Showing posts with label rehoboth beach. Show all posts
Showing posts with label rehoboth beach. Show all posts

Thursday, May 19, 2016

I'm here to tell you it's HARD


B.Chavez,
©2016 Evil Genius Sports Performance


will ferrell erection anchorman.jpg
………....to pull with a stiff bar............and it should be! Whimsical titles aside I really do believe in the premise of using the LEAST Advantageous lifting conditions for base (off Season) training.

The late great genius A.Jones of Nautilus Sports Medicine fame was quoted many times saying "never make an exercise easier, make it harder!". Safety is one thing, but if you are using a specific piece of lifting apparatus just to be able to say your training weight is 700lbs rather than 650lbs you could be (ARE) setting yourself up for heartache on event day. Especially if you're forced to do things the "HARD WAY".

We seem to have entered an era where weight on the bar is far more of a prize than progress at one chosen endeavor!

Growing muscle and developing strength beyond the physiological norm is about applying stresses not finding clever ways to avoid them! I'm not campaigning against the use of flexible deadlift bars................ I'm merely trying to point out that by avoiding and even criticizing stiff bar pulls I have seen of late on many different social media outlets you are most certainly putting your long-term progress at a distinct disadvantage.Picture.jpeg

I have even recently witnessed vids of famous puller (and his washing machine) doing 2-inch deficit deadlifts while using a bar with 3 inches of bend! Is behavior such as this good for pulling progress or just good for social media attention?

Individual criticism aside, my strong suggestion to you dear reader is to stop making TRAINING depressions based on load used and/or facebook likes and seek out HARDER MORE CHALLENGING modes of training! If you are truly strong come event day no apparatus or lifting condition will be a disadvantage!

B.Chavez is available for programming and nutritional consultations Email: EvilGSP@gmail.com
Or Find Us On The Web At:

Sunday, April 17, 2016

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!


Find Us On The Web At:
http://www.youtube.com/EvilGSP 
http://www.facebook.com/TeamEvilGSP  
https://www.google.com/+Evilgsp 
http://www.instagram.com/teamevilgsp  
https://twitter.com/TeamEvilGSP 

Wednesday, March 30, 2016

A review of Strongman Eddie

Strongman Eddie is not just a good movie, it may well be the best muscle - head film since Pumping Iron!

Being Full length, well produced, with well thought out storytelling makes the film solid in every way. Eddie Hall and the rest of the strongman universe makes this film engaging and fun.

Covering almost every aspect of the life from work to workouts, home life (and home trials) to the absurdity of international travel at 300+ lbs.

All told Eddie Strongman is a must own bit of muscle history.


B.Chavez is available for programming and nutritional consultations Email: EvilGSP@gmail.com Or Find Us On The Web At:
http://www.youtube.com/EvilGSP 
http://www.facebook.com/TeamEvilGSP   
https://www.google.com/+Evilgsp 
http://www.instagram.com/teamevilgsp  
https://twitter.com/TeamEvilGSP 

Tuesday, December 22, 2015

EDDIE - Strongman

An EvilGSP MUST SEE!

Truck mechanic, husband and father of two, Eddie Hall wants to be the World’s Strongest Man. This feature documentary vividly illustrates the sacrifices that this extremely driven man must make to chase his dream. He will stop at nothing. He trains, eats, sleeps and breathes strongman, competing all over the world and breaking records. He faces not only gargantuan competitors, but his own inner demons as he strives to leave behind the scars of his teenage years.

This film gets under the skin of a man totally dedicated to becoming the greatest and offers an engrossing snapshot of an unforgettable character, Eddie - Strongman.

Featuring appearances from Arnold Schwarzenegger, Hafthor Bjornsson ("Man Mountain" from Game of Thrones) and multiple World’s Strongest Man winners Bill Kazmaier, Geoff Capes, Brian Shaw and Zydrunas Savickas.

Monday, December 7, 2015

STRONGMAN NIRVANA!

B.Chavez,
©2015 Evil Genius Sports Performance

OK, the smart people (ME) have been polled and the vote is in .........YES, YOU DO NEED TO DEADLIFT.

How much of this vile thing must I do you may (should)  be asking yourself. Sadly the answer to that is not simple, straightforward or uniform. To begin to answer, I will state that I'm going to limit the majority of my discussion to the sport of competitive strongman for many reasons including the forum and the fact the Deadlift protocol for general strength training and powerlifting vary vastly from one another much less from competitive Strongman.

Powerlifting prowess is tested in a very uniform and systematic manner. Powerlifters are tested in the three competitive lifts ONLY (a major reason I'm suspicious of training methods that measure progress in "special" or non-contest lifts) this makes preparing much more simplistic and streamlined.  Strongman, on the other hand, is just the opposite, the events are in fact and by design derivatives of uniform lifts. A strongman events will have "a press", "a squat", "a deadlift" and so on. This obvious but somehow overlooked point should be proof enough that a strongman competitor needs far greater with and berth "pulling prowess" than any other variety of strength athlete.

ASIDE from the Variety within the individual events themselves (axles, logs, odd objects etc) take the moment to look at the knee-hip angles involved in most strongman events and you will see much more deadlift-like mechanics than you might initially believe.

  • Log & axel cleans begin with a ground-based pull.
  • The low position of a stone lift is surely deadlift-like
  • The Tire flip is a "pulling based" movement!
  • The "pick" and setup in the farmers-walk is more like a deadlift that not.
  • Even a loading medley has deadlift like ground-based lifting.
  • A yoke walk outwardly resembles the squat, but the shallow knee-hip angle and extreme torso stabilization rings of DEADLIFT strength!

All the above points SHOULD lead one to believe the deadlift is not just needed but fundamental integral to a well-designed strongman training regimen. As to how much daily, weekly, monthly pulling a prospective athlete needs to do........................that is a very (necessarily) individual question! That is not to say the answer is whatever you want it to be.........................IT MEANS YOU NEED TO THINK! Like any SCIENCE based subject, there is a rough formula that when "filled-in" you get a very solid starting point towards a refined applicable answer.

Things you may need to consider before developing you Strongman Deadlift Protocol:

  • Are you presently a good Puller? (you may not need to spend additional resources on something you are already "good" at)
  • Age (age can vastly affect recovery rates)
  • Experience as a strength athlete (Do you have well-developed motor pathways?)
  • Limb length/body type (would excessive pulling be damaging to you "structure"?)
  • Nutritional status (again a recovery issue)
  • Pharmacological status (drugs=Recovery)
  • General health (yet another recovery based consideration)
  • Any other relevant (to you) factor.

With a rough understanding of the above points (and others), you should be able to begin to see an outline for your protocol emerge from the data. If you are young, healthy and have a "safe" pulling body -type it would not be unreasonable to be doing a deadlift derivative almost every single training session! On the other hand, if you are older, "clean" or have a very unfriendly pulling body-type you may only be able to effectively deadlift once per week. Consider the HONEST data and follow it where it leads and you will likely find the path ends at or near STRONGMAN NIRVANA!

B.Chavez is available for programing and nutritional consultations Email: EvilGSP@gmail.com
Or Find Us On The Web At:
https://twitter.com/TeamEvilGSP

Friday, November 20, 2015

Building Blocks!

B.Chavez,
©2015 Evil Genius Sports Performance
The tried and true methods of block periodization have gained and lost favor in a strangely rhythmic cycle over the last 5 decades. Block periodization gave way to a dozen (or more) derivatives some having value others......well not so much!

Evil Genius Sports Performance has spent years developing training strategies predicated on  the basic ideas of BLOCK periodization. Sure there are other viable  periodized models, but the ㏄simplicity of the basic block model is so modular and adaptable it has almost infinite applications.



To properly explain Block Periodization and its near infinite applications would take volumes well beyond this modest article, but in its most simplistic form "B.P." is just breaking training into BLOCKS of time with definite and singular goals assigned to each. This simple yet powerful strategy makes training by definition very focused, allowing for very precise tracking and measurements of training variables (load, volume, duration, etc). The purpose of each BLOCK is to strategically enhance some aspect of ability or performance characteristic that can and (ideally) will result in peak competitive performance on "game day".

The focus of this particular article is something we at EvilGSP affectionately call a "Building Block". Tricky DB (douchebag) name aside a building block is most likely the singular most valuable tool available to aspiring early and intermediate athletes of almost every sport.

What is a BUILDING BLOCK you ask? An EvilGSP "BB" is a block of training time dedicated purely to the BUILDING of lean mass and "strength potential" in the fundamental athletic muscle systems. Ok, I can hear you now "You can’t re-brand Bodybuilding" and sell it as something new and clever! To this, I say YOU ARE CORRECT, a properly designed and applied BB does take its cues (at least fundamentally) from classic Bodybuilding but is and must be far more specific and focused. Classical bodybuilding (should) give no regard to athletic performance just the building and presentation of the lean muscular form, A noble and interesting goal for sure but of little value to sports performance you say? Yet again I say, "You are Correct", but the tools and techniques bodybuilders have developed over the last century should not be dismissed so lightly.

Who can argue that at least to a degree (a sizable one at that) muscular size predicts contractile force? Lever and neurological differences make size strength comparisons between differing subjects impossible, but if YOU get BIGGER you got STRONGER! With the above statement in place, who knows the techniques of "bigger" better than the world of Bodybuilding. I'm not suggesting that strength athlete much less athlete at large stop what they're doing and become closet bodybuilders, just that they recognize the wealth of hypertrophy based knowledge bodybuilding  has to offer!

So the amalgamation, the synthesis of Strength Training, Periodization & Bodybuilding leads to the EvilGSP "Building Block". Not the indiscriminate offseason bodybuilding type acquisition of mass but the very precise and discriminant accumulation (hypertrophy) of sport specific muscle systems! As an example let's say an early intermediate powerlifter was to implement a 10-14 week "Building Block" as part of a larger (periodized) off-season training plan. This protocol would actually begin during the last competitive cycle, with careful evaluation of relative strengths and weaknesses in the 3 lifts. After identifying what needs to "Grow" (triceps, mid back, glutes, etc) a hypertrophy based training scheme borrowing deeply from tried and true bodybuilding strategies would be designed to target (very specifically) the outlined "weaknesses".

General Building Block (bodybuilding) training protocols
  • A higher degree of Muscular isolation
  • high volume training(20-30 sets per muscle/session
  • High training frequency (2-3 sessions per muscle /per week)
  • Low training loads (%40-%60 of max)
  • High training pace (low rests periods 60-90 seconds)
  • Reduced repetition speed (high time under tension)
  • Full and even exaggerated range of motion
  • Accentuated eccentric contractions
  • the integrated nutrition and restoration to support the above points

The above protocols would then be employed in the creation of a coherent and highly targeted hypertrophy centric training cycle or “Building Block”.

*A word of caution with this and any block periodized training model, the acquisition of lean mass and strength potential does not ensure the effective utilization of said potential. Transitional and Preparatory blocks should be employed to effectively bring the newly acquired hypertrophy to bare on your chosen athletic endeavor.

B.Chavez is available for programing and nutritional consultations Email: EvilGSP@gmail.com
Or Find Us On The Web At:

Saturday, September 12, 2015

Top Down Deadlifts



Top Down Deadlifts Explained By B."EvilGenius"Chavez And Demonstrated BY Big Kevin Murphy Of TeamEvilGSP

Team EvilGSP Defined:
As well as being Delaware’s premier strength and power team, Team EvilGSP is the practical arm and test bed for Evil Genius Sports Performance. Through constant experimentation and methodical data collection, EvilGSP is able to develop new training strategies as well as refine existing protocols to meet the demands of modern high level athletics. 

Cutting edge training and nutritional science wrapped in a %100 hard-core attitude! 
  • • Powerlifting
  • • StrongMan
  • • Weightlifting
  • • Athletics Programing
  • • BodyBuilding
  • • Nutrition/Supplementation 
Evil Genius Sports Performance is dedicated to the pursuit of “ULTIMATE SPORTS PERFORMANCE”.

Tuesday, March 24, 2015

"Nutritional Diversity"



Another edition of the EvilGSP video Blog

Some thoughts on "Nutritional Diversity" and its benefits to your sports performance goals!


B."EvilGenius"Chavez

For More TeamEvilGSP Visit:



Tuesday, January 13, 2015

How To Tear Your Pec And Love It or If you never fail and fail spectacularly you simply are not trying hard enough!



..............Ok, Ok love it is a bit of an embellishment, but despite the pain and disruption to my future training I don't HATE IT! No being hurt isn't "cool" or make me  a "tough guy" but it does prove (to me)  that I am pushing myself to the brink and even beyond!

When I was 15 years old I was fortunate enough to spend some time with Thomas Steven Platz. That time was life changing and without a doubt life and future shaping! I clearly remember Tom saying time and time again "the only way to be certain you did all you can do is to attempt the one(s) you can not do!". In context Tom was talking about training in general and sets of multi-reps for sure, but the mind set of acheiving failure to PROVE SUCCESS is one I came to hold very near and dear to my very way of life!

Though the career in bodybuilding I and many others thought I would peruse (at the time) didn't materialize, I took much if not all my guiding principles, thoughts and attitudes away from Tom and others in the bodybuilding world. Yes powerlifting and strength training are MUCH different than bodybuilding, but so much of the mental and even spiritual traits need to succeed are shared by all high level endeavors! 

Tom and so many other bodybuilders from the late 70's and early 80's that inspired me, lived this attitude to the fullest every single day! They risked health and sanity with nutritional, pharmacological and training practices that bordered on pure madness but not because they wanted to but because they couldn't live with the failure of not trying! 

With all of the above in mind I would like to point out that 10 min before the 495 bench press attempt that left me injured I did a life time best 455 Raw @235lb and 43 years of age! 

Rest assured this time next year I will one again be staring down the bench at 5 plates (or more) and feeling fully justified and confident in my reckless abandon!

See you next year!


Tuesday, March 11, 2014

Binding Proteins


SHBG
Sex hormone-binding globulin (SHBG) is a glycoprotein that binds at the plasma level (in the blood) to sex hormones, specifically testosterone and estradiol based hormones. Other steroid hormones such as progesterone, cortisol, and other corticosteroids are bound by transcortin (a plasma marker of overtraining).

Transport of Sex hormones
These sex hormones circulate in the bloodstream, bound mostly to SHBG and to some degree bound to serum albumin. Only a small fraction is unbound, or "free," and thus biologically active and able to enter a cell and activate its receptor. The SHBG inhibits the function of these hormones. The binding globulin then releases the hormonal compound at a controlled rate (the decay of the SHBG protein).Thus bioavailability of sex hormones is influenced by the level of SHBG.

Production
SHBG is produced by the liver cells and is released into the bloodstream. Other sites that produce SHBG are the brain, uterus, and placenta and vagina. In addition SHBG is produced by the testes; testes-produced SHBG is also called androgen-binding protein.

Regulation
SHBG levels appear to be controlled by a delicate balance of up and down regulating mechanisms. Its level is decreased by high levels of insulin and insulin-like growth factor 1 (IGF-1) and possibly Growth Hormone. Also, high androgen levels decrease SHBG, while high estrogen and thyroxine levels

Plasma Levels
When determining levels of circulating estradiol or testosterone, either a total measurement could be done that includes the "free" and the bound fractions, or only the "free" hormone could be measured. A free androgen index expresses the ratio of testosterone to the sex hormone binding globulin and can be used to summarize the activity of free testosterone. Sex hormone binding globulin can be measured separate from the total fraction of testosterone, however the total testosterone is likely the most accurate measurement of plasma androgen levels.


ABP
Androgen-binding protein (ABP) is a glycoprotein (beta-globulin) produced by the Sertoli cells in the seminiferous tubules of the testis that binds specifically to testosterone (T), dihydrotestosterone (DHT), and 17-beta-estradiol.By binding to T and DHT these hormones are made less lipophilic and become concentrated within the luminal fluid of the seminiferous tubules. The higher levels of these hormones enable spermatogenesis in the seminiferous tubules and sperm maturation in the epididymis.ABP has the same amino acid sequence as sex hormone-binding globulin (SHBG); the difference is the site of production and the addition of different sugar moieties. ABP’s production is regulated under influence of FSH on Sertoli cell, enhanced by insulin, retinol, and testosterone.

Summery
Binding proteins are likely simultaneously the most important, misunderstood and ignored aspect of hormonal application/manipulation. Binding globulins like SHBG (and others) act as a buffer or time release mechanism to “prevent” a large (sudden) influx of hormone to its target tissue.

With a little thought and imagination a perspective “endocrinologist” can begin to see the pointlessness of many of the common practices in sports performance. Tapering, Front-Loading and many other misguided practices can be “explained away” once binding proteins are fully considered.

Maintaining elevated plasma Insulin levels (hard for the low carb contingent!) and minimizing catecholamine production (overtraining) are simple non-pharmacological means of maintaining a positive bound of unbound sex hormone ratio.
    

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

Thursday, March 6, 2014

%2


I squat once per week, always have.
With only 52 weeks in a year and 2 spent on taper/event....that leaves effectively 50 training se
ssions per year. Simple math shows us that each weekly squat session is %2 of my yearly progress.
When you dwell on this point it realy begins to dawn on you the urgency of each and every session! If I was to miss even one session %98 of my potential is the MOST i could hope to achieve. Sobering thout isnt it?
No one can totaly avoid the ocasional "off" day where things are tougher than normal, but with %2 of your yearly gains at stake who can afford to turn an "off" day into a day off?.
I'll see you at the squat rack! My %2 isnt an option it is a certainty!

B."EvilGenius"Chavez
www.EvilGSP.com.
www.YouTube.com/EvilGSP
www.FaceBook.com/TeamEvilGSP

Thursday, August 23, 2012

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