicit insulin responses that were disproportionately higher than their glycemic responses." They also conclude that insulin indices may be useful for dietary management and avoidance of non-insulin-dependent diabetes mellitus and hyperlipidemia.

Explanation of Index
The insulin index shows how much insulin is present in a subject’s blood as a result of particular food consumption, the glucose index shows how much glucose is present in the blood as a result of a particular food, and the satiety index shows how much a particular food decreases one's propensity to eat more.

Glucose (glycemic) and insulin scores were determined by feeding 1000 kilojoules (239 kilocalories) of the food to the participants and recording the area under the glucose/insulin curve for 120 minutes then dividing by the area under the glucose/insulin curve for white bread. The result being that all scores are relative to white bread. The satiety score was determined by comparing how much food was eaten by participants at a buffet after being fed a fixed number of calories of a particular food while blindfolded (to ensure food appearance was not a factor), then dividing that number by the amount eaten by participants after eating white bread. White bread serves as the baseline of 100. In other words, foods scoring higher than 100 are more satisfying than white bread and those under 100 are less satisfying.

Limitations And Criticisms

• The glycemic index does not take into account other factors other than glycemic response, such as insulin response, which is measured by the insulin index and can be more appropriate in representing the effects from some food contents other than carbohydrates.
• The glycemic index is significantly altered by the type of food, its ripeness, processing, the length of storage, cooking methods, and its variety
• The glycemic response is different from one person to another and even in the same person from day to day, depending on blood glucose levels, insulin resistance, and other factors.
• The number of grams of carbohydrate impacts blood sugar levels more than the glycemic index.
• Lowering glycemic index leads to small (momentary) improvements in blood sugar levels, but consuming fewer total carbohydrates would benefit the blood glucose profile much more.
• Carbohydrate impacts glucose levels most profoundly, and two foods with the same carbohydrate content are generally comparable in their effects on blood sugar. A food with a low glycemic index may have high carbohydrate content or vice versa; this can be accounted for with the glycemic load.
• Most of the values on the glycemic index do not show the impact on glucose levels after two hours.
• The GI of foods is determined under experimental conditions after an overnight fast (with only 10 test subjects), and might not apply to foods consumed later during the day because glycemic response is strongly influenced by the composition of the previous meal.

Relevance And Application
The Glycemic Index holds extraordinary relevance to a diabetic subject (or anyone using exogenous insulin). The ability to comparatively rate the release rates of dietary glucose holds life saving value to the clinical diabetic.

For non diabetic and non insulin using subjects the value of such data is questionable at best. The Glycemic Index holds almost no valuable info for the non insulin using athlete. Food volume and meal frequency has a far greater “GI” slowing effect than the carbohydrate bearing matrix or starch chemistry.

As the above overview illustrates dietary carbohydrate quantity dictates the total daily plasma insulin volume. The simple conclusion is that over consumption of carbohydrates not the comparative GI of said carbohydrate is the larger problem.

B.”EvilGenius”Chavez
www.EvilGSP.com

Pause for Some Inspiration

I maintain an online training journal @ www.evilarchives.blogspot.com   with the purpose of  illustrating my training ideas, successes and  failures. Today's installment is more of a broad generalization than a success or failure, but helpful (I think) none the less.

Trainees are always asking about training "variety" and how to "Change it up".............

Exercise selection is in fact a way to change your workout, but changing a major "core" movement like the squat is in my view not feasible since you only have 52 weeks per year to develop your squat!

If replacement isn't an option then what, modification?

No, modification is the neurological equivalent of replacement! (Take a moment and think about that!!!)

Golfers don't hit baseballs / Squatters don't do leg presses

The only real means of variety available to a dedicated strength athlete is rep range and the rarely used rep cadence!

Rep range is malleable to a degree but being a "strength" athlete requires certain constraints on per set volumes! So any meaningful changes in "Workout structure" must be within the confines of major "core" moments and withing prescribed rep ranges.

Repetition cadence is a hugely under valued aspect of modern strength training! Bar speed as well as turnaround time (starting strength) can be enormously dynamic variables in ones training regimen.

Options available are, but not limited to:

• Fast Positives - Slow Negatives
• Fast Positives - Fast Negatives
• Slow Positives - Slow Negatives
• Paused Repetitions!
• Repetitions with no Pause or stop!
• any combination you can think of!

STOP CONJUGATING AND START THINKING

B."EvilGenius"Chavez

www.EvilGSP.com 

Hypertension and Anabolic Steroids: A New Pathway?

Here is a great new science piece on AS and Hypertension from our good friend Pat Arnold. This is a must read for gear users!

Hypertension and Anabolic Steroids: A New Pathway?

October 30, 2012 ,

by Patrick Arnold

People familiar with the use of anabolic steroids know that water retention and hypertension (high blood pressure) are potential side effects. This is due to the fact that all androgenic hormones have the capacity to cause some sodium retention (and hence water retention) through direct action via androgen receptors in the kidneys. Furthermore, anabolic steroids that are estrogenic or can convert to estrogens can cause even more sodium retention via additional interaction with renal (kidney) estrogen receptors. So it’s often thought that an anabolic steroids propensity for water retention is related to its potency both as an androgen and as an estrogen (manifested via aromatization to estrogenic metabolites).

Read the full txt @ http://www.ironmagazine.com/blog/2012/hypertension-and-anabolic-steroids-a-new-pathway/ 

Fructose

Fructose (also levulose or laevulose) is a simple sugar (monosaccharide) found in many foods and is one of the three important dietary monosaccharides along with glucose and galactose. Honey, tree fruits, berries, melons, and some root vegetables, such as beets, sweet potatoes, parsnips, and onions, contain fructose, usually in combination with glucose in the form of sucrose. Fructose is also derived from the digestion of granulated table sugar (sucrose), a disaccharide consisting of glucose and fructose, and high-fructose corn syrup (HFCS). Crystalline fructose and high-fructose corn syrup are often mistakenly confused as the same product. The former is simply pure (100%) fructose. The latter is composed of nearly equal amounts of fructose and glucose.
Classification And Structure
Fructose also referred to as fruit sugar is a simple monosaccharide with a ketone functional group. Fructose is an isomer of glucose with the same molecular formula (C6H12O6) but with a different structure. Fructose is a 6-carbon polyhydroxyketone. When dissolved in solution, it forms ring structures similar to glucose, which are classified as cyclic hemiketals as opposed to the cyclic hemiacetals formed by aldoses such as glucose. When fructose forms a 5-member ring, the OH group on the fifth carbon atom attaches to the carbonyl group that is on the second carbon atom (D-Fructofuranose). Alternatively, the OH group on the sixth carbon may attach to the carbonyl carbon to form a 6-member ring (D-Fructopyranose).

Sugar Content In Common Foods (g/100g)

Food Item	Total Carbohydrate	Total Sugars	Free Fructose	Free Glucose	Sucrose	Fructose / Glucose Ratio	Sucrose as a % of Total Sugars
Fruit
Apple	13.8	10.4	5.9	2.4	2.1	2.0	19.9
Apricot	11.1	9.2	0.9	2.4	5.9	0.7	63.5
Banana	22.8	12.2	4.9	5.0	2.4	1.0	20.0
Grapes	18.1	15.5	8.1	7.2	0.2	1.1	1.0
Peach	9.5	8.4	1.5	2.0	4.8	0.9	56.7
Pear	15.5	9.8	6.2	2.8	0.8	2.1	8.0
Vegetables
Beet, Red	9.6	6.8	0.1	0.1	6.5	1.0	96.2
Carrot	9.6	4.7	0.6	0.6	3.6	1.0	70.0
Corn, Sweet	19.0	3.2	0.5	0.5	2.1	1.0	64.0
Red Pepper, Sweet	6.0	4.2	2.3	1.9	0.0	1.2	0.0
Onion, Sweet	7.6	5.0	2.0	2.3	0.7	0.9	14.3
Sweet Potato	20.1	4.2	0.7	1.0	2.5	0.9	60.3
Yam	27.9	0.5	tr	tr	tr	na	tr
Sugar Cane		13 - 18	0.2 – 1.0	0.2 – 1.0	11 - 16	1.0	100
Sugar Beet		17 - 18	0.1 – 0.5	0.1 – 0.5	16 - 17	1.0	100

Data obtained at http://www.nal.usda.gov/fnic/foodcomp/search/
Metabolism
Fructose is readily absorbed and rapidly metabolized by the human liver. For thousands of years humans consumed fructose amounting to 16–25 grams per day, largely from fresh fruits. Westernization of diets has resulted in significant increases fructose consumption, leading to typical daily ingestion of 85–100 grams of fructose. The (over) exposure of the liver to such large quantities of fructose leads to rapid stimulation of lipogenesis and TG accumulation, which in turn contributes to reduced insulin sensitivity and hepatic insulin resistance/glucose intolerance. These negative effects of fructose are the reason that fructose metabolism has gained recent research attention.

Interestingly, small catalytic quantities of fructose can have positive effects, and actually decrease the glycemic response to glucose loads, and improve glucose tolerance. These effects are also observed without any changes in insulin responses and non-esterified fatty acid (NEFA) and TG levels. In 1976, sugar substitutes such as fructose had been found to offer the 'advantage' of a 'better' utilization in conditions of limited insulin production. Fructose had a smaller influence on serum insulin concentrations than glucose, and no influence on plasma glucose levels. At that time, this evidence was considered to support fructose as a positive treatment for diabetic control. Even with the early positive results, researchers noticed accompanying "unfavorable" influences of these so-called diabetic sugars on obesity and weight gain. Certain metabolic differences exist between glucose and fructose, and the results that were once thought favorable, proved exacerbating to insulin resistance and obesity. In a study comparing normal and diabetic patients, glycemic effects of HFCS were compared to glucose. The negative results of HFCS on immunoreactive insulin, glycemic effect, and immunoreactive C-peptide did not support its use as a substitute for glucose in diabetic patients.

Research in the metabolism of fructose has left more questions about the difference between short-term positive effects, and the negative effects of chronic, long-term use of fructose sugars. The long-term negative effects can include changes in digestion, absorption, plasma hormone levels, appetite, and hepatic metabolism, leading to development of insulin resistance, diabetes, obesity, and inevitably cardiovascular disease. When the metabolic pathways and characteristics of fructose are examined more closely, many of the questions about its positive and negative effects can be answered. Fructose is a potent regulator of glycogen synthesis and liver glucose uptake. Therefore any catalytic improvements are due to hepatic glucokinase and glucose uptake facilitation. However, as mentioned, the beneficial effects do not continue with chronic fructose utilization. Because of its lipogenic properties, excess fructose in the diet can cause glucose and fructose malabsorption, and greater elevations in TG and cholesterol compared to other carbohydrates. There are key differences in the metabolic pathways that glucose and fructose follow. Upon gastric absorption both fructose and glucose are delivered via the portal vein to the liver. It is believed that the ability of the liver to metabolize high doses of fructose is responsible for the disruption in energy stores and fuel metabolism observed. In the liver, fructose is metabolized into glyceraldehyde and dihydroxyacetone phosphate. These particular fructose end products can then readily converge with the glycolytic pathway. Of key importance is the ability of fructose to by-pass the main regulatory step of glycolysis, the conversion of glucose-6-phosphate to fructose 1,6-bisphosphate, controlled by phosphofructokinase. Thus, while glucose metabolism is negatively regulated by phosphofructokinase, fructose can continuously enter the glycolytic pathway. Therefore, fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG.

The glycemic index (GI) has been commonly used to differentiate and compare various nutrients, as well as to describe how different foods produce different plasma glucose levels after ingestion. The GI can range from 100 for glucose and baked potato compared to approximately 20 for fructose and whole barley. Foods with varying GIs have different time courses associated with satiety. High GI carbohydrates have been reported to reduce appetite in the short term, whereas low GI carbohydrates possess a more delayed effect on energy intake controls. Fructose appears to have differing effects on appetite compared to glucose, contributing to its negative properties. Anderson et al. determined the association between food intake and blood glucose, comparing glucose and a fructose mixture. Glucose was administered as a high GI preload, which resulted in lower mealtime energy intakes compared to the low GI preload of the glucose-fructose mixture. An inverse relationship was seen between GI (and blood glucose concentrations), and appetite with consequent increased food intakes seen with fructose. In 2002, Vozzo et al. studied the comparative effects of glucose and fructose on blood glucose, insulin, and acute food intake. When subjects drank equienergetic preloads of glucose or fructose before an ad libidum buffet lunch, glucose concentrations were lower in the fructose group compared to glucose, and insulin concentrations were 50% higher in the fructose group in type 2 diabetics than in non-diabetics. The authors concluded that fructose may be a suitable replacement for glucose in diabetic patients – although it was found that satiating efficiencies of fructose certainly offered no advantages. This study differs from others with regards to insulin secretion, but the trend is clear between GI, glucose concentrations, and appetite. An explanation for the variation in glucose and fructose glycemic responses appears to be dependent on rates of hydrolysis and absorption of glucose, and gastric emptying. The variations observed in GI and appetite control of glucose and fructose can also be explained by differences in stimulation of insulin and leptin, important players in the long-term regulation of energy homeostasis.

Fructose will generally produce smaller insulin excursions upon consumption because it does not stimulate the secretion of insulin from pancreatic beta cells, whereas glucose does. Insulin-regulated leptin will also have a reduced concentration and a decreased net effect on reducing appetite. Limited effects on appetite suppression, combined with the fact that fructose is favored by the liver to be metabolized into lipid, will subsequently lead to weight gain, hyperinsulinemia, and the associated insulin resistance. Glucose and fructose comparison studies continued examining new hormonal targets. In 2004, Teff et al. showed that subjects served meals with either 30% glucose beverages, or 30% fructose beverages, had differing hormonal and metabolic responses. Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects. There was a concomitant reduction in circulating leptin both in the short and long-term as well as a 30% reduction in ghrelin (an orexigenic gastroenteric hormone) in the fructose group compared to the glucose group. A prolonged elevation of TG was also seen in the high fructose subjects. The insulin sensitizer agonist, peroxisome proliferator-activated receptor-gamma, stimulates adiponectin production and adiponectin is in fact thought to be part of this agonist's mechanism lowering circulating fatty acids and increasing fat oxidation. The net effect is to decrease liver TG and increase insulin sensitivity.

Insulin Resistance
Increasingly, questions have been raised as to whether dietary carbohydrate and fructose intake are directly related to the development of type 2 diabetes. As insulin resistance is often associated with circulating C-peptide concentrations, a cross-sectional study was performed to assess dietary fructose and carbohydrate, and glycemic loads related to C-peptide concentrations. It was found that the highest quintile of fructose intake had 13.9% higher C-peptide concentrations than the lowest quintile. Of note, subjects with high intakes of cereal fiber had 15.6% lower C-peptide concentrations, indicating that these types of nutrients may have opposing roles in the development of insulin resistance. A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia, which is associated with cardiovascular and cerebrovascular diseases.

Although fructose does not appear to acutely increase insulin levels, chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms. One proposed mechanism involves GLUT5, a fructose transporter that is found to have significantly higher expression levels in young Zucker obese rats compared to lean controls. As the rats age and become diabetic, GLUT5 abundance and activity is compromised, causing an even more marked insulin resistance over lean rats, implying a possible role of GLUT5 receptors in the pathology of metabolic syndrome associated with fructose feeding and insulin resistance. In rats fed 66% fructose for 2 weeks, insulin receptor mRNA, and subsequent insulin receptor numbers in skeletal muscle and liver were significantly lower compared to rats fed a standard chow diet. Also, blood pressure and plasma TG increased in the fructose-fed rats, even though there was no change in plasma insulin, glucose, or body weight. Evidence shows these early steps in insulin signaling are important for insulin's metabolic effects. In a different study, it was found that after 28 days of fructose feeding there were no changes in insulin receptor concentration, but, insulin stimulated autophosphorylation, a mechanism necessary for insulin action, was reduced to 72% in the liver.

Lipogenic Nutrient?
There is considerable evidence supporting the ability of high fructose diets to up regulate the lipogenesis pathway, leading to increased TG production. Insulin and glucose are known to directly regulate lipid synthesis and secretion. Insulin controls hepatic sterol regulatory element binding protein (SREBP) expression, which is a key transcription factor responsible for regulating fatty acid and cholesterol biosynthesis. SREBP binds to sterol responsive elements (SRE) found on multiple genes, and can activate a cascade of enzymes involved in cholesterol biosynthetic pathways. Miyazaki et al. reported an induction of the hepatic SREBP-1 isoform and lipogenic gene expression including FAS, acetyl-CoA carboxylase (ACC), and stearoyl-CoA desaturase (SCD) in mice following 7 days on a 60% fructose diet. It is known that SREBPs are regulated by intracellular sterol concentrations. However, more recently, it has been established that hormones such as insulin and platelet derived growth factor play a role in regulating these transcription factors. Expression of SREBP is enhanced by insulin in all three major insulin target tissues, liver, fat, and skeletal muscle. Similarly, levels of SREBP are enhanced in the presence of hyperinsulinemia. There is evidence that the insulin-mediated stimulation of SREBP occurs through the MAP kinase pathway, with ERK1/2 being shown to activate the SREBP-1a isoform by phosphorylating serine 117). Despite the fact that SREBP-1 is directly stimulated via insulin signaling, the depletion of insulin and insulin signaling through streptozotocin (STZ) treatment paradoxically induces SREBP-1c expression upon glucose, fructose, or sucrose feeding. It would have been expected that SREBP-1c would be downregulated concomitantly along with the reduced insulin availability, but this is not the case. Glucose feeding causes a short-term peak induction, whereas fructose caused a gradual extended increase in SREBP-1c activity, providing evidence that lipogenesis can be independent of insulin signaling, given carbohydrate, and particularly fructose, availability.
Heath Based Concluding Remarks
The alarming increase in fructose consumption may be an important contributor to the epidemic of obesity and insulin resistant diabetes in both pediatric and adult populations. For thousands of years, the human diet contained a relatively small amount of naturally occurring fructose from fruits and other complex foods. Adaptation of humans to a high glucose/low fructose diet has meant that hepatic carbohydrate metabolism is designed to actively metabolize glucose with a limited capacity for metabolizing a small daily intake of fructose. The increasing application of high fructose sweeteners over the past few decades has resulted in a considerable rise in the dietary intake of fructose. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to (potentially) major health consequences.
Performance Based Concluding Remarks
Due to its diverged chemistry and metabolic pathways fructose has major applications in blood sugar management and glycogen repletion in context of high intensity strength training. Fructose could be used as a non-insulin dependent hepatic CHO source for rapid repletion of liver glycogen, potentially making workout period recovery times more brief! Quicker more complete hepatic glycogen re-synthesis could unlock the potential for more frequent training sessions……………..there for more monthly/yearly training volume.

B.”EvilGenius”Chavez
www.EvilGSP.com